Santiago v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

Filed: July 8, 2026

*************************

PATRICIA SANTIAGO, * PUBLISHED

*

Petitioner, * No. 21-1562V

*

v. * Special Master Nora Beth Dorsey

*

SECRETARY OF HEALTH * Dismissal; Influenza (“Flu”) Vaccine;

AND HUMAN SERVICES, * Idiopathic Thrombocytopenia Purpura

* (“ITP”); Severity Requirement; One Day

Respondent. * Onset.

*

*************************

Laura Levenberg, Muller Brazil, LLP, Dresher, PA, for Petitioner.

Alexa Roggenkamp, U.S. Department of Justice, Washington, DC, for Respondent.

DECISION 1

On July 9, 2021, Patricia Santiago (“Petitioner”) filed a petition for compensation under

the National Vaccine Injury Compensation Program (“Vaccine Act” or “the Program”), 42

U.S.C. § 300aa-10 et seq. (2018). 2 Petitioner alleges that she suffered idiopathic

thrombocytopenia purpura (“ITP”) as a result of an influenza (“flu”) vaccine she received on

October 16, 2019. Petition at Preamble (ECF No. 1). Respondent argued against compensation,

stating that “this case is not appropriate for compensation under the terms of the Vaccine Act.”

Respondent’s Report (“Resp. Rept.”) at 2 (ECF No. 13). Respondent argued this case should “be

1

Because this Decision contains a reasoned explanation for the action in this case, the

undersigned is required to post it on the United States Court of Federal Claims’ website and/or at

https://www.govinfo.gov/app/collection/uscourts/national/cofc in accordance with the E-

Government Act of 2002. 44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of

Electronic Government Services). This means the Decision will be available to anyone with

access to the Internet. In accordance with Vaccine Rule 18(b), Petitioner has 14 days to

identify and move to redact medical or other information, the disclosure of which would

constitute an unwarranted invasion of privacy. If, upon review, the undersigned agrees that the

identified material fits within this definition, the undersigned will redact such material from

public access.

2

The National Vaccine Injury Compensation Program is set forth in Part 2 of the National

Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755, codified as amended,

42 U.S.C. §§ 300aa-10 to -34 (2018). All citations in this Decision to individual sections of the

Vaccine Act are to 42 U.S.C. § 300aa.

dismissed for failure to satisfy [§11(c)(1)(D)],” hereinafter referred to as the severity requirement

under the Vaccine Act. Id. Respondent also argued Petitioner failed to “offer reliable evidence

to establish a causal relationship” between the flu vaccination and her alleged injury of ITP. Id.

at 15.

After carefully analyzing and weighing the evidence presented in this case in accordance

with the applicable legal standards, 3 the undersigned finds that Petitioner met the severity

requirement under § 11(c)(1)(D) of the Vaccine Act but has failed to provide preponderant

evidence that her flu vaccine caused her ITP. Thus, Petitioner has failed to satisfy her burden of

proof under Althen v. Secretary of Health & Human Services, 418 F.3d 1274, 1280 (Fed. Cir.

2005). Accordingly, the petition must be dismissed.

I. ISSUES TO BE DECIDED

“The parties stipulate that Petitioner received a[] [flu] vaccination on October 16, 2019.”

Joint Pre-Hearing Submission, filed Jan. 28, 2025, at 1 (ECF No. 81). Petitioner’s diagnosis of

ITP 4 is not in dispute. Id.; Petitioner’s Exhibit (“Pet. Ex.”) 10 at 6; Resp. Ex. A at 5.

The parties dispute whether the statutory severity requirement was met. Joint Pre-

Hearing Submission at 2. Specifically, under § 11(c)(1)(D), the parties dispute “whether

[P]etitioner has had residual effects of ITP for longer than six months.” Id.

The parties also dispute causation, specifically all three Althen prongs: “(1) whether the

[flu] vaccine administered to Petitioner can cause ITP; (2) whether Petitioner’s ITP was caused

by receipt of the vaccination at issue, [and] (3) whether the time between Petitioner’s

vaccinations and the onset of symptoms would be considered medically acceptable to infer

causation-in-fact.” Joint Pre-Hearing Submission at 2.

3

While the undersigned has reviewed all the information filed in this case, only those filings and

records that are most relevant will be discussed. See Moriarty v. Sec’y of Health & Hum. Servs.,

844 F.3d 1322, 1328 (Fed. Cir. 2016) (“We generally presume that a special master considered

the relevant record evidence even though [s]he does not explicitly reference such evidence in

h[er] decision.”); Simanski v. Sec’y of Health & Hum. Servs., 115 Fed. Cl. 407, 436 (2014)

(“[A] Special Master is ‘not required to discuss every piece of evidence or testimony in her

decision.’” (citation omitted)), aff’d, 601 F. App’x 982 (Fed. Cir. 2015); Paterek v. Sec’y of

Health & Hum. Servs., 527 F. App’x 875, 884 (Fed. Cir. 2013) (“Finding certain information not

relevant does not lead to—and likely undermines—the conclusion that it was not considered.”).

4

To avoid confusion, the undersigned will refer to immune thrombocytopenia, idiopathic

thrombocytopenia purpura, and immune thrombocytopenia purpura as ITP throughout this

Decision. ITP “has been found to be an autoimmune condition, caused by antigens against

platelets, resulting in ecchymoses, petechiae, and other bleeding.” Idiopathic Purpura, Dorland’s

Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=101150 (last

visited June 17, 2026).

2

II. BACKGROUND

A. Procedural History

Petitioner filed her petition along with medical records 5 and a declaration on July 9,

2021. Petition; Pet. Exs. 1-7. This case was assigned to the undersigned on January 4, 2022.

Notice of Reassignment dated Jan. 4, 2022 (ECF No. 9). Respondent filed his Rule 4(c) report

on March 7, 2022, arguing compensation should be denied and this case should be dismissed for

failure to meet the severity requirement under the Vaccine Act. Resp. Rept. at 2.

The undersigned held a status conference on May 24, 2022 to address the issues raised in

Respondent’s Rule 4(c) report. Order dated May 24, 2022 (ECF No. 17). The undersigned

explained that she required expert opinion on the question of severity in this case. Id. at 1. From

September 2022 to September 2023, Petitioner filed expert reports from Dr. Abhimanyu Ghose

and Dr. Omid Akbari and Respondent filed expert reports from Dr. Lisa Baumann Kreuziger and

Dr. You-Wen He. Pet. Exs. 10, 40, 72; Resp. Exs. A, C-D.

Thereafter, pursuant to the parties’ request, the undersigned held a Rule 5 Conference on

November 28, 2023. Rule 5 Order dated Nov. 28, 2023 (ECF No. 41). The undersigned

indicated that she was unable to provide her preliminary opinions and findings in this case. Id. at

2. Because there was litigative risk for both parties, the undersigned recommended informal

settlement discussions. Id. at 2-3.

Respondent indicated he was not interested in settlement, and the matter was scheduled

for an entitlement hearing in March 2025. Order dated Feb. 20, 2024 (ECF No. 47); Prehearing

Order dated Mar. 22, 2024 (ECF No. 50). Over the next year, prior to the entitlement hearing,

additional expert reports from Dr. Akbari and Dr. He were filed. Pet. Exs. 88, 115; Resp. Ex. F.

An entitlement hearing was held from March 4 to March 6, 2025. Order dated Mar. 6,

2025 (ECF No. 102). Petitioner, Dr. Ghose, Dr. Akbari, Dr. Baumann, and Dr. He testified at

the hearing. Transcript (“Tr.”) 3, 149, 272. Thereafter, Petitioner requested post-hearing

briefing. Order dated Mar. 13, 2025 (ECF No. 105).

Petitioner filed her post-hearing brief on July 10, 2025. Pet. Post-Hearing Brief (“Br.”),

filed July 10, 2025 (ECF No. 114). On August 8, 2025, Respondent filed a status report

indicating that he “does not intend to file a post-hearing brief.” Resp. Status Rept., filed Aug. 6,

2025 (ECF No. 115).

This matter is now ripe for adjudication.

5

Medical records were filed throughout litigation.

3

B. Factual History

1. Medical History 6

a. Pre-Vaccination Medical History

On March 7, 2016, Petitioner saw Dr. Shana Weiss, her primary care physician (“PCP”),

for an annual physical examination. Pet. Ex. 2 at 5. Petitioner’s physical examination was

normal, and her platelet count was 369 K/uL (reference range: 140-400 K/uL). Id. at 5-6.

On September 5, 2017, Petitioner saw Dr. Sarah Peterson, allergist, to establish care as a

new patient. Pet. Ex. 3 at 39. She reported having nasal allergies for “years” as well as adult-

onset asthma. Id. She reported that full tabs of antihistamines made her drowsy so she was

taking half-tabs of Zyrtec. Id. An examination found Petitioner was allergic to dogs, cats,

feather mix, trees, grass, Bermuda grass, and mold. Id. at 40.

On March 9, 2018, Petitioner saw Dr. Peterson for an “increase in asthma symptoms in

recent weeks/months.” Pet. Ex. 3 at 20. Petitioner noted that antihistamines would lead to

“significant grogginess” where she would feel “drunk.” Id. She was applying for FMLA, as the

medications would not allow her to drive to work safely. Id. She also stated that she had

experienced drowsiness in response to Singulair in the past. Id. at 22. Dr. Peterson filled out

Petitioner’s FMLA paperwork, planned to repeat labs, and prescribed Petitioner one-half tab

Zyrtec daily. Id.

On October 16, 2019, Petitioner underwent a pre-employment screening determination at

Saint Anthony Hospital. Pet. Ex. 1 at 6-22. She was certified as able to perform essential

functions of the job as per the job description. Id. at 10. Her physical was normal. Id. at 11-19.

She noted that she had suffered from allergic reactions that interfered with her breathing along

with asthma in the past but indicated that she did not currently suffer from breathing problems.

Id. at 16-17. She was using an albuterol inhaler for breathing problems. Id. at 11, 17. The

remainder of Petitioner’s pre-employment screening was normal. Id.

b. Post-Vaccination Medical History

On October 16, 2019, at 57 years old, Petitioner received a quadrivalent flu vaccination

(Flucelvax) as part of her medical clearance as a new employee (registered nurse) at Saint

Anthony’s Hospital. Pet. Ex. 1 at 8-9, 26.

On October 17, 2019, Petitioner saw Dr. Peterson for a follow up of her allergic rhinitis,

asthma, and hives. Pet. Ex. 2 at 91. Petitioner reported receiving her flu shot the day prior, and

“about an hour later when she got home she [] [felt] shaky and cold. She then developed

6

This summary of medical records is largely taken from the parties’ prehearing briefs, as the

undersigned finds the parties provided an accurate representation of the records. See Pet. Mot. at

2-3; Resp. Response at 3-9. The undersigned has made edits, deleted less relevant entries, and

has included additional information.

4

petechiae[7] at the site of the injection as well as a few on her opposite arm, on her face, and

inside her mouth.” Id. Petitioner also reported “[one] episode of dyspnea [that] morning,

[which] resolv[ed] with albuterol.” Id. On examination, Petitioner had a “few petechiae in

buccal membrane and [one] on tongue.” Id. at 92. Petitioner also had one petechia on her right

deltoid, one on her nose, and a few scattered on her left forearm. Id. Her heart was “mildly

[tachycardic].” Id. Dr. Peterson diagnosed Petitioner with a “[r]eaction to [the] flu vaccine” and

recommended that she undergo lab testing, start a Medrol Dose pack (low-dose steroids), and

return if her symptoms worsened or failed to improve. Id.; Pet. Ex. 3 at 9. A complete blood

count (“CBC”) performed on October 17, 2019 was abnormal, showing a platelet count of 5

K/uL (reference range: 131-340 K/uL). Pet. Ex. 3 at 2.

The following day, around 10:00 AM on Friday, October 18, 2019, Petitioner presented

to the emergency department (“ED”) at Northwestern Medical Center at the advice of her

allergist. Pet. Ex. 4 at 65-66. She was contacted regarding her platelet count of 5 and instructed

to present to the ED. Id. at 66. She was seen by emergency medicine physician Steven W.

Hodges, M.D. around 11:30 AM. Id. at 65. Petitioner described being in her “usual state of

health” when she received a flu vaccination two days earlier, and “within ten minutes of the

injection, she was tachycardiac. [Petitioner] later went home and noted muscle aches and chills

on the drive home, and when she arrived home, her husband noted significant shivering and

rigors that continued for about one hour.” Id. at 65-66. Petitioner reported having a fever of

103º Fahrenheit and petechiae around the area of injection, her face, and in her mouth. Id. at 66.

When she presented to her allergist the day prior, she had “more isolated petechiae on arm, chest,

and face and was prescribed a Medrol dose pack and labs were drawn.” Id. Petitioner had taken

two doses of the Medrol dose pack and has “noticed a decrease in the darkness of petechial

lesions.” Id.

Repeat labs were ordered in the ED. Pet. Ex. 4 at 68. Petitioner’s platelets were low at

39 K/uL (reference range: 140-390 K/uL). Id. Her C-reactive protein (“CRP”) level was

elevated at 2.4 (reference range: 0.0-0.5 mg/dL) and her erythrocyte sedimentation rate (“ESR”)

was also elevated at 100 (reference range: 0-30 mm/hour). Id. at 69, 76. A peripheral blood

smear taken at approximately 1:00 PM that day confirmed thrombocytopenia 8 and no platelet

clumping was observed. Id. at 76. Hematology and oncology were consulted, Petitioner was

given steroids, and repeat labs were recommended. Id. Repeat labs showed an increase in

Petitioner’s platelet count to 50 K/uL. Id. at 76, 113. Petitioner was discharged from the ED

with instructions to continue taking prednisone for four days and to follow up with hematology

on Monday (October 21, 2019). Id. at 76.

7

Petechia is “a pinpoint, nonraised, perfectly round, purplish red spot caused by intradermal or

submucous hemorrhage.” Petechia, Dorland’s Med. Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=38200 (last visited June 17, 2026).

8

Thrombocytopenia refers to a decrease in platelets. Thrombocytopenia, Dorland’s Med.

Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=49875 (last visited

June 17, 2026).

5

A report to Vaccine Adverse Event Report System (“VAERS”) was submitted on

October 18 on Petitioner’s behalf by Phyllis Murillo, who appears to work at Petitioner’s

employer, Saint Anthony’s Hospital. Pet. Ex. 1 at 26.

On October 23, 2019, Petitioner presented to hematologist Daniel Dammrich, M.D., for

an initial appointment. Pet. Ex. 4 at 61. Petitioner reported that she received a “flu shot last

week and immediately after develop[ed] shaking chills. She went on to develop petechiae on her

face and hands and most prominently in her buccal mucosa.” Id. She also reported her visits to

her allergist and the ED and that she completed her steroids that day (October 23). Id. at 61-62.

Dr. Dammrich ordered labs that day, October 23, which showed Petitioner’s platelets had

“normaliz[ed]” to 323 K/uL (reference range: 140-390 K/uL). Id. at 57, 62. Dr. Dammrich

diagnosed Petitioner with ITP that was “possibly a reaction to flu shot as it happened

immediately after.” Id. at 63. He further opined that Petitioner’s ITP was “[l]ikely precipitated

by vaccination given the timing of onset.” Id. He noted that Petitioner had a “[g]reat response to

steroids.” Id. Petitioner was prescribed a three-day regimen of dexamethasone (a steroid) and

Dr. Dammrich planned to “recheck [her platelet count] in [one] month since platelets have

already normalized.” Id.

On November 25, 2019, Petitioner followed up with Dr. Dammrich. Pet. Ex. 4 at 41.

Petitioner’s platelet count was 391 K/uL (reference range: 140-390 K/uL). Id. at 33. Petitioner

complained of fatigue, occasional shortness of breath, and possible tachycardia. Id. at 42. Dr.

Dammrich ordered a thyroid stimulating hormone (“TSH”) test and an EKG and noted that if

those tests were unremarkable, then Petitioner would follow up with her PCP the next week. 9 Id.

at 43. Petitioner was also instructed to follow up with Dr. Dammrich in six months. Id.

On December 28, 2019, Petitioner saw Dr. Weiss, her PCP, for a possible ear infection.

Pet. Ex. 2 at 27. The visit notes document Petitioner’s ITP diagnosis in October 2019. Id. No

report of fatigue was documented. Id. at 27-28.

Petitioner saw nurse practitioner Ellen Verlen, at her PCP’s office, on April 17, 2020 via

telehealth for a possible Covid-19 infection. Pet. Ex. 2 at 30. Petitioner stated that she was

working as a nurse and that one of her coworkers had died that week. Id. She further stated that

she had been sleeping poorly as her sister had died from Covid the previous week. Id.

Petitioner’s ITP, or any related sequela, was not mentioned. Id. at 30-31.

On May 20, 2020, Petitioner saw Dr. Dammrich for follow-up via telemedicine. Pet. Ex.

4 at 28. Fatigue was not mentioned or documented at this visit. Id. at 28-30. Dr. Dammrich

ordered labs, which returned on May 26, 2020 and showed a platelet count of 375 K/uL

(reference range: 140-390 K/uL). Id. at 16-17, 31.

On May 27, 2020, Petitioner emailed counsel and stated that her platelets were above

370,000 K/uL and that she was “still tired at times but otherwise [she was] doing ok.” Pet. Ex. 6

at 1. She also noted that her hematologist “want[ed] [her] to continue to follow[] up in [six]

months due to possibilities of [her] ITP rebounding.” Id.

9

Her TSH was normal at 1.75 (reference range: 0.40-4.00 uIU/ML). Pet. Ex. 4 at 37.

6

Petitioner’s platelet count remained normal for the remainder of 2020, with no reports of

related bruising, bleeding, or fatigue. See Pet. Ex. 2 at 34-35, 39-40 (reporting insomnia but

“thinks it might [be] related to comfort with new knee [post-surgery]” and denying fatigue under

review of systems), 80; Pet. Ex. 4 at 8-10, 13-14 (“Her platelet count has remained normal as of

end of May and she has no symptoms to suggest that it has fallen.”); Pet. Ex. 8 at 32; Pet. Ex. 9

at 54.

Petitioner called her hematologist’s office on October 30, 2020, requesting a written

statement for her employer that “she cannot take flu shots.” Pet. Ex. 5 at 8. Registered nurse

Abigail I. Vollmer indicated that a letter was faxed to Petitioner as requested. 10 Id.

The medical records do not show that Petitioner had any recurrence of her ITP.

No additional relevant medical records were provided.

2. Petitioner’s Declaration and Hearing Testimony

Petitioner has worked as a registered nurse since 1990. Tr. 153-54.

She received the subject flu vaccination on October 16, 2019, in the afternoon. Tr. 157,

176-77. Following her vaccination, she had an hour drive home. Tr. 158. On her drive home,

she started feeling “really bad” about 20 minutes into the drive, or about 30 minutes after

vaccination, which she described as uneasiness and shortness of breath. Tr. 158, 160-61, 177-80.

When she got home, she had chills, shakiness, and body cramps. Tr. 158-61, 179.

When she woke the next morning, October 17, around 8:00 A.M. or 9:00 A.M., she

“didn’t feel bad,” but saw petechiae/“blood blisters” on her face, chest, and legs and inside her

mouth. Tr. 159, 162, 180-82. That afternoon, she presented to her allergist, Dr. Peterson. Tr.

158, 162, 182-83. Blood work was ordered and Petitioner was started on a Medrol dose pack

(low-dose steroids). Tr. 183-84.

The following day, October 18, she drove to the ER on instruction of her allergist due to

her platelet level of five. 11 Tr. 164. She was treated with dexamethasone, a high-dose steroid,

and she quickly started to improve. Tr. 164-65. She was discharged that day 12 and instructed to

continue with steroids and to see a hematologist. Tr. 165-68, 187-88.

10

It does not appear that a copy of the letter was filed.

11

In her declaration, Petitioner averred her symptoms began “[w]ithin forty-eight (48) hours of

[flu] vaccination.” Pet. Ex. 7 at ¶ 3.

12

Petitioner explained that the ER physicians wanted to admit her, but she “beg[ged]” to go

home as she had already been there for hours. Tr. 185. She indicated she would return if

needed, referring to her knowledge as a registered nurse. Id. She further testified that she, like

other nurses, “are probably some of the worst patients.” Id.

7

She then began care with hematologist Dr. Dammrich. Tr. 165-68. Her platelets were

considered normal at her first visit with Dr. Dammrich in October. Tr. 188-89. She continued to

follow up with Dr. Dammrich. Tr. 190. In November 2019, her platelets remained normal

despite her continuing fatigue. Tr. 191, 198.

She testified that she consistently complained of fatigue at her visits with Dr. Dammrich.

Tr. 165-66, 170. Petitioner averred she reported fatigue at her visit with Dr. Dammrich on May

20, 2020, despite no documentation of such complaint in his record. Pet. Ex. 7 at ¶ 6; see also

Tr. 170. She “always felt like his only concern was what [her] platelet count reading was at each

visit.” Pet. Ex. 7 at ¶ 6.

As of July 8, 2021, the date on which Petitioner’s declaration was executed, she

continued to “feel overly fatigued at times.” Pet. Ex. 7 at ¶ 7; see also Tr. 168 (testifying that her

fatigue “probably” lasted “a year or more” and would fluctuate). At the entitlement hearing in

March 2025, she testified that the fatigue would affect her daily life. Tr. 171. She has been

taking vitamins and supplements to counteract her fatigue. Tr. 198. Petitioner was unable to

work for two weeks after her diagnosis of ITP, but she was able to return to work full-time

thereafter. Tr. 170-71.

She testified that she had received flu vaccines in prior years and never experienced these

symptoms following vaccination. Tr. 157-58, 161. She reported experiencing fatigue when she

was sick with the flu or Covid as well as during the Covid pandemic during which time she was

working as a nurse. Tr. 167-68, 202-05. She also reported grogginess on a half-tab of Zyrtec,

which she has taken daily since approximately 2017. Tr. 199-201.

C. Expert Reports 13

1. Petitioner’s Expert, Dr. Abhimanyu Ghose 14

a. Background and Qualifications

Dr. Ghose is board certified in internal medicine and hematology and oncology. Pet. Ex.

10 at 1; Pet. Ex. 157 at 9. After receiving his M.B.B.S. in 2007 from Nilratan Sircar Medical

College in India, he worked in India as a physician before beginning an internal medicine

residency in 2009 at the University of Toledo, Ohio. Pet. Ex. 10 at 1-2; Pet. Ex. 157 at 1-2. He

then completed a fellowship in hematology-oncology in 2015 at the University of Cincinnati in

Ohio. Pet. Ex. 10 at 1; Pet. Ex. 157 at 1. He currently works at Arizona Center for Cancer Care/

Honorhealth Virginia G. Piper Cancer Care Network and is a clinical assistant professor of

13

For the sake of brevity and clarity, the undersigned does not summarize all of the experts’

opinions or testimony and attempts to limit this Decision to the most material and relevant

opinions.

14

Dr. Ghose provided two expert reports and testified at the entitlement hearing. Pet. Exs. 10,

72; Tr. 3.

8

Internal Medicine, Hematology Oncology at A.T. Still University School of Osteopathic

Medicine and Grand Canyon University in Arizona. Pet. Ex. 10 at 1; Pet. Ex. 157 at 1. He

previously worked Arizona Oncology/US Oncology Network as a principal investigator for

multiple clinical trials. Pet. Ex. 10 at 1; Pet. Ex. 157 at 1. Dr. Ghose has been an expert witness

on more than 20 cases including Vaccine Program cases. Pet. Ex. 157 at 1. He is a member of

and has served on various societies and boards, and he has authored or co-authored over 30

publications, abstracts, and presentations focused on hematology and oncology. Id. at 4-9; Pet.

Ex. 10 at 1; Tr. 8.

Dr. Ghose is “an expert in hematological disorders including [ITP].” Pet. Ex. 10 at 2.

Since 2015, he has worked in private practice treating hematological patients and he “sees

patients with ITP on a regular basis.” Pet. Ex. 10 at 2; see also Tr. 7. Dr. Ghose was offered and

admitted as an expert in hematology without objection. Tr. 9. Dr. Ghose was not admitted as an

expert in immunology. Tr. 74-75.

b. Opinion

i. Severity Requirement

Dr. Ghose opined Petitioner “more likely than not” met the six-month severity

requirement because she continued to experience fatigue as a result of her ITP despite her

normalized platelet counts. Tr. 11, 19-20; Pet. Ex. 10 at 3-4.

He explained that ITP is an immune-mediated disorder that leads to the destruction of

platelets. Tr. 11-12. Patients with ITP “present with bleeding manifestations” including

bruising, petechiae, and bleeding. Tr. 12-13. Dr. Ghose explained that “ITP is not only a disease

of platelets but also a plethora of residual symptoms,” including fatigue, which “can affect

[patients’] daily activities” as well as their work and social life. Pet. Ex. 10 at 7; Tr. 13; see also

Pet. Ex. 10 at 5 (noting fatigue as a “consequence[] of ITP”); Pet. Ex. 72 at 3 (“Tiredness or

fatigue is a known debilitating symptom of ITP.”).

He cited various articles to support fatigue as a residual sequela of ITP. McMillian et

15

al., for example, evaluated health-related quality of life in 73 adults with chronic ITP and found

the health-related quality of life of adult ITP patients is “significantly worse” than that of the

general U.S. population. Pet. Ex. 12 at 1; see also Pet. Ex. 10 at 4-5. The authors acknowledged

that they were unable to examine whether a correlation between platelet counts and health-

related quality of life scores existed. Pet. Ex. 12 at 4.

15

Robert McMillian et al., Self-Reported Health-Related Quality of Life in Adults with Chronic

Immune Thrombocytopenic Purpura, 83 Am. J. Hematol. 150 (2008).

9

Dr. Ghose also cited Mathias et al., 16 who showed ITP “affects many other facets of life,”

including fatigue. Tr. 17-19 (citing Pet. Ex. 148); see also Pet. Ex. 10 at 6. In three focus groups

of 23 total ITP patients, fatigue was reported as well as the effects of fatigue on daily activities

and work. Pet. Ex. 148 at 5, 6 tbl.1. In two of the focus groups, totaling 15 participants, fatigue

was reported by 14 of the 15 participants (93%). Id. at 5, 7, 7 tbl. 2. One of those participants

characterized fatigue as the “number one [issue].” Id. at 8, 9 tbl. 3. Other patients reported their

daily activities were limited due to fatigue. Id. at 10.

Hill and Newland 17 examined fatigue in ITP patients. Pet. Ex. 63 at 1. They indicated

“[f]atigue is an important aspect of health-related quality of life from the patient perspective” and

“a significant number of both adults and children with [ITP] suffer from fatigue.” Id. Hill and

Newland summarized previous studies that reported fatigue in patients with ITP, including

Mathias et al. Id. at 2. The authors also noted “[i]t is less clear whether fatigue is associated

with disease severity as measured by the platelet count” and summarized studies that have found

fatigue did and did not correlate to platelet count. Id.

Grace et al. 18 also studied fatigue in ITP patients, though specifically children and

adolescents with ITP. Pet. Ex. 153 at 1. The authors found “[c]hildren and adolescents with ITP

reported a similarly high level of fatigue [at study entry] with 54% (29/54) of children and 62%

(26/42) of adolescents reporting moderate-to-severe fatigue.” Id. at 1, 3. They further noted

fatigue scores, which were measured at study entry (baseline), one month after treatment began,

and 12 months after treatment began, “did not correlate with bleeding symptoms, platelet count,

or platelet response to treatment.” Id. at 1, 4 tbl. II, 5-6 (“Fatigue scores [] did not differ based

on platelet response to treatment at [one] or 12 months. In addition, fatigue scores did not

correlate with the most recent platelet counts at baseline, [one] month, or 12 months after starting

treatment.” (internal citations and data omitted)).

Zhang et al. 19 focused on changes in fatigue among Chinese ITP adults. Pet. Ex. 154 at

2. Zhang et al., like Hill and Newland and Grace et al., examined whether there was a

correlation between fatigue and platelet count. Id. at 8. They concluded that in their study with

175 patients, there was “[n]o relationship [] found between platelet count and fatigue . . . , which

16

Susan D. Mathias et al., Impact of Chronic Immune Thrombocytopenic Purpura (ITP) on

Health-Related Quality of Life: A Conceptual Model Starting with the Patient Perspective, 6

Health Qual. Life Outcomes 1 (2008).

17

Quentin A. Hill & Adrian C. Newland, Fatigue in Immune Thrombocytopenia, 170 Br. J.

Haematol. 141 (2015).

18

Rachael F. Grace et al., Fatigue in Children and Adolescents with Immune Thrombocytopenia,

191 Br. J. Haematol. 98 (2020). Grace et al. cited a study that examined fatigue in 34 adults with

ITP and determined fatigue was not related to disease severity or affected by therapy. Pet. Ex.

153 at 2. This study was not filed in this case.

19

Wenhui Zhang et al., Fatigue and Health-Related Quality of Life in Patients with Immune

Thrombocytopenia: A Longitudinal Assessment in China, 16 Expert Rev. Hematol. 1125 (2023).

10

was consistent with previous studies that showed that platelet counts were not associated with

fatigue in ITP patients.” Id. Zhang et al. also determined that their patients’ fatigue improved at

discharge but worsened at three months after discharge. Id. at 1, 9.

Cooper et al. 20 also examined the effects of ITP on quality of life and concluded

“[p]hysicians should be aware not only of platelet counts and bleeding but also the multi-

dimensional impact of ITP on patients’ lives as an integral component of disease management.”

Pet. Ex. 152 at 1. They documented patients reported their “ITP reduced their energy levels

(85% of patients), capacity to exercise (77%), and limited their ability to perform daily tasks

(75%).” Id. Fifty percent of patients reported fatigue, while 38% of physicians reported their

patients felt fatigued, with 46% of these patients at a “high level of fatigue.” Id. at 3. Viana et

al. 21 similarly found half of their patients (49.9%) were experiencing fatigue. Pet. Ex. 151 at 7, 8

tbl. 3.

Although some of these studies focused on patients with chronic ITP, and Petitioner had

acute ITP, Dr. Ghose opined these studies are still relevant and apply to Petitioner as the

distinction of chronic versus acute is based on the length of time platelets are low. Tr. 50.

Moreover, these studies, according to Dr. Ghose, “haven’t actually said that fatigue happens only

in chronic ITP patients.” Tr. 57.

Despite the fact that Petitioner’s platelets normalized in October 2019, she continued to

experience fatigue, which Dr. Ghose opined was a residual symptom of her ITP. Tr. 11, 39

(testifying that because of her continued symptoms of fatigue, Petitioner had not fully recovered

clinically). Dr. Ghose explained that patients can continue to experience fatigue even when

platelets have normalized. Tr. 19, 42. For support, he cited to Petitioner’s affidavit and email to

counsel, which reported continued complaints of fatigue through May 2020, despite a normal

platelet count. Pet. Ex. 10 at 4 (citing Pet. Ex. 4 at 20; Pet. Ex. 6 at 1; Pet. Ex. 7 at 1). Hill and

Newland noted studies that have found fatigue did not correlate to platelet count. Pet. Ex. 63 at

2. In Grace et al., the authors determined fatigue scores “did not correlate with bleeding

symptoms, platelet count, or platelet response to treatment.” Pet. Ex. 153 at 1. And Zhang et al.

found “[n]o relationship . . . between platelet count and fatigue.” Pet. Ex. 154 at 8.

With regard to Petitioner’s complaints of sleeping poorly in April 2020 due to the Covid

pandemic and her sister’s death, Dr. Ghose testified that he cannot say whether her fatigue would

be due to her sleeping poorly or her ITP at this time. Tr. 61. He opined, “more likely than not,”

Petitioner’s complaints of fatigue to Dr. Dammrich in November 2019 as well as in May 2020,

as also evidenced by Petitioner’s email and testimony, was a residual symptom of her ITP. Tr.

19-20; Pet. Ex. 10 at 3-4.

20

Nicola Cooper, Immune Thrombocytopenia (ITP) World Impact Survey (I-WISh): Impact of

ITP on Health-Related Quality of Life, 96 Am. J. Hematol. 199 (2021).

21

Ricardo Viana et al., Psychometric Evaluation of ITP Life Quality Index (ILQI) in a Global

Survey of Patients with Immune Thrombocytopenia, 38 Adv. Ther. 5791 (2021).

11

As to any lack of documentation of fatigue in Petitioner’s medical records, Dr. Ghose

explained that fatigue “[is] not measured objectively in routine visits by physicians and [is] often

missed.” Pet. Ex. 72 at 3; see also Pet. Ex. 148 at 11 (“[D]espite [] finding that over 90% of the

patients in [two] focus groups mentioned fatigue, currently fatigue is not sufficiently often

considered by clinicians who manage persons with ITP. In fact, fatigue is seldom recorded as an

adverse event in clinical trials of ITP patients.”). He explained that hematologists focus on

measuring patient’s platelet counts as it is an objective measurement that can be corrected. Tr.

20-21; see also Tr. 23 (noting platelet counts are “what [hematologists] go by”); Pet. Ex. 12 at 2

(“Physicians caring for ITP patients tend to focus on the platelet count and may fail to appreciate

the magnitude of the effect of ITP and its treatment on their patients’ quality of life.”); Pet. Ex.

148 at 7 (“Platelet counts, with or without the presence of any signs or symptoms, are often the

only determinant of treatment decisions and are also used to establish whether the patient has

responded to treatment and whether the response is considered complete, partial, or minimal.”).

Fatigue, on the other hand, “is not easy to correct” and thus, “the focus is on whether the

platelets have normalized.” Tr. 21; see also Tr. 55-56; Pet. Ex. 151 at 3 (“The International

Consensus Report has mentioned that severe fatigue is the most difficult ITP symptom to treat,

experienced by 39–59% of adult patients, yet it is under-recognized by healthcare practitioners.

Further, physicians primarily focus on platelet count whereas fatigue and [other] symptoms . . .

are often the more primary concerns of patients.”); Pet. Ex. 148 at 11 (“[P]latelet counts, with or

without the presence of symptoms, can dictate whether to treat ITP.”). Moreover, certain

documentations in medical records are not often updated and therefore “they don’t completely

reflect what the patient may be saying or may not be saying. So a lot of times physicians focus

just on platelets[] [and] they don’t update the notes.” Tr. 64.

ii. Althen Prong One

Dr. Ghose opined that the flu vaccine can cause ITP via “[m]olecular mimicry to the

proteins in the vaccine with that of platelets, causing the body to generate antibodies against it.”

Pet. Ex. 10 at 4, 7. In other words, “antibodies against . . . vaccine antigens cross-react with

normal platelet antigens,” which “causes a drop in platelets as the platelets are falsely recognized

as foreign to the body.” Id. at 4. He opined molecular mimicry was “the most plausible

explanation.” 22 Id. at 7; see also Pet. Ex. 17 at 1-2 (stating molecular mimicry is the “most

likely” theory by which vaccines induce ITP). 23

22

Dr. Ghose also noted another mechanism in his first report: “an immune alteration where there

is loss of self tolerance and body’s development of self-reactive antibodies are promoted like in

hematological malignancies like [Chronic Lymphocytic Leukemia] and autoimmune diseases.”

Pet. Ex. 10 at 4. Dr. Ghose did not discuss this theory further, and thus, the undersigned finds it

was not developed and will not be discused. In his second expert report, Dr. Ghose adopted Dr.

Akbari’s inflammasome and hypersensitivity theories. Pet. Ex. 72 at 2. Because these theories

will be discussed in more detail below in Dr. Akbari’s expert section, the undersigned does not

discuss these opinions here.

23

Carlo Perricone et al., Immune Thrombocytopenic Purpura (ITP) Associated with

Vaccinations: A Review of Reported Cases, 60 Immunologic Rsch. 226 (2014). This was also

filed as Pet. Ex. 107.

12

In Perricone et al., the authors offered molecular mimicry as the process by which

“[a]ntibodies responsible for the clearance of virus antigens may cross-react with antigens

naturally present on platelets.” Pet. Ex. 17 at 2. The authors hypothesized that with the flu

vaccine, “the target of molecular mimicry probably involves hemagglutinin” (“HA”), “the main

antigen in [flu] vaccines.” Id. at 4. According to Perricone et al., HA has been shown to “bind[]

to platelets, through receptors bearing a terminal N-acetyl neuraminic acid group displayed on

their surface. Consequently, the membrane-bound HA can be recognized by the anti-HA

antibodies, triggering activation of the complement cascade which induces platelet lysis and

thrombocytopenia.” Id. While molecular mimicry is the current prevailing theory, the authors

acknowledged that the pathogenic mechanisms of ITP have not been fully explained. Id. at 2.

Dr. Ghose opined infections and vaccinations, including the flu infection and vaccination,

have been associated with ITP in the literature. 24 Pet. Ex. 10 at 4-5; Pet. Ex. 72 at 1; Tr. 12, 16;

see, e.g., Pet. Ex. 16 at 3-12 (describing infectious agents and vaccinations that have been

associated with ITP); 25 Pet. Ex. 17 at 2-7 (same). Rinaldi et al. explained “[t]he vaccines-

autoimmunity interplay is very similar to the established association between infections and

autoimmunity. Infectious agents can cause or trigger autoimmunity through several mechanisms

such as molecular mimicry . . . . .” Pet. Ex. 16 at 8; see also Pet. Ex. 17 at 2.

24

The undersigned does not discuss literature that does not address the flu vaccine or flu

infection for the sake of brevity and due to lack of relevance. See Pet. Ex. 14 (E. Miller et al.,

Idiopathic Thrombocytopenic Purpura and MMR Vaccine, 84 Arch. Dis. Child. 227 (2001))

(also filed as Pet. Ex. 27); Pet. Ex. 22 (Laura J. Sauvé & David Scheifele, Do Childhood

Vaccines Cause Thrombocytopenia?, 14 Paediatr. & Child Health 31 (2009)); Pet. Ex. 24 (Eric

K. France et al., Risk of Immune Thrombocytopenic Purpura After Measles-Mumps-Rubella

Immunization in Children, 121 Pediatrics e687 (2008)); Pet. Ex. 25 (Corri Black et al., MMR

Vaccine and Idiopathic Thrombocytopaenic Purpura, 55 Brit. J. Clin. Pharmacol. 107 (2003));

Pet. Ex. 26 (Annie P. Jonville-Bera et al., Thrombocytopenic Purpura After Measles, Mumps and

Rubella Vaccination: A Retrospective Survey by the French Regional Pharmacovigilance

Centres and Pasteur-Merieux Serums et Vaccins, 15 Pediatr. Infect. Dis. J. 44 (1996)); Pet. Ex.

28 (Laura J. Sauvé et al., Postvaccination Thrombocytopenia in Canada, 29 Pediatr. Infect. Dis.

J. 559 (2010)) (also filed as Resp. Ex. A10); Pet. Ex. 29 (Judy Beeler et al., Thrombocytopenia

After Immunization with Measles Vaccines: Review of the Vaccine Adverse Events Reporting

System (1990 to 1994), 15 Pedistr. Infect. Dis. J. 88 (1996)) (also filed as Pet. Ex. 77); Pet. Ex.

30 (Vasiliki Vlacha et al., Recurrent Thrombocytopenic Purpura After Repeated Measles-

Mumps-Rubella Vaccination, 97 Pediatrics 738 (1996)); Pet. Ex. 34 (Eun-Ju Lee et al.,

Thrombocytopenia Following Pfizer and Moderna SARS-CoV-2 Vaccination, 96 Am. J.

Hematol. 534 (2021)) (also filed as Pet. Ex. 84); Pet. Ex. 73 (Anna C. Bibby et al., Is MMR

Immunisation Safe in Chronic Idiopathic Thrombocytopenic Purpura?, 93 Arch. Dis. Child. 354

(2008)).

25

M. Rinaldi et al., Immune Thrombocytopaenic Purpura: An Autoimmune Cross-Link Between

Infections and Vaccines, 23 Lupus 554 (2014).

13

Isai et al. 26 reviewed a database of reports of suspected adverse reactions in the European

Union from October 2009 to December 2010 for adjuvanted and non-adjuvanted pandemic flu

A/H1N1 vaccines. Pet. Ex. 79 at 1. The data included reports of autoimmune adverse reactions

where an adjuvanted or unadjuvanted A/H1N1 vaccine was reported as suspect, interacting, or

concomitant. Id. at 2. The authors reported that ITP was the third most common autoimmune

condition following flu vaccination. Id. at 3 tbl.2.

Perricone et al. summarized articles describing an association between the flu vaccine

and ITP. Pet. Ex. 17 at 4, 5 tbl.1. For example, “Garbe et al. found that [flu] vaccine has a

‘probable’ causality to induce ITP.” Id. at 4 (citing Pet. Ex. 53 at 1-2, 9). 27 Garbe et al. was a

large case-control surveillance study that used data from Berlin hospitals on adults from 2000 to

2009. Pet. Ex. 53 at 1. Ninety of the 169 total cases of ITP were determined to be drug-related,

and these included vaccines. Id. at 1-2, 9. Three of the cases were related to the flu vaccine. Id.

Vaccine causality was determined to be “probable” using the World Health Organization

(“WHO”) standardized causality assessment tool. 28 Id. at 9. The “[flu] vaccination was

associated with a statistically significant [four]-fold risk.” Id.

Jadavji et al. 29 reported on data obtained from 12 pediatric centers in Canada from 1992

to 2001. Pet. Ex. 23 at 1. The authors identified 61 patients who had decreased platelet counts

within 30 days of vaccination. Id. Two of the patients developed thrombocytopenia after the flu

vaccine, at 10 and 14 days post-vaccination. 30 Id. at 2, 2 tbl. 1.

26

Alina Isai et al., Autoimmune Disorders After Immunisation with Influenza A/H1N1 Vaccines

with and Without Adjuvant: EudraVigilance Data and Literature Review, 30 Vaccine 7123

(2012).

27

Edeltraut Garbe et al., Drug-Induced Immune Thrombocytopaenia: Results from the Berlin

Case-Control Surveillance Study, 68 Eur. J. Clin. Pharmacol. 821 (2012). This was also filed as

Pet. Exs. 104, 147.

28

The WHO assessment of causality includes the categories certain, probable, possible, unlikely,

unclassified, and unclassifiable. Pet. Ex. 53 at 3. “A drug reaction was evaluated as ‘probable’

when the ITP occurred with a reasonable time [after] administration[,] . . . was unlikely to be

attributed to other causes, and a positive dechallenge reaction was observed on drug

withdrawal.” Id. at 3-4.

29

Taj Jadavji et al., Thrombocytopenia After Immunization of Canadian Children, 1992 to 2001,

22 Pediatr. Infect. Dis. J. 119 (2003). This was also filed as Pet. Ex. 35.

30

Of note, the authors noted a limitation of the study, in that the majority of patients with post-

vaccination thrombocytopenia also had a viral infection or exposure to medication that could

suggest an alternate cause of the illness. Pet. Ex. 23 at 3.

14

For further support, he cited numerous case reports of ITP post-flu vaccination. Tishler

31

et al. reported on a 68-year-old patient who developed severe thrombocytopenia 14 days

following receipt of a flu vaccine. Pet. Ex. 18 at 1. Regarding causation, the authors explained

that “[t]he most popular hypothetical mechanism for the triggering of autoimmunity by an

infectious agent is that of molecular mimicry.” Id.

Ohta and Sano 32 described a case of acute onset ITP in an 88-year-old male four days

after receiving a flu vaccination. Pet. Ex. 20 at 1. He was diagnosed with “[flu] vaccine-induced

severe ITP,” and the authors noted his case “suggest[ed] that [flu] vaccines can be associated

with ITP.” Id. at 3. The authors did not discuss any mechanisms by which the flu vaccine can

cause ITP.

Nagasaki et al. 33 reported ITP four to five weeks following flu vaccination in three

elderly patients, ages 75, 81, and 87. Pet. Ex. 21 at 1-2. The authors concluded that “[v]accine-

associated ITP [was] probably caused by molecular mimicry.” Id. at 2. They also concluded

that ITP was “strongly suspected” to be associated with the flu vaccine. Id. at 4.

Shalmovitz and Johar 34 described a 50-year-old man who developed Evans’ syndrome,

which is the combination of ITP and autoimmune hemolytic anemia with no known underlying

cause. Pet. Ex. 32 at 1. The patient had received a flu vaccine four days before his onset of

symptoms. Id. The authors postulated that the flu vaccine, through molecular mimicry, may

have been the cause of the patients Evans’ syndrome. Id. at 2. The authors performed a

PubMed 35 search and came across eight case reports of patients who developed ITP after

receiving a flu vaccine. Id. The authors opined that these case reports “suggest [] immunizations

may provide a trigger for the development of autoimmune disease in susceptible individuals.”

Id.

31

Moshe Tishler et al., Immune Thrombocytopenic Purpura Following Influenza Vaccination, 8

IMAJ 322 (2006).

32

Ryuichi Ohta & Chiaki Sano, Severe Immune Thrombocytopenic Purpura Following Influenza

Vaccination: A Case Report, 14 Cureus 1 (2022).

33

Joji Nagasaki et al., Postinfluenza Vaccination Idiopathic Thrombocytopenic Purpura in Three

Elderly Patients, 2016 Case Reps. Hematol. 1. This was also filed as Pet. Exs. 33, 83.

34

Gil Z. Shlamovitz & Sandeep Johar, A Case of Evans’ Syndrome Following Influenza

Vaccine, 44 J. Emerg. Med. e149 (2013). This was also filed as Pet. Exs. 39, 82.

35

“PubMed is a free resource supporting the search and retrieval of biomedical and life sciences

literature . . . . PubMed contains more than 40 million citations and abstracts of biomedical

literature.” Nat’l Libr. Med., Nat’l Ctr. for Biotechnology Info., About PubMed,

https://pubmed.ncbi.nlm.nih.gov/about/ (last visited June 17, 2026).

15

Mantadakis et al. 36 described a case report of a three-year-old boy who developed ITP 26

days after his second dose of the flu vaccine. Pet. Ex. 38 at 1. They postulated that the

mechanism of thrombocytopenia following flu infection was most likely due to molecular

mimicry. Id. at 2. The authors concluded that while there was a risk of ITP within six to eight

weeks following the measles-mumps-rubella (“MMR”) vaccine, more evidence was needed to

explore the connection between the flu vaccine and ITP. Id. at 2-3 (“In conclusion, although the

link between ITP and [flu] vaccination is biologically plausible, there is insufficient evidence to

indicate a causal relationship between [flu] vaccine and symptomatic thrombocytopenia.”).

And Hamiel et al. 37 described a four-and-one-half-year-old boy who presented in October

2013 with bleeding and his platelet count was severely decreased at 17,000. Pet. Ex. 76 at 1. A

review of the child’s past medical records revealed that he had previously been hospitalized at

age one-and-one-half years and three-and-one-half years of age with similar symptoms of

bleeding. Id. at 2. All three of the child’s hospital admissions for ITP had taken place within

one week of receiving a flu vaccine. Id. And all three times the child received the Fluarix

trivalent flu vaccine. Id. After the last occurrence, the child did not receive any further annual

flu vaccines, and no recurrences of ITP were observed. Id. Using the WHO standardized case

causality assessment, the flu vaccine was determined to fall into the category of “certain”

causality. Id.

Lastly, Dr. Ghose cited two cases where immunosuppressed patients developed ITP

following flu vaccination. See Pet. Ex. 36; 38 Pet. Ex. 37. 39 However, there is no evidence

36

Elpis Mantadakis et al., A Case of Immune Thrombocytopenic Purpura After Influenza

Vaccination: Consequence or Coincidence?, 32 J. Pediatr. Hematol. Oncol. e227 (2010). This

was also filed as Pet. Ex. 106.

37

Uri Hamiel et al., Recurrent Immune Thrombocytopenia After Influenza Vaccination: A Case

Report, 138 Pediatrics e1 (2016).

38

K. Ikegame et al., Idiopathic Thrombocytopenic Purpura After Influenza Vaccination in a

Bone Marrow Transplantation Recipient, 38 Bone Marrow Transplant. 323 (2006). Ikegame et

al. discussed a bone marrow transplant recipient whose platelet count rapidly decreased two

weeks after flu vaccination. Pet. Ex. 36 at 1-2. At the time of vaccination, the patient was

receiving low doses of tracrolimus (1.7 mg/day) (immunosuppressant) and prednisone (7

mg/day). Id. at 1. The authors suggested that the causal theory was molecular mimicry, stating

“[a]cute ITP may [] occur after vaccination” because “[a]ntibodies responsible for the clearance

of virus antigens may cross-react with antigens naturally present on platelets.” Id. at 2.

39

Satoshi Mamori et al., Thrombocytopenic Purpura After the Administration of an Influenza

Vaccine in a Patient with Autoimmune Liver Disease, 77 Digestion 159 (2008). Mamori et al.

described a 75-year-old patient with autoimmune liver disease (“AILD”) who received a flu

vaccine. Pet. Ex. 37 at 1. One week after vaccination, the patient began experiencing symptoms

and was diagnosed with ITP. Id. The authors concluded that “the [flu] vaccine can exacerbate

potential immune-mediated platelet destruction in AILD patients, thus leading to severe

autoimmune side effects.” Id. at 2.

16

Petitioner here was immunosuppressed at the time of vaccination, and thus, the relevance of

these cases is unclear.

iii. Althen Prongs Two and Three

Dr. Ghose agreed Petitioner suffered acute ITP in October 2019 and opined her “flu

vaccine more likely than not caused [her] ITP.” Tr. 11, 13; see also Pet. Ex. 10 at 6

(“Undoubtedly [Petitioner] developed acute ITP secondary to [flu] vaccination.”); Pet. Ex. 72 at

3 (“It is more likely than not that [Petitioner] developed ITP and chronic fatigue from the flu

vaccine administered on October 16, 2019.”).

Dr. Ghose explained that “the flu vaccine caused [Petitioner’s] ITP because the very next

day [after vaccination,] she started not feeling well and her platelets started dropping.” Tr. 14,

16. Thus, “before the vaccine, she was perfectly fine. Just after it, her platelets dropped and she

started having . . . signs and symptoms [of ITP]. So it was . . . very obvious that . . . here, a

vaccine led to the issue . . . .” Tr. 16.

He opined Petitioner did not have any previous medical history or precipitating events,

other than the flu vaccination, that could have caused her ITP. Tr. 13-14; Pet. Ex. 10 at 6; Pet.

Ex. 72 at 3.

He also cited to statements from Petitioner’s treating hematologist, Dr. Dammrich, who

first saw Petitioner on October 23, 2019, and attributed Petitioner’s ITP to her flu vaccination,

which he believed was significant. Pet. Ex. 10 at 3-4, 6; Tr. 15-17, 39. Petitioner continued to

see Dr. Dammrich over the ensuing months, and he continued to attribute Petitioner’s ITP to her

vaccination. Pet. Ex. 10 at 3-4, 6.

As to timing, Dr. Ghose opined Petitioner’s ITP onset was “within [one] day of receiving

the [f]lu vaccine on October 16[,] 2019,” when her platelets dropped and she developed bruising

and petechiae on her body and face and in her mouth. Pet. Ex. 10 at 6-7; Tr. 24-25, 27

(testifying Petitioner’s ITP symptoms began “[w]ithin a day” of her flu vaccination, “when the

platelets drop[ped] significantly”).

On cross-examination, Dr. Ghose agreed Petitioner “began developing symptoms that

eventually led to ITP” within ten minutes of vaccination when she developed tachycardia, and

that her subsequent symptoms (e.g., chills, shakiness, shortness of breath) were also related to

her ITP. Tr. 27-33. He clarified that these symptoms were evidence of “a strong immunological

response” to the flu vaccine, meaning they are “related” to ITP “but [] not a symptom of ITP.”

Tr. 29-30; see also Pet. Ex. 72 at 2-3 (classifying Petitioner’s initial symptoms as evidence of a

hypersensitivity reaction 40 to the flu vaccine, which was then followed by a rapid drop in

platelets). He agreed Petitioner developed ITP the same day as her flu vaccination. Tr. 35. He

explained that Petitioner had petechiae at the site of injection, on her opposite arm, her face, and

inside her mouth, which showed that her ITP developed the same day as the vaccination. Tr. 36.

40

Dr. Ghose does not define hypersensitivity reaction and appears to be relying on Dr. Akbari’s

expert reports in making this statement. See supra note 22; infra Section II.C.2.b.

17

This timing, according to Dr. Ghose, “is characteristic of the autoimmune nature of the

disease and confirms the causal relationship to the vaccine which caused the immune mediated

drop in platelets.” Pet. Ex. 10 at 6-7 (“The fact that the platelets dropped within [one to two]

days of the vaccination [] confirms the immune mediated nature of the disease that characterizes

ITP.”). Additionally, because Petitioner had received prior flu vaccinations, Dr. Ghose opined

her previous exposures “might be a reason why she developed an immediate hypersensitivity

reaction.” Pet. Ex. 73 at 3.

Additionally, he asserted the literature shows ITP can develop between one and 35 days

after vaccination. Pet. Ex. 10 at 6; Pet. Ex. 72 at 2-3. However, Dr. Ghose did not provide any

literature to support an onset of ITP on the same day as flu vaccination, or within one day of flu

vaccination, or that a one-day onset was an appropriate temporal interval for his posited theory of

molecular mimicry.

A review of his literature shows cases of ITP post-flu vaccination occurring between four

days and five weeks after vaccination. Jadavji et al. reported two cases of ITP, 10 and 14 days

post-flu vaccination. Pet. Ex. 23 at 2, 2 tbl. 1. Tishler et al. reported a case of ITP 14 days after

flu vaccination. Pet. Ex. 18 at 1. Ohta and Sano’s case of ITP occurred four days after a flu

vaccination. Pet. Ex. 20 at 1. Nagasaki et al. described three cases of ITP occurring four to five

weeks post-flu vaccination. Pet. Ex. 21 at 1-2. The patient discussed by Shalmovitz and Johar

developed Evans’ syndrome four days after receiving a flu vaccine. Pet. Ex. 32 at 1.

Mantadakis et al. described a child who developed ITP 26 days after his second flu vaccine. Pet.

Ex. 38 at 1. And Hamiel et al. reported a child whose ITP symptoms began within one week of a

flu vaccine on three separate occasions. Pet. Ex. 76 at 2.

2. Petitioner’s Expert, Dr. Omid Akbari 41

a. Background and Qualifications

Dr. Akbari is a Professor of Immunology at the University of Southern California, Keck

School of Medicine. Pet. Ex. 40 at 2; Pet. Ex. 156 at 2. He received a Ph.D. in cellular and

molecular immunology at the National Institute for Medical Research in London, United

Kingdom. Pet. Ex. 156 at 1. Thereafter, he completed a postdoctoral fellowship at Stanford

41

Dr. Akbari provided three expert reports and testified at the entitlement hearing. Pet. Exs. 40,

88, 115; Tr. 3, 272. For sake of brevity, the undersigned does not discuss literature previously

discussed above in Dr. Ghose’s expert section or literature that is not relevant to this case (i.e.,

literature that does not pertain to the flu vaccine or ITP). See, e.g., Pet. Ex. 69 (Sonal Prasad et

al., Immune Thrombocytopenia Following COVID-19 Vaccine, 2022 Case Reps. Hematol. 1)

(addressing a case of ITP following COVID vaccination); Pet. Ex. 71 (Meirong Zhu et al., IL-18

and IL-35 in the Serum of Patients with Sepsis Thrombocytopenia and the Clinical Significance,

19 Exp. & Ther. Med. 1251 (2020)) (examining IL-18 and IL-35 levels in the serum of patients

with sepsis, with and without thrombocytopenia). Further, the undersigned does not discuss all

aspects of Dr. Akbari’s reports and testimony and attempts to limit this Decision to only those

aspects that are relevant.

18

University. Id. Dr. Akbari’s research focuses on the “the role of immune tolerance and how

immune cells induce autoimmune and allergic diseases.” Pet. Ex. 40 at 2; see also Pet. Ex. 156

at 6-7. His laboratory research includes multiple studies regarding “how a vaccination can result

in an appropriate or dysregulated immune response.” Pet. Ex. 40 at 2; see also Pet. Ex. 156 at 6-

7. Dr. Akbari serves as an associate editor and reviewer on several journals. Pet. Ex. 40 at 2;

Pet. Ex. 156 at 5-6. He has authored or co-authored over 100 publications. Pet. Ex. 156 at 15-

34.

Dr. Akbari is not a medical doctor and thus, he does not diagnose or treat patients with

ITP. See Pet. Ex. 156 at 1. He was admitted as an expert in immunology without objection. Tr.

82.

b. Opinion

i. Severity Requirement

Dr. Akbari agreed with Dr. Ghose that fatigue, an important aspect of health-related

quality of life, can affect adults with ITP, even when in remission. Pet. Ex. 40 at 13. He opined

Petitioner’s “persistent fatigue” was associated with her ITP. Id. at 4.

Dr. Akbari explained that induction of inflammasomes and the subsequent induction of

molecular mimicry can lead to persistent fatigue in ITP patients. Pet. Ex. 40 at 13-14. He

summarized that after flu vaccination, cytokines and inflammasomes are induced, which causes

immune dysregulation that in turn induces fatigue in patients with ITP. Id. at 15.

He cited and discussed literature to support the association between fatigue and ITP. Pet.

Ex. 40 at 13-14; Tr. 133-38. Newton et al., 42 for example, examined fatigue in adult ITP

patients, both with active disease and non-active disease, in the US and UK, to determine patient

characteristics associated with fatigue. Pet. Ex. 64 at 1-2. The authors noted that although

patients with primary ITP often report fatigue, hematologists rarely consider fatigue as a

manifestation of ITP. Id. at 1. Newton et al. concluded that “[f]atigue is a common symptom

among patients with ITP.” Id. Univariate analysis showed patient characteristics significantly

associated with fatigue included platelet count, steroid treatment, and more, while duration of

ITP was not associated with fatigue. Id. at 5. “Although the presence of fatigue was

significantly associated with lower platelet counts, the relative frequency of fatigue among

patients with platelet counts ≥ 100[,]000/µL[43] was also significantly greater than expected for

normal subjects.” Id. at 5, 5 tbl. 2 (finding 32% of the UK cohort and 9% of the US cohort with

a platelet count ≥ 100,000/µL reported fatigue, both of which were “significantly greater” than

the expected frequency in normal subjects (2.5%)).

42

Julia N. Newton et al., Fatigue in Adult Patients with Primary Immune Thrombocytopenia, 86

Eur. J. Haematol. 420 (2011).

43

Patients’ platelet counts were based on patient recall. Pet. Ex. 64 at 2. Patients who reported

“normal” platelet counts were considered to have a platelet count > 100,000/µL. Id.

19

ii. Althen Prong One

1. Overview

Dr. Akbari began by explaining how vaccines and the immune system work. Generally,

after vaccination, there is a local inflammatory response mediated by cells involved in the innate

immune system, which functions as a general, nonspecific response to activate the adaptive

immune system, which in turn involve B and T cells (memory cells) that protect against

subsequent exposures. Pet. Ex. 40 at 5; Tr. 84; see also Pet. Ex. 42 (generally describing how

vaccines induce immune responses). 44 Upon flu vaccine administration specifically,

inflammasomes are induced (e.g., IL-1 and IL-18) at the site of vaccination, which “starts a

series of cascades that trigger more immune cells to the site” of vaccination, leading to an

adaptive immune response where CD4 and CD8 T cells are activated and become memory cells

within approximately two weeks. Tr. 85.

Dr. Akbari opined ITP is an immune-mediated disorder whose pathogenesis “has not

been complete elucidated.” Pet. Ex. 40 at 6, 10; see also Pet. Ex. 88 at 14 (noting the

pathogenesis of vaccine-related ITP “remains incompletely understood”). He explained ITP can

occur immediately, “mainly mediated through innate induction of immune system,” or ITP can

be explained “with induction of adaptive immune responses, including induction of B and T cells

mainly through mechanism of molecular mimicry.” Pet. Ex. 40 at 6.

Dr. Akbari’s theory, summarized in the image below, involves both the innate and

adaptive immune system:

44

Claire-Anne Siegrist, Vaccine Immunology, in Plotkin’s Vaccines 16 (7th ed. 2018).

20

Pet. Ex. 155. 45

To summarize, Dr. Akbari explained the first step after flu vaccination is activation of

inflammasomes. Tr. 331.

Then, in the second step, inflammasome activation via dendritic cells (an antigen-

presenting cell or “APCs”) leads to “two pathways:” one is immediate hypersensitivity and the

second affects platelets and megakaryocytes, which have IL-1 receptors that are recognized by

dendritic cells for binding. Tr. 331-32, 334. IL-1β is a cytokine, a product of inflammasomes,

and part of the innate immune system. Tr. 335, 337. IL-1β binds to the IL-1 receptors on

platelets and megakaryocytes, which leads to apoptosis (cell death). Id. (explaining the IL-1β

“cytokine can directly bind on the receptor and start the cascade that change the homeostasis of

platelets” (citing Pet. Ex. 128)); see also Pet. Ex. 115 at 10.

The second pathway of step two (inflammasome activation and IL-1 receptors on

platelets and megakaryocytes are recognized by dendritic cells (APCs) for binding) then leads to

the third step of Dr. Akbari’s theory, which is when inflammasomes activate autoreactive B

cells. Tr. 332. The IL-1β receptor is “very highly expressed on autoreactive B cells.” Tr. 335.

He acknowledged that “it takes several days for conventional naïve B cells to get activated and

produce IgM,” however, “for autoreactive B cell[s], . . . the activation threshold is very low,” and

thus, activation would be faster. Tr. 332; see also Pet. Ex. 115 at 2-3. Dr. Akbari agreed that the

third step, involving autoreactive B cells, is part of the adaptive immune system. Tr. 336.

The fourth and final step of his theory is the “production of IgM and direct activation of

inflammasome binding to megakaryocytes and platelets to cause acute ITP.” Tr. 333, 336.

Thus, both the innate immune response and the adaptive immune response are involved

in Dr. Akbari’s theory. Tr. 337; see also Pet. Ex. 88 at 8.

2. Innate Immune System, Inflammasomes, and

Cytokines

Dr. Akbari opined he is “very [] certain that induction of inflammasome[46] by vaccines

play[s] an important role as [an] initial trigger for the development of ITP.” Pet. Ex. 40 at 6; see

also Tr. 84-86.

45

Dr. Akbari prepared this slide for the hearing. Tr. 331.

46

For more information on inflammasomes, see, for example, Pet. Ex. 88 at 8-9.

21

For support, he cited literature reporting activation of inflammasomes after flu

vaccination. 47 Pet. Ex. 40 at 6-8 (citing, e.g., Pet. Ex. 43); 48 see also Tr. 86. In Crooke et al., Dr.

Akbari opined the authors demonstrated “inflammasome and subsequent production of IL-1 and

related genes get sufficiently triggered[] by the flu vaccination[] in the absence of adjuvants.”

Pet. Ex. 40 at 7 (citing Pet. Ex. 43 at 9). Crooke et al. evaluated inflammasome activity at

baseline, 24 hours after flu vaccination, and 28 days after flu vaccination. Resp. Ex. 43 at 2.

The authors noted “[flu] vaccination did not appear to have an immediate effect on macrophage

inflammasome activity, although IL-1β levels were slightly elevated in unstimulated

macrophages 24 h[ours] postvaccination compared to baseline.” Id. at 4. Additionally, “IL-1β

secretion in response to [flu] stimulation at 24 h[ours] post-vaccination was higher in older

adults.” Id. at 7. No “associations between inflammasome-mediated cytokine production and

change in [HA inhibition] titer after vaccination” were observed. Id. at 6. Crooke et al. did not

study or discuss ITP.

During the hearing, Dr. Akbari noted he and Dr. He agreed the flu vaccine is capable of

inducing inflammasomes, and individuals’ responses to such inflammasomes can differ. Tr. 87-

88, 330; see Pet. Ex. 88 at 5-7; Pet. Ex. 96 at 1 (“[T]here was no evidence for a ‘universal

signature’ that predicted antibody response to all vaccines.”). 49

He also cited literature, including Qiao et al., 50 to show “inflammasome[s] directly play a

role in induction of ITP.” Tr. 87 (citing Pet. Ex. 47); see also Pet. Ex. 40 at 8. Of note, Qiao et

al. stated that ITP is an “immune dysregulation-related disorder,” involving “dysregulation of T

cell activity and related cytokines,” along with “the development of autoreactive B cells.” Pet.

Ex. 47 at 1-2. They further explained that the decreased platelet count is a result of an “anti-

platelet autoantibody-mediated immune response, leading to accelerated platelet destruction and

impaired platelet production.” Id. at 5. The study provided evidence of a higher expression of

inflammasomes (NLRP3 and others), suggesting that NLRP3 activation may play “a regulatory

role . . . in inflammation and adaptive immune response.” Id. The authors concluded that

47

Dr. Akbari cited Wan et al. to show the flu infection can induce inflammasomes. Pet. Ex. 40

at 8; Tr. 87 (citing Pet. Ex. 44 (Pin Wan et al., AP-1 Signaling Pathway Promotes Pro-IL-1β

Transcription to Facilitate NLRPP3 Inflammasome Activation upon Influenza A Virus Infection,

13 Virulence 502 (2022))). However, he did not explain how this information pertains to a flu

vaccine considering the flu vaccine given here did not contain the live virus flu infection. See

Tr. 139.

48

Stephen N. Crooke et al., Inflammasome Activity in Response to Influenza Vaccination Is

Maintained in Monocyte-Derived Peripheral Blood Macrophages in Older Adults, 2 Front.

Aging 1 (2021). This was also filed as Pet. Ex. 90.

49

Thomas Hagan et al., Transcriptional Atlas of the Human Immune Response to 13 Vaccines

Reveals a Common Predictor of Vaccine-Induced Antibody Responses, 23 Nature Immunol.

1788 (2022).

50

Jianlin Qiao et al., Elevated Expression of NLRP3 in Patients with Immune

Thrombocytopenia, 64 Immunol. Res. 431 (2016).

22

“NLRP3 activation might be involved in the pathogenesis of ITP.” Id. at 6. However, the

authors did not suggest that inflammasomes directly induce platelet destruction or that platelet

destruction could occur absent the adaptive immune response.

Dr. Akbari also cited medical literature showing the flu vaccine increases levels of

proinflammatory cytokines, which may be associated with local and systemic responses that

occur shortly after vaccination. Pet. Ex. 40 at 9-10, 14. Christian et al., 51 for example, studied

post-flu vaccination proinflammatory cytokine responses. Pet. Ex. 48 at 1. Serum cytokines

were tested at days one through three after vaccination. Id. Injection site soreness and increases

in two cytokines tested were elevated at one day post-vaccination. Id. Illness-like symptoms

and serum cytokines were elevated at two days post-vaccination. Id. at 1-2. Christian et al. does

not mention ITP.

Cytokines, Dr. Akbari explained, “play an important role in the induction of Th17 cells,”

which are elevated in patients with ITP. Pet. Ex. 40 at 14. In a supplemental expert report, Dr.

Akbari opined “Th17 cells have the potential to trigger ITP.” Pet. Ex. 88 at 9. He explained that

flu vaccination activates inflammasomes, which releases IL-1, “a pivotal cytokine that plays a

central role in the differentiation and proliferation of Th17 cells.” Id. at 10. Th17 cells are

“armed with the potential to cause ITP and contribute to pathological processes,” according to

Dr. Akbari. 52 Id.

He cited Zhang et al., 53 who explained T cell abnormalities are important in the

pathogenesis of chronic ITP. Pet. Ex. 66 at 1. Th17 cells are characterized by the production of

IL-17, 54 and Th17 has been linked to the development of autoimmune diseases. Id. Zhang et al.

suggested Th17 and Th1 cells “may” play a role in the pathogenic mechanism of ITP (whether

that be cooperative or synergetic) and Th17 cells, which promote a cytokine imbalance, “may

induce ITP.” Id. at 2-3. Further, they indicated their data “strongly supported the hypothesis that

51

Lisa M. Christian et al., Proinflammatory Cytokine Responses Correspond with Subjective

Side Effects After Influenza Virus Vaccination, 33 Vaccine 3360 (2015). This was also filed as

Pet. Ex. 91.

52

For more information about Th17 cells responses in the context of flu vaccination, see Pet. Ex.

88 at 10-11. Overall, Dr. Akbari opined Th17 cells have a “pivotal role” in the efficacy of

vaccination. Pet. Ex. 88 at 11. Dr. Akbari also discussed regulatory T cells. See id. at 11-14.

53

Jingbo Zhang et al., Elevated Profile of Th17, Th1 and Tc1 Cells in Patients with Immune

Thrombocytopenic Purpura, 94 Haematologica 1326 (2009).

54

See Pet. Ex. 68 (Yinyao Lin et al., Th17 Cytokines and Vaccine Induced Immunity, 32 Semin

Immunopathol. 79 (2010)).

23

cytotoxic T lymphocyte-mediated cytotoxicity[55] was an alternative mechanism for platelet

destruction in ITP.” Id. at 3.

2. Adaptive Immune System and Molecular

Mimicry

Dr. Akbari opined “molecular mimicry is accepted as a theory to explain causation of

autoimmune disease such as ITP.” 56 Pet. Ex. 40 at 11. He explained molecular mimicry is an

“immunological process of cross-reactivity” or the “sharing of antigens between a host and a

microorganism.” Id. He defined molecular mimicry as a “mechanism by which an immune

stimulated response by infection or other method, i.e. vaccination, can trigger cross-reactive

antibodies or T cells that cause the symptoms of autoimmune disease.” Id.

Dr. Akbari acknowledged that direct sequence homology between the flu vaccine and

ITP is not known. Pet. Ex. 40 at 11-2. But “despite no obvious amino acid sequence similarity,”

he asserted “mimicry can still happen at the host level.” Id. at 12. “Molecular mimicry is thus

occurring between two recognized peptides that have similar antigenic surfaces in the absence of

primary sequence homology.” Id. at 13.

Specific to this case, Dr. Akbari testified that the inflammasomes induced by the flu

vaccine directly activate autoreactive B cells 57 which produce IgM. Tr. 92. “Then[,] at the same

time, . . . inflammatory induction not only help[s] these autoreactive B cells and T cells, [] they

can [also] directly affect the generation and homeostasis of platelets.” Tr. 92-93. On cross-

examination, he specified that the molecular mimicry aspect of his theory focuses on IgM

produced from autoreactive B cells. Tr. 116; see also Pet. Ex. 155 (step three).

He opined severe and persistent cases of ITP are associated with T cells, while cases like

Petitioner’s are not due to “B cells lack[ing] adequate T cell assistance.” Pet. Ex. 88 at 15-16.

He explained that “B cells and antibodies may recognize self-proteins shortly after their

formation. Unlike T cells, B cells do not require antigen-presenting cells for activation and can

directly bind antigens with membrane-bound antibodies. Significantly, B cells also function as

55

Cytotoxic T lymphocyte-mediated cytotoxicity is an immune process by which T cells kill

their targets (other cells) by inducing apoptosis (cell death). T Cell-Mediated Immunity, in

Immunobiology: The Immune System in Health and Disease (Charles A. Janeway et al. eds., 5th

ed. 2001), https://www.ncbi.nlm.nih.gov/books/NBK27101/; Glossary, in Immunobiology: The

Immune System in Health and Disease, supra, https://www.ncbi.nlm.nih.gov/books/NBK10759/.

56

For general information on molecular mimicry, see, for example, Pet. Ex. 55 (Molecular

Mimicry: Infection-Inducing Autoimmune Disease (M.B.A. Oldstone ed., 2005)); Pet. Ex. 56

(Robert S. Fujinami et al., Molecular Mimicry, Bystander Activation or Viral Persistence:

Infections and Autoimmune Disease, 19 Clin. Microbiol. Revs. 80 (2006)).

57

Autoreactive B cells recognize and respond to self-antigens (autoantigens). See Autoreactive,

Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=5033

(last visited June 17, 2026).

24

antigen-presenting cells.” Id. at 16. This, according to Dr. Akbari, leads to ITP, albeit less

persistent cases of ITP due to the lack of T cell involvement, “within hours in some individuals.”

Id.; Pet. Ex. 115 at 6-7. Dr. Akbari provided no support for his opinion that onset of ITP could

occur within 24 hours if there is a lack of T cell involvement, or that molecular mimicry could

induce platelet destruction within one day.

Dr. Akbari summarized

the mechanism underlying this rapid response involves the complex interplay

between the innate and adaptive immune systems. The inflammasome arm, a

component of the innate immune system, when activated by vaccines, can

enhance the activity of autoreactive B cells. These B cells, part of the adaptive

immune system, produce antibodies that mistakenly target the body’s own tissues,

leading to adverse outcomes within [a] few hours.

Pet. Ex. 88 at 16 (emphasis omitted).

In his third report, he provided additional information to support his proposed mechanism

of autoreactive B cell molecular mimicry. Pet. Ex. 115 at 2-8. He explained that autoreactive B

cells and conventional B cells are distinct. Id. at 2-3; Tr. 93-94. Conventional B cells are part of

the adaptive immune system, are “responsible for producing antibodies that specifically target

and neutralize pathogens,” and antibody production and response “takes several days.” Pet. Ex.

115 at 2-3. In contrast, he opined that autoreactive B cells “mistakenly recognize and react

against the body’s own tissues, leading to autoimmunity,” and can be “[f]ast-acting.” Id. Dr.

Akbari added that conventional B cells “usually require help from T cells to become fully

activated,” while autoreactive B cells do not. Id. at 3.

Citing van den Broek et al., 58 Dr. Akbari opined “the process of autoreactive B cells

responding to antigen and contributing to the immune response can occur within a few hours.”

Pet. Ex. 115 at 3 (citing Pet. Ex. 116). However, the authors do not make this finding, they do

not discuss vaccination or flu vaccination, nor is ITP mentioned. Thus, the relevancy of this

article is unclear. And Dr. Akbari did not provide any other literature to support these opinions.

At the hearing, Dr. Akbari again opined autoreactive B cells act within minutes. Tr. 94.

For support, he explained autoreactive B cells produce IgM and cited a figure in Cines et al. 59

showing IgM levels in ITP patients. Tr. 94-95; Pet. Ex. 115 at 5; Pet. Ex. 117 at 5 fig.7. Dr.

Akbari opined that this figure suggested “IgM fast-producing antibodies from autoreactive B

cells are basically associated with ITP.” Tr. 95. However, the study was not related to how long

it took autoreactive B cells to act/activate. The authors studied ITP patients “for the presence of

58

T. van den Broek et al., Invasion of Spontaneous Germinal Centers by Naïve B Cells Is Rapid

and Persistent, 2023 bioRxiv [Preprint] 1, https://www.biorxiv.org/content/10.1101/2023.05.30.

542805v2. This appears to be a preprint and the source is not clear.

59

Douglas B. Cines et al., Platelet Antibodies of the IgM Class in Immune Thrombocytopenic

Purpura, 75 J. Clin. Invest. 1183 (1985).

25

IgM anti-platelet antibodies” and found these antibodies in some of the patients with ITP. Pet.

Ex. 117 at 1. The study does not support rapid onset of ITP consistent with the facts of this case.

Further, it does not relate to vaccination.

3. Additional Medical Literature

Dr. Akbari agreed ITP post-flu vaccination is rare, but emphasized that “rarity does not

negate the potential for adverse effects.” Pet. Ex. 88 at 15.

Like Dr. Ghose, Dr. Akbari cited to Garbe et al. and Mantadakis et al. as support that the

flu vaccine can cause ITP. Pet. Ex. 40 at 10 (citing Pet. Ex. 53); Pet. Ex. 88 at 14; see also Tr.

99-101 (citing Pet. Exs. 38, 53).

He also cited a study from Huang et al., 60 which examined passive reports of adverse

events following the 2009 H1N1 vaccine in Taiwan. Pet. Ex. 40 at 10 (citing Pet. Ex. 52 at 1);

Pet. Ex. 88 at 14. ITP was included as an adverse event. Pet. Ex. 52 at 2. The authors made no

findings or conclusions about an association between ITP and the H1N1 vaccine or increased

risk of ITP post-H1N1 vaccination.

The authors in Cecinati et al. 61 noted that “[v]accine-related thrombocytopenia is

considered to be of immune origin because antibodies can be detected on platelets in about 79%

of cases.” Pet. Ex. 105 at 1. Based on data from surveillance systems, they reported that cases

of ITP following vaccination are generally infrequent and less severe. Id. at 2. The authors also

noted that the “[t]rivalent inactivated [flu] vaccine [] has been associated with ITP in a very

small number of adult case reports,” as well as a surveillance study by Garbe et al. Id. at 3

(citing Pet. Ex. 53).

Dr. Akbari also cited Nakayama and Onoda, 62 who examined cases reported in the post-

marketing surveillance of the Kitasato Institute and noted two ITP cases were reported among

38.02 million doses of the flu vaccine. Pet. Ex. 108 at 1, 5. The authors made no findings

related to flu vaccination and ITP.

60

Wan-Ting Huang et al., The Reporting Completeness of a Passive Safety Surveillance System

for Pandemic (H1N1) 2009 Vaccines: A Capture–Recapture Analysis, 30 Vaccine 2168 (2012).

This was also filed as Pet. Exs. 103, 146.

61

Valerio Cecinati et al., Vaccine Administration and the Development of Immune

Thrombocytopenic Purpura in Children, 9 Hum. Vaccines & Immunotherapeutics 1158 (2013).

62

Tetsuo Nakayama & Kazumasa Onoda, Vaccine Adverse Events Reported in Post-Marketing

Study of the Kitasato Institute from 1994 to 2004, 25 Vaccine 570 (2007).

26

Lastly, Dr. Akbari cited a case report from Yamamoto et al. 63 of severe

thrombocytopenia within one day of flu vaccine with diffuse alveolar hemorrhage leading to

respiratory failure. Pet. Ex. 115 at 17 (citing Pet. Ex. 145). The authors stated that “[t]he onset

of vaccine-related ITP has a strict time relationship, developing within 4-35 days after [flu]

vaccination.” Pet. Ex. 145 at 4. Theu further noted that “although [the patient] had potentially

been sensitized by [a] previous vaccination, vaccine-related ITP may also have been

incompatible given the too-short latency time. Other pathogeneses of thrombocytopenia might

therefore have been involved; however, the pathogenesis of vaccine-related thrombocytopenia

remains unknown.” Id. They concluded that the role of the flu vaccine “remains unclear, and

further investigations are required.” Id.

iii. Althen Prongs Two and Three

Dr. Akbari opined “more likely than not” the flu vaccination caused Petitioner’s ITP via

molecular mimicry and induction of inflammasomes. Tr. 80; Pet. Ex. 40 at 1; Pet. Ex. 88 at 27;

Pet. Ex. 115 at 18.

He summarized that “[Petitioner,] as a result of receiving a[] [flu] vaccine on October 16,

2019, first developed immediate hypersensitivity,[64] as evident by symptoms such as shivering,

petechiae at the site of the injection, on her face, and inside her mouth,” which are “signs []

associated with induction of inflammasome and related pathways, induced by [flu] vaccine,” and

which resulted in ITP. Pet. Ex. 40 at 4, 17-18; see also Tr. 98-99, 114-15. Dr. Akbari added that

delayed hypersensitivity reactions 65 in ITP (e.g., petechiae, chills, fever, fatigue, nausea, and

tachycardia), often occur within hours or days after vaccine administration and are accompanied

by a variety of cytokines, chemokines, and complements. Pet. Ex. 40 at 5; see also Tr. 103-04.

Dr. Akbari opined this timing supports the flu vaccine as the most logical sequence of

cause and effect. Pet. Ex. 40 at 17-18. He postulated that ITP occurring within one day of flu

vaccination “suggests that either autoreactive B cells and/or innate cells were involved in the

induction of ITP.” Pet. Ex. 115 at 6-7; see also Tr. 122; Pet. Ex. 88 at 27 (concluding “the

timing between the vaccine administration and the symptom development aligns with the role of

63

Yuji Yamamoto et al., Influenza Vaccination-Associated Acute Thrombocytopenia and

Diffuse Alveolar Hemorrhage, 59 Intern. Med. 1633 (2020).

64

An immediate hypersensitivity reaction is a “mediated by antibodies and develop[s] rapidly,

generally in minutes to hours,” and can be “distinguished from those mediated by T lymphocytes

and macrophages and generally requiring 24 to 72 hours to develop ( . . . sometimes called

delayed hypersensitivity [reactions]).” Immediate Hypersensitivity Reaction, Dorland’s Med.

Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=102389 (last visited

June 17, 2026).

65

A delayed hypersensitivity reaction is “a reaction of cell-mediated immunity, named in

contrast to immediate hypersensitivity reactions because its onset is 24 to 72 hours after the

antigenic challenge.” Delayed Hypersensitivity Reaction, Dorland’s Med. Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=102357 (last visited June 17, 2026).

27

B cells and induction of inflammasome, establishing a logical sequence of cause and effect

between [Petitioner’s] vaccination and [her] subsequent adverse reactions”). “The rapid

induction of inflammasome within a short timeframe leads to robust immune responses triggered

by molecular mimicry, which can subsequently aggregate symptoms associated with ITP.” Pet.

Ex. 88 at 27.

Dr. Akbari opined Petitioner’s vaccine contained HA from several strains of the flu virus,

including the H1N1 proteins measured in Crooke et al. Pet. Ex. 40 at 8. However, he did not

cite any support for this statement. At the hearing, Dr. Akbari agreed Petitioner’s flu vaccine did

not contain a live virus. Tr. 139. Although Petitioner’s vaccine record indicated she received a

quadrivalent flu vaccination (Flucelvax), no package insert was provided to show the viral strains

or specific ingredients of Petitioner’s vaccine. See Tr. 139-40; Pet. Ex. 1 at 26.

Additionally, Dr. Akbari testified that there was no alternative cause for Petitioner’s ITP.

Tr. 101.

As to timing, Dr. Akbari opined Petitioner’s onset of symptoms was a “few hours” after

her flu vaccination as evidenced by her hypersensitivity reactions. Pet. Ex. 40 at 18; Tr. 102-03.

The hypersensitivity reactions were then “followed by induction of ITP [a] few days after

administration of flu vaccine.” Pet. Ex. 40 at 18.

At the hearing, however, he placed onset of Petitioner’s ITP when Petitioner’s blood

work showed her low platelet level, which was within or around one day but not within hours.

Tr. 107, 126. He opined Petitioner did not have ITP prior to receiving her platelet count of five

the day after vaccination. Tr. 126.

He testified that this timing (one day) is medically appropriate because inflammasomes,

which are part of the innate immune system, peak at one day. Tr. 107, 120; Pet. Ex. 40 at 18.

He cited Christian et al. to support a one-day onset. Tr. 104-06 (citing Pet. Ex. 48 at 11 fig. 1).

However, Christian et al. examined only local reactions post-vaccination and serum

proinflammatory cytokines when finding cytokines elevated one-day post-vaccination. See Pet.

Ex. 48 at 11 fig. 1. Timing as it relates to an adaptive immune response was not discussed or

studied in Christian et al. See id. Dr. Akbari did not acknowledge the other steps of his theory

that he asserted must take place in order for platelets to be destroyed, including aspects that

require induction of the adaptive immune system. See, e.g., Pet. Ex. 155 (demonstrative

showing Dr. Akbari’s four-step theory).

Additionally, he testified that the timing between vaccination and onset depends on the

type of vaccine and patient; “it can happen within a few minutes to . . . a few months.” Tr. 102-

03. However, he also testified that several reports of ITP following various vaccinations have

shown an acceptable time frame to be “within one day to a few weeks.” Tr. 107.

Dr. Akbari acknowledged “a primary antibody response is evident within one to two

weeks after vaccination. During this period, . . .autoreactive B cells, if present, can also become

activated. This rapid response is crucial for providing immediate protection against the virus but

also means that any potential autoreactivity can manifest relatively quickly.” Pet. Ex. 115 at 6.

28

However, Petitioner’s “rapid response” was within one day, not one to two weeks post-

vaccination.

Lastly, Dr. Akbari admitted that “[he] believe[d], the significance of a temporal

relationship, denoting a close proximity in time between vaccination and the emergence of

symptoms or injury, stands out as one of the most compelling aspects in the context of this case.”

Pet. Ex. 115 at 17.

3. Respondent’s Expert, Dr. Lisa Baumann Kreuziger 66

a. Background and Qualifications

Dr. Baumann is board certified in hematology and oncology. Resp. Ex. A at 1; Resp. Ex.

H at 3. She graduated from the University of Wisconsin-Madison, School of Medicine and

Public Health in 2006 with her M.D. and thereafter completed an internal medicine residency at

the Mayo Clinic, a fellowship at the University of Minnesota, and an M.S. in clinical research at

the University of Minnesota. Resp. Ex. H at 1. Since 2013, Dr. Baumann has held various

faculty, administrative, and hospital staff appointments. Id. at 2. She has authored or co-

authored over 100 publications. Id. at 19-29.

Dr. Baumann “routinely care[s] for patients with hematologic disorders including [ITP]”

and “ha[s] treated over 30 patients with ITP.” Resp. Ex. A at 1. She was admitted, without

objection, as an expert in hematology and epidemiology. Tr. 279.

b. Opinion

i. Severity Requirement

Dr. Baumann explained that “ITP is an autoimmune disorder where the immune system is

activated against and destroys platelets.” Tr. 279. Clinically, ITP manifests with low platelet

counts and bleeding. Tr. 280. According to Dr. Baumann, ITP patients are considered to have

“active ITP” when their platelet counts are low. Tr. 308, 314. Thus, “[w]hen platelet counts are

normal, ITP is not active.” Tr. 314.

First, Dr. Baumann does not dispute that “fatigue is associated with active ITP.” Tr. 308;

see also Tr. 312 (agreeing “[f]atigue is a symptom of active ITP”). She noted she routinely

questions her patients about fatigue. Tr. 288. She explained that “when platelet counts are low,

fatigue can be present,” and the fatigue could be due to the disease or disease-related treatment.

Tr. 288-89. However, she opined that when patients do not have active disease (i.e., when

platelet counts are normal), complaints of fatigue are not due to ITP. Tr. 290, 313-14 (testifying

that “if somebody would tell [her] that they had fatigue and their platelet count was normal, []

[she] would tell them [] that their fatigue is not due to ITP”).

66

Dr. Baumann provided two expert reports and testified at the entitlement hearing. Resp. Exs.

A, C; Tr. 272.

29

She explained that if an ITP patient is complaining of fatigue when they have normal

platelet counts, “[she] would look at the patient’s hemoglobin, because anemia or low

hemoglobin can also cause fatigue. If that’s also normal, [she] would . . . look at iron, [and] the

other things that are within the hematology purview that cause fatigue.” Tr. 289. If those are

also normal, she would then tell her patients that there is not a “blood reason for [their] fatigue”

and other, non-blood related reasons could be a potential cause of their fatigue, as “fatigue is

caused by a lot of things.” Tr. 288-89.

As to Petitioner specifically, Dr. Baumann opined Petitioner “experienced acute ITP . . .

from 10/17/19 to 10/23/19,” a total of six days, and since then, she “has had normal platelet

counts and no further reports of petechiae, spontaneous bruising, or gum bleeding.” Resp. Ex. A

at 5, 9; see also Resp. Ex. C at 7-8; Tr. 285-86. Thus, Dr. Baumann opined Petitioner has not

suffered from active ITP since October 23, 2019. Tr. 286, 288, 294.

Regarding Petitioner’s argument that she had fatigue due to her ITP that lasted more than

six months, Dr. Baumann disagreed and opined “[f]atigue was noted intermittently prior to

vaccination and the assertion that it persisted [more than] [six] months after vaccination was not

corroborated by [Petitioner’s] physicians or in the documentation she filled out prior to physical

therapy” in June 2020 for an unrelated issue. Resp. Ex. A at 6, 9; see also Resp. Ex. C at 6-8.

She first noted “[f]atigue can be due to multiple factors” and Petitioner had documented

episodic fatigue prior to her flu vaccination. Resp. Ex. A at 6 (citing Pet. Ex. 2 at 2, 6, 18); Resp.

Ex. C at 6 (“The symptom of fatigue reported by [Petitioner] does not correlate to the

pathophysiology of fatigue in ITP due to activation of the inflammasome because fatigue

preceded her diagnosis of ITP . . . .”).

Next, Dr. Baumann discussed how the medical records do not support Petitioner’s

assertion that she experienced fatigue for more than six months. Resp. Ex. A at 6; Resp. Ex. C at

6-7; Tr. 296-99. In May 2020, fatigue was not mentioned or documented during a telehealth

visit with Dr. Dammrich, though an email from Petitioner to her counsel later that month did

document fatigue. Resp. Ex. C at 7 (citing Pet. Ex. 5 at 36-37; Pet. Ex. 6 at 1). In June 2020,

Petitioner filled out records for her knee surgery, and in these handwritten records, she did not

mark she was suffering from “fatigue.” Tr. 296-98 (citing Pet. Ex. 8 at 32; Pet. Ex. 9 at 54);

Resp. Ex. C at 7. Because “she had the ability . . . to write [fatigue] herself, and it was not

noted,” Dr. Baumann opined Petitioner was not suffering from fatigue in June 2020. Tr. 298-99.

And at another visits with Dr. Dammrich in June 2020, he wrote Petitioner’s “platelet count has

remained normal as of end of May and she has no symptoms to suggest it has fallen.” Resp. Ex.

C at 7 (quoting Pet. Ex. 4 at 14). Fatigue was not mentioned at that visit. Id.

Thus, she concluded “there is not corroborated evidence that an effect of ITP persisted

for [six] months, particularly in the continued presence of normal platelet counts” as well as a

lack of need for medication. Resp. Ex. A at 6; see also Resp. Ex. C at 7.

Dr. Baumann acknowledged that Petitioner complained of fatigue in November 25, 2019,

as documented in her medical records, despite having normal platelet counts and no longer

30

receiving ITP treatment (steroids) at that time. Tr. 316. She did not further comment on this

record.

Lastly, Dr. Baumann addressed literature cited by Dr. Ghose regarding fatigue in the

presence of ITP. Dr. Baumann opined that Dr. Ghose’s literature linking fatigue to ITP applies

to only those with active ITP. Tr. 308, 314. And this literature, Dr. Baumann added, pertains

only to patients with chronic ITP, as they are “easier to study.” Tr. 309; see also Resp. Ex. A at

5. Thus, she opined that this literature only “tells us [] that when ITP is active, there is evidence

of impacts on fatigue and quality of life,” which she does not dispute. Tr. 308-09, 312.

For example, Dr. Baumann noted McMillan et al., cited by Dr. Ghose, was a study that

examined impact to quality of life in patients with chronic ITP. Resp. Ex. A at 6 (citing Pet. Ex.

12). She noted that the authors documented study limitations, including the failure of the study

to look at “how much of the reduced [health related quality of life] in ITP was related to the

disease itself (e.g., lack of energy that is often reported by patients and appears to be related to a

low platelet count) rather than effects of treatment.” Id. (quoting Pet. Ex. 12 at 4). “In addition,

measurement of platelet counts was not one of the study assessments, thus correlations between

platelet counts and [health related quality of life] scores could not be examined.” Pet. Ex. 12 at

4. McMillan et al. do not indicate their study pertains only to patients with chronic ITP.

On cross-examination, Dr. Baumann was questioned about a review from Al-Samkari

and Kuter. 67 Tr. 314-15 (citing Resp. Ex. A2). The authors noted fatigue was “[t]he most

common symptom in ITP aside from bleeding” and is seen in 20-40% of patients. Resp. Ex. A2

at 2. They further wrote, “[a]lthough the etiology is not entirely clear, fatigue can markedly

affect quality of life in ITP patients and may even be an indication for treatment, which may be

very effective at alleviating fatigue.” Id. Dr. Baumann maintained that fatigue resolved with

higher platelet counts. Tr. 315.

Dr. Baumann was also questioned on cross-examination about Grace et al. and agreed

that the authors surveyed both acute and chronic ITP patients. Tr. 316 (citing Pet. Ex. 153). She

further agreed that the authors noted “[f]atigue scores at [one] and 12 months did not differ

significantly depending on whether patients were platelet responders to therapy.” Tr. 317

(quoting Pet. Ex. 153 at 6).

ii. Althen Prong One

According to Dr. Baumann, “ITP is an autoimmune disorder and why autoimmunity

occurs is not fully understood for most autoimmune diseases.” Tr. 311; see also Resp. Ex. A at

6.

Dr. Baumann explained “[t]he autoimmune mechanism at play in ITP is an activation of

[] T cells, which can directly kill platelets, and [] B cells, which produce autoantibodies against

67

Hanny Al-Samkari & David J. Kuter, Immune Thrombocytopenia in Adults: Modern

Approaches to Diagnosis and Treatment, 46 Semin. Thromb. Hemost. 275 (2020).

31

platelets. Anything with an antibody on it, [the] body then recognizes that to be destroyed.” Tr.

318. T cells “can kill platelets once they’re activated,” which “generally takes minimum of

[five] to 10 to 14 days” with the adaptive immune system. Tr. 318-19. With autoantibodies, the

timing of their production depends on whether it is a primary exposure (seven to 14 days) or

secondary exposure (about three days). Tr. 319-20. She opined the mechanism by which ITP

occurs would be the same regardless of the inciting agent. 68 Tr. 322.

As for Dr. Ghose’s theory of molecular mimicry, Dr. Baumann opined “molecular

mimicry is not a scientifically reliable mechanism by which [the flu] vaccine could cause ITP.”

Resp. Ex. A at 8. She took issue with the fact that Dr. Ghose did not provide any information as

to how molecular mimicry could occur, or more specifically, that he did not indicate a similar

molecular structure between the flu vaccine and platelet antigens, which she acknowledged has

not been identified despite extensive research. Id.

Dr. Akbari and Dr. Ghose also posited a hypersensitivity/inflammasome theory to

account for Petitioner’s symptoms beginning within 24 hours of vaccination, which Dr.

Baumann also disagreed with. Resp. Ex. C at 5-6. She cited to Siegrist to show the process by

which the immune system responds to vaccination, which “extends well beyond 24 hours.” Id. at

5 (citing Pet. Ex. 42 at 6 fig. 2.1, 9 fig. 2.3). Specifically, Siegrist explained the process that

occurs following vaccination:

Following injection (1), the pathogen-associated patterns contained in vaccine

antigens attract dendritic cells, monocytes, and neutrophils that patrol throughout

the body (2). Elicitation of sufficient “danger signals” by the vaccine antigens

[]/adjuvants [] activates monocytes and dendritic cells (3); the activation changes

their surface receptors and induces their migration along lymphatic vessels (4), to

the draining lymph nodes (5) where the activation of T and B lymphocytes will

take place.

Pet. Ex. 42 at 6 fig. 2.1.

Dr. Baumann also criticized other literature from Dr. Akbari and Dr. Ghose and opined

“a reliable and more likely than not mechanism of how inflammasome activation leads to

thrombocytopenia within 24 hours was not provided.” Id. at 6.

Even though she agreed there is an “associated link” between the MMR vaccine and ITP,

Dr. Baumann opined it is not permissible to impute that data to other vaccines like the flu

vaccine, in part because the MMR vaccine is a live vaccine and the flu vaccine is not. Tr. 300-

68

For more information on the mechanism by which platelets are destroyed and produced, see,

for example, Resp. Ex. A1 (Maurice Swinkles et al., Emerging Concepts in Immune

Thrombocytopenia, 9 Front. Immunol. 1 (2018)); Resp. Ex. A15 (Renata Grozovsky et al.,

Regulating Billions of Blood Platelets: Glycans and Beyond, 126 Blood 1877 (2015)).

32

01; Resp. Ex. A at 8; see also Resp. Ex. A17 (reviewing how different vaccine types generate

immune responses). 69

She agreed the flu infection, as well as other infections, can cause ITP. Tr. 311-12; Resp.

Ex. A at 6. As to flu infection specifically, she cited literature that has shown the flu virus must

be present for thrombocytopenia to occur. Resp. Ex. A at 8 (citing Resp. Ex. A16). 70

Kazatchkine et al. evaluated how antibodies could cause complement-mediated platelet lysis.

Resp. Ex. A16 at 1. Their study showed “incubation of human platelets with suspensions of [flu]

virus, but not with bacterial neuraminidase, results in completement and antibody-mediated lysis

of platelets . . . [with] [t]he crucial event [being] the interaction of immunoglobulins with a viral

[HA] present on the platelet membrane.” Id. at 1-2. Dr. Baumann cited this article to show

“[v]iral replication does not occur after [flu] vaccination because [the vaccine uses] an

inactivated virus and thus viral [HA] is not present in significant amounts to bind to the platelet

surface.” Resp. Ex. A at 8 (citing Resp. Ex. A16). Therefore, the flu vaccine is not likely to

cause ITP because it is an inactivated vaccine. Id.

Next, Dr. Baumann addressed the epidemiological evidence between the flu vaccine and

ITP and concluded “the preponderance of evidence from well controlled and large studies has

not found as association between [flu] vaccination and ITP.” Resp. Ex. A at 7; see also Tr. 303.

She acknowledged there was one study (Garbe et al.) that suggested a “potential association,”

however, she opined “there were biases within that study” 71 and subsequent studies have not

shown an association between the flu vaccine and ITP. Tr. 303 (citing Pet. Ex. 53); see also

Resp. Ex. C at 4.

Dr. Baumann discussed a large case control study by Grimaldi-Bensouda et al. 72 that did

not find an association between the flu vaccine and ITP. Tr. 306-07 (citing Resp. Ex. A9).

Grimaldi-Bensouda et al. conducted a large case control study in France with 198 ITP cases and

878 controls, of which 66 ITP cases and 303 controls received a vaccination within 12 months of

“index date” (i.e., symptom onset). Resp. Ex. A9 at 1, 3. There was no evidence of an increase

in ITP after vaccination in the previous six and 12 months, and though there was a higher odds

ratio for all vaccines within the two-month period of onset, the increase was not statistically

significant. Id. at 1, 3-4, 5 tbl. 3. The authors concluded that common vaccines, including the flu

vaccine, are not associated with a risk of developing ITP. Id. at 1, 5.

69

David Baxter, Active and Passive Immunity, Vaccine Types, Excipients and Licensing, 57

Occup. Med. 552 (2007).

70

Michel D. Kazatchkine et al., Membrane-Bound Hemagglutinin Mediates Antibody and

Complement-Dependent Lysis of Influenza Virus-Treated Human Platelets in Autologous

Serum, 74 J. Clin. Invest. 976 (1984).

71

For these biases, see Tr. 305-06; Resp. Ex. C at 4.

72

Lamiae Grimaldi-Bensouda et al., A Case-Control Study to Assess the Risk of Immune

Thrombocytopenia Associated with Vaccines, 120 Blood 4938 (2012). This was also filed as

Resp. Ex. D6.

33

Dr. Baumann next cited Rajantie et al. 73 Resp. Ex. A11. In Rajantie et al., 506 Nordic

children (up to age 14) were diagnosed with ITP during a three-year period. Id. at 1. The

authors studied only those patients whose onset of ITP occurred within one month of vaccination

(35 total patients). Id. at 1-2. None of the children received the flu vaccine. 74 Id. at 2. Thus, the

relevancy of this study to this case is not clear.

O’Leary et al. 75 examined the risk of ITP after childhood vaccinations other than MMR.

Resp. Ex. A12 at 1. The authors identified a cohort of 1.8 million children aged six weeks to 17

years, and within that cohort, there were 197 confirmed cases of ITP. Id. at 1-3. The authors

found “no increased risk of ITP after vaccines other than MMR in young children.” Id. at 1. In

older children, they found “ITP may occur after certain other vaccines,” however, this did not

include the flu vaccine. Id. at 1, 6. For cases of ITP after the trivalent flu vaccine specifically,

the authors found “several [incident rate ratios] that approached statistical significance in older

children,” though “estimates in older children are less stable because there are fewer cases of ITP

on which to perform analyses.” Id. at 4.

And lastly, she cited Lafaurie et al., 76 a French study that found no increased risk of ITP

following flu vaccination when using three different designs and multiple sensitivity analyses.

Resp. Ex. C at 4 (citing Resp. Ex. C1). Their main limitation, according to the authors, was that

the patients in their study were those with the “most severe” ITP, while mild and transient ITP

patients were not included. Resp. Ex. C1 at 2.

Overall, she summarized that there was “one flawed case control study [that] suggested

an association between [flu] vaccination and ITP” and “three large case-control studies and one

cohort study [that] did not find an association.” Resp. Ex. C at 4. Dr. Baumann concluded

“these large well controlled studies are evidence that there is more likely than not no association

between [flu] vaccination and ITP.” Id.

As for Dr. Ghose’s case reports, she testified that case reports are not sufficient to show

an association between an inciting event and an outcome; they are used to “generate hypotheses”

73

J. Rajantie et al., Vaccination Associated Thrombocytopenic Purpura in Children, 25 Vaccine

838 (2007).

74

In Nordic countries, “[p]ersons 65 years and above, pregnant women[,] and persons with

certain underlying diseases (including children) are recommended [to have] annual, seasonal

vaccination against [flu].” Recommended Vaccinations, Publ. Health Agency Swed.,

https://www.folkhalsomyndigheten.se/the-public-health-agency-of-sweden/communicable-

disease-control/vaccinations/recommended-vaccinations/ (last updated Sept. 1, 2025).

75

Sean T. O’Leary et al., The Risk of Immune Thrombocytopenic Purpura After Vaccination in

Children and Adults, 129 Pediatrics 248 (2012).

76

Margaux Lafaurie et al., Risk of Immune Thrombocytopenia After Influenza Vaccine, 182

JAMA Internal Med. 444 (2022). This was also filed as Resp. Ex. D5.

34

and to show the scientific community what needs to be looked into further. Tr. 300; see also

Resp. Ex. A at 7, 9. Thus, she opined that case reports do not show causation between the flu

vaccine and ITP. Tr. 302. She concluded “the weight of the medical literature does not support

an association between the [flu] vaccination and ITP.” Resp. Ex. A at 9.

iii. Althen Prongs Two and Three

Dr. Baumann opined Petitioner’s October 16, 2019 flu vaccination did not cause her to

develop ITP. Tr. 309-10; Resp. Ex. A at 7, 9; Resp. Ex. C at 8. Her opinion is based on three

reasons: (1) “there is no reliable and more likely than not mechanism demonstrated by which the

[flu] vaccination can cause ITP;” (2) “the timing of onset does not support the association

between vaccination and ITP for [Petitioner];” and (3) the “weight of medical literature favors

that there is no relationship between ITP and the [flu] vaccine.” Resp. Ex. A at 7.

She agreed Petitioner did not have any pre-existing conditions, infections, or other

etiologies that could have caused her ITP, although “[she] was not tested for viral infections or

other underlying etiologies.” Resp. Ex. A at 6 (“Without a known association, she would be

considered to have primary ITP.”); see also Tr. 312.

As for timing, Dr. Baumann opined Petitioner developed ITP “within 24 hours after [flu]

vaccination,” and this “timing of onset is faster than immune system activation and platelet

clearance would allow” and “is not supported by the proposed mechanism.” Resp. Ex. C at 6, 8;

see also Resp. Ex. A at 9 (“This timing is shorter than would be expected for an association

between antibody production after vaccination and development of ITP.”).

While Petitioner testified that she had received prior flu vaccinations, Dr. Baumann

opined that she did not know the flu strains in the prior vaccinations. Tr. 320. Dr. Baumann

testified that it depends on what flu vaccines she had previously received, and the strains in those

vaccines. 77 Id. “[I]f the same strains were [received] and [] an autoantibody was produced from

that specific strain, [the timing] still would be three days” for a secondary exposure. Id.

Dr. Baumann testified that symptoms like petechiae generally “take[] days, if not longer”

to manifest. Tr. 321. Thus, she disagreed with Dr. Ghose’s assertion that Petitioner’s platelet

decrease within one to two days of vaccination “confirm[ed] the immune mediated nature of the

disease that characterizes ITP.” Resp. Ex. A at 8 (quoting Pet. Ex. 10 at 6).

In her first report, she explained the events that occur in order for petechiae to develop in

ITP:

[A]utoantibodies to platelets are produced, platelets are cleared from the blood

stream, and spontaneous bleeding into the skin occurs from damage to the blood

vessels. When the body is exposed to an inactivated vaccine such as the [flu]

vaccine, the virus is phagocytosed by dendritic cells. Antigen fragments are

presented on the cell surface of the dendritic cell. TH2-cells and B-cells will

77

This information was not provided.

35

become activated upon binding to the dendritic cell. The activated TH2 cell

produces cytokines which allow B-cells to differentiate and proliferate. B-cells

then produce antibodies against the foreign antigen (i.e. [flu]). This process takes

10-14 days.

Resp. Ex. A at 8; see also Resp. Ex. C at 5 (“For symptoms of ITP to occur, the immune system

is activated against platelets, platelets need to be cleared from the system, and petechia need to

form by breaking small blood vessels.”). Therefore, Petitioner’s timing of less than 24 hours

after vaccination “is shorter than would be expected for an association between antibody

production after vaccination and development of ITP.” Resp. Ex. A at 9.

Overall, Dr. Baumann concluded “the timing is insufficient for the purported mechanism

and does not reliably explain how a six-day episode of ITP [from] October 17, 2019[] to October

23, 2019 could result in alleged persistent fatigue in the absence of any other evidence of ITP.”

Resp. Ex. C at 7.

4. Respondent’s Expert, Dr. You-Wen He 78

a. Background and Qualifications

Dr. He is currently a Professor of Integrated Immunobiology at Duke University Medical

Center. Resp. Ex. G at 1. Dr. He received his M.D. from the Fourth Military Medical University

in Xian, China and his Ph.D. in Microbiology and Immunology from the University of Miami

School of Medicine in Miami, Florida. Id. His research areas include “innate and adaptive

immunity against viral and bacterial infections, as well as tumors.” Resp. Ex. D at 1. He has

conducted research on human immune responses to viral infections and is currently a Co-

Principal Investigator for clinical trials focusing on cancer immunotherapy. Id. Dr. He has

reviewed National Institutes of Health studies, served on editorial boards, and has authored or

co-authored numerous publications. Id. at 1-2; Resp. Ex. G at 2-3, 7-17.

Dr. He is not a hematologist. Tr. 211. He does not have experience treating ITP patients.

Tr. 211, 259. He does not treat patients in the United States, but does see patients in his home

country of China. Tr. 211. Dr. He has not published on ITP, nor has his research focused on ITP

or platelets. Tr. 259. Dr. He was admitted as an expert in immunology, without objection, with

his testimony focusing on the theory presented and related research. Tr. 211-12.

b. Opinion

Dr. He opined “to a reasonable degree of medical certainty[,] that there is no reliable

evidence to support [Petitioner’s] theory that the [flu] vaccine caused [Petitioner’s] ITP.” Resp.

Ex. D at 26; see also Resp. Ex. F at 21-22.

78

Dr. He provided two expert reports and testified at the entitlement hearing. Resp. Exs. D, F;

Tr. 149, 272.

36

i. Althen Prong One

Dr. He opined the flu vaccine cannot cause ITP and there is no evidence to support a

causal link between flu vaccination and ITP. Tr. 259; Resp. Ex. at 4.

He explained the innate immune system is the “first line of defense” and acts as a signal

to activate an adaptive immune response, which provides protection from the antigen/stimulus.

Tr. 215; see also Resp. Ex. F8 at 1. 79 During an innate immune response, various cells are

involved and over the course of approximately three days, these cells are activated and send

signals to the T and B lymphocytes to activate the adaptive immune response, which provides a

host’s immune system with “memory” to enable a more rapid and efficient immune response

upon subsequent exposures. Tr. 215-18; see also Resp. Ex. F8 at 1-2, 4. Thus, with an adaptive

immune response, there is a lag time between antigen exposure and response, which typically

takes five to 10 days. Resp. Ex. F at 14; see also Resp. Ex. F8 at 1. This timing is faster with a

memory response (i.e., a response to a previously encountered stimulus) than a primary response

(i.e., a response to a newly encountered stimulus). Tr. 218; Resp. Ex. F at 14-15 (“The time for

antigen-specific B cells to be activated and become antibody secreting cells [] upon primary

vaccination takes 8-10 days while the time for secondary vaccination takes 5-7 days.”).

Although “[t]he pathogenesis of primary ITP remains to be fully understood,” Dr. He

opined both the innate and adaptive immune responses are involved. Resp. Ex. D at 3; see also

Resp. Ex. F at 13-14, 21-22; Tr. 213. Dr. He found no literature or evidence showing that any

cells involved in the innate immune response destroy platelets. Tr. 216-17; Resp. Ex. F at 13.

Dr. He testified that from his review of the literature, it is “very clear” that ITP is an adaptive

immune-mediated response. Tr. 213; see also Resp. Ex. F at 13-14.

He explained that “[t]he predominant cause of thrombocytopenia is due to reduced

platelet lifespan caused by autoimmune reactions including autoantibodies and autoreactive

cytotoxic T cells against platelets as well as humoral and cellular autoimmunity against

megakaryocytes.” Resp. Ex. D at 3 (citing Resp. Ex. D1 at 1, 4). 80 The autoantibodies targeting

79

Jean S. Marshall et al., An Introduction to Immunology and Immunopathology, 14 Allergy

Asthma Clin. Immunol. 5 (2018).

80

Donald M. Arnold & Adam Cuker, Immune Thrombocytopenia (ITP) in Adults: Clinical

Manifestations and Diagnosis, UpToDate, https://www.uptodate.com/contents/immune-

thrombocytopenia-itp-in-adults-clinical-manifestations-and-diagnosis (last updated July 5, 2023).

An updated version (last updated July 26, 2023) was filed as Resp. Ex. F6.

37

platelets or platelet antigens destroy circulating platelets “through Fc-mediated phagocytosis[81]

in the spleen and other reticuloendothelial tissues,” leading to reduced platelet production. Id.

(citing Resp. Ex. D2 at 2). 82 He added that cytotoxic T cells may have a direct lytic effect. Id.

(citing Resp. Ex. D2 at 2). Thus, because “the pathogenesis of ITP is mediated by anti-platelet

autoantibodies and autoreactive antigen specific cytotoxic T cells,” both the innate immune

system and the adaptive immune systems are at play. Id. at 9; see also Tr. 213; Resp. Ex. F8

(providing an overview of innate and adaptive immunity).

Dr. He next addressed the literature, opining there is no evidence causally linking the flu

vaccine to ITP. Resp. Ex. D at 3, 26. For support, he cited a vaccine safety review from Dudley

et al. 83 that used data compiled in the 2012 Institute of Medicine (“IOM”) Report and the 2014

Agency for Healthcare Research and Quality (“AHRQ”) Report to assess causal associations of

adverse events post-vaccination. Resp. Ex. D3 at 1 (citing Resp. Ex. D7; 84 Resp. Ex. D8; 85

Resp. Ex. D9). 86 Dr. He noted that the study did not identify an association between the flu

vaccine and ITP. Resp. Ex. D at 4 (citing Resp. Ex. D3 at 4, 4 tbl. 1). However, Dudley et al.

acknowledged that the 2012 IOM Report and the AHRQ Report did not assess a relationship

between ITP and flu vaccination. See Resp. Ex. D3 at 7 (“The IOM report only assessed the

81

Fc receptors are “specific cell-surface receptors for antigen-antibody complexes or aggregated

immunoglobulins that bind a site in the Fc portion of the immunoglobulin molecule and may

exhibit specificity for particular immunoglobulin classes. Fc receptors are found on B cells, K

cells, macrophages, neutrophils, and eosinophils, and, during some developmental stages, on T

cells; those on K cells, macrophages, and neutrophils bind to opsonizing antibodies bound to

antigens and trigger phagocytosis of the antigen.” Fc Receptors, Dorland’s Med. Dictionary

Online, https://www.dorlandsonline.com/dorland/definition?id=102550 (last visited June 17,

2026). Phagocytosis refers to the internalization or endocytosis of particulate matter, such as

microorganisms or cell fragments, and results in the material being engulfed and killed.

Phagocytosis, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/

dorland/definition?id=38307 (last visited June 17, 2026); Glossary, supra note 55.

82

Syed Mahamad et al., Proceedings of the Immune Thrombocytopenia Summit: New Concepts

in Mechanisms, Diagnosis, and Management, 7 Res. Pract. Thromb. Haemost. 1 (2023).

83

Matthew Z. Dudley et al., The Safety of Vaccine Safety Science: Systematic Reviews of the

Evidence, 20 Lancet Infect. Dis. e80 (2020).

84

Inst. of Med., Adverse Effects of Vaccines: Evidence and Causality (Kathleen Stratton et al.

eds., 2012).

85

Margaret A. Maglione et al., Safety of Vaccines Used for Routine Immunization of US

Children: A Systematic Review, 134 Pediatrics 325 (2014).

86

Agency for Healthcare Rsch. & Quality, Safety of Vaccines Used for Routine Immunization in

the United States (Apr. 6, 2020), https://effectivehealthcare.ahrq.gov/products/safety-

vaccines/protocol. The 2014 version was cited in Dr. He’s report; however, the 2020 research

protocol version was filed in this case.

38

relationship between [ITP] and tetanus, diphtheria, or pertussis containing vaccines, and the

AHRQ report concluded that [strength of evidence] was moderate for an association between

MMR vaccine and [ITP]. Our Review has concluded that the MMR vaccine can very rarely

cause [ITP] in children.”). And thus, Dr. He’s reliance on this literature appears misplaced.

Dr. He next cited an updated report from AHRQ published in May 2021. Resp. Ex. D4. 87

Based on additional evidence, the study found no evidence of an increased risk of ITP with flu

vaccination. Id. at 16 tbl. A. Dr. He, like Dr. Baumann, also relied upon Grimaldi-Bensouda et

al. and Lafaurie et al., and neither study found an association between flu vaccination and ITP.

Resp. Ex. D at 4 (citing Resp. Exs. A9, C1).

Overall, he opined that “these systemic studies have concluded that there is no evidence

to link [flu] vaccine with ITP development,” and given the large numbers of flu vaccinations

administered each year, “the lack of any reliable evidence to associate [flu] vaccine with ITP

strongly indicates that the [flu] vaccine more likely than not does not cause ITP.” Resp. Ex. D at

4.

Next, Dr. He addressed aspects of Petitioner’s experts’ reports. First, as to Dr. Ghose’s

proposed theory of molecular mimicry, Dr. He opined there were insufficient details to support

the theory. Resp. Ex. D at 9; Tr. 229-30. Dr. He explained Dr. Ghose did not provide homology

between the flu vaccine and platelets, and Dr. He is not aware of any relevant homology between

the two. Tr. 230. Dr. He also noted that sequence homology alone cannot cause ITP. Resp. Ex.

F at 21.

With regard to Dr. Ghose’s literature, he disagreed that it showed an association between

the flu vaccine and ITP. Resp. Ex. D at 5-8. Dr. He criticized Dr. Ghose’s literature references

as “completely lacking in reliable scientific strength.” Id. at 5. As to the case reports

specifically, Dr. He opined the case reports (1) show “a simple temporal relationship” that is

insufficient for causation; (2) span more than 30 years, despite the regularity of the

administration of the flu vaccine, and thus “it cannot be reliably concluded that the [flu] vaccine

was more likely than not the cause;” and (3) do no support an onset of one day or less, and

instead report onset intervals between four days and five weeks. Id. at 6, 8-9; see also Tr. 265.

Some of Dr. Ghose’s literature also focused on infections or vaccines other than the flu vaccine,

or they were factually different from this case. Resp. Ex. D at 8.

Dr. He also addressed Dr. Akbari’s proposed theory and literature. 88 Overall, Dr. He

opined Dr. Akbari “only provided scientific studies reporting activation of inflammasome

pathway, cytokine production[,] and Th17 differentiation upon [flu] vaccination,” which are part

of a normal immune response, and failed to provide evidence that the flu vaccine “could have

87

Agency for Healthcare Rsch. & Quality, Safety of Vaccines Used for Routine Immunization in

the United States: An Update (May 25, 2021), https://effectivehealthcare.ahrq.gov/products/

safety-vaccines/research.

88

For some of Dr. He’s criticisms of Dr. Akbari’s literature, see Resp. Ex. D at 13-16; Resp. Ex.

F at 2-3, 5-8, 11-12.

39

induced strong immune responses to break the host immune tolerance mechanisms to cause ITP

in [Petitioner].” Resp. Ex. F at 21.

Dr. He agreed with Dr. Akbari that the flu vaccine activates inflammasomes within hours,

which is step one of his theory. Tr. 340 (citing Pet. Ex. 155); see also Resp. Ex. D at 13 (“[I]t is

entirely expected that both [flu] virus infection and [flu] vaccinations will activate the

inflammasomes and produce inflammatory cytokines including IL-1β. Without proper activation

of the innate immunity, vaccines will not work as intended to induce adaptive immunity.”);

Resp. Ex. F at 2-4; Tr. 244 (agreeing with Dr. Akbari that inflammasomes are part of the innate

immune systems and be activated “very quickly”). But Dr. He added that “[i]nflammasome

itself is not going to be able to attack platelets.” Tr. 243.

Part two of this process involves the activation of antigen presenting cells by

inflammasomes, which Dr. Akbari testified could occur within hours. Tr. 340-41. Dr. He agreed

that IL-1β “could affect homeostasis” but opined it would “take days,” and not be as rapid as Dr.

Akbari posited. Tr. 341-42. Additionally, Dr. He noted there is no evidence that IL-1β kills

platelets directly. Tr. 341, 344; see also Resp. Ex. D at 13. And because of this, to affect

homeostasis, other cells would have to help facilitate the destruction of the platelets, which

would take “at least more than three days” and would “never[] [be] within 24 hours.” Tr. 342-

43. Thus, Dr. He opined there is no evidence to support ITP can be caused by immediate

reactions mediated through the innate immune system like Dr. Akbari asserted, or that

inflammasomes, cytokines, and other innate immune cells play a direct role in ITP. Resp. Ex. D

at 11, 13-14; Resp. Ex. F at 6-11; see also Tr. 235-37, 247-48.

As to step three (activation of autoreactive B cells), Dr. He testified that IL-1β, other

cytokines, or antigen-presenting cells activate autoreactive B cells and conventional naïve B

cells. Tr. 343. However, “it will never happen within one day or two days.” Id. Autoreactive B

cells, like memory B cells, have a lower threshold, leading to a faster response; however, this

only speeds up the process by two to three days, and never to the point of one day or less. Tr.

231-32, 343-44. Thus, he explained autoreactive B cells cannot produce antibody, bind to

platelets, and cause destruction within one day. Tr. 231-32, 344-45.

On cross-examination, Dr. He agreed B cells produce IgM antibodies and that IgM and

IgG antibodies can cause platelet destruction. Tr. 262-63. However, it would take “at least []

three days,” according to Dr. He, for these antibodies to be detected after vaccination. Id. He

maintained IgM, which is produced before IgG, 89 cannot peak within one to two days. Tr. 263.

In response to molecular mimicry, Dr. He took issue with the fact that Dr. Akbari did not

provide any details on any alleged amino acid sequence similarity between flu vaccine antigens

89

“IgM antibodies are produced as a body’s first response to a new infection, and increase for

several weeks and then decline as IgG production begins. IgG antibodies are produced during an

initial infection or other antigen exposure, rising a few weeks after it begins, then decreasing and

stabilizing.” Blender v. Sec’y of Health & Hum. Servs., No. 16-1308V, 2021 WL 1096662, at

*4 n.13 (Fed. Cl. Spec. Mstr. Feb. 26, 2021) (internal quotation marks and citation omitted).

40

and platelet proteins. Resp. Ex. D at 18, 22. He opined that molecular mimicry requires either

structural or sequence homology. Tr. 264-65.

Overall, Dr. He opined that although “inflammasome activation is an essential part of

host innate immune activation[,] Dr. Akbari did not substantiate how inflammasome activation

would have caused ITP.” Resp. Ex. D at 22; see also Tr. 255 (testifying that he has not seen

evidence of a connection between activation of inflammasome and destruction of platelets). “Dr.

Akbari also hypothesized molecular mimic theory without providing any molecular details,

either amino acid sequence homology or structural homology, between [flu] vaccine and

platelet.” Resp. Ex. D at 22. Dr. He maintained ITP is not mediated by the innate immune

system alone, and requires the adaptive immune system. Id. at 23; Resp. Ex. F at 13.

ii. Althen Prongs Two and Three

Dr. He summarized Petitioner’s clinical course: “[Petitioner] received a[] [flu] vaccine on

October 16, 2019 and felt shaky and cold at about [one] hour after the vaccination. She had a

platelet count of [five] on October 17, 2019 and [was diagnosed with and treated for] ITP. Her

platelet count returned to normal level shortly after treatment.” Resp. Ex. D at 3; see also Tr.

227-28. Dr. He opined “the timing between receipt of the vaccine and development of ITP in

[Petitioner] is not consistent with the cause and effect of immunizations with flu vaccine and the

subsequent development of ITP.” Resp. Ex. D at 24.

Dr. He disagreed with Dr. Ghose’s assertion that Petitioner’s ITP was “[u]ndoubtedly”

due to her flu vaccination as well as Dr. Ghose’s assertion that a rapid platelet drop as seen in

Petitioner “confirms the immune mediated nature” of ITP as neither are consistent with the

evidence in this case nor immunology. Resp. Ex. D at 7 (quoting Pet. Ex. 10 at 6-7). He

testified that no immunological process can explain how Petitioner’s clinical course led to ITP

within 24 hours of vaccination. Tr. 229.

Dr. He opined none of the literature supports a time frame consistent with the one day

onset seen in Petitioner. Resp. Ex. D at 6, 8-9. Further, the rapid onset directly counters

immunologic principles. Id. at 9, 22-23. Dr. He explained

[t]he timeframe for innate immunity to activate and play its function is within the

first 3-5 days after vaccination while the adaptive immunity is not fully activated

until day 7-10 after infection or vaccination. The adaptive immune response then

undergoes contraction to form a stable memory pool by day 25. As the

pathogenesis of ITP is mediated by anti-platelet autoantibodies and autoreactive

antigen-specific cytotoxic T cells, both essential components of the host adaptive

immune responses, the claim that [Petitioner’s] ITP is due to [flu] vaccination

induced adaptive immune responses cannot stand. It is simply impossible for the

adaptive immune system to produce anti-platelet autoantibodies or autoreactive

cytotoxic T lymphocytes within [one]-day upon [flu] vaccination.

41

Id. at 9 (citing Resp. Ex. D10 at 2 fig. 1); 90 see also Tr. 215; Resp. Ex. F at 13-15. Thus, he

concluded that a one-day onset is not characteristic of ITP “and certainly argues against any

causal relationship to the vaccine.” Resp. Ex. D at 10, 26; see also Tr. 214 (testifying that it is

“impossible to activate the adaptive immune system” within one day); Resp. Ex. F at 14-15 (“[I]t

is impossible for T and B cells to be activated within [one] day upon [flu] vaccination to cause

[Petitioner’s] ITP.”).

For further support, Dr. He referenced a graph from Carter et al. 91 to show the timeline of

antigen-specific antibodies after exposure to infection and primary and secondary vaccination:

Resp. Ex. F at 15 (citing Resp. Ex. F10 at 9 fig. 2); see also Tr. 219-21 (discussing this chart).

He testified that this chart shows the time it takes for the production of antigen-specific

antibodies. Tr. 222. He opined there is no evidence as illustrated by this chart to indicate an

adaptive immune response could occur within one day. Tr. 221; see also Resp. Ex. F at 21-22.

And even with a memory response, an adaptive immune response cannot be shortened to one

day. Tr. 225.

Therefore, because ITP involves the adaptive immune system, which requires a minimum

of five days to be mounted, “[i]t is impossible for adaptive immunity to be induced in one day by

[flu] vaccination to cause ITP.” Resp. Ex. F at 21-22.

90

Matthew A. Williams & Michael J. Bevan, Effector and Memory CTL Differentiation, 25

Annu. Rev. Immunol. 171 (2007).

91

Michael J. Carter et al., The Antibody-Secreting Cell Response to Infection: Kinetics and

Clinical Applications, 8 Front. Immunol. 1 (2017).

42

III. DISCUSSION

A. Standards for Adjudication

The Vaccine Act was established to compensate vaccine-related injuries and deaths. §

10(a). “Congress designed the Vaccine Program to supplement the state law civil tort system as

a simple, fair and expeditious means for compensating vaccine-related injured persons. The

Program was established to award ‘vaccine-injured persons quickly, easily, and with certainty

and generosity.’” Rooks v. Sec’y of Health & Hum. Servs., 35 Fed. Cl. 1, 7 (1996) (quoting

H.R. Rep. No. 908 at 3, reprinted in 1986 U.S.C.C.A.N. at 6287, 6344).

Petitioner’s burden of proof is by a preponderance of the evidence. § 13(a)(1). The

preponderance standard requires a petitioner to demonstrate that it is more likely than not that the

vaccine at issue caused the injury. Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315,

1322 n.2 (Fed. Cir. 2010). Proof of medical certainty is not required. Bunting v. Sec’y of Health

& Hum. Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). Petitioner need not make a specific type of

evidentiary showing, i.e., “epidemiologic studies, rechallenge, the presence of pathological

markers or genetic predisposition, or general acceptance in the scientific or medical communities

to establish a logical sequence of cause and effect.” Capizzano v. Sec’y of Health & Hum.

Servs., 440 F.3d 1317, 1325 (Fed. Cir. 2006). Instead, Petitioner may satisfy her burden by

presenting circumstantial evidence and reliable medical opinions. Id. at 1325-26.

In particular, Petitioner must prove that the vaccine was “not only [the] but-for cause of

the injury but also a substantial factor in bringing about the injury.” Moberly, 592 F.3d at 1321

(quoting Shyface v. Sec’y of Health & Hum. Servs., 165 F.3d 1344, 1352-53 (Fed. Cir. 1999));

see also Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). The

received vaccine, however, need not be the predominant cause of the injury. Shyface, 165 F.3d

at 1351. A petitioner who satisfies this burden is entitled to compensation unless Respondent

can prove, by a preponderance of the evidence, that the vaccinee’s injury is “due to factors

unrelated to the administration of the vaccine.” § 13(a)(1)(B). However, if a petitioner fails to

establish a prima facie case, the burden does not shift. Bradley v. Sec’y of Health & Hum.

Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).

“Regardless of whether the burden ever shifts to the [R]espondent, the special master

may consider the evidence presented by the [R]espondent in determining whether the [P]etitioner

has established a prima facie case.” Flores v. Sec’y of Health & Hum. Servs., 115 Fed. Cl. 157,

162-63 (2014); see also Stone v. Sec’y of Health & Hum. Servs., 676 F.3d 1373, 1379 (Fed. Cir.

2012) (“[E]vidence of other possible sources of injury can be relevant not only to the ‘factors

unrelated’ defense, but also to whether a prima facie showing has been made that the vaccine

was a substantial factor in causing the injury in question.”); de Bazan v. Sec’y of Health & Hum.

Servs., 539 F.3d 1347, 1353 (Fed. Cir. 2008) (“The government, like any defendant, is permitted

to offer evidence to demonstrate the inadequacy of the [P]etitioner’s evidence on a requisite

element of the [P]etitioner’s case-in-chief.”); Pafford, 451 F.3d at 1358-59 (“[T]he presence of

multiple potential causative agents makes it difficult to attribute ‘but for’ causation to the

vaccination. . . . [T]he Special Master properly introduced the presence of the other unrelated

contemporaneous events as just as likely to have been the triggering event as the vaccinations.”).

43

B. Factual Issues

A petitioner must prove, by a preponderance of the evidence, the factual circumstances

surrounding her claim. § 13(a)(1)(A). To resolve factual issues, the special master must weigh

the evidence presented, which may include contemporaneous medical records and testimony.

See Burns v. Sec’y of Health & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (explaining that a

special master must decide what weight to give evidence including oral testimony and

contemporaneous medical records). Contemporaneous medical records, “in general, warrant

consideration as trustworthy evidence.” Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d

1525, 1528 (Fed. Cir. 1993). But see Kirby v. Sec’y of Health & Hum. Servs., 997 F.3d 1378,

1382 (Fed. Cir. 2021) (rejecting the presumption that “medical records are accurate and complete

as to all the patient’s physical conditions”); Shapiro v. Sec’y of Health & Hum. Servs., 101 Fed.

Cl. 532, 538 (2011) (“[T]he absence of a reference to a condition or circumstance is much less

significant than a reference which negates the existence of the condition or circumstance.”

(quoting Murphy v. Sec’y of Health & Hum. Servs., 23 Cl. Ct. 726, 733 (1991), aff’d per curiam,

968 F.2d 1226 (Fed. Cir. 1992))), recons. den’d after remand, 105 Fed. Cl. 353 (2012), aff’d

mem., 503 F. App’x 952 (Fed. Cir. 2013).

There are situations in which compelling testimony may be more persuasive than written

records, such as where records are deemed to be incomplete or inaccurate. Campbell v. Sec’y of

Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“[L]ike any norm based upon common

sense and experience, this rule should not be treated as an absolute and must yield where the

factual predicates for its application are weak or lacking.”); Lowrie v. Sec’y of Health & Hum.

Servs., No. 03-1585V, 2005 WL 6117475, at *19 (Fed. Cl. Spec. Mstr. Dec. 12, 2005)

(“[W]ritten records which are, themselves, inconsistent, should be accorded less deference than

those which are internally consistent.” (quoting Murphy, 23 Cl. Ct. at 733)). Ultimately, a

determination regarding a witness’s credibility is needed when determining the weight that such

testimony should be afforded. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1379

(Fed. Cir. 2009); Bradley, 991 F.2d at 1575.

Despite the weight afforded to medical records, special masters are not rigidly bound by

those records in determining onset of a petitioner’s symptoms. Valenzuela v. Sec’y of Health &

Hum. Servs., No. 90-1002V, 1991 WL 182241, at *3 (Fed. Cl. Spec. Mstr. Aug. 30, 1991); see

also Eng v. Sec’y of Health & Hum. Servs., No. 90-1754V, 1994 WL 67704, at *3 (Fed. Cl.

Spec. Mstr. Feb. 18, 1994) (noting Section 13(b)(2) “must be construed so as to give effect also

to § 13(b)(1) which directs the special master or court to consider the medical records (reports,

diagnosis, conclusions, medical judgment, test reports, etc.), but does not require the special

master or court to be bound by them”).

C. Causation

To receive compensation through the Program, Petitioner must prove either (1) that she

suffered a “Table Injury”—i.e., an injury listed on the Vaccine Injury Table—corresponding to a

vaccine that she received, or (2) that she suffered an injury that was actually caused by a

vaccination. See §§ 11(c)(1), 13(a)(1)(A); Capizzano, 440 F.3d at 1319-20. Petitioner must

44

show that the vaccine was “not only a but-for cause of the injury but also a substantial factor in

bringing about the injury.” Moberly, 592 F.3d at 1321 (quoting Shyface, 165 F.3d at 1352-53).

Because Petitioner does not allege she suffered a Table Injury, she must prove a vaccine

she received caused her injury. To do so, Petitioner must establish, by preponderant evidence:

“(1) a medical theory causally connecting the vaccination and the injury; (2) a logical sequence

of cause and effect showing that the vaccination was the reason for the injury; and (3) a showing

of a proximate temporal relationship between vaccination and injury.” Althen, 418 F.3d at 1278.

The causation theory must relate to the injury alleged. Petitioner must provide a sound

and reliable medical or scientific explanation that pertains specifically to this case, although the

explanation need only be “legally probable, not medically or scientifically certain.” Knudsen v.

Sec’y of Health & Hum. Servs., 35 F.3d. 543, 548-49 (Fed. Cir. 1994). Petitioner cannot

establish entitlement to compensation based solely on her assertions; rather, a vaccine claim must

be supported either by medical records or by the opinion of a medical doctor. § 13(a)(1). In

determining whether a petitioner is entitled to compensation, the special master shall consider all

material in the record, including “any . . . conclusion, [or] medical judgment . . . which is

contained in the record regarding . . . causation.” § 13(b)(1)(A). The undersigned must weigh

the submitted evidence and the testimony of the parties’ proffered experts and rule in Petitioner’s

favor when the evidence weighs in her favor. See Moberly, 592 F.3d at 1325-26 (“Finders of

fact are entitled—indeed, expected—to make determinations as to the reliability of the evidence

presented to them and, if appropriate, as to the credibility of the persons presenting that

evidence.”); Althen, 418 F.3d at 1280 (noting that “close calls” are resolved in Petitioner’s

favor).

Testimony that merely expresses the possibility—not the probability—is insufficient, by

itself, to substantiate a claim that such an injury occurred. See Waterman v. Sec’y of Health &

Hum. Servs., 123 Fed. Cl. 564, 573-74 (2015) (denying Petitioner’s motion for review and

noting that a possible causal link was not sufficient to meet the preponderance standard). The

Federal Circuit has made clear that the mere possibility of a link between a vaccination and a

petitioner’s injury is not sufficient to satisfy the preponderance standard. Moberly, 592 F.3d at

1322 (emphasizing that “proof of a ‘plausible’ or ‘possible’ causal link between the vaccine and

the injury” does not equate to proof of causation by a preponderance of the evidence); Boatmon

v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, 1359-60 (Fed. Cir. 2019). While certainty is

by no means required, a possible mechanism does not rise to the level of preponderance.

Moberly, 592 F.3d at 1322; see also de Bazan, 539 F.3d at 1351.

IV. SEVERITY REQUIREMENT ANALYSIS

To receive compensation, Petitioner must show that she

(i) suffered the residual effects or complications of [her] illness, disability, injury,

or condition for more than six months after the administration of the vaccine, or

(ii) died from the administration of the vaccine, or (iii) suffered such illness,

disability, injury, or condition from the vaccine which resulted in inpatient

hospitalization and surgical intervention.

45

§ 11(c)(1)(D).

Compensation is not available under the Vaccine Act for minor illness which are short-

lived. Wright v. Sec’y of Health & Hum. Servs., 22 F.4th 999, 1001-04 (Fed. Cir. 2022). Cases

may appropriately be dismissed for failure to substantiate the severity requirement. See, e.g.,

Hinnefeld v. Sec’y of Health & Hum. Servs., No. 11-328V, 2012 WL 1608839, at *4-5 (Fed. Cl.

Spec. Mstr. Mar. 30, 2012) (dismissing case where medical history revealed that petitioner’s

GBS resolved less than two months after onset). It is Petitioner’s burden to prove her case,

including the six-month requirement, by a preponderance of the evidence. See § 13(a)(1)(A).

To satisfy the six-month requirement, “[a] potential petitioner must do something more than

merely submit a petition and an affidavit parroting the words of the statute.” Faup v. Sec’y of

Health & Hum. Servs., No. 12-87V, 2015 WL 443802, at *3 (quoting Black v. Sec’y of Health &

Hum. Servs., 33 Fed. Cl. 546, 550 (1995), aff’d, 93 F.3d 784, 792 (Fed. Cir. 1996)). A petitioner

cannot establish the length or ongoing nature of an injury merely through their own statements,

but rather is required to “submit supporting documentation which reasonably demonstrates that

the alleged injury or its sequelae lasted more than six months.” Black, 33 Fed. Cl. at 550; see

also Lett v. Sec’y of Health & Hum. Servs., 39 Fed. Cl. 259, 260-61 (1997) (“Section 300aa-

13(a)(1) provides that a special master may not award compensation ‘based on the claims of [a]

petitioner alone, unsubstantiated by medical records or by medical opinion.’”).

The Federal Circuit recently addressed the six-month severity requirement in Wright. 22

F.4th at 1001. The petitioner’s child suffered ITP, a condition characterized by abnormally low

platelet counts, bruising, and bleeding, after receipt of the MMR vaccination. Id. The child’s

ITP resolved in less than three months, and although he had later episodes of bruising, testing

showed that his platelet count remained normal. Id. at 1003-04. The Circuit held that the

petitioner failed to satisfy the six-month requirement when the platelet count normalized less

than three months post-ITP onset because “relatively non-invasive ongoing [platelet]

monitoring” was not a “residual effect” pursuant to § 11(c)(1)(D)(i). Id. at 1001, 1003, 1006-07.

The Circuit noted that the child’s later bruising was not related to his vaccine injury and that

ongoing testing “did not reveal, constitute, or cause any somatic change.” Id. at 1001.

Defining the language in § 11(c)(1)(D)(i), the Circuit ruled that “[t]he term ‘residual

effects’ . . . requires a change within the patient that is caused by the vaccine injury.” Wright, 22

F.4th at 1004. It continued, stating that “‘[r]esidual’ suggests something remaining or left behind

from a vaccine injury . . . . Because vaccine injuries are somatic conditions defined by their

signs and symptoms within the patient, . . . their residues are similarly defined.” Id. at 1005-06

(internal citations omitted). Further, the words “suffered” and “complication” in association with

“residual effects” in § 11(c)(1)(D)(i) “suggest that Congress contemplated residual effects to be

detrimental conditions within the patient, such as lingering or recurring signs and symptoms.”

Id. at 1006. The Circuit concluded that “[r]ead together, ‘residual effects’ and ‘complications’

appear to both refer to conditions within the patient, with ‘residual effects’ focused on lingering

signs, symptoms, or sequelae characteristic of the course of the original vaccine injury, and

‘complications’ encompassing conditions that may not be ‘essential part[s] of the disease’ or

may be outside the ordinary progression of the vaccine injury.” Id.

46

Considering and weighing all of the evidence, the undersigned finds it preponderates in

favor of a finding that Petitioner “suffered the residual effects or complications of [her] [ITP] for

more than six months after the administration of the vaccine.” § 11(c)(1)(D)(i).

Petitioner received the flu vaccine at issue on October 16, 2019 and her onset manifested

within one day, by October 17. Thus, to satisfy the six-month severity requirement, Petitioner

would have to provide preponderant evidence that she suffered from the residual effects of her

ITP until mid-April 2020. To satisfy the severity requirement, Petitioner contends she suffered

from ITP-related fatigue for more than six months.

First, the undersigned notes the experts agree that fatigue can be associated with ITP and

the literature supports the finding that fatigue is a residual effect of ITP.

Second, the undersigned finds there is evidence to support a finding that Petitioner

experienced fatigue past mid-April 2020. Here, Petitioner provided evidence that she was

suffering from fatigue until at least May 2020, as evidenced by her email to her attorney.

Specifically, Petitioner wrote on May 27, 2020 that her platelets were above 370,000 K/uL but

that she was “still tired at times but otherwise [she was] doing ok.” Pet. Ex. 6 at 1. The

undersigned finds this is not negated by a lack of reference of fatigue in Dr. Dammrich’s records

during this time. See Shapiro, 101 Fed. Cl. at 538 (“[T]he absence of a reference to a condition

or circumstance is much less significant than a reference which negates the existence of the

condition or circumstance.” (quoting Murphy, 23 Cl. Ct. at 733, aff’d per curiam, 968 F.2d 1226

(Fed. Cir. 1992))), recons. den’d after remand, 105 Fed. Cl. 353 (2012), aff’d mem., 503 F.

App’x 952 (Fed. Cir. 2013).

Third, the undersigned finds Respondent’s arguments for why Petitioner’s fatigue was

not due to her ITP not persuasive.

Respondent argues that Petitioner’s fatigue was due to other reasons, including Covid and

her sister’s death in April 2020. However, this would not explain ongoing fatigue which began

after vaccination and was still present in April 2020. Moreover, in her email to her attorney,

Petitioner is referencing her ITP, and notes she was “still tired at times but otherwise [she was]

doing ok.” Pet. Ex. 6 at 1. The reasonable inference is that she attributes her fatigue to her prior

ITP. Respondent’s assertions that Petitioner’s fatigue was due to Covid or her sister’s death is

not supported by any evidence. Because “close calls” are resolved in Petitioner’s favor, and

Respondent failed to provide evidence that Petitioner’s ITP was not the reason for her fatigue,

the undersigned does not find Respondent’s argument persuasive. Althen, 418 F.3d at 1280.

Respondent also argues that fatigue is a residual effect in only those ITP patients with

chronic and active ITP (as evidence by low platelets), not patients like Petitioner, whose platelet

levels had normalized. However, Respondent did not cite to an article supporting this narrow

finding. Overall, the literature shows ITP patients complain of fatigue, which can be associated

but is not always correlated with platelet levels. See, e.g., Pet. Ex. 63 at 2 (noting “[i]t is less

clear whether fatigue is associated with disease severity as measured by the platelet count” and

summarized studies that have found fatigue did and did not correlate to platelet count); Pet. Ex.

47

153 at 5 (finding “fatigue scores did not correlate with the most recent platelet counts at

baseline”).

In conclusion, the undersigned finds that Petitioner did experience fatigue, which was a

residual effect of her ITP, for longer than six months. Therefore, she does meet the severity

requirement set forth in the Vaccine Act. However, as discussed below, Petitioner has not

satisfied all three Althen prongs.

V. CAUSATION ANALYSIS

A. Althen Prong One

Under Althen prong one, Petitioner must set forth a medical theory explaining how the

received vaccine could have caused the sustained injury. Andreu, 569 F.3d at 1375; Pafford, 451

F.3d at 1355-56. Petitioner’s theory of causation need not be medically or scientifically certain,

but it must be informed by a “sound and reliable” medical or scientific explanation. Boatmon,

941 F.3d at 1359; see also Knudsen, 35 F.3d at 548; Veryzer v. Sec’y of Health & Hum. Servs.,

98 Fed. Cl. 214, 223 (2011) (noting that special masters are bound by both § 13(b)(1) and

Vaccine Rule 8(b)(1) to consider only evidence that is both “relevant” and “reliable”). If

Petitioner relies upon a medical opinion to support her theory, the basis for the opinion and the

reliability of that basis must be considered in the determination of how much weight to afford the

offered opinion. See Broekelschen v. Sec’y of Health & Hum. Servs., 618 F.3d 1339, 1347 (Fed.

Cir. 2010) (“The special master’s decision often times is based on the credibility of the experts

and the relative persuasiveness of their competing theories.”); Perreira v. Sec’y of Health &

Hum. Servs., 33 F.3d 1375, 1377 n.6 (Fed. Cir. 1994) (stating that an “expert opinion is no better

than the soundness of the reasons supporting it” (citing Fehrs v. United States, 620 F.2d 255, 265

(Ct. Cl. 1980))).

In her pre-hearing brief, Petitioner contends she presented evidence of a “biologically

plausible mechanism” 92 which “is based on molecular mimicry.” 93 Pet. Pre-Hearing Br., filed

Jan. 7, 2025, at 6-9 (ECF No. 70) (“Here, Petitioner has presented a biologically plausible theory

to explain how the [flu] vaccination provoked an autoimmune response which caused ITP by

molecular mimicry.”). Petitioner’s post-hearing brief maintains Petitioner presented a “sound

92

Petitioner’s theory must be “sound and reliable.” Boatmon, 941 F.3d at 1359. “[P]etitioner

must do more than demonstrate a ‘plausible’ or ‘possible’ causal link between the vaccination

and the injury; [s]he must prove [her] case by a preponderance of the evidence.” W.C. v. Sec’y

of Health & Hum. Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013).

93

“Molecular mimicry is sequence and/or conformational homology between an exogenous

agent (foreign antigen) and self-antigen leading to the development of tissue damage and clinical

disease from antibodies and T cells directed initially against the exogenous agent that also react

against self-antigen.” Resp. Ex. D7 at 99. Dr. Akbari agreed molecular mimicry is part of the

adaptive immune system. See, e.g., Pet. Ex. 88 at 16 (explaining “B cells, part of the adaptive

immune system, produce antibodies that mistakenly target the body’s own tissues, leading to

adverse outcomes”).

48

and reliable medical theory in which the flu vaccine can cause ITP . . . based on molecular

mimicry.” Pet. Post-Hearing Br. at 8-11. 94

The experts all appear to agree that the adaptive immune system is responsible for

causing platelet destruction. Dr. He explained that ITP is thought to be caused by autoimmune

reactions including autoantibodies and autoreactive cytotoxic T cells against platelets, as well as

humoral and cellular autoimmunity against megakaryocytes. The autoantibodies targeting

platelets or platelet antigens destroy circulating platelets and cause reduced platelet production.

Because ITP is mediated by anti-platelet autoantibodies and autoreactive antigen specific

cytotoxic T cells, both the innate immune system and the adaptive immune systems play a role in

the pathogenesis of ITP.

Dr. Akbari’s expert reports and testimony was more difficult to follow. He appears to

suggest a combination of theories, implicating a type of hypersensitivity/inflammasome reaction

and molecular mimicry, which he opines involves both the innate and adaptive immune systems.

Therefore, consistent with both parties’ experts, the undersigned finds that both the innate

and adaptive immune systems play a role in the pathogenesis of ITP.

Assuming Petitioner has proven a sound and reliable causal mechanism under Althen

prong one, the undersigned finds Petitioner did not provide preponderant evidence of a logical

sequence of cause and effect or a proximate temporal relationship between the flu vaccination

and Petitioner’s ITP. Due to the facts and circumstances of this case, specifically the fact that

Petitioner developed symptoms within one day after receipt of a flu vaccine, the undersigned’s

determination as to causation turns on an analysis of Althen prongs two and three, and thus, the

undersigned focuses on Althen prongs two and three. See Vaughan ex rel. A.H. v. Sec’y of

Health & Hum. Servs., 107 Fed. Cl. 212, 221-22 (2012) (finding the special master’s failure to

rule on Althen prong one not fatal to his decision because Althen prong two was fatal to

Petitioner’s case); Hibbard v. Sec’y of Health & Hum. Servs., 698 F.3d 1355, 1364 (Fed. Cir.

2012) (“discern[ing] no error in the manner in which the special master chose to address the

Althen [prongs]” when he focused on Althen prong two after “assuming the medical viability of

[the] theory of causation”).

While the undersigned is not making a finding as to whether Petitioner has provided

preponderant evidence of Althen prong one, a one-day onset is not compatible with a theory

based on the finding that ITP is caused by the innate and adaptive immune systems. This is

because, as explained by Dr. He, the pathogenesis involves autoimmune reactions including

autoantibodies and autoreactive cytotoxic T cells against platelets, as well as humoral and

cellular autoimmunity against megakaryocytes. The autoantibodies targeting platelets or platelet

antigens destroy circulating platelets and cause reduced platelet production.

94

Petitioner described her theory as both “sound and reliable” and “biologically plausible” in her

post-hearing brief. Pet. Post-Hearing Br. at 8, 11.

49

Again, as explained by Dr. He, in an adaptive immune response there is a lag time

between antigen exposure and response, which typically takes five to 10 days. This timing is

faster with a memory response, so for a secondary vaccination it would take five to seven days.

Dr. Akbari provided no foundational support to show how a response involving both the

innate and adaptive immune response can occur within 24 hours.

Case law illustrates that an adaptive immune response does not occur within one day.

See, e.g., Forrest v. Sec’y of Health & Hum. Servs., No. 14-1046V, 2019 WL 925495, at *6, *8

(Fed. Cl. Spec. Mstr. Jan. 28, 2019) (finding “a preponderance of the evidence shows that

molecular mimicry is not likely to happen within 36 hours, even for a recall response,” as

molecular mimicry is an adaptive immune response); Martinez ex rel. W.M. v. Sec’y of Health

& Hum. Servs., No. 16-738V, 2022 WL 4884923, at *27 (Fed. Cl. Spec. Mstr. Sept. 9, 2022)

(finding “a relative short onset” of one day “not medically acceptable” in an “an autoimmune

reaction involving antibodies or other immune cells associated with the adaptive[] [] immune

response in reaction to antigenic exposure” (emphasis omitted)), mot. for rev. denied, 165 Fed.

Cl. 76 (2023); Langert v. Sec’y of Health & Hum. Servs., No. 22-809V, 2025 WL 1892418, at

*6, *8 (Fed. Cl. Spec. Mstr. June 13, 2025) (“Such a short, one-day onset timeframe is not

consistent with Petitioner’s causation theory . . . [which] involves the adaptive immune system—

the secondary immune arm, which does not immediately respond to a vaccine upon

administration. Rather, this process takes more than a day to result in the production of

antibodies capable of a cross-reactive, autoimmune attack.” (internal citations omitted)); see also

Brancheau v. Sec’y of Health & Hum. Servs., No. 21-1209V, 2024 WL 1619606, at *23-24

(Fed. Cl. Spec. Mstr. Mar. 21, 2024) (detailing the timing involved in the latency period between

antigen exposure and peak adaptive immune response); infra Part V.C (analyzing Althen prong

three).

B. Althen Prong Two

Under Althen prong two, Petitioner must prove by a preponderance of the evidence that

there is a “logical sequence of cause and effect showing that the vaccination was the reason for

the injury.” Capizzano, 440 F.3d at 1324 (quoting Althen, 418 F.3d at 1278). “Petitioner must

show that the vaccine was the ‘but for’ cause of the harm . . . or in other words, that the vaccine

was the ‘reason for the injury.’” Pafford, 451 F.3d at 1356 (internal citations omitted).

In evaluating whether this prong is satisfied, the opinions and views of the vaccinee’s

treating physicians are entitled to some weight. Andreu, 569 F.3d at 1367; Capizzano, 440 F.3d

at 1326 (“[M]edical records and medical opinion testimony are favored in vaccine cases, as

treating physicians are likely to be in the best position to determine whether a ‘logical sequence

of cause and effect show[s] that the vaccination was the reason for the injury.’” (quoting Althen,

418 F.3d at 1280)). Medical records are generally viewed as trustworthy evidence, since they are

created contemporaneously with the treatment of the vaccinee. Cucuras, 993 F.2d at 1528.

Petitioner need not make a specific type of evidentiary showing, i.e., “epidemiologic studies,

rechallenge, the presence of pathological markers or genetic predisposition, or general

acceptance in the scientific or medical communities to establish a logical sequence of cause and

50

effect.” Capizzano, 440 F.3d at 1325. Instead, Petitioner may satisfy her burden by presenting

circumstantial evidence and reliable medical opinions. Id. at 1325-26.

The undersigned finds there is not preponderant

This text is long and has been trimmed here. Open the source document for the complete record.