VICP Registry Case Source Bundle
Canonical URL: https://vicp-registry.org/case/USCOURTS-cofc-1_17-vv-01367
Package ID: USCOURTS-cofc-1_17-vv-01367
Petitioner: BENJAMIN S. MAXWELL
Filed: 2017-09-28
Decided: 2025-05-02
Vaccine: influenza
Vaccination date: 2014-10-05
Condition: seronegative rheumatoid arthritis
Outcome: denied
Award amount USD: 

AI-assisted case summary:
Benjamin S. Maxwell filed a petition alleging that an influenza vaccination he received on October 5, 2014, caused him to develop seronegative rheumatoid arthritis (RA) or significantly aggravated a preexisting condition. Mr. Maxwell was 28 years old at the time of vaccination. He reported experiencing flu-like symptoms, including fever and body aches, two days after the vaccination, which later progressed to joint stiffness and pain. He was diagnosed with inflammatory arthritis and later seronegative RA by his treating physicians. The respondent, the Secretary of Health and Human Services, recommended denial of entitlement. The case involved extensive expert testimony and medical literature regarding the diagnosis of seronegative RA and its potential causation by the flu vaccine. The court considered the opinions of Dr. Eric Gershwin for the petitioner and Drs. Chester Oddis and You-Wen He for the respondent. Ultimately, the Special Master found that while Mr. Maxwell may have seronegative RA, he failed to establish a sound and reliable medical theory connecting the flu vaccine to his condition. The court noted the lack of supporting epidemiological data and the inadequacy of the mechanistic evidence presented. Furthermore, the court found that the petitioner did not prove a logical sequence of cause and effect, particularly due to the consistent absence of inflammatory markers in his bloodwork over an eight-year period, despite his symptoms and treatments. Although the temporal proximity of two days for initial symptoms was deemed medically acceptable for an innate immune response, this alone was insufficient to prove causation. The petition was denied.

Theory of causation field:
Off-Table

Public staged source text:

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DOCUMENT 1: USCOURTS-cofc-1_17-vv-01367-1
Date issued/filed: 2025-05-02
Pages: 39
Docket text: PUBLIC DECISION (Originally filed: 3/26/2025) regarding 93 DECISION Dismissing Petition. Signed by Special Master Jennifer A. Shah. (am) Service on parties made.
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Case 1:17-vv-01367-UNJ Document 96 Filed 05/02/25 Page 1 of 39
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 17-1367
Filed: March 26, 2025
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BENJAMIN S. MAXWELL,
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Petitioner, *
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v.
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SECRETARY OF HEALTH AND *
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HUMAN SERVICES,
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Respondent. *
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Elizabeth Martin Muldowney, Sands Anderson, PC, Richmond, VA, for Petitioner.
Dorian Hurley, U.S. Department of Justice, Washington, DC, for Respondent.
DECISION DENYING ENTITLEMENT1
Shah, Special Master:
On September 28, 2017, Benjamin Maxwell (“Petitioner”) filed a petition for compensation
under the National Vaccine Injury Compensation Program, 42 U.S.C. § 300aa-10, et seq.2 (the
“Vaccine Act” or “Program”). The petition alleges that Petitioner suffered from an inflammatory
polyarthropathy and/or rheumatoid arthritis (“RA”) caused by an influenza (“flu”) vaccination he
received on October 5, 2014. Pet. at 1 (ECF No. 1). The petition alternatively alleges that the
vaccination significantly aggravated an unnamed preexisting condition. Id. Throughout the course
1 Because this Decision contains a reasoned explanation for the action in this case, it must be made publicly
accessible and will be posted on the United States Court of Federal Claims's 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, I agree that
the identified material fits within this definition, I will redact such material from public access.
2 National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755. For ease of citation,
all “§” references to the Vaccine Act will be to the pertinent subparagraph of 42 U.S.C. § 300aa (2012).

Case 1:17-vv-01367-UNJ Document 96 Filed 05/02/25 Page 2 of 39
of the litigation, Petitioner has clarified that he alleges he developed seronegative RA caused by
the subject flu vaccination. See, e.g., Ex. 18 (report of Petitioner’s expert, Dr. M. Eric Gershwin).
Upon review of the evidence in this case, I find that Petitioner has failed to preponderantly
demonstrate that the flu vaccination in question caused him to develop seronegative RA. The
petition is accordingly dismissed.
I. PROCEDURAL HISTORY
After filing the petition, Petitioner filed affidavits and medical records. Exs. 1-17. On
June 18, 2018, Respondent filed a Rule 4(c) Report (“Report”), recommending that entitlement be
denied. Report at 1 (ECF No. 18).
Petitioner filed an expert report by M. Eric Gershwin, M.D., MACR, MACP, along with
Dr. Gershwin’s curriculum vitae and medical literature, on October 16, 2018. Exs. 18-26. On
February 27, 2019, Respondent filed expert reports from Chester Oddis, M.D., and You-Wen He,
M.D., Ph.D., along with their curricula vitae and medical literature. Exs. A & Tabs 1-4, B, C &
Tabs 1-13, D.
On March 4, 2019, former Special Master Katherine E. Oler ordered Petitioner to file a
second expert report from Dr. Gershwin addressing Dr. Oddis’s opinion concerning Petitioner’s
diagnosis and Dr. He’s opinion concerning the appropriate onset for the alleged condition.
Petitioner filed a second expert report and literature from Dr. Gershwin addressing these issues.
Exs. 29-30. Respondent filed responsive reports from Drs. Oddis and He on August 7, 2019. Exs.
E, F.
On August 22, 2019, Special Master Oler held a status conference at which she advised the
parties that the issues in dispute appeared to be diagnosis and causation. In Special Master Oler’s
view, based on the diagnostic criteria for RA, the evidence indicated that diagnosis was
appropriate. As such, she encouraged the parties to discuss settlement. ECF No. 37.
Petitioner filed a third expert report and additional literature from Dr. Gershwin on October
15, 2019. Exs. 34-37. Respondent filed responsive expert reports and literature from Drs. Oddis
and He on March 6, 2020. Exs. G & Tabs 1-2, H. Petitioner filed a fourth report and an article
from Dr. Gershwin on April 3, 2020. Exs. 38-39.
The parties could not informally resolve the case, and it was scheduled for an entitlement
hearing. See ECF No. 57. On February 1 and April 26, 2022, Petitioner filed additional medical
records. Exs. 40-48. Petitioner filed additional literature on August 23, 2022. Exs. 49-52.
Prehearing briefs were filed on August 24 and September 8, 2022. ECF Nos. 66, 75.
Special Master Oler conducted an entitlement hearing on September 21, 2022, at which
Drs. Gershwin, Oddis, and He testified. After the hearing, the parties filed further expert reports
and literature. Exs. 53-62; L-R. The parties filed post-hearing briefs on February 7, April 10, and
June 2, 2023. ECF Nos. 85, 86, 88.
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Both parties agreed that the record was complete on June 20, 2023. ECF No. 89. This
matter is now ripe for adjudication.
II. FACT EVIDENCE
Petitioner served in the Army National Guard. See Ex. 1. Prior to the subject vaccination,
he had a medical history notable for hernia surgery in 2011; he was also diagnosed with anxiety,
major depression, and PTSD. See Ex. 5 at 3; Ex. 9 at 1; Ex. 10 at 24, 28, 33, 41. He was 28
years old when he received a flu vaccine on October 5, 2014, during a monthly Army National
Guard drill. Ex. 11 at 1. He was attending the University of Idaho at the time. Ex. 1 at 2.
According to his affidavit, executed on September 26, 2017, Petitioner had no immediate
reaction to the vaccination. Ex. 1 at 1. But two days later, he woke up with a fever of 102
degrees, along with chills, stiffness, and achiness throughout his body. Id. He missed two days
of school. Id. Four days after the vaccination, the symptoms had subsided except for joint
stiffness and achiness. Id. Petitioner did not seek medical attention at the time because his
symptoms did not limit his mobility and were controlled with ibuprofen. Id. By the next week,
however, his achiness and stiffness worsened, and he started having pain in both shoulders. Id.
Petitioner’s wife, Mrs. Tabitha Maxwell, also submitted an affidavit executed September
26, 2017. Ex. 2. Mrs. Maxwell stated that the day after the vaccination, Petitioner was tired
but was able to attend classes. Id. at 1. The next morning, however, he “woke up with a fever
and body aches and was not able to attend school for the next two days because of his
symptoms.” Id. By October 9, 2014, he was feeling better but still complained of discomfort
in his right rotator cuff. Id.
Petitioner and Mrs. Maxwell stated that later in October 2014, he began experiencing
pain in both knees, which prevented him from sleeping in his bed. Ex. 1 at 1; Ex. 2 at 1. By
the end of October, his pain precluded him from standing or walking. Ex. 1 at 1. He made an
appointment to see his primary care provider (“PCP”). Id. at 2.
The medical records show that Petitioner presented to his PCP, Physician’s Assistant
(“PA”) Todd Bledsoe, on November 7, 2014, for pain in all his joints that had been ongoing for
the past month. Ex. 13 at 1. He reported the pain “all started after his flu shot” and that he had
been in his “usual good state of health” before the vaccination. Id. He said two days after he
received the vaccine, he developed flu-like symptoms, including fever and body aches. Id.
His muscle aches resolved, but he continued to have joint aches, which were getting worse. Id.
He reported having hand and wrist swelling in the morning, with redness in his knuckles and
finger joints. Id. The symptoms would ease as the day went on. Id. He also complained of
pain with movement after prolonged immobility of any joint. Id. He denied any prior history
of these symptoms, but he noted he had a cousin with RA. Id.
On exam, Petitioner had no swelling, redness, or warmth in his extremities. Ex. 13 at 1.
He had pain with range of motion (“ROM”) in all of the joints of his fingers and in his knees,
elbows, and hips. Id. PA Bledsoe diagnosed Petitioner with polyarthropathy, ordered lab tests,
and prescribed ibuprofen 800mg. Id. at 2. He provided a note releasing Petitioner from all
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military activities until further notice. Id.
On November 12, 2014, Petitioner returned to PA Bledsoe to follow up on his lab tests.
Ex. 13 at 3. His joint pain was worse. Id. His erythrocyte sedimentation rate (“ESR”),3
antinuclear antibody (“ANA”),4 and C-reactive protein (“CRP”)5 results were negative. Id. at
4-5. His white blood cell (“WBC”) count was normal. Id. at 4. PA Bledsoe commented that
“notably, all his connective tissue panel and inflammatory markers are [negative].” Id. at 3.
His exam showed no evidence of “swelling, redness, or warmth of the extremities” but revealed
pain on ROM of the hands, knees, hips, and elbows. Id. at 5. PA Bledsoe diagnosed arthralgia,
suspecting Petitioner had experienced an allergic reaction to the flu shot. Id. He referred
Petitioner to rheumatology and started him on a prednisone taper. Id.
In a follow-up appointment on November 19, 2014, Petitioner reported 60% relief of
his symptoms with prednisone, but he had pain after prolonged sitting and was unable to attend
classes. Ex. 13 at 7. He had discontinued his military training exercises and was in the process
of withdrawing from school for the semester. Id. An exam showed full ROM in all extremities,
with pain in standing up from a prolonged sitting position and mild pain with ROM in his wrists
and fingers. Id. He was continued on the prednisone taper. Id. at 7-8.
On November 25, 2014, 51 days after the vaccination, Petitioner saw rheumatologist
Dustin Dinning, D.O. Ex. 14 at 1. He reported bilateral hand pain with sudden onset that was
relieved with medications. Id. He also reported fatigue, decreased mobility, nocturnal
awakening, nocturnal pain, spasms, and swelling. Id. On exam, he had swelling in both
hands, but no observations of redness or warmth were documented. Id. at 3. Dr. Dinning
diagnosed inflammatory arthritis, which he suspected was caused either by a virus or the flu
3 Erythrocyte sedimentation rate: the rate at which erythrocytes precipitate out from a well-mixed specimen
of venous blood, measured by the distance the top of the column of erythrocytes falls in a given time interval
under specified conditions; an increase in rate is usually due to elevated levels of plasma proteins, especially
fibrinogen and immunoglobulins, which decrease the zeta potential on erythrocytes by dielectric shielding
and thus promote rouleau formation. It is increased in monoclonal gammopathy, hypergammaglobulinemia
due to inflammatory disease, hyperfibrinogenemia, active inflammatory disease, and anemia.
DORLAND’S MEDICAL DICTIONARY ONLINE,
https://www.dorlandsonline.com/dorland/definition?id=102146&searchterm=erythrocyte+sedimentation+
rate (last visited March 19, 2025) (“DORLAND’S”).
4 Antinuclear Antibody: antibodies directed against nuclear antigens; ones against a variety of different
antigens are almost invariably found in systemic lupus erythematosus and are frequently found in
rheumatoid arthritis, scleroderma (systemic sclerosis), Sjögren syndrome, and mixed connective tissue
disease. Antinuclear antibodies may be detected by immunofluorescent staining. Serologic tests are also
used to determine antibody titers against specific antigens. DORLAND’S,
https://www.dorlandsonline.com/dorland/definition?id=56804&searchterm=antinuclear+antibodies (last
visited March 19, 2025).
5 C-reactive protein: a globulin that forms a precipitate with the somatic C-polysaccharide of the
pneumococcus in vitro; it is the most predominant of the acute-phase proteins. DORLAND’S,
https://www.dorlandsonline.com/dorland/definition?id=100489&searchterm=C-reactive%20protein (last
visited March 19, 2025).
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vaccine. Id. He ordered additional lab tests, including for cytomegalovirus, Epstein-Barr virus,
and parvovirus B19. Id. The plan was to continue to slowly wean Petitioner off the prednisone.
Id.
Petitioner’s affidavit said his symptoms continued to worsen during December 2014.
Ex. 1 at 3. Mrs. Maxwell stated that, around this time, Petitioner was unable to “do anything
more than basic actions such as walking to the bathroom or getting something to eat.” Ex. 2 at
2.
On December 31, 2014, Petitioner saw Dr. Dinning. Ex. 14 at 7. Petitioner described
his symptoms as “constant,” leading Dr. Dinning to suspect he might be developing a chronic
inflammatory arthritis, such as RA. Id. On exam, Dr. Dinning observed swelling in the bilateral
hands, knees, feet, and ankles. Id. at 8-9. No redness or warmth of the joints was observed. Id.
Dr. Dinning noted that Petitioner’s lab work showed a negative rheumatoid factor (“RF”). Id.
at 7. He pondered whether a cyclic citrullinated peptide (“CCP”)6 test would be positive, given
the involvement of Petitioner’s large joints. Id. He diagnosed chronic inflammatory arthritis,
prescribed weekly methotrexate injections, and advised Petitioner to continue prednisone. Id.
at 8.
On January 7, 2015, Petitioner returned to PA Bledsoe. Ex. 13 at 9. His current pain
level was 7/10. Id. His ROM was slow due to pain. Id. That month, he returned to school
but was using a cane. Ex. 1 at 3. According to his affidavit, he was unable to type or write due
to the inflammation in his hands, and he had to use voice command software to complete
assignments. Id. at 2. He needed assistance getting to class. Id.
On February 10, 2015, Petitioner returned to Dr. Dinning for worsening pain. Ex. 14
at 13. He had swelling in the hands and knees. Id. at 15. He was diagnosed with RA, and
Humira was added to his medications. Id. The same day, Petitioner had x-rays of his bilateral
knees and hands, which showed no joint abnormality, soft tissue abnormality, or significant
joint effusion. Ex. 8 at 2-5.
On February 18, 2015, Petitioner returned to PA Bledsoe with complaints of lumps on
the backs of his knees. Ex. 13 at 11. Petitioner reported he was feeling much better since
starting prednisone and methotrexate, with minimal joint pain in the hands and wrists in the
morning. Id. He was diagnosed with bilateral Baker’s cysts7 of the knee and was instructed to
6 Cyclic citrullinated peptide: a synthetic, citrulline-containing peptide with a cyclic structure, used in assays
for rheumatoid arthritis; the presence of antibodies to this peptide is highly specific for rheumatoid arthritis.
DORLAND’S,
https://www.dorlandsonline.com/dorland/definition?id=97140&searchterm=cyclic+citrullinated+peptide
(last visited March 12, 2025).
7 Baker Cyst: a swelling behind the knee, caused by escape of synovial fluid that becomes enclosed in a
membranous sac; called also popliteal c.
DORLAND’S, https://www.dorlandsonline.com/dorland/definition?id=68277&searchterm=Baker%20cyst
(last visited March 12, 2025).
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ice the area and return if the pain worsened. Id.
On March 11, 2015, Petitioner filed a VAERS report. Ex. 12 at 1. He described the
onset of flu-like symptoms beginning October 7, 2015, two days after vaccination. Id.
On March 26, 2015, Dr. Dinning completed a Veterans Administration (“VA”) disability
benefits form stating that Petitioner had experienced the “sudden, explosive onset of joint
pain/swelling/stiffness/fever two days after flu vaccination” and had been diagnosed with RA.
Ex. 4 at 187-92.
On May 4, 2015, occupational health specialist Laurie Duran at the Naval Medical
Center in San Diego had a telephone consultation with Petitioner on behalf of the Defense
Health Agency, Immunization Healthcare Branch (“DHA-IHB”). Ex. 4 at 47. Petitioner
discussed his medical history and reported that he had experienced mild symptoms with
previous vaccinations. Id. at 49. He reported that his first cousin and great aunt had been
diagnosed with RA. Id. Additionally, in February 2015, his brother was diagnosed with
arthritis that was attributed to a 2010 exposure to hydraulic fluid. Id.
Bloodwork completed May 11, 2015, was positive for Epstein-Barr virus.8 Ex. 14 at 26.
On June 19, 2015, the DHA-IHB issued a “causality assessment” of Petitioner’s case.
Ex. 4 at 53. The committee found Petitioner had seronegative RA, which was acquired in the
line of duty, but it declared that the relationship between that condition and his flu vaccine was
“indeterminate.” Id. at 54. That same day, Petitioner saw Ms. Duran, who advised that
Petitioner should continue to follow with his rheumatologist and also see a military
rheumatologist. Id. at 53. Ms. Duran noted that Petitioner should approach live vaccines “with
caution” in light of the “theoretical risk” of exacerbating his condition. Id. at 54.
On June 29, 2015, Petitioner had a follow-up appointment with Dr. Dinning and
reported that the severity of his pain had decreased, but he was experiencing joint swelling and
fatigue. Ex. 14 at 29. An exam documented swelling in both hands, knees, and ankles. Id.
at 31. Dr. Dinning increased the Humira dosage. Id. at 32.
On August 28, 2015, Petitioner saw PCP Deborah Collins, M.D., for knee stiffness,
popping, and “giving out.” Ex. 13 at 18. He was using a cane and having difficulty walking.
Id. He reported pain ranging from 3-8/10 in severity. Id. On exam, he had mild tenderness to
palpation (“TTP”) and crepitus in both knees. Id. He had very little ability to bear weight on
the right knee. Id. at 19. Dr. Collins recommended starting naproxen and obtaining x-rays of
the knees, but she suspected that Petitioner more likely had a “soft tissue pathology.” Id.
On September 4, 2015, Petitioner saw psychologist Jane Barga, Ph.D., for reported
8 Epstein-Barr virus: a virus of the genus Lymphocryptovirus that causes infectious mononucleosis and is
associated with Burkitt lymphoma and nasopharyngeal carcinoma. DORLAND’S,
Https://www.dorlandsonline.com/dorland/definition?id=80849 (last visited December 20, 2024).
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anxiety associated with his RA diagnosis. Ex. 9 at 6.9
On September 28, 2015, Petitioner saw orthopedist Steven Pennington, M.D., for
bilateral knee pain. Ex. 15 at 1. Petitioner reported that the Humira had eased his symptoms
in all joints except his knees. Id. He was walking with a cane. Id. An MRI of his knee was
normal, but his knees were stiff on exam. Id. He inquired about the possibility of undergoing
a synovectomy (a surgery to address intractable knee pain), but Dr. Pennington did not think
that was indicated. Id. Dr. Pennington administered a right knee corticosteroid injection. Id.
Petitioner’s affidavit states that the Army and the VA conducted medical evaluations in
November 2015. Ex. 1 at 3. The Army gave Petitioner a 90% disability rating, and the VA gave
him an 80% disability rating, which was deemed to be service related. Id. Petitioner was placed
on the Army's Permanent Disability Retired List, and he medically retired on February 18, 2016.
Id.
Petitioner saw Dr. Collins on August 4, 2016, to secure a disability letter for his school.
Ex. 13 at 26. He reported that his symptoms were much better and controlled with Humira and
etodolac (an NSAID used to treat arthritis). Id. The diagnosis was RA. Id.
Petitioner moved to Tempe, Arizona, in July 2017 to start a graduate degree. Ex. 1 at 3.
Shortly thereafter, he developed shingles, which required him to suspend Humira treatment for six
weeks. Id.
On June 22, 2018, Petitioner saw internist Sriharsha Vajjala, M.D., at Marana Main
Health Center in Marana, Arizona, to establish care as a new patient. Ex. 27 at 1. Petitioner
reported that he had recently moved to the area and that he had been diagnosed in 2015 with
“chronic RA,” for which he had been on Humira for the “past [three] years and prednisone as
needed.” Id. His exam was normal. Id. at 3. Petitioner stated that he believed his RA
medications were losing efficacy, so Dr. Vajjala gave him a rheumatology referral. Id.
On July 20, 2018, nearly four years after his vaccination, Petitioner presented to
rheumatologist Jeffrey Loomer, M.D. Ex. 28 at 1. He reported that he was diagnosed with
seronegative RA in 2014 and had been followed by Dr. Dinning.10 Id. His symptoms would “flare
up” every four to six weeks, affecting his knees, wrists, ankles, and elbows. Id. He attributed his
condition to the flu vaccination, but he was not certain he had RA. Id. He reported that he had a
“big family history of RA and [ankylosing spondylitis] with [his] brother and three cousins who[]
were all diagnosed in [their] late twenties.” Id. He reported that all of his relatives with RA
“started out seronegative then would ‘turn’ seropositive after 1-2 years after their diagnosis, but
[he had] not.” Id. He requested additional laboratory testing before resuming taking RA
medications. Id.
9 Petitioner continued to see a psychologist for his anxiety and his other preexisting mental health issues
through December 2015 and again in July 2016. See generally Ex. 9.
10 Petitioner reported that his last appointment with Dr. Dinning was in June of 2017. Ex. 28 at 1. The
record before me, however, does not contain any notes from such a visit.
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On the day of the visit with Dr. Loomer, Petitioner was “coming out of a flare, which
put him down in bed for two days.” Ex. 28 at 1. He had not taken the Humira for three weeks
due to a rash he had developed. Id. A review of systems “(ROS”) was positive for fatigue,
heartburn, rash, low back pain, joint pain, joint swelling, morning stiffness, neck pain, and
muscle pain. Id. at 2. A joint exam documented 24 tender joints and 23 swollen joints. Id.
at 3. Dr. Loomer observed signs of a fungal rash. Id. at 2. He ordered lab tests and x-rays of
the ankles, chest, feet, hands, wrists, and lumbar and sacroiliac spine. Id. at 4. He believed
that Petitioner had RA but indicated that he would “take a fresh look at serologies and x-rays to
formulate a most accurate diagnosis.” Id.
Petitioner followed up with Dr. Loomer on August 6, 2018. Ex. 28 at 6. He continued
to be off of the Humira, and he felt “no wor[s]e off this medication (it was not working).” Id.
at 7. His lab results, dated July 21, 2018, were negative for RF, CCP, or elevated ESR or CRP,
and were otherwise normal. Id. at 12. His hand, wrist, foot, and ankle x-rays were negative
for inflammatory changes, and his lumbosacral spine and sacroiliac joints were negative for
degenerative or inflammatory changes. Id. He complained of abdominal pain. Id. at 7. He
had mild TTP of the joints on exam. Id. at 8. Dr. Loomer assessed seronegative RA,
commenting on Petitioner’s “strong” family history of the disease. Id. at 12. He prescribed
sulfasalazine. Id.
On August 19, 2018, Petitioner presented to Estela Rutiaga, M.D., at Dove Mountain
Urgent Care, complaining of a rash and a flareup of his RA symptoms. Ex. 27 at 15. He had
been off of the Humira for the past six weeks. Id. He had discontinued use of the sulfasalazine
after two days when he developed a rash, and he had discontinued the prednisone due to
abdominal pain. Id. A ROS was negative for joint pains, muscle weakness, inflammation,
tenderness, or swelling. Id. at 16. An exam showed mild TTP to the right lower quadrant but
was otherwise normal. Id. Dr. Rutiaga assessed Petitioner with a rash. Id. She advised him to
discontinue the sulfasalazine, gave Petitioner a “GI cocktail” in the office, and administered a
Kenalog injection for the rash. Id.
On August 22, 2018, Petitioner returned to Dr. Loomer after his urgent care visit. Ex.
28 at 14. On exam, Dr. Loomer observed tenderness in 16 joints in Petitioner’s elbows, wrists,
hands, and knees. Id. at 16. Petitioner’s ankles were tender and swollen. Id. at 17. Dr. Loomer
started Petitioner on Simponi Aria infusions. Id. at 20.
On August 30, 2018, Petitioner returned to Dr. Loomer sooner than anticipated due to
worsening abdominal discomfort and rash. Ex. 28 at 22. Dr. Loomer felt the rash was caused
by the sulfasalazine. Id. at 27. He prescribed a low dose of prednisone. Id.
Petitioner had his first Simponi Aria infusion on September 20, 2018. Ex. 28 at 29. He
had a second infusion on October 18, 2018. Id. at 32.
Petitioner relocated to New England. On September 19, 2019, he presented to
rheumatology fellow Elizabeth Graef, D.O., at Beth Israel Deaconess Medical Center, to
establish care. Ex. 45 at 8. He reported “notable improvement” on Simponi Aria, but he was
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still experiencing recurrent morning stiffness affecting the metacarpophalangeal joints,
proximal interphalangeal joints, and knees. Id. at 9. His exam showed no signs of synovitis
but did show tenderness in several bilateral metacarpophalangeal joints. Id. at 11-12. Dr. Graef
opined that Petitioner’s history was “somewhat atypical” and commented that she would
“consider seronegative spondyloarthropathy though symmetric small joint involvement was
more consistent with RA.” Id. at 12. She referred Petitioner to allergy and immunology for
testing. Id. at 13.
Dr. Graef’s exam was reviewed by attending rheumatologist Robert Shmerling, M.D.
Ex. 45 at 14. Dr. Shmerling’s impression was “[History] of seronegative RA – details uncertain.
Will check xrays, labs . . . consider past fungal exposure given time spent in Arizona, Idaho;
vaccination [history] reviewed.” Id. His plan was to closely follow Petitioner and review his
medical records. Id.
Petitioner’s lab tests from September 19, 2019, were negative for RF or CCP. Ex. 45 at
3, 8. X-rays of the hands and knees were normal. Id. at 54.
On September 26, 2019, Petitioner presented to allergist Qura Rashid, M.D., for a
consult relating to a possible vaccine allergy. Ex. 45 at 15. Dr. Rashid advised Petitioner that
“there is no way to test for [a] [non-IgE] mediated allergic reaction.” Id. at 18. He
recommended that Petitioner receive the intranasal flu vaccine, as he had previously tolerated
that formulation of the vaccine. Id.
Petitioner resumed Simponi Aria infusions on October 3, 2019, and continued to receive
them regularly. See generally Ex. 45.
On December 12, 2019, Petitioner saw Drs. Graef and Shmerling. Ex. 45 at 23.
Petitioner reported that his breakthrough arthralgias had resolved with the infusions. Id. at 24.
The only symptom he reported was mild achiness in his hands and knees when outside during
cold weather. Id. at 25. An exam revealed no synovitis. Id. Petitioner was advised to continue
the current regimen. Id. at 26.
Petitioner had a telephonic appointment with Dr. Graef on April 30, 2020, with
complaints that his hands felt stiffer two to three days a week and were worse at the end of the
day after extensive typing. Ex. 45 at 34. Dr. Graef concluded that his symptoms were likely
due to poor ergonomics while working. Id. at 35. She ordered a trial of Voltaren gel. Id.
On August 5, 2020, Petitioner saw rheumatology fellow Afroditi Boulougoura, M.D.,
and attending rheumatologist Kristie Pepper, D.O. Ex. 45 at 41. Petitioner’s RA was noted to
be in remission, and his treatment plan remained unchanged. Id. On November 3, 2020,
Petitioner returned to Dr. Boulougoura, reporting a three-week history of pain in his hands and
knees with tenderness in the bilateral fourth metacarpophalangeal joints and proximal
interphalangeal joints, left wrist, and bilateral knees. Id. at 51. His exam showed tenderness of
several joints but no synovitis. Id. at 53. Repeat labs were normal. Id. At that time, the plan
was to continue the Simponi Aria infusions every eight weeks, start naproxen and omeprazole,
and return for a follow-up in six weeks. Id. at 54.
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Petitioner’s last appointment with Dr. Boulougoura was on February 24, 2021, as he
was preparing to move back to Idaho. Ex. 45 at 66. Petitioner was to continue with the
treatment plan and was strongly advised to make an appointment with a rheumatologist in
Idaho. Id.
On September 23, 2021, Petitioner was seen by PCP Amanda Berbert, M.D., at Family
Medicine Health Center, seeking a referral to continue the Simponi Aria infusions. Ex. 47 at
11. On October 12, 2021, he returned to Dr. Berbert because he was unable to get a
rheumatology appointment until December. Ex. 47 at 5-7. Dr. Berbert noted that Petitioner
was due for an infusion on October 8, 2021, and she prescribed prednisone as needed for RA
flareups. Id.
On November 3, 2021, Petitioner saw rheumatologist Achini Dingman, M.D. Ex. 48 at
25-29, 51-56. He reported increased joint pain involving his hands and knees, noting that he
was taking prednisone for the pain. Id. at 25-26. An exam was negative for synovitis, but Dr.
Dingman observed “notable warmth” with “mild fullness” over the right wrist. Id. at 28.
Petitioner denied significant pain in the wrists. Id. Dr. Dingman administered an intramuscular
steroid injection for Petitioner’s knee pain. Id.
On February 7, 2022, Petitioner presented to Dr. Dingman for a follow-up appointment.
Ex. 48 at 1. He was doing well on the Simponi Aria infusions. Id. at 3. There are no further
relevant treatment records.
III. EXPERT EVIDENCE
A. Pre-Hearing Expert Reports
1. Eric Gershwin, M.D., MACR, MACP: First Expert Report
Dr. Gershwin submitted five reports in this case. Ex. 18 (“First Gershwin Rep.”); Ex. 29
(“Second Gershwin Rep.”); Ex. 34 (“Third Gershwin Rep.”); Ex. 38 (“Fourth Gershwin Rep.”);
Ex. 53 (“Fifth Gershwin Rep.”). He also testified at the entitlement hearing. Tr. at 7-95, 163-67.
Dr. Gershwin earned his M.D. from Stanford University in 1971 and is board certified in
internal medicine, rheumatology, and allergy/clinical immunology. Tr. at 8; Ex. 19 (“Gershwin
CV”) at 1-2. He is a Master of the American College of Rheumatology and a Master of the
American College of Physicians, the highest clinical honors a rheumatologist/internal medicine
specialist can receive in the United States. Tr. at 11; Gershwin CV at 1. He is currently the Jack
and Donald Chia Professor of Medicine and a Distinguished Professor of Medicine at the
University of California, Davis. Tr. at 8; Gershwin CV at 1. He serves as the editor-in-chief for
Clinical Reviews in Allergy, Reviews in Autoimmunity, Autoimmunity Reviews, and the Journal of
Autoimmunity, and as an ad hoc editor for numerous other publications. Gershwin CV at 5-7. He
has written and edited 1,000 peer-reviewed experimental papers, several hundred book chapters
and book reviews, and at least 50 books. Tr. at 910.
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Dr. Gershwin concluded that Petitioner suffered from seronegative RA. First Gershwin
Rep. at 1. RA is “an inflammatory arthropathy that leads to significant inflammation, and, if
unresponsive, joint destruction and reduction in physical function.” Id. at 2. The disease affects
women over men at a ratio of at least 4-5:1. Id. at 1. In men, RA is most often seen in those with
a history of smoking. Id. at 2. Severe periodontal disease is also a risk factor. Id. at 3. In 80-90%
of patients, serology will eventually be positive for antibodies to RF and/or CCP antigens. Id. at
2. It is unusual to see a male, non-smoking, seronegative RA patient without any history of
periodontal disease. Id. at 2-3.
The diagnosis of RA includes blood testing and examination for synovitis, or swelling of
the synovium. First Gershwin Rep. at 2. Patients often respond to drugs that inhibit a pro-
inflammatory cytokine response. Id. at 3. Here, Petitioner showed evidence of joint swelling and
responded to anti-inflammatory treatments, but he had neither a positive RF nor antibodies to CCP,
so the proper diagnosis was seronegative RA. Id. at 1-3.
Dr. Gershwin disavowed a causal connection between seropositive RA and vaccination.
First Gershwin Rep. at 2. He stated that, if Petitioner had been seropositive, he would not have
offered an opinion supporting vaccine causation. Id. However, seronegative RA “should be
considered a distinct clinical pathologic entity.” Id; Firestein & McInnes, Immunopathogenesis of
Rheumatoid Arthritis, 46 IMMUNITY REV. 183, 185 (2017) (Ex. 20) (“Firestein & McInnes”).
Specifically, the environmental risks, disease severity, and overall clinical outcome are different
for seropositive and seronegative RA patients. First Gershwin Rep. at 2. Genetic factors likely
account for these differences. Id.
Dr. Gershwin noted that “[t]here is considerably less epidemiology on seronegative disease
following vaccination and, in fact, there is no significant power calculations that I am aware of for
the presence of seronegative [RA] in a young, non-smoking male following influenza
vaccination.” First Gershwin Rep. at 2. Nonetheless, he opined that there was a reliable
mechanistic theory linking seronegative RA and the flu vaccination. Id. These patients experience
“intense cellular infiltrates” that result from activation of both the innate and adaptive immune
responses. Id. The innate response would “include activation of cytokines and complement and
the adaptive response would include an immune response to self-proteins.” Id. The initial RA
presentation (within 48 hours) would result from the innate response, while the adaptive response
would follow and perpetuate the disease. Id.
Whether or not B cells are producing antibody or only acting as
antigen-presenting cells, and/or producers of inflammatory
cytokines, is also less clear. What is clear, however, is that patients
are treated and often respond to drugs that inhibit a pro-
inflammatory cytokine response and this indeed is the treatment that
has been given to [Petitioner].
Id. at 2-3.
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Dr. Gershwin concluded that Petitioner developed an acute inflammatory arthritis 48 hours
after his flu vaccination, which was caused by an innate immune cell activation due to the vaccine
and subsequently evolved into seronegative RA. First Gershwin Rep. at 3.
2. Chester V. Oddis, M.D.: First Expert Report
Dr. Oddis submitted four reports in this case. Ex. A (“First Oddis Rep.”); Ex. E (“Second
Oddis Rep.”); Ex. G (“Third Oddis Rep.”); Ex. R (“Fourth Oddis Rep.”). He also testified at the
entitlement hearing. Tr. at 96-136.
Dr. Oddis earned his M.D. from Pennsylvania State University College of Medicine, where
he also completed his residency in internal medicine. Tr. at 97; Ex. B (“Oddis CV”) at 1. He is
board certified in internal medicine and rheumatology. Tr. at 97; Oddis CV at 3. In 1987, he
completed a fellowship in rheumatology at the University of Pittsburgh, where he currently serves
as a Professor of Medicine in the Division of Rheumatology and Clinical Immunology. Tr. at 97;
Oddis CV at 1-2. Outside of teaching, Dr. Oddis performs clinical research and maintains a clinical
practice, spending half his time seeing patients with a variety of conditions, from autoimmune
diseases like myositis to rheumatological diseases. Tr. at 98-99. He sees about 40-45 RA patients
monthly, fewer than 10% of whom are seronegative. Tr. at 99-100. He has published about 150
peer-reviewed articles. Id. at 101; Oddis CV at 4-13.
Dr. Oddis opined that Petitioner did not have seronegative RA. First Oddis Rep. at 3. At
the time of his initial presentation in November 2014, his lab results were “completely normal.”
Id. Additionally, his musculoskeletal exam revealed no joint swelling. Id. Consistent with these
observations, the initial diagnosis was polyarthropathy, indicating joint pain, not polyarthritis,
which would have signified an inflammatory condition. Id. When Petitioner was seen by
rheumatologist Dr. Dinning in late November 2014, he still had no objective lab evidence of any
inflammatory condition. Id. Petitioner’s ESR and CRP findings were normal to low-normal,
which is “distinctly unusual in a patient with RA.” Id. The only evidence of any joint abnormality
was swelling of the hands, which was repeated in a template form in Dr. Dinning’s notes. Id.
Dr. Oddis commented that there were “other peculiar findings in this patient.” First Oddis
Rep. at 3. When Petitioner saw PCP Dr. Collins on August 28, 2015, he complained of his knee
“popping out” and reported an 8/10 pain level, but he had a normal exam and was assessed with a
“likely soft tissue pathology,” which was inconsistent with RA. Id. at 2-3. When he saw
orthopedist Dr. Pennington on September 28, 2015, he was using a cane and asked about a
synovectomy, but his examination was normal. Id. at 3; Ex. 15 at 1. Dr. Oddis concluded that
Petitioner experienced “a subjective over-reaction to pain which likely forced the hand of the
rheumatologist to pursue a treatment approach that was more aggressive than was clinically
indicated.” First Oddis Rep. at 4. He was not surprised that Petitioner responded to RA therapies,
noting that there was a documented placebo response in the clinical trials. Id.; Azais et al, Meta-
Analysis of The Clinical Efficacy of The Placebo Effect from Tumour-Necrosis-Factor Inhibitors
to Treat Rheumatoid Arthritis After Methotrexate Failure, 2 J. RHEUMATIC DISEASES &
TREATMENT 1, 4 (2016) (Ex. A, Tab 1) (“Azais”); Abdullah, Placebo Effect in The Treatment of
Rheumatoid Arthritis: A Systematic Review and Meta-Analysis of Randomized Controlled Trials,
SCI. ABSTRACTS 263, 263 (2015) (Ex. A, Tab 2) (“Abdullah”).
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Dr. Oddis disagreed with Dr. Gershwin’s statement that seronegative RA patients can
become positive for RF and CCP antibodies over time. First Oddis Rep. at 4. To the contrary, the
prevailing view is that “autoantibody positivity actually develops before the clinical manifestations
of RA,” which is referred to as “preclinical” RA. Id. (emphasis in original); Deane & El-
Gabalawy, Pathogenesis and Prevention of Rheumatic Disease: Focus on Preclinical RA and SLE,
10 NATURE REV.’S RHEUMATOLOGY 212, 212 (2014) (Ex. A, Tab 3) (“Deane & El-Gabalawy”);
Deane, Preclinical Rheumatoid Arthritis (Autoantibodies): An Updated Review, 16 CURRENT
RHEUMATOLOGY REP.’S 1, 1 (2014) (Ex. A, Tab 4) (“Deane”).
Dr. Oddis opined that if Petitioner’s inflammatory response was as intense as Dr. Gershwin
described, he “would have expected elevated inflammatory markers.” First Oddis Rep. at 4. These
were never observed. Id. Dr. Oddis also disagreed with Dr. Gershwin’s theory of how Petitioner
developed acute inflammatory polyarthritis 48 hours after vaccination, as Petitioner never had an
acute polyarthritis and, in particular, presented in November 2014 with a normal examination and
laboratory findings. Id.
3. You-Wen He, M.D., Ph.D.: First Expert Report
Dr. He submitted three reports in this case. Ex. C (“First He Rep.”); Ex. F (“Second He
Rep.”); Ex. H (“Third He Rep.”). He also testified at the entitlement hearing. Tr. at 136-62.
Dr. He received his medical degree in China from the Fourth Military Medical University
and his Ph.D. from the University of Miami School of Medicine. Tr. at 138-39; Ex. D (“He CV”)
at 1. He has been a Professor of Immunology in the Department of Immunology at Duke
University Medical Center since 2000. Tr. at 137; He CV at 1. About 80-85% percent of his work
is focused on research, with the remaining time spent on teaching and consultations. Tr. at 137.
He also serves as a Principal Investigator in four clinical trials testing cancer immunotherapies.
Tr. at 137-38. He has published more than 135 peer-reviewed articles. Id. at 138; He CV at 8-15.
Dr. He deferred to Dr. Oddis on Petitioner’s diagnosis and focused his report on causation.
First He Rep. at 2. He defined RA as a chronic inflammatory autoimmune disease primarily
affecting joints. Id.; Firestein & McInnes at 183; Klareskog et al., Rheumatoid arthritis, 373
LANCET 659, 659 (2009) (Ex. C, Tab 2) (“Klareskog”). The disease can take many years to
develop. First He Rep. at 4. A major feature of RA is the development of autoantibodies to
immunoglobin and anti-citrullinated proteins, which are the autoimmune responses considered to
cause self-destructive damage in RA. First He Rep. at 2. Seropositive patients have detectable
RF and CCP antibodies, while patients without detectable amounts of these substances are
classified as seronegative. Id.; Pratt & Isaacs, Seronegative Rheumatoid Arthritis: Pathogenetic
and Therapeutic Aspects, 28 BEST PRACTICE & RES. CLINICAL RHEUMATOLOGY 651, 651-52
(2014) (Ex. C, Tab 3) (“Pratt”). Only a small fraction of RA patients are seronegative. First He
Rep. at 2.
Dr. He explained that although the etiology of RA is still unclear, genetic predisposition
and environmental factors are considered the probable root causes. First He Rep. at 2; Firestein &
McInnes at 183; Klareskog at 659; Pratt at 653. There are also differences in the genetic
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backgrounds, risk factors, and clinical courses for seronegative and seropositive RA patients. First
He Rep. at 3, 5; Pratt at 653. Identified risk factors for RA include “certain human MHC
haplotypes, some epigenetic markers, smoking, microbiota,” and female sex. Id. at 2. However,
microbes and smoking are established risk factors for seropositive RA only, not seronegative RA.
Id. at 5.
Dr. He opined that there is no causal relationship between either serotype of RA and the
flu vaccine. First He Rep. at 3. Population-based studies showed that “different influenza vaccines
did not enhance the incidence of [RA].” Id.; Kurland et al., Lack of Association of Swine Flu
Vaccine and Rheumatoid Arthritis, 59 MAYO CLINIC PROC. 816, 820 (1984) (Ex. C, Tab 4)
(“Kurland”); Bardage et al., Neurological and Autoimmune Disorders After Vaccination Against
Pandemic Influenza A (H1N1) With a Monovalent Adjuvanted Vaccine: Population Based Cohort
Study in Stockholm, Sweden, BMJ 1, 4-5 (2011) (Ex. C, Tab 5) (“Bardage”). Studies also found
the flu vaccine was safe for RA patients. First He Rep. at 3.
Dr. He disagreed with Dr. Gershwin’s theory that innate immune cell activation alone could
lead to RA. First He Rep. at 6. Rather, the development of RA is gradual, beginning with
citrullination of host proteins, which leads to the presentation of antigens, activation of T
lymphocytes, and production of antibodies that recognize self-proteins. Id. at 2. This autoimmune
response induces synovial inflammation and produces inflammatory cytokines, such as TNF, IL-
1, IL-6, and IL-8, which cause tissue damage. Id. at 2-3. “Thus, the treatment based on blockage
of inflammatory cytokines is effective to relieve symptoms and reduce tissue damage.” Id. at 3.
Both innate and adaptive cellular responses are involved in the process. Id. at 4.
In this case, Petitioner’s ESR and CRP levels were normal, indicating that there was no
systemic inflammation. First He Rep. at 4. The lack of systemic inflammation made it unlikely
that activation of innate immunity alone was the cause of his severe joint pain. Id. at 5. Moreover,
the onset of Petitioner’s symptoms within 48 hours was inconsistent with an adaptive immune
reaction causing severe tissue damage. Id. at 4. In a typical immune response, the initiation of
innate immune response is rapid, occurring within the first three days of vaccination. Id. The
adaptive immune response then takes between 7-15 days, as the anti-joint tissue T lymphocytes
and B cell-produced autoantibodies take time to develop and induce tissue damage. Id. at 4-5. For
flu vaccines specifically, it would take two to four weeks to develop detectable anti-influenza
antibodies. Id. at 4. Given the time needed for an adaptive immune response, Petitioner’s acute
onset of symptoms could not have been induced by the flu vaccine. Id. at 5.
4. Dr. Gershwin’s Second Expert Report
In response to Dr. Oddis, Dr. Gershwin noted that in 2018, a second rheumatologist, Dr.
Loomer, agreed with Petitioner’s seronegative RA diagnosis. Second Gershwin Rep. at 1; Ex.
28. In fact, none of Petitioner’s treating physicians questioned the initial RA diagnosis assigned
by Dr. Dinning. Second Gershwin Rep. at 2. Furthermore, Dr. Dinning observed synovitis
following the vaccination, supporting the RA diagnosis. Id.; Ex. 14 at 2-3. Also, Petitioner’s
negative CRP and ESR tests did not rule out a RA diagnosis; instead, those tests reflected the
relative mildness of his condition. Second Gershwin Rep. at 2.
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Dr. Gershwin agreed with Dr. Oddis that RA antibodies can develop before clinical
symptoms in seropositive RA, but a patient with seronegative RA will not develop detectable
autoantibodies. Second Gershwin Rep. at 2; Venables, Diagnosis and Differential Diagnosis of
Rheumatoid Arthritis, UPTODATE 1, 3 (2018) (Ex. 30) (“Venables”) (noting that both the RF and
anti-CCP antibody tests “are negative on presentation in up to 50 percent of patients and remain
negative during follow-up in 20 percent of patients with RA”).
Responding to Dr. He on the question of onset, Dr. Gershwin pointed out that they agreed
that the “initiation of an innate immune response is rapid, occurring within the first [three] days,”
with the adaptive immune response trailing later. Second Gershwin Rep. at 2. Petitioner’s clinical
course indicates he had an initial, rapid innate response. Id. However, Dr. Gershwin could not
point to evidence of an adaptive immune response because Petitioner had seronegative RA, which
is a complex disease that is not fully understood. Id. at 2-3. Nonetheless, the innate immune
response was what initially triggered Petitioner’s disease. Id.
5. Dr. Oddis’s Second Expert Report
In his second report, Dr. Oddis again explained that Petitioner’s initial exam in November
2014 “never documented joint swelling, and, as previously summarized, [Petitioner] has never
once had elevated inflammatory markers commonly seen with RA.” Second Oddis Rep. at 1.
Later, when Petitioner saw Dr. Loomer in July 2018, he complained of a recent flare of his arthritis
that rendered him bedridden for two days. Id. at 2-3. However, extensive lab testing at that time
was completely normal, despite the fact that his blood was “drawn at a time when [Petitioner] was
completely off all medications for [RA] for several weeks.” Id. at 1 (emphasis in original). Dr.
Oddis could not recall any of his RA patients with normal lab results being bedridden. Id. at 2-3.
Furthermore, four years after the onset of Petitioner’s symptoms, he continued to have negative
RF and anti-CCP autoantibodies, and every musculoskeletal examination by Dr. Loomer was
negative for swelling of the joints. Id.at 1; Ex. 28 at 8, 16, 23, 35.
Dr. Oddis questioned the relevance of Petitioner’s family history of RA, because it was
unverified and because a family history is only relevant in patients with seropositive RA. Second
Oddis Rep. at 2. He pointed out that the Venables article, which discussed seronegative RA, noted
that the diagnosis requires that the patient exhibit characteristics of RA, which Petitioner never
had. Id.; Venables at 7. In Dr. Oddis’s opinion, Petitioner consistently exhibited a subjective over-
reaction to pain and had a chronic pain syndrome, not RA. Second Oddis Rep. at 2.
6. Dr. He’s Second Expert Report
Dr. He opined that, for RA to develop, both the innate and adaptive immune systems would
need to be activated. Second He Rep. at 2. Activation of innate immunity would exhibit as acute
inflammation and disappear in a few days. Id. Activation of adaptive immunity would take
“much longer than the 2 days that was exhibited in [Petitioner’s] disease course.” Id. An
autoimmune response to the joints would not occur without subsequent development of
autoreactive adaptive antibody and/or T lymphocyte responses. Id. Because Petitioner’s T
lymphocytes were not assayed, it is unknown whether he had such a response. Id. Dr. Gershwin’s
complete reliance on activation of innate response was not scientifically sound and not supported
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by the literature. Id.
7. Dr. Gershwin’s Third Expert Report
Dr. Gershwin reiterated that two qualified rheumatologists agreed with the seronegative
RA diagnosis and treated Petitioner for that condition. Third Gershwin Rep. at 1. He
acknowledged that Petitioner did not have positive inflammatory markers and might have had an
overreaction to his pain, but that did not necessarily obviate the RA diagnosis. Id.
Dr. Gershwin disagreed with Dr. He that innate immunity was not an essential component
of RA. Third Gershwin Rep. at 1. Indeed, it is impossible to develop an adaptive immune
response without an innate immune response. Id. Also, Dr. Gershwin pointed to “multiple
studies reflecting that effector cells and molecules of the innate immune system are locally
recruited into the synovium, as evidenced by macrophage expression of TNFalpha, IL-1 and IL-
6.” Id.; Gierut et al., Innate Immunity and Rheumatoid Arthritis, 36 RHEUMATIC DISEASE CLINICS
N. AM. 271, 271 (2010) (Ex. 35) (“Gierut”); Firestein, Evolving Concepts of Rheumatoid
Arthritis, 423 NATURE 356, 360 (2003) (Ex. 36) (“Firestein”); Hong et al., Arthritis Critically
Dependent on Innate Immune System Players, 16 IMMUNITY 157, 157-58 (2002) (Ex. 37)
(“Hong”).
8. Dr. Oddis’s Third Expert Report
Dr. Oddis pointed out that, because Petitioner had normal inflammatory markers over the
course of his then six-year diagnosis, the articles discussing innate immunity leading to an
inflammatory state were irrelevant. Third Oddis Rep. at 1.
Dr. Oddis responded to Special Master Oler’s September 4, 2019 Order, in which she stated
her preliminary opinion that Petitioner’s condition satisfied the American College of
Rheumatology’s criteria for RA (“ACR Criteria”). Third Oddis Rep. at 1; Aletaha & Smolen,
2010 Rheumatoid Arthritis Classification Criteria, 62 ARTHRITIS & RHEUMATISM, 2569, 2569
(2010) (Ex. G, Tab 1) (“Aletaha”). Dr. Oddis disagreed, explaining that the classification criteria
were used in clinical trials and were not appropriate for diagnosing an individual patient. Third
Oddis Rep. at 1; see Aletaha at 2572.
Furthermore, regardless of the intended use of the ACR Criteria, Dr. Oddis explained that
Petitioner would not meet the standards to enter a clinical trial based on the criteria. Third Oddis
Rep. at 2. In fact, Petitioner would only score a “1” based on the duration of his symptoms, given
his normal lab results and lack of joint inflammation. Id.; see Aletaha at 2574.
9. Dr. He’s Third Expert Report
Dr. He reiterated his position that the innate immune response alone would not be sufficient
to cause RA. Third He Rep. at 2. RA, as he described, is a chronic disease, which evolves slowly,
involving both an innate and an adaptive immune cellular response. Id. Two days is insufficient
for the initiation of the adaptive immune cellular response; therefore, the subject vaccine is not a
plausible cause of Petitioner’s condition. Id. at 3.
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10. Dr. Gershwin’s Fourth Expert Report
Dr. Gershwin agreed with Dr. He’s statement that an adaptive immune response could not
occur within 2 days. Fourth Gershwin Rep. at 1. However, Dr. He based his opinion “on the
presence of a typical adaptive immune response in seropositive [RA],” but since Petitioner was
seronegative, this opinion was irrelevant. Id.; Firestein at 358.
Dr. Gershwin also disagreed with Dr. Oddis’s suggestion that Petitioner had a
psychosomatic illness. Fourth Gershwin Rep. at 1-2. He opined that the medical records did not
support such an alternative diagnosis, and he reiterated that Petitioner’s treating physicians
diagnosed and treated Petitioner for seronegative RA. Id. at 2.
B. Expert Testimony
1. Dr. Gershwin’s Testimony
Dr. Gershwin opined that Petitioner was correctly diagnosed with seronegative RA. Tr. at
14-15. The onset of Petitioner’s symptoms was abrupt, suggesting that there was an environmental
factor that triggered the condition. Id. Also, Petitioner experienced morning stiffness, pain, and
swelling of his joints in a distribution compatible with RA. Id. at 15, 18-19, 26, 71; Ex. 4 at 384-
86 (December 7, 2015 visit); Ex. 14 at 1-2 (November 25, 2014 visit); 7-12 (December 31, 2014
visit); 29-32 (June 29, 2015 visit). On at least one exam, he had swelling in multiple joints, but
not in the distal interphalangeal joints (“DIP joints”),11 which is noteworthy because in RA those
joints remain disease-free. Tr. at 15, 20-23, 26; Ex. 28 at 1-5 (July 20, 2018 visit). Erythema,12
another characteristic of RA, was also documented.13 Tr. at 21-23, 26, 69; Ex. 13 at 1-2 (November
7, 2014 visit); Ex. 14 at 1-2. The treating physicians uniformly believed Petitioner had
seronegative RA, and that diagnosis was confirmed by a military review panel. Tr. at 15, 53, 67.
He was prescribed steroids and biologics, common RA therapies. Id. at 15-16. The treating
physicians would not have prescribed these therapies absent a definitive RA diagnosis. Id. at 29.
Dr. Gershwin differentiated between seropositive and seronegative RA, stating that the
serotypes are likely different diseases, with seropositive RA characterized by the presence of
antibodies against proteins like CCP, fibrinogen, vimentin, alpha-enolase, and RF, in contrast to
seronegative RA. Tr. at 31-32, 51-52, 77-78. The treatment protocols for seronegative and
11 DIP joint: the interphalangeal joint located distally on any digit. DORLAND’S,
https://www.dorlandsonline.com/dorland/definition?id=83515&searchterm=DIP+joint (last visited March
19, 2025).
12 Erythema: a redness of the skin produced by congestion of the capillaries. DORLAND’S,
https://www.dorlandsonline.com/dorland/definition?id=17187 (last visited March 19, 2025).
13 Dr. Gershwin admitted on cross examination that the medical record in question documented a general
finding of skin “redness” without specifying that the finding applied to the joints; he assumed that was what
was meant. Tr. at 58-59; see Ex. 14 at 2.
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seropositive RA may be similar. Id. at 32.
Petitioner met the published diagnostic criteria for RA. Tr. at 16; Kay & Upchurch,
ACR/EULAR 2010 Rheumatoid Arthritis Classification Criteria, 51 RHEUMATOLOGY 1, 1 (2012)
(Ex. 52) (“Kay”). A rheumatologist would not need to determine a patient met these criteria to
diagnose RA in the clinical setting. Tr. at 16. Nonetheless, Petitioner satisfied the criteria because
he had symptoms across multiple, symmetric joints, while sparing the DIP joints.14 Id.; Kay at 4
(Table 2).
Further, although Petitioner’s ESR and CRP levels were normal, that would not rule out a
diagnosis of RA.15 Tr. at 23-24, 73. Instead, they signified that his disease was mild. Id. at 24,
54, 75. Moreover, because Petitioner was treated with biologics and steroids, his signs, symptoms,
and inflammatory markers were likely suppressed to some extent. Id. at 15-16, 23-26. These
treatments also helped alleviate Petitioner’s condition, further supporting the diagnosis. Id. at 26-
28; see Ex. 15 at 1 (September 28, 2015 visit); Ex. 28 at 1-5 (July 20, 2018 visit). Dr. Gershwin
did not believe Petitioner’s response to these treatments was a mere placebo reaction. Tr. at 26.
Dr. Gershwin testified that RA is caused by a combination of genetic and environmental
factors. Tr. at 29-30, 63. The flu vaccine can cause seronegative RA in a genetically predisposed
person through the innate immune response. Id. at 40-45. After vaccination, there is an initial
innate immune response. Id. at 35-39; Firestein at 356; Hervé et al., The How’s and What’s of
Vaccine Reactogenicity, 4 NPJ VACCINES 1, 2 (2019) (Ex. 49) (“Hervé”). As part of that response,
cytokines and prostaglandins are released and can activate the innate immune cells in the
synovium. Tr. at 34-35; Hervé at 2-4; see Tu et al., A Tale of Two Immune Cells in Rheumatoid
Arthritis: The Crosstalk Between Macrophages and T Cells in the Synovium, 12 FRONTIERS
IMMUNOLOGY 1, 1 (2021) (Ex. 51) (“a variety of immune cells are involved in the pathogenesis of
RA [], including cells from the innate immune system”). This causes the local production of
inflammatory factors and “[c]ould amplify innate cytokine expression to promote disease.” Tr. at
38. Innate immunity is sufficient to trigger an inflammatory disease like seronegative RA. Id. at
44, 48-51. Although adaptive autoimmunity also likely develops as part of the natural history of
seronegative RA, the host tissues against which those autoantibodies or cytotoxic T cells are
directed have not been identified. Id. at 77.
Dr. Gershwin commented that shortly after vaccination, Petitioner exhibited signs of fever
and body, joint, and muscle aches, which grew progressively worse. Tr. at 32-33, 45; Ex. 13 at 2.
This was a sign that the resident innate cells already in Petitioner’s synovium had begun to activate.
Tr. at 43-45, 81. The fever and polyarthralgias evolved over multiple visits and with no other
preexisting evidence of RA. Id. at 41-42, 81. Further, the onset of Petitioner’s symptoms two
14 On cross examination, Dr. Gershwin was shown an article he co-authored discussing the diagnostic
parameters of RA. Tr. at 68; Greenspan & Gershwin, IMAGING IN RHEUMATOLOGY: A CLINICAL
APPROACH 1, 93 (2018) (Ex. L) (“Greenspan & Gershwin”). Dr. Gershwin testified that these criteria
reinforced his diagnosis of Petitioner. Tr. at 69-71; Greenspan & Gershwin at 3, 5.
15 Dr. Gershwin explained that Petitioner’s normal ESR and CRP results would result in the deduction of
points on the ACR classification scale, but that would not rule out an RA diagnosis. Tr. at 91.
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days after vaccination was medically acceptable, because innate immune responses can occur
within a few hours. Id. at 45.
On cross examination, Dr. Gershwin agreed that Petitioner’s blood tests did not show signs
of inflammation at any time, even when he was not being treated with biologic therapies. Tr. at
54-57, 59-62; Ex. 13 at 2 (November 7, 2014 visit), 5-6 (November 12, 2014 visit); Ex. 28 at 2, 9-
13 (July 20, 2018 visit). Additionally, Petitioner’s imaging studies did not show signs of erosion,
effusions, synovitis, or other characteristics of RA. Tr. at 76. However, in Dr. Gershwin’s opinion,
these facts did not exclude an RA diagnosis. Tr. at 57, 73.
Under questioning by Special Master Oler, Dr. Gershwin clarified that in general, he did
not believe that seropositive RA could be vaccine caused. Tr. at 82. The serotype was important
because there is a clearly defined preclinical phase in seropositive RA, whereas there is no
evidence of such a stage in seronegative RA. Id. at 83.
Dr. Gershwin testified that although Petitioner lacked the expected imaging changes one
would see in progressive, untreated RA, he was taking biologics and steroids, which were used to
prevent joint destruction. Tr. at 84-85, 93-94. This explains why he experienced swelling and
pain but had no imaging showing any type of synovial erosion. Id. at 85, 94. Furthermore, some
RA patients do not experience joint erosions. Id. at 85.
Special Master Oler inquired about Petitioner’s July 20, 2018 visit with rheumatologist Dr.
Loomer, who noted:
Known diagnosis of RA and strong [four-year] history of Humira
use which most recently has been minimally effective. . . Based on
our clinical and historical finding today, we do believe patient has
autoimmune condition (RA), but we will take a fresh look at
serologies and [x-rays] to formulate a most accurate diagnosis.
Ex. 28 at 4. Dr. Gershwin did not believe this record indicated doubt about the RA diagnosis;
instead, he believed Dr. Loomer wished to confirm the diagnosis was accurate, because using
biologics without a clear diagnosis was below the standard of care. Tr. at 87.
Special Master Oler asked how the innate immune response could lead to a chronic disease.
Tr. at 87-88. Dr. Gershwin explained that the innate immune response initiated the disease process,
and the adaptive response followed with autoantibodies, which are not identified in patients with
seronegative RA. Id. Although the perpetuation of the disease required an adaptive response, the
innate immune response would not disappear; it would simply have continued with the production
of inflammatory mediators. Id. at 88. Here, Petitioner’s reaction occurred after two days, which
was “highly consistent with an immune response.” Id. at 83.
2. Dr. Oddis’s Testimony
Dr. Oddis testified that RA involves the symmetric onset of inflammation affecting the
small joints of the hands and feet, usually in association with elevated inflammatory markers and
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the presence of RF and/or anti-CCP antibody positivity. Tr. at 109-10. ESR and CRP are markers
for inflammation. Id. at 118-19. The cause of RA is unknown, but there is typically a genetic
predisposition along with an environmental insult, such as an infection, which together trigger an
inflammatory response. Id. at 116-17. The flu vaccine has never been identified as a risk factor
for either seropositive or seronegative RA. Id. at 117.
There are key differences between seropositive and seronegative RA patients. Tr. at 110-
11. Seropositive patients normally have more overt and serious symptoms of swelling and
inflammation in their synovia, along with abnormal lab tests. Id. at 110. Seropositive and
seronegative RA are similarly treated with potent biologic agents and steroids, making it critically
important to ensure that a seronegative RA patient actually has the disease:
If you’re going to call somebody seronegative [RA], you better
make doggone sure that that’s the diagnosis, and it helps to follow
these patients over time so that there is [sic] more objective
manifestations of an inflammatory state, because, as I said, if you
are going to call it seronegative [RA], you are going to use the
medications that we have available, which means they are going to
be aggressively treated with steroids and some point, maybe low
dose, maybe higher dose, along with immunosuppressive drugs,
along with biologic agents that target particular cytokines that are
indicated in the pathogenesis of [RA], be it seronegative or
seropositive.
Id. at 110-11. To diagnose seronegative RA, one would consider clinical exams of the small joints
of the hands and feet, lab tests for inflammatory markers, and imaging. Id. at 115-16.
According to Dr. Oddis, the classification criteria for RA were intended to be used in
clinical trials to ensure participants truly have that diagnosis. Tr. at 112. There is a significant
placebo effect with treatments tested in clinical trials. Id. As such, to avoid distortion of clinical
trial results, it is critical to measure participants against the RA criteria to ensure they actually have
RA. Id.
Dr. Oddis testified that, after considering Petitioner’s overall clinical course, he did not
agree with the diagnosis of seronegative RA. Tr. at 104. Within 48 hours of his flu vaccination,
Petitioner did have some acute symptoms of joint aches and pains. Id. at 106. His lab tests,
however, did not show any evidence of inflammation over the course of eight years. Id. Although
he had intermittent treatment with biologics and steroids, which might have affected his lab
findings, it is still significant that his results were consistently normal over his eight-year course.
Id. Furthermore, Petitioner’s first rheumatologist, Dr. Dinning, appears to have “plugged”
abnormal exam findings into a template record, suggesting that these observations were not
actually made during multiple visits. Id. at 107. Also, when Petitioner saw the second
rheumatologist, Dr. Loomer, on July 20, 2018, Dr. Loomer documented 47 swollen or tender joints
– indicative of “a lot of inflammation” – but Petitioner’s ESR and CRP remained normal, showing
an ”undetectable” level of inflammation, in tests taken the next day. Id. at 108-09. Dr. Oddis
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concluded: “I don’t see this in seronegative [RA], I don’t see this in seropositive [RA], I don’t see
this in any disorder where there is concomitant inflammation.” Id. at 109.
Also notable was Petitioner’s report during the July 2018 visit that a flare-up caused him
to stay bedridden for two days. Tr. at 123. “[V]ery rarely does a patient [of Petitioner’s age] put
themselves in bed.” Id. Further, Petitioner was not convinced he had RA even after four years of
treatment. Id. at 123-24. This belief was “the reverse of what we normally see these days,” making
Dr. Oddis “very skeptical of that history.” Id. at 124.
Apart from disputing the diagnosis, Dr. Oddis did not believe that there was a reliable
theory for how the flu vaccine could cause seronegative RA. Tr. at 125. The flu vaccine was not
known to cause, exacerbate, or induce any form of RA. Id. at 117. Furthermore, although
Petitioner might have had normal, transient symptoms in the days after the vaccination, there was
no evidence in the medical records that he had an ongoing inflammatory response consistent with
seronegative RA. Id. at 127. Finally, the 2-day timeframe was inappropriate for the development
of seronegative RA. Id. at 126-27.
On cross examination, Dr. Oddis was asked to provide an alternative diagnosis for
Petitioner, but he was unable to conclusively opine on this. Tr. at 131-32. Petitioner’s actions
were overdramatic. Id. At his visit with orthopedist Dr. Pennington, he was using a cane for
reported knee inflammation but had a normal examination. Id. at 131. Also, despite the normal
examination, Petitioner made the unusual request for an aggressive operative procedure known as
synovectomy, which is used for uncontrolled inflammation in the knee joint. Id. at 131-32.
Dr. Oddis acknowledged that elevated ESR and CRP are not required to make a diagnosis
of seronegative RA; instead, those measurements are part of the classification criteria for the
disease. Tr. at 132.
Responding to Special Master Oler, Dr. Oddis testified that the biologic and steroidal
treatments Petitioner took might have suppressed inflammation, but “over a period of six to eight
years, never having an elevated inflammatory marker at a time when the joints are visibly noted to
be abnormal, would be distinctly unusual in my opinion.” Tr. at 134. Additionally, if the
treatments were effectively suppressing Petitioner’s inflammatory markers, he would have
expected Petitioner’s physical symptoms, such as swelling, to correspondingly abate, but that was
not seen. Id.
3. Dr. He’s Testimony
Dr. He testified that RA is a chronic, systemic autoimmune inflammatory disorder, for
which the etiology is unknown. Tr. at 141-42. The pathogenesis for the seropositive and
seronegative serotypes is the same, but the bloodwork of seronegative RA patients does not contain
RF or anti-CCP factors.16 Id. at 142, 144-45; Firestein at 357 (Fig. 1). There is no reputable
theory as to how the flu vaccine can cause either form of RA. Tr. at 153, 159. There are no
epidemiologic studies or case reports supporting such a theory. Id. at 146. To the contrary, “the
16 Dr. He explained that there are other autoantibodies that might be detected in seronegative RA, such as
anti-MDA, anti-MAA, and anti-AIAT. Tr. at 143.
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evidence is very extensive . . . to show . . . unequivocally that influenza vaccine – there is no
relation between influenza vaccine and RA.” Id. at 147.
Dr. He opined that it would be impossible for innate immune activation alone to cause
seronegative RA, based on the pathways that drive RA development. Tr. at 148-49. If the innate
immune system alone is activated after vaccination, the patient might suffer two to three days of
fever and discomfort, which will then dissipate. Id. at 151. But RA is mediated by antibodies, and
it also requires the activation of T lymphocytes, which attack joint tissue. Id. at 150. Those could
not be produced and cause damage within 48 hours, as alleged here. Id. at 149. A full-blown
autoimmune response would take seven to ten days. Id. at 153.
Finally, Dr. He agreed with Dr. Oddis that Petitioner’s ESR and CRP levels remained
normal, and he had no evidence of joint damage, suggesting there was not an abnormal activation
of his immune system. Tr. at 148, 156.
On cross, Dr. He acknowledged that a two-day timeframe would be sufficient for activation
of the innate immune response. Tr. at 160. He also claimed that newer literature has discussed a
“preclinical” phase of seronegative RA. Id. at 160-61.
4. Dr. Gershwin’s Rebuttal Testimony
On rebuttal, Dr. Gershwin testified that he was skeptical of the notion that there is a
preclinical phase of seronegative RA. Tr. at 163. This is because a preclinical phase is
characterized by the presence of antibodies without clinical symptoms, but there are no detectable
antibodies in seronegative RA. Id.
Dr. Gershwin disagreed with Dr. He that RA symptoms could not manifest without an
adaptive immune response. Tr. at 164. He noted that the innate immune response is powerful,
and the drugs used to treat RA fight the cytokines that are produced by that response. Id. at 164-
65. The evidence here indicates that Petitioner experienced an innate immune response within two
days of vaccination, after which the adaptive immune response facilitated the continuation of
disease. Id. at 166.
C. Post-Hearing Expert Reports
1. Dr. Oddis’s Fourth Expert Report
Dr. Oddis continued to disagree with the seronegative RA diagnosis, noting that the
identification of a preclinical biomarker in seronegative RA “has absolutely nothing to do with
whether [Petitioner] has seronegative RA.” Fourth Oddis Rep. at 1. He found the most recent
literature filed by Dr. Gershwin “irrelevant” to his testimony. Id.
2. Dr. Gershwin’s Fifth Expert Report
In his final report, Dr. Gershwin discussed literature filed by Dr. He after the hearing. See
Exs. M-Q. He opined that these papers failed to support the notion of a preclinical biomarker of
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seronegative RA. Fifth Gershwin Rep. at 1-3. Several of them explicitly concerned seropositive
RA or patients who had RA symptoms and thus were not in a “preclinical” phase of the disease.
Id. at 1-2. Furthermore, the literature supported Dr. Gershwin’s view that the innate immune
system could largely drive the development of RA. Id. at 3 (referencing paper stating that the
immunopathology of seronegative RA “is greatly driven by synovial stromal and myeloid cells,
with minor involvement of adaptive immune cells”); see Li et al., ACPA-Negative Rheumatoid
Arthritis: From Immune Mechanisms to Clinical Translation, 83 EBIOMEDICINE 1, 1, 6 (2022)
(Ex. M) (“Li”)).
IV. APPLICABLE LAW
A. Petitioner’s Burden in Vaccine Program Cases
Under the Vaccine Act, a petitioner may prevail in one of two ways. First, he may show
that he suffered a Table injury within the time provided in the Table. § 11(c)(1)(C)(i). “In such a
case, causation is presumed.” Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1320
(Fed. Cir. 2006); see § 13(a)(1)(B). Second, where the alleged injury is not listed in the Table, he
may demonstrate that he suffered an “off-Table” injury that was caused-in-fact by his vaccination.
§ 11(c)(1)(C)(ii).
For both Table and non-Table claims, Vaccine Program petitioners bear a “preponderance
of the evidence” burden of proof. § 13(a)(1). That is, a petitioner must offer evidence that leads
the “trier of fact to believe that the existence of a fact is more probable than its nonexistence before
[he] may find in favor of the party who has the burden to persuade the judge of the fact’s
existence.” Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1322 n.24 (Fed. Cir. 2010);
see also Snowbank Enter. v. United States, 6 Cl. Ct. 476, 486 (1984) (mere conjecture or
speculation is insufficient under a preponderance standard). The petitioner must demonstrate 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 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352,
1355 (Fed. Cir. 2006). A petitioner may not receive a Vaccine Program award based solely on his
assertions; rather, the petition must be supported by either medical records or the opinion of a
competent physician. § 13(a)(1).
In attempting to establish entitlement to a Vaccine Program award of compensation for a
non-Table claim, a petitioner must satisfy all three of the elements established by the Federal
Circuit in Althen v. Secretary of Health and Human Services. 418 F.3d 1274 (Fed. Cir. 2005).
Althen requires a petitioner to establish by preponderant evidence that the vaccination caused his
injury “by providing: (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.” Id. at
1278.
Each of the Althen prongs requires a different showing. Under Althen prong one, a
petitioner must provide a “reputable medical theory” demonstrating that the vaccine received can
cause the type of injury alleged. Pafford, 451 F.3d at 1355-56 (citations omitted). To satisfy this
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prong, a petitioner’s theory must be based on a “sound and reliable medical or scientific
explanation.” Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). Such
a theory must only be “legally probable, not medically or scientifically certain.” Id. at 548-49;
Bunting v. Sec’y of Health & Hum. Servs., 931 F.2d 867, 873 (Fed. Cir. 1991).
A petitioner may satisfy the first Althen prong without resort to medical literature,
epidemiological studies, demonstration of a specific mechanism, or a generally accepted medical
theory. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1378-79 (Fed. Cir. 2009) (citing
Capizzano, 440 F.3d at 1325-26). Despite their expertise, special masters are not empowered by
statute to conclusively resolve what are complex scientific and medical questions, and thus
scientific evidence offered to establish Althen prong one is viewed “not through the lens of the
laboratorian, but instead from the vantage point of the Vaccine Act’s preponderant evidence
standard.” Id. at 1380. However, this does not negate or reduce a petitioner’s ultimate burden to
establish his entitlement to damages by preponderant evidence. W.C. v. Sec’y of Health & Hum.
Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013) (citations omitted).
The second Althen prong requires proof of a logical sequence of cause and effect, usually
supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; Andreu,
569 F.3d at 1375-77; Capizzano, 440 F.3d at 1326 (stating that “medical 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 particularly trustworthy evidence because they are created contemporaneously with the
treatment of the patient. Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed.
Cir. 1993). However, the existence of medical records and/or statements of treating physician
views does not require the special master to adopt their conclusions per se. § 13(b)(1) (providing
that “[a]ny such diagnosis, conclusion, judgment, test result, report, or summary shall not be
binding on the special master or court”); Snyder v. Sec’y of Health & Hum. Servs., 88 Fed. Cl. 706,
746 n.67 (2009) (“[T]here is nothing … that mandates that the testimony of a treating physician is
sacrosanct–that it must be accepted in its entirety and cannot be rebutted.”). As with expert
testimony offered to establish a theory of causation, the opinions or diagnoses of treating
physicians are only as trustworthy as the reasonableness of their suppositions or bases. The views
of treating physicians should also be weighed against other, contrary evidence in the record—
including conflicting opinions among such individuals. Hibbard v. Sec’y of Health & Hum. Servs.,
100 Fed. Cl. 742, 749 (2011) (it was not arbitrary or capricious for special master to weigh
competing treating physicians’ conclusions against each other), aff’d, 698 F.3d 1355 (Fed. Cir.
2012); Caves v. Sec’y of Health & Hum. Servs., No. 06-522V 2011 WL 1935813, *17 (Fed. Cl.
Spec. Mstr. Apr. 29, 2011), mot. for review den’d, 100 Fed. Cl. 344, 356 (2011), aff’d without
opinion, 475 Fed. App’x 765 (Fed. Cir. 2012).
The third Althen prong requires establishing a “proximate temporal relationship” between
the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to
the phrase “medically acceptable temporal relationship.” Id. Thus, a petitioner must offer
“preponderant proof that the onset of symptoms occurred within a timeframe which, given the
medical understanding of the disorder’s etiology, it is medically acceptable to infer causation.” de
Bazan v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation
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for what is a medically acceptable timeframe must also be consistent with the theory for how the
relevant vaccine can cause the alleged injury (Althen prong one’s requirement). Id. at 1352;
Shapiro v. Sec’y of Health & Hum. Servs., 101 Fed. Cl. 532, 542 (2011), recons. denied after
remand on other grounds, 105 Fed. Cl. 353 (2012), aff’d without op., 503 F. App’x 952 (Fed. Cir.
2013); Koehn v. Sec’y of Health & Hum. Servs., No. 11-355V, 2013 WL 3214877 (Fed. Cl. Spec.
Mstr. May 30, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).
B. Law Governing Analysis of Fact Evidence
The process for making factual determinations in Vaccine Program cases begins with
analyzing the medical records, which are required to be filed with the petition. §11(c)(2). The
special master is required to consider “all [] relevant medical and scientific evidence contained in
the record,” including “any diagnosis, conclusion, medical judgment, or autopsy or coroner’s
report which is contained in the record regarding the nature, causation, and aggravation of the
petitioner’s illness, disability, injury, condition, or death,” as well as the “results of any diagnostic
or evaluative test which are contained in the record and the summaries and conclusions.”
§13(b)(1)(A). The special master is then required to weigh the evidence presented, including
contemporaneous medical records and testimony. See Burns v. Sec’y of Health & Hum. Servs., 3
F.3d 413, 417 (Fed. Cir. 1993) (it is within the special master’s discretion to determine whether to
afford greater weight to contemporaneous medical records than to other evidence, such as oral
testimony surrounding the events in question that was given at a later date, provided that such
determination is based on a rational analysis).
Medical records created contemporaneously with the events they describe are generally
trustworthy, because they “contain information supplied to or by health professionals to facilitate
diagnosis and treatment of medical conditions,” where “accuracy has an extra premium.” Kirby
v. Sec’y of Health & Hum. Servs., 997 F.3d 1378, 1382 (Fed. Cir. 2021) (citing Cucuras, 993 F.2d
at 1528). Accordingly, if the medical records are clear, consistent, and complete, then they should
be afforded substantial weight. See generally Lowrie v. Sec’y of Health & Hum. Servs., No. 03-
1585V, 2005 WL 6117475 at *19 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous
medical records are often found to be deserving of greater evidentiary weight than oral testimony,
especially where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528;
see also 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), cert. den’d, Murphy v. Sullivan, 506 U.S. 974 (1992) (citing United
States v. U.S. Gypsum Co., 333 U.S. 364, 396 (1947) (“[i]t has generally been held that oral
testimony which is in conflict with contemporaneous documents is entitled to little evidentiary
weight.”)).
However, there are situations in which compelling oral testimony could be more persuasive
than written medical 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, 2005 WL 6117475,
at *19 (“Written records which are, themselves, inconsistent, should be accorded less deference
than those which are internally consistent.”) (quoting Murphy, 23 Cl. Ct. at 733)). Ultimately, the
special master should assess each witness’s credibility when determining the weight their
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testimony should be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec’y of Health & Hum.
Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).
In determining the accuracy and completeness of medical records, the Court of Federal
Claims has listed four possible explanations for inconsistencies between contemporaneously
created medical records and later testimony: (1) a person’s failure to recount to the medical
professional everything that happened during the relevant time period; (2) the medical
professional’s failure to document everything reported to her or him; (3) a person’s faulty
recollection of the events when presenting testimony; or (4) a person’s purposeful recounting of
symptoms that did not exist. LaLonde v. Sec’y of Health & Hum. Servs., 110 Fed. Cl. 184, 203-
04 (2013), aff’d, 746 F.3d 1334 (Fed. Cir. 2014). In deciding whether to afford greater weight to
contemporaneous medical records or other evidence, such as testimony, a rational analysis must
be explicated. Burns, 3 F.3d at 417.
C. Analysis of Expert Testimony
Establishing a sound and reliable medical theory connecting the vaccine to the injury often
requires a petitioner to present expert testimony in support of his or her claim. Lampe v. Sec’y of
Health & Hum. Servs., 219 F.3d 1357, 1361 (Fed. Cir. 2000). Vaccine Program expert testimony
is usually evaluated according to the factors for analyzing scientific reliability set forth in Daubert
v. Merrell Dow Pharm., Inc., 509 U.S. 579, 594-96 (1993); see Cedillo v. Sec’y of Health & Hum.
Servs., 617 F.3d 1328, 1339 (Fed. Cir. 2010) (citing Terran v. Sec’y of Health & Hum. Servs., 195
F.3d 1302, 1316 (Fed. Cir. 1999)). “The Daubert factors for analyzing the reliability of testimony
are: (1) whether a theory or technique can be (and has been) tested; (2) whether the theory or
technique has been subjected to peer review and publication; (3) whether there is a known or
potential rate of error and whether there are standards for controlling the error; and (4) whether the
theory or technique enjoys general acceptance within a relevant scientific community.” Terran,
195 F.3d at 1316 n.2 (citing Daubert, 509 U.S. at 592-95).
The Daubert factors play a slightly different role in Vaccine Program cases than they do in
other federal judicial proceedings. Those factors are employed by judges to exclude evidence that
is unreliable and potentially confusing to a jury. In Vaccine Program cases, the factors are
generally used to assess the reliability and weight of scientific evidence. Davis v. Sec’y of Health
& Hum. Servs., 94 Fed. Cl. 53, 66-67 (2010) (“[U]niquely in this Circuit, the Daubert factors have
been employed also as an acceptable evidentiary-gauging tool with respect to persuasiveness of
expert testimony already admitted[.]”). The flexible use of the Daubert factors to evaluate
persuasiveness and reliability of expert testimony has routinely been upheld. See, e.g., Snyder, 88
Fed. Cl. at 743.
Respondent frequently offers one or more experts of his own to rebut a petitioner’s case.
Where both sides offer expert testimony, a special master’s decision may be “based on the
credibility of the experts and the relative persuasiveness of their competing theories.”
Broekelschen v. Sec’y of Health & Hum. Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing
Lampe, 219 F.3d at 1362). Nothing requires the acceptance of an expert’s conclusion “connected
to existing data only by the ipse dixit of the expert,” especially if “there is simply too great an
analytical gap between the data and the opinion proffered.” Snyder, 88 Fed. Cl. at 743 (quoting
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Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)). A “special master is entitled to require some
indicia of reliability to support the assertion of the expert witness.” Moberly, 592 F.3d at 1324.
Weighing the relative persuasiveness of competing expert testimony, based on a particular expert’s
credibility, is part of the overall reliability analysis special masters must employ in Vaccine
Program cases. Id. at 1325-26 (“[a]ssessments as to the reliability of expert testimony often turn
on credibility determinations”); see also Porter v. Sec’y of Health & Hum. Servs., 663 F.3d 1242,
1250 (Fed. Cir. 2011) (“[T]his court has unambiguously explained that special masters are
expected to consider the credibility of expert witnesses in evaluating petitions for compensation
under the Vaccine Act”).
D. Consideration of Medical Literature
Finally, although this decision discusses some but not all the medical literature in detail, I
have reviewed and considered all the medical records and literature submitted in this matter. 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).
V. ANALYSIS
A. Diagnosis
As a threshold matter, a petitioner must establish that he suffered the injury for which he
seeks compensation. Broekelschen, 618 F.3d at 1346. “The function of a special master is not to
‘diagnose’ vaccine-related injuries, but instead to determine ‘based on the record as a whole and
the totality of the case, whether it has been shown by a preponderance of the evidence that a vaccine
caused the [petitioner]’s injury.’” Andreu, 569 F.3d at 1382 (quoting Knudsen, 35 F.3d at 549).
“Although the Vaccine Act does not require absolute precision, it does require the petitioner to
establish an injury – the Act specifically creates a claim for compensation for ‘vaccine-related
injury or death.’” Stillwell v. Sec’y of Health & Hum. Servs., 118 Fed. Cl. 47, 56 (2014) (quoting
42.U.S.C. § 300aa-11(c)). Accordingly, the Federal Circuit has concluded that it is “appropriate
for the special master to first determine what injury, if any, [is] supported by the evidence presented
in the record” before applying a causation analysis pursuant to Althen. Lombardi v. Sec’y of Health
& Hum. Servs., 656 F.3d 1343, 1351-53 (Fed. Cir. 2011).
Petitioner alleges he developed seronegative RA. Respondent disputes this diagnosis.
Ultimately, it is not necessary to resolve whether Petitioner proved he has seronegative RA,
because even assuming he did, he failed to prove his flu vaccination could have or did cause that
condition.
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B. Althen Prong One
In the context of the Program, “to establish causation, the standard of proof is
preponderance of evidence, not scientific certainty.” Langland v. Sec’y of Health & Hum. Serv.,
109 Fed. Cl. 421, 441 (Fed Cir. 2013). Petitioner’s burden under Althen’s first prong is to provide
a medical theory causally connecting the vaccination and the injury. Id. This theory must be sound
and reliable. Boatmon v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019).
For the reasons discussed below, even assuming the appropriate diagnosis for Petitioner was
seronegative RA, I conclude that Petitioner has not provided a sound and reliable medical theory
causally connecting the flu vaccine to that condition.
1. Seronegative Rheumatoid Arthritis
RA is an inflammatory disease of the joints. See First Gershwin Rep. at 2; see also, e.g.,
Firestein & McInnes at 183 (noting that RA is the “most common inflammatory arthropathy” and
is thought to be immune mediated); Aletaha at 2570 (“RA is a chronic inflammatory disease
characterized by joint swelling, joint tenderness, and destruction of synovial joints[.]”); Klareskog
at 659 (RA is a “systemic, inflammatory, autoimmune disorder”). Dr. Oddis testified that RA is
characterized by “the symmetric onset of an inflammatory arthritis, [mainly] affecting the small
joints of the hands and the feet, usually in association with elevated inflammatory markers and the
presence of rheumatoid factor and/or anti-CCP antibody positivity.” Tr. at 109-10. To diagnose
RA, a clinician will consider exam findings concerning the small joints of the hands and feet, lab
tests, and imaging. Id. at 115-16 (Dr. Oddis’s testimony); see also First Gershwin Rep. at 2 (noting
that diagnosis of RA includes “determination of whether synovitis . . . is present . . . [and] testing
for both rheumatoid factor and antibodies to CCP.”). In evaluating the joints, the key signs of
inflammation to look for are swelling, warmth, redness, and pain. See Greenspan & Gershwin at
3. With respect to lab tests, RF and CCP are found in seropositive RA, but are undetectable in
seronegative disease. First Gershwin Rep. at 2; Tr. at 31-32; 109-10. Also, ESR and CRP are
markers for inflammation and are usually elevated in RA, although levels might decrease with
treatment. Tr. at 23-24, 118-19; see also, e.g., Venables at 7 (“Normal acute phase reactants [e.g.,
ESR/CRP] may occur in untreated patients with RA, but such findings are very infrequent.”).
Treatment for RA typically includes the use of Disease-Modifying Antirheumatic Drugs
(“DMARDs”), including methotrexate, sulfasalazine, hydroxychloroquine, leflunomide, and
glucocorticoids, and/or tumor necrosis factor (“TNF”) blockers like infliximab, etanercept, and
adalimumab (Humira). See Klareskog at 666-67; see also Aletaha at 2571 (noting that the optimal
use of these treatments has “dramatically enhanced the success of RA management”).
As the experts agreed, the etiology of RA is not well understood, but the disease is
commonly believed to be caused by a combination of genetic and environmental factors. See Tr.
at 29-30 (Dr. Gershwin); 116-17 (Dr. Oddis); 141-42 (Dr. He). The experts noted that the female
sex, cigarette smoking, and periodontal disease are risk factors for RA. See First Gershwin Rep.
at 1-3; First He Rep. at 5. Additionally, silica dust, mineral oils, and other airway exposures are
considered potential environmental risk factors. Klareskog at 661; see also id. (Table 2)
(identifying genetic and environmental factors associated with seropositive and seronegative RA);
Haville et al., Pre-RA: Can early diagnosis lead to prevention?, 36 BEST PRAC. & RSCH. CLINICAL
RHEUMATOLOGY 1, 4 (Table 1) (2022) (Ex. 56) (“Haville”).
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Seronegative RA is thought to be clinically and pathogenetically distinct from seropositive
disease. See, e.g., Firestein & McInnes at 185 (stating that “meta-analyses of patients with
[seronegative RA] show some differences from [seropositive RA] disease, consistent with the idea
that ‘seronegative RA’ should be considered a distinct clinical pathologic entity”); Aletaha at 2578
(seropositive and seronegative patients “have been shown to differ from a pathogenetic, clinical,
and prognostic perspective”); Klareskog at 660 (“growing evidence shows that the disease consists
of at least two subsets, with different causes and severity . . . increasingly the separation is made
on the basis of presence or absence of antibodies to citrullinated protein antigen (ACPA),
sometimes referred to as anti-CCP (cyclic citrullinated peptide)”); Li at 1 (seropositive and
seronegative RA are “two distinct disease entities with differential underlying pathophysiology”).
2. Causation Theory17
Dr. Gershwin opined that the scientific evidence would not support a claim that the flu
vaccine can cause seropositive RA. See First Gershwin Rep. at 2. As discussed below, this
position is borne out by the epidemiologic evidence in the record concerning flu vaccine and “RA”
broadly. Dr. Gershwin contended, however, that seronegative RA is a distinct entity from
seropositive RA, with different environmental risk factors and a different expected clinical course
than seropositive RA. See First Gershwin Rep. at 2. Thus, he came to a different conclusion
concerning whether the flu vaccine can cause seronegative RA.
Dr. Gershwin admitted that “we know very little about the earliest events in the
development of either seropositive or seronegative patients.” First Gershwin Rep. at 2. He opined,
though, that seronegative RA is initially driven by a pathogenic innate immune response in the
synovial tissue. Tr. at 40. Dr. Gershwin elaborated, stating that, in seronegative RA specifically,
the pathogenic innate immune response is characterized by the innate immune system’s ongoing
production of inflammatory mediators, as well as a pathogenic adaptive immune response. He
testified:
Well, the innate immune response starts this disease off, and the
innate immune response is required for an adaptive response. The
adaptive response, if seronegative, will include autoantibodies that
have yet to be identified, but people believe they exist, and some
people have shown them to exist using phased display systems and
to include cytotoxic T cells.
If you think of a clock, you’ve got two cog wheels. Innate immunity
is a cog on the left. Adaptive is a cog on the right. The innate
17 I note that Dr. Gershwin’s theory was described in a very short and cursory manner. In his first report,
Dr. Gershwin dedicated approximately one page of his two-page report (excluding the list of cited medical
literature and letterhead) to his causation theory. First Gershwin Rep. at 2-3. Dr. Gershwin filed four more
reports that did not elaborate on his causation theory, totaling seven pages. See Second, Third, Fourth, and
Fifth Gershwin Reps. This lack of detail lessened the persuasiveness of his opinions. See Dotson v. Sec’y
of Health & Hum. Servs., No. 17-637V, 2025 WL 354801, at *28 (Fed. Cl. Spec. Mstr. Jan. 10, 2025)
(criticizing Dr. Gershwin’s theories for lack of “sufficient development”).
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immunity turns and starts the adaptive response. So the perpetuation
of the disease requires an adaptive response, but the innate immune
response doesn’t disappear, and we continue to see production of
inflammatory mediators by the innate response.
Tr. at 87-88 (emphasis added). The Li article further explained that, in seronegative RA,
fibroblast-like synoviocytes in the synovium secrete a variety of cytokines, chemokines, and pro-
angiogenic factors to “recruit immune cells to perpetuate joint inflammation.” Li at 5.
Dr. Gershwin cited to a number of pieces of medical literature to support his broad theory.
I note that many of the papers address RA generally; Li was one of the few that discussed the
pathogenesis of seronegative RA. In the Gierut paper, the authors described the contributions of
innate immune system components, concluding that “[i]nnate immunity, with macrophages
playing a central role, is critically important in the pathogenesis of RA.” Gierut at 14. Similarly,
the Firestein paper proposed that RA involves activation of the innate immune response “by
stimulating dendritic cells, macrophages, fibroblasts and mast cells,” which then migrate into the
synovium, creating an opportunity for an adaptive immune response in individuals with genetic
susceptibility. Firestein at 359 (Fig. 3); see also Edilova et al., Innate Immunity Drives
Pathogenesis of Rheumatoid Arthritis, 44 BIOMEDICAL J. 172, 173 (2021) (Ex. 50) (“Edilova”)
(“Various innate immune cells including monocytes, macrophages and dendritic cells are involved
in inflammatory responses seen in RA patients as well as in driving the activation of the adaptive
immune system, which plays a major role in the later stages of the disease.”).
Concerning the potential role of the flu vaccine in causing this pathogenic immune
response, Dr. Gershwin opined that vaccination can cause the release of cytokines and
prostaglandins into the blood, which can in turn activate innate immune cells, including in the
synovium. Tr. at 34-35. Dr. Gershwin submitted the Hervé paper to support this opinion. In
Hervé, the authors explained that vaccines contain antigens that are recognized as potential
pathogens by circulating immune cells. Hervé at 2. This stimulates the innate immune system to
produce cytokines and chemokines, activate complement, and signal for cellular recruitment. Id.
These substances can enter the bloodstream and cause systemic side-effects such as fever, fatigue,
and headache. Id. The Hervé authors stated that studies of non-adjuvanted vaccines18
“consistently described a slight and short-lived increase in inflammatory mediators in blood
following vaccination, in particular, an increase in CRP and IL-6. The level and kinetics of the
inflammatory markers depended on the type of vaccine used and the population studied.” Id. at 4.
With respect to the flu vaccine, the Hervé paper cited a study that found the non-adjuvanted
seasonal flu vaccine produced a “mild and transient increase in circulating IL-6 and TNF-α” in
pregnant women. Id.
Hervé is inadequate to substantiate Petitioner’s claim that the seasonal flu vaccine can
cause an abnormal, ongoing innate immune reaction leading to pathogenic inflammation of the
synovium, as is believed to occur in seronegative RA. Nothing in Hervé suggests that the flu
vaccine can cause an abnormal inflammatory innate response, particularly an ongoing one. At
best, Hervé reports only that the vaccine produces transient and mild systemic inflammation. In
fact, none of the literature in the record addresses any potential mechanistic connection between
18 The subject vaccine in this case was non-adjuvanted. See Tr. at 36.
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the flu vaccine and a pathogenic innate immune response leading to (and perpetuating)
seronegative RA.
Another component to Dr. Gershwin’s theory was that the innate immune system attacks
the synovium/joints, yet he did not articulate how this happens. First Gershwin Rep. at 2. He
testified: “[Petitioner has] got these resident cells in his synovium, and they are activated by virtue
of a genetic predisposition, and he gets the inflammation that was described 48 hours later.” Tr.
at 42. But Dr. Gershwin did not explain how the flu vaccine activates the synovial cells.
Also, Petitioner admittedly did not propose what the pathogenic adaptive immune response
in seronegative RA might be, even though Dr. Gershwin acknowledged that such a response would
be necessary to produce the disease. Dr. Gershwin testified that the role of the adaptive immune
system is unknown in seronegative RA. Tr. at 43-44, 77, 87-88. Thus, even accepting that
seronegative RA is initially driven by an abnormal innate immune response, and even accepting
that the flu vaccine induces some innate immune response, Petitioner failed to produce reliable
evidence of a link between the flu vaccine and a pathogenic, ongoing innate response, or the
abnormal adaptive immune response, that purportedly causes seronegative RA.
3. Epidemiologic Data
Epidemiologic evidence is not required to prove a Vaccine Act case. It is appropriate,
however, for a special master to consider such evidence as part of the overall assessment of the
case. See Druery v. Sec’y of Health & Hum. Servs., No. 17-1213V, 2023 WL 5094088, at *17
(Fed. Cl. July 11, 2023), mot. for rev. den’d, 169 Fed. Cl. 557 (2024) (observing that “[n]othing in
Althen or Capizzano requires the Special Master to ignore probative epidemiological evidence that
undermines petitioner's theory.”) (quoting D’Tiole v. Sec’y of Health & Hum. Servs., 726 F. App’x
809, 811 (Fed. Cir. 2018)). “Although Althen and Capizzano make clear that a claimant need not
produce medical literature or epidemiological evidence to establish causation under the Vaccine
Act, where such evidence is submitted, the Special Master can consider it in reaching an informed
judgment as to whether a particular vaccination likely caused a particular injury.” Andreu, 569
F.3d at 1379; see also Tullio v. Sec’y of Health & Hum. Servs., No. 15-51V, 2019 WL 7580149,
*5-8 (Fed. Cl. Spec. Mstr. Dec. 19, 2019), aff’d, 149 Fed. Cl. 448 (2020) (in a case alleging a flu
vaccination caused RA, discussing at length the proposition that it is appropriate for a special
master to consider and give weight to relevant epidemiologic studies, even if they are not
dispositive of Althen prong one).
Petitioner did not submit any epidemiologic data relating to a potential association between
flu vaccination and seronegative RA. Dr. Gershwin acknowledged that there is “considerably less
epidemiology on seronegative disease following vaccination,” suggesting that it would be difficult
to conduct a sufficiently powered study to provide a reliable result for patients like Petitioner. First
Gershwin Rep. at 2 (“[T]here is no significant power calculations that I am aware of for the
presence of seronegative rheumatoid arthritis in a young, non-smoking male following influenza
vaccination.”).19 Petitioner also did not identify any case reports describing seronegative RA
following flu vaccination.
19 This claim is not entirely persuasive. The literature showed that RA is the most common inflammatory
arthropathy and affects about 0.5-1% of the total population. Firestein & McInnes at 1; Firestein at 356.
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Respondent submitted several epidemiologic studies concerning RA generally and flu
vaccination. These studies did not differentiate between seropositive and seronegative RA
patients, and they assessed different flu vaccines than the one at issue here, so they are not entirely
on point in assessing the particular claim advanced here. Nonetheless, they clearly reported no
causal association between any type of RA and any type of flu vaccine, and Dr. Gershwin did not
dispute their findings or methodologies.
a. Kurland
In Kurland, published in 1984, the investigators performed three separate analyses. First,
they studied the incidence of RA following the 1976 swine flu vaccination campaign in patients
from the Mayo Clinic who had been diagnosed with RA between 1976 and 1980. Kurland at 818.
Of the patients living in Minnesota (the Mayo Clinic’s location), 66% had been vaccinated against
the swine flu. Id. Patients living in adjacent states had a swine flu vaccination rate of 54%. Id.
A comparison of the rates of RA in various time periods before and after vaccination showed no
increase in the risk of RA following vaccination. Id.
Second, the Kurland investigators considered the rates of RA in 682,000 U.S. Army
servicemembers who had received the swine flu vaccine in the fourth quarter of 1976. Kurland at
818-19. The investigators found no significant increase in the risk of RA after vaccination in this
population. Id. at 819.
Third, the investigators reviewed other studies of the swine flu vaccine and rheumatologic
disorders, including RA. Kurland at 819-20. Again, none of those studies found a significantly
increased risk of developing RA or flareups of symptoms following the vaccination. Id. The
authors stated:
We can conclude from the review of the available literature that RA
has not been associated with past influenza vaccination programs,
including the national swine flu vaccination program of 1976. . . .
We conclude from the epidemiologic and clinical data that no
evidence indicates that the swine flu vaccine is a risk factor for new
or existing cases of RA.
Id. at 820.
b. Bardage
The Bardage study, published in 2011, evaluated the effects of the H1N1 swine flu vaccine
(developed in response to the 2009 H1N1 swine flu pandemic), considering a variety of potential
associations, including with RA. Bardage at 1. More than one million patients from a Swedish
Of that group, about 10-20% have seronegative RA. Firestein & McInnes at 8. This likely represents a
fairly large potential dataset of patients, even if one further narrows it to young, non-smoking males. Still,
neither party provided any epidemiologic data specifically evaluating a potential association between flu
vaccination and seronegative RA.
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health database were included in the analysis. Id. at 2. The investigators found no significantly
increased risk of RA following H1N1 vaccination compared to controls, either during the first 45
days following vaccination or during the period thereafter. Id. at 4, 9 (Table 2).
c. Studies of flu vaccination in RA patients
Respondent also submitted a number of studies evaluating the effects of flu vaccination in
already-diagnosed RA patients. Each of these studies found that flu vaccination was safe and/or
was not significantly associated with clinical exacerbations of RA, providing additional reassuring
evidence. See Herron et al., Influenza Vaccination in Patients With Rheumatic Diseases, 242
JAMA 53 (1979) (Ex. C, Tab 6) (“Herron”) (administration of the seasonal flu vaccine to patients
with RA did not result in a significantly increased risk of symptom flareup); Del Porto et al.,
Influenza vaccine administration in patients with systemic lupus erythematosus and rheumatoid
arthritis, 24 VACCINE 3217 (2006) (Ex. C, Tab 7) (“Del Porto”) (no significant difference in
clinical activity of RA in patients versus controls following seasonal flu vaccination); Ori
Elkayam, Safety and efficacy of vaccination against influenza in patients with rheumatoid arthritis,
13 CLINICAL & DEV. IMMUNOLOGY 349 (2006) (Ex. C, Tab 8) (“Elkayam”) (literature review
showed that the flu vaccine “does not induce clinical exacerbation of RA”); Elkayam et al.,
Efficacy and Safety of Vaccination Against Pandemic 2009 Influenza A (H1N1) Virus Among
Patients With Rheumatic Diseases, 63 ARTHRITIS CARE & RSCH. 1062 (2011) (Ex. C, Tab 9)
(“Elkayam II”) (study finding that vaccination with an adjuvanted H1N1 flu vaccination was safe
in RA patients); Saad et al., Immunogenicity and safety of the 2009 non-adjuvanted influenza
A/H1N1 vaccine in a large cohort of autoimmune rheumatic diseases, 70 ANN RHEUM DIS 1068
(2011) (Ex. C, Tab 10) (“Saad”) (no moderate or severe side effects of seasonal flu vaccination in
patients with autoimmune rheumatic diseases, including RA); Milanovic et al., Influenza
Vaccination in Autoimmune Rheumatic Disease Patients, 229 TOHOKU J. EXP. MED. 29 (2013)
(Ex. C, Tab 11) (“Milanovic”) (administration of seasonal flu vaccine to RA patients did not result
in any exacerbation of disease); Milanetti et al., Safety and immunogenicity of co-administered
MF59-adjuvanted 2009 pandemic and plain 2009–10 seasonal influenza vaccines in rheumatoid
arthritis patients on biologicals, 177 THE J. OF TRANSLATIONAL IMMUNOLOGY 287 (2014) (Ex. C,
Tab 12) (“Milanetti”) (study of adjuvanted H1N1 flu vaccine in RA patients showed no significant
increase in disease activity; a slight increase in activated interferon-γ, TNF-α, or IL-17A-secreting
T cells was observed a one month post-vaccination, followed by a reduction in such cells by six
months post-vaccination).
In sum, Petitioner successfully showed that seronegative RA is a distinct clinical entity
from seropositive RA and that it is characterized at least in part by a pathogenic innate immune
response. But he failed to provide any relevant clinical data on this question, and the epidemiologic
evidence in the record does not support the claim that the vaccine significantly increases the risk
of developing RA generally. Also, the mechanistic evidence Petitioner supplied did not adequately
substantiate that the flu vaccine could cause the abnormal innate immune response in the joints
that is thought to drive seronegative RA. Further, Petitioner provided no reliable evidence at all
concerning the potential pathogenic adaptive immune response in seronegative RA, nor how the
flu vaccine could cause that response. Thus, after careful review of the record, I conclude that
Petitioner has not presented preponderant evidence in the form of a sound and reliable theory that
the flu vaccine can cause seronegative RA.
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C. Althen Prong Two
Under Althen’s second prong, a petitioner must “prove a logical sequence of cause and
effect showing that the vaccination was the reason for the injury.” Althen, 418 F.3d at 1278. The
sequence of cause and effect must be “‘logical’ and legally probable, not medically or scientifically
certain." Andreu, 569 F.3d at 1380 (quoting Knudsen, 35 F.3d at 548-49). A petitioner is not
required to show “epidemiologic studies, rechallenge, the presence of pathological markers or
genetic disposition, or general acceptance in the scientific or medical communities to establish a
logical sequence of cause and effect.” Capizzano, 440 F.3d at 1325. Instead, circumstantial
evidence and reliable medical opinions may be sufficient to satisfy the second Althen prong. Id.
Further, special masters are expected to consider the views of treating doctors. Id. at 1326. Such
views are often persuasive because the doctors have direct experience with the patient whom they
are diagnosing -- but they are not necessarily dispositive of the causation question. See McCulloch
v. Sec’y of Health & Hum. Servs., No. 09-293V, 2015 WL 3640610, at *20 (Fed. Cl. Spec. Mstr.
May 22, 2015).
The medical records indicate that PA Bledsoe and Dr. Dinning both initially suspected
Petitioner’s presentation had a vaccine and/or viral cause. These suspicions were recorded very
early in Petitioner’s course and before he was formally diagnosed with RA or tested for objective
signs of inflammatory disease. When PA Bledsoe initially saw Petitioner on November 7, 2014,
he wrote that he suspected Petitioner suffered an “allergic” reaction to the vaccine. Ex. 13 at 5.
He did not diagnose Petitioner with RA, though; instead, he diagnosed arthralgia. Id. Also, when
Dr. Dinning first saw Petitioner on November 25, 2014, he suspected his “inflammatory arthritis”
had either a viral cause or was “associated with flu vaccine.” Ex. 14 at 3. Again, however, at that
time Dr. Dinning had not yet diagnosed Petitioner with RA or completed additional lab testing.
When Dr. Dinning first diagnosed Petitioner with RA on February 10, 2015, he did not repeat his
suspicion that the condition was caused by the flu vaccine, though he did reference the temporal
relationship between the vaccination and the onset of symptoms in the disability form completed
March 26, 2015. See id. at 14; Ex. 4 at 187-92. Overall, these preliminary statements are not
persuasive evidence of vaccine causation.
Moreover, other aspects of the record are unsupportive of the proposition that there is a
logical connection between the vaccine and Petitioner’s condition, and these factors outweigh the
initial suspicions of the treating providers. Most notably, Petitioner’s imaging and bloodwork
never showed any indication of inflammation throughout his eight-year course, belying the
argument that he experienced a vaccine-induced, ongoing inflammatory reaction, as Dr. Gershwin
contended. Petitioner’s x-rays over the span of four and a half years were always unremarkable.
Ex. 8 at 2-5 (February 10, 2015 x-rays of hands and knees); Ex. 28 at 12 (August 6, 2018 x-rays
of hands, feet, wrists, ankles, lumbosacral spine, and sacroiliac joint); Ex. 45 at 54 (September 19,
2019 x-rays of hands and knees). Also, the biomarkers used to assess inflammation, ESR and
CRP, were consistently normal, or even low-normal. Significantly, this was true even during
periods when Petitioner was not undergoing any kind of treatment for RA that might have masked
inflammation. When Petitioner was seen by PA Bledsoe for his joint pain (and before he began
any treatment for RA), his ESR and CRP levels were measured and were normal. Ex. 13 at 3-4.
Similarly, when he first saw Dr. Loomer on July 20, 2018, he reported that he had discontinued
his Humira treatment for the previous three weeks due to a fungal rash. Ex. 28 at 1. But despite
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this pause in treatment, bloodwork done the next day showed an “undetectable” CRP level and a
normal ESR level. Ex. 28 at 12. Dr. Oddis testified:
So at a time when this patient has 47 tender or swollen joints, he’s
got absolutely no evidence of any inflammation in his – in his blood,
and if you go through the entire period of this patient’s presentation
with many different physicians, you will never find an elevated
inflammatory marker, and not only are they normal, they are well
within the normal range. In fact, they are in the low normal and
sometimes undetectable range.
I don’t see this in seronegative rheumatoid arthritis, I don’t see this
in seropositive rheumatoid arthritis, I don’t see this in any disorder
where there is concomitant inflammation.
Tr. at 109. These facts strongly pull against the theory that Petitioner suffered an ongoing
inflammatory response to the flu vaccine, as posited by Dr. Gershwin. See also First He Rep. at 5
(opining that the lack of systemic inflammation made it unlikely that an abnormal innate immune
response caused Petitioner’s joint symptoms).
As such, I conclude that Petitioner has not presented preponderant evidence in support of
Althen’s second prong.
D. Althen Prong Three
The timing prong contains two parts. First, a petitioner must establish the “timeframe for
which it is medically acceptable to infer causation,” and second, he must demonstrate that the onset
of the disease occurred in this period. Shapiro, 101 Fed. Cl. at 542-43.
The record reflects, and the parties agree, that Petitioner experienced flu-like symptoms
two days after vaccination. ECF No. 85 (“Petitioner’s Post-Hearing Brief”) at 17-18; ECF No. 86
(“Respondent’s Post-Hearing Brief”) at 29. The question is whether those symptoms represented
the onset of seronegative RA, and whether a two-day timeframe for development of initial
symptoms is medically appropriate.
Dr. Gershwin posited that Petitioner’s seronegative RA was initially caused by an abnormal
innate response triggered by the flu vaccine. He further opined that two days was an appropriate
timeframe for an innate immune reaction to a vaccination. Tr. at 45-46. At some later point, the
abnormal activation of the innate immune response in turn activated an (unknown) adaptive
response that led to Petitioner’s chronic RA. Id. at 88. Dr. Gershwin did not present an opinion
on when the adaptive response would initiate, but I do not believe that level of specificity was
required in light of the mechanistic theory he proposed, which, as noted, relied on an ongoing
innate immune response occurring to some extent in parallel with the adaptive response.
Respondent did not refute the proposition that two days would be a medically acceptable
timeframe for an innate immune response. Dr. He, in fact, admitted this. Tr. at 160. Dr. He
instead focused his opinion on whether an adaptive immune response could manifest in this time;
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he maintained that two days was not a medically acceptable timeframe for that response. First He
Rep. at 4; Second He Rep. at 2; Tr. at 150.
Given Respondent’s failure to refute Dr. Gershwin’s point, I conclude that Petitioner has
met Althen prong three based on the record before me and the causation theory he advanced. But
since he has failed to satisfy either prong one or prong two, his overall claim for relief must be
denied. 20 Grant v. Sec’y of Dep’t of Health & Hum. Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992)
(“a proximate temporal association alone does not suffice to show a causal link between the
vaccination and the injury.”); see also Althen, 418 F.3d at 1278.
E. Other Rheumatoid Arthritis Cases
Although the decisions of other special masters are not binding in this case, they are
instructive. I note that Program petitioners asserting RA as a vaccine injury, including
seronegative RA, have mostly failed.
1. Cases involving seronegative RA
Cases alleging seronegative RA as a vaccine injury have been uniformly disfavored in the
Program. In Seivwright, the petitioner alleged that a flu vaccination caused her to develop
seronegative RA. Seivwright v. Sec’y of Health & Hum. Servs., No. 19-1398V, 2023 WL 3197267,
20 Dr. He testified that some literature supports the existence of a preclinical biomarker for seronegative
RA. Tr. at 160-61. He filed several papers purportedly showing this. Exs. M-Q. The identification of a
preclinical marker might suggest a genetic cause of seronegative RA and also would raise the possibility
that Petitioner’s condition began before his vaccination. However, as Dr. Gershwin pointed out, several of
the papers submitted by Dr. He concerned studies in patients already diagnosed with arthritis, so they did
not concern a putative preclinical biomarker. Fifth Gershwin Rep. at 1-2; see Pratt et al., A CD4 T cell gene
signature for early rheumatoid arthritis implicates interleukin 6-mediated STAT3 signalling, particularly
in anti-citrullinated peptide antibody-negative disease, 71 ANN. RHEUM. DIS. 1374, 1374 (2011) (Ex. P)
(“Pratt”); Anderson et al., IL-6-driven STAT signalling in circulating CD4+ lymphocytes is a marker for
early anticitrullinated peptide antibody-negative rheumatoid arthritis, 75 ANN. RHEUM. DIS. 466, 466
(2014) (Ex. Q) (“Anderson”). Another study, using a proprietary assay, identified a protein signature for
seronegative RA in a Native American population consisting of first-degree relatives of RA patients.
O’Neil et al., Association of a Serum Protein Signature With Rheumatoid Arthritis Development, 73
ARTHRITIS & RHEUMATOLOGY, 78, 78 (2020) (Ex. O) (“O’Neil”). Dr. Gershwin acknowledged that
the study was “potentially exciting but only illustrate[d] a genetic predisposition to develop disease,” which
would not preclude vaccine causation. Fifth Gershwin Rep. at 2. He also pointed out that the proteins
identified in the study were involved in the innate immune system, purportedly supporting his causal theory.
Id.
Although at least some of the literature filed by Dr. He supported the hypothesis that a biomarker
for seronegative RA might be identified in patients who have not yet developed the disease, the data on that
topic appear to be nascent. More fundamentally, it is unknown whether Petitioner had any such biomarker
or a genetic predisposition to RA; thus, it is speculative to infer that Petitioner’s condition was genetic
and/or predated the vaccination. The only clinical evidence I have showed an onset of symptoms beginning
two days after vaccination, and Dr. Gershwin’s opinion that a two-day onset of innate immunity was
medically appropriate was unrefuted. Thus, I still conclude on this record that Petitioner satisfied Althen
prong three.
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at *1 (Fed. Cl. Spec. Mstr. May 2, 2023). She offered expert opinion from Dr. Gershwin;
Respondent offered a responsive opinion from Dr. Oddis. Id. The special master issued a tentative
finding that the petitioner was unlikely to prove entitlement to compensation. Id. He specifically
rejected Dr. Gershwin’s theory of causation “involving somatic changes invoking the adaptive
immune system” and cytokine-driven inflammation. Id. at *2. He further noted that special
masters had “consistently rejected a theory based upon cytokines.” Id. (citing Hock v. Sec’y of
Health & Hum. Servs., No. 17-168V, 2020 WL 6392770, at *29 (Fed. Cl. Spec. Mstr. Sept. 30,
2020); Olson v. Sec’y of Health & Hum. Servs., No. 13-493V, 2017 WL 3624085, at *20 (Fed. Cl.
Spec. Mstr. July 14, 2017), mot. for rev. den’d, 758 F. App’x 919 (Fed. Cir. 2018)). He granted
the petitioner’s motion to voluntarily dismiss her claim. Id. at *3.
Tullio is also instructive. There, the petitioner’s RA diagnosis was seronegative because
he did not have detectable anti-CCP antibodies. 2019 WL 7580149, at *2. But unlike here, he
had elevated ESR and CRP levels, signifying that he was experiencing inflammation. Id. The
petitioner’s experts articulated a theory based on an abnormal adaptive immune response, opining
that the flu vaccine could cause RA through molecular mimicry, resulting in an attack on the
collagen within the joints. Id. at *5. The special master concluded that the petitioner had failed to
preponderantly prove that pathogenic molecular mimicry between the flu vaccine and collagen
could cause RA. Id. at *22. The special master also examined substantial epidemiologic data
showing no causal association between the flu vaccine and RA. Id. at *9-11.
In C.P., the special master rejected a causation theory of seronegative RA based on
molecular mimicry between an unknown tissue and the flu vaccine. C.P. v. Sec’y of Health &
Human Servs., No. 14-917V, 2019 WL 5483621, at *29 (Fed. Cl. Spec. Mstr. Aug. 21, 2019). The
petitioner also failed to present a reliable causation theory based on a vaccine-driven T cell
response in the synovium. Id. at *26. Molecular mimicry theories of flu vaccine-caused
seronegative RA were also rejected in Gauvin and McGuinness. Gauvin v. Sec’y of Health & Hum.
Servs. No. 18-480V, 2024 WL 5346729 (Fed. Cl. Spec. Mstr. Dec. 27, 2024); McGuinness v. Sec’y
of Health & Hum. Servs., No. 17-954V, 2021 WL 5292343 (Fed. Cl. Spec. Mstr. Oct. 20, 2021).
2. Cases involving similar causation theories
As noted above, theories of vaccine-caused RA based on cytokine response have been
rejected. Seivwright, 2023 WL 3197267, at *2. In Hock, the Chief Special Master rejected the
petitioner’s theory that the flu vaccine caused him to develop seropositive RA. 2020 WL 6392770,
at *1. The petitioner’s expert offered the theory the vaccine elicits the secretion of
proinflammatory cytokines, which can then build up over time and cause RA. Id. at *5-6. That
process, the expert opined, is followed by bystander activation of autoreactive cells, along with
molecular mimicry between the vaccine components and autoantibodies, leading to tissue damage.
Id. The Chief Special Master concluded that the petitioner had failed to substantiate this theory
with scientific evidence showing how this process occurs or the role of the flu vaccine in triggering
it. Id. at *26.
In Olson, the petitioner alleged an HPV vaccine caused her to develop RA. 2017 WL
3624085, at *19. Her causation theory centered on the claim that the alum used as an adjuvant in
the vaccine was associated with the production of inflammatory cytokines. Id. at *20. The Chief
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Special Master noted that the petitioner had failed to demonstrate “that cytokine upregulation
allegedly resulting from vaccine administration is itself a trigger for RA, rather than either a
byproduct or subsequent component of the disease.” Id. (emphasis in original). She also failed to
establish that the alum adjuvant was causally associated with RA or a similar autoimmune disease.
Id. “The articles referencing the general capacity of alum to stimulate inflammasomes, or the
possibly pathogenic role of over-stimulation of inflammasomes,” were insufficient to support this
theory. Id. at *21.
3. Cases involving seropositive RA
There are also several cases involving seropositive RA purportedly caused by vaccines in
which entitlement has been denied. See, e.g., Wilson v. Sec’y of Health & Hum. Servs., No. 17-
1264V, 2023 WL 9053671, at *12 (Fed. Cl. Spec. Mstr. Dec. 7, 2023) (dismissing petitioner’s
claim that she suffered from seropositive RA as a result of the flu vaccine); Clark v. Sec’y of Health
& Hum. Servs., No. 17-1553V, 2023 WL 4897284, at *28-32 (Fed. Cl. Spec. Mstr. June 16, 2023)
(concluding that the flu vaccine did not significantly aggravate or exacerbate petitioner’s RA,
along with other associated injuries); Moran v. Sec’y of Health & Hum. Servs., No. 16-538V, 2021
WL 4853544, slip. op., at 23-24 (Fed. Cl. Spec. Mstr. Oct. 4, 2021) (denying entitlement for a
petitioner asserting the flu vaccine caused him to develop symptoms of RA after three days);
Monzon v. Sec’y of Health & Hum. Servs., No. 17-1055V, 2021 WL 2711289, at *21-23 (Fed. Cl.
Spec. Mstr. June 2, 2021) (denying entitlement for a petitioner alleging Tdap vaccine caused her
to develop RA after 10 days); Bean-Sasser v. Sec’y of Health & Hum. Servs., No. 13-326V, 2016
WL 1649355, at *9-11 (Fed. Cl. Spec. Mstr. April 5, 2016), (denying entitlement to a petitioner
alleging the hepatitis B vaccine caused her to manifest symptoms of RA approximately eleven
hours later), aff’d, 127 Fed. Cl. 161 (2016).
Lastly, I have identified only two cases alleging RA as a vaccine injury in which
entitlement was granted, and only one involving the flu vaccine. In Campbell, the court vacated
the special master’s denial of a claim that the flu vaccine caused seropositive RA. Campbell v.
Sec’y of Health & Hum. Servs., 97 Fed. Cl. 650, 673-74 (2011). The court found that the petitioner
had proven the biologic plausibility of a theory that molecular mimicry and/or immune complexes
could cause RA following flu vaccination and had submitted case reports and review articles
supporting that theory. Id. at 673. The court also relied on the “strong temporal proximity between
the vaccination and the onset of her symptoms, and the statements of her treating physicians[.]”
Id. Federal Circuit decisions, however, have clarified that the proper burden of proof is
preponderance, not biologic plausibility. See Boatmon, 941 F.3d at 1360 (“We have consistently
rejected theories that the vaccine only ‘likely caused’ the injury and reiterated that a ‘plausible’ or
‘possible’ causal theory does not satisfy the standard.”) (citing Moberly, 592 F.3d at 1322). Thus,
to the extent it applies a plausibility standard for satisfaction of Althen prong one, Campbell is
unpersuasive. It is also distinct from this case, in that it involved seropositive RA. 97 Fed. Cl. at
654; see also H.J. v. Sec’y of Health & Hum. Servs., No. 11-301V, 2015 WL 6848357, at *9, 12
(Fed. Cl. Spec. Mstr. Nov. 6, 2015) (finding the petitioner had shown she was predisposed to RA
by virtue of having preclinical RA and “overlap syndrome,” and that the Tdap vaccine she received
caused her RA).
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VI. CONCLUSION
Upon careful evaluation of all the evidence submitted in this matter, including the medical
records, the testimony, the experts’ opinions, and the medical literature, I conclude that Petitioner
has not shown by preponderant evidence that he is entitled to compensation under the Vaccine
Act. His petition is therefore DISMISSED. The clerk shall enter judgment accordingly.21
IT IS SO ORDERED.
s/ Jennifer A. Shah
Jennifer A. Shah
Special Master
21 Pursuant to Vaccine Rule 11(a), the parties may expedite entry of judgment by each filing (either jointly
or separately) a notice renouncing their right to seek review.
39