Monzon v. Secretary of Health and Human Services

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 17-1055V
(to be published)

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ROSA MONZON, *
*
Petitioner, * Chief Special Master Corcoran
*
v. *
* Filed: June 2, 2021
SECRETARY OF HEALTH AND *
HUMAN SERVICES, *
*
Respondent. *
*
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Joseph Vuckovich, Maglio Christopher & Toale, P.A., Washington, DC, for Petitioner

Dhairya Jani, U.S. Dep’t of Justice, Washington, DC, for Respondent

ENTITLEMENT DECISION 1

On August 4, 2017, Rosa Monzon filed a petition seeking compensation under the National
Vaccine Injury Compensation Program (the “Vaccine Program”) 2 alleging that the tetanus-
diphtheria-acellular pertussis (“Tdap”) vaccine that she received on April 12, 2016, caused her to
develop polymyalgia rheumatica (“PMR”). See Petition (“Pet.”) at 2. Petitioner’s diagnosis was
subsequently changed to rheumatoid arthritis (“RA”), and RA is the asserted injury in this case.
Ex. 13 at 2; Petitioner’s Prehearing Brief at 1.

1 This Decision will be posted on the United States Court of Federal Claims’ website in accordance with the E-
Government Act of 2002, 44 U.S.C. § 3501 (2012). This means the Decision will be available to anyone with access
to the internet. As provided by 42 U.S.C. § 300aa-12(d)(4)(B), however, the parties may object to the published
Decision’s inclusion of certain kinds of confidential information. Specifically, under Vaccine Rule 18(b), each party
has fourteen (14) days within which to request redaction “of any information furnished by that party: (1) that is a trade
secret or commercial or financial in substance and is privileged or confidential; or (2) that includes medical files or
similar files, the disclosure of which would constitute a clearly unwarranted invasion of privacy.” Vaccine Rule 18(b).
Otherwise, the entire Decision will be available to the public in its current form. Id.
2The Vaccine Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660,
100 Stat. 3755 (codified as amended at 42 U.S.C. §§ 300aa-10–34 (2012)) (hereinafter “Vaccine Act” or “the Act”).
All subsequent references to sections of the Vaccine Act shall be to the pertinent subparagraph of 42 U.S.C. § 300aa.
 An entitlement hearing was held in this matter on February 5, 2021. After consideration of
the record and testimony provided at hearing, I deny entitlement in this case. As discussed in more
detail below, Petitioner has not preponderantly established that she likely experienced RA, rather
than the preclinical version of it. At best, Petitioner experienced some post-vaccination symptoms
likely attributable to the vaccine, but they did not reflect her claimed injury. And even if I had
found that she likely did experience RA, she has not established that the Tdap vaccine could cause
it, or that it did so in this case.

I. Medical History

A. Medical History Prior to Vaccination

Prior to her vaccination, Ms. Monzon was a healthy and active fifty-five-year-old woman
with a medical history of hypertension, dyslipidemia, and irritable bowel syndrome, and no history
of symptoms that could be deemed harbingers of RA. Pet. at 1; Ex. 2 at 2. On April 12, 2016, she
visited Dr. Amir Goldenberg, her primary care physician, to establish care and receive treatment
for hypertension. Ex. 2 at 15-17. At this same visit, she received the Tdap vaccine in her left
deltoid. Ex. 1 at 1.

B. Onset of Symptoms

Ten days later, on April 22, 2016, Ms. Monzon presented to Memorial Healthcare System
urgent care center in East Hollywood, Florida with complaints of generalized fatigue, neck pain,
arm pain, a small hematoma at the Tdap injection site, and bilateral leg pain that she stated had
“started after getting her tetanus vaccine.” Ex. 2 at 35. She reported no fever, chills, paresthesia,
or rash, however. Id. On exam, Petitioner had normal range of motion in her neck and extremities.
Id. at 37. She was assessed with a “small Hematoma at site of injection of TDAP injection done
one week ago” with reports of “associated fatigue and weakness,” was prescribed steroidal
medication, and instructed to return to the clinic in one week Id. at 38.

On May 4, 2016 (now approximately three weeks since the relevant vaccination), Petitioner
was seen by Dr. Goldenberg for complaints of neck and lower back pain that she reported had
returned two days following her completion of the steroidal medication. Ex. 2 at 52. Dr.
Goldenberg’s notes indicate that Petitioner’s neck and back pain was reported to have “started 2
days after Tdap injection on 4/12/2016. She developed a small hematoma on the deltoid area but
no surrounding erythema, fever or chills.” Id. On exam, Petitioner had normal range of motion in
her hips, but her cervical spine showed decreased range of motion with tenderness and spasm. Id.
at 53-54. Dr. Goldenberg diagnosed a mild reaction to Tdap, cervicalgia, and lumbago that
“[s]tarted after recent daily [sic] vaccination, likely adverse effect, flu like reaction.” Id. at 55. He
prescribed NSAIDs and local heat for the hematoma, a muscle relaxant, and administered an
injection of Toradol, a pain killer. Id.

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 Ms. Monzon returned to urgent care on May 21, 2016, for evaluation of whole body
weakness, aches, and pain that was mainly localized to her neck, buttocks, and posterior thighs.
Ex. 2 at 74. She now reported that she could not bend over to pick anything up from the ground
due to pain. Id. On exam, she had decreased range of motion in her neck, diffuse body muscle
aches on palpation mainly in the posterior thigh, posterior neck, and gluteal muscles. Id. at 75. The
diagnosis was cervicalgia and “adverse effect of pertussis vaccine.” Id. at 76-77. She was
prescribed an oral steroid and referred for a rheumatology consult. Id.

On May 31, 2016, Petitioner completed a Vaccine Adverse Event Reporting System
(“VAERS”) form reporting the date of vaccination and onset of alleged adverse event as April 14,
2016 (hence two days after vaccination) at 5:00 a.m. Ex. 9. On June 9, 2016, Petitioner returned
to Dr. Goldenberg, who observed from lab testing an elevated erythrocyte sedimentation rate—a
biomarker for the presentation of inflammation—and joint pain. Ex. 2 at 108. He urged her to
consult with a rheumatologist. Id.

On June 16, 2016, Petitioner presented to rheumatologist Zabeth Cure Lopez, M.D., for
evaluation. Ex. 10 at 171. Ms. Monzon now reported a two-month history of left arm pain
following receipt of a Tdap vaccine, adding that she was fatigued because her neck pain disturbed
her sleep, and also complained of myalgia, muscle cramps, numbness, and tingling. Id. On exam,
she had full range of motion in all joints, negative fibromyalgia trigger points, bilateral trapezius
spasm, and tenderness in her neck with related decreased range of motion. Id. Petitioner was
diagnosed with low back pain, neck pain that “started after Tdap,” and myalgia that was prominent
in the neck and back. Id. Dr. Lopez ordered blood labs and recommended a neurological consult
for possible Guillain-Barré syndrome (“GBS”). Id.

On June 23, 2016, Petitioner was seen by a neurologist, Adnan Subei, D.O., who concluded
that Petitioner was not likely suffering from GBS. Ex. 11 at 10. However, Dr. Subei did “think she
developed some kind of an inflammatory reaction from the vaccine given her symptoms and lab
markers.” Id. He ordered an EMG/NCS of select muscles in the left arm to evaluate for
mononeuropathy multiplex or demyelinating polyneuropathy (although no EMG/NCS
results/records have been filed) and instructed Petitioner to continue follow-up with rheumatology.
Id. On July 7, 2016, Petitioner returned to Dr. Lopez, who noted that Petitioner’s exam results
were consistent with her June 16, 2016 presentation. Ex. 3 at 2. The diagnosis was polymyalgia
rheumatica (“PMR”), and Petitioner was prescribed Prednisone, to be taken twice a day for 30
days. Id.

Petitioner returned to Dr. Lopez for a follow-up visit on July 7, 2016. Ex. 3 at 2. Dr. Lopez
noted that Petitioner’s exam was unchanged since June 2016, and diagnosed Petitioner with PMR.
Id. On August 11, 2016, however, Dr. Lopez amended the notes to Petitioner’s medical record
based on previously-ordered test results. Id. at 5-6. Her assessment was now (for the first time in
the record) RA, based on “increased inflammatory markers and +CCP high titer.” Ex. 6 at 7-10.
As discussed below, the anti-cyclic citrullinated protein (“anti-CCP” or “+CCP”) antibody is

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highly associated with RA.

C. Subsequent Treatment

Petitioner continued to visit Dr. Lopez throughout the balance of 2016 and into mid-2017.
Ex. 6 at 2, 5; Ex. 7 at 3; Ex. 10 at 175, 178, 181, 186, 278. On November 16, 2016, Dr. Lopez
noted that Petitioner appeared to have no complaints. Ex. 7 at 1. In addition, exam revealed full
range of motion in all joints with no synovitis. However, the typical tender points for fibromyalgia
were positive. Id. at 3. Petitioner’s diagnosis remained RA, but because there was “no clinical or
laboratory evidence for disease activity,” Dr. Lopez proposed to maintain existing treatment while
tapering the Prednisone. Id. In keeping with this treatment plan, on February 9, 2017, Petitioner’s
dosage of Prednisone was reduced to 1 mg per day, and ceased entirely by April. Ex. 10 at 175,
178. Petitioner continued to take other prescription medications for treatment of fibromyalgia,
however. Id.

On May 22, 2017—now a little more than a year since her symptoms began—Petitioner
saw Dr. Goldenberg and reported that her RA was mostly controlled, and that she was no longer
taking Prednisone. Ex. 10 at 300. Petitioner returned to Dr. Lopez on August 7, 2017, at which
time she was without complaints of lower back pain, and she denied arthralgias or morning
stiffness in her shoulders or hips. Id. at 183.

On May 5, 2018, Petitioner visited Dr. Gladys Nogueiras at MD Healthcare Hollywood in
Hollywood, Florida for the first time. Ex. 44 at 178. Dr. Nogueiras took a medical history and
noted that Petitioner had “no new complaints.” Id. A physical exam revealed full range of motion
in all extremities and no swelling. Id. at 182. Dr. Nogueiras noted that Petitioner’s RA was stable,
in treatment with Methotrexate (a common and effective RA-specific drug), and her fibromyalgia
was stable in treatment with Duloxetine—both prescribed by her rheumatologist Dr. Lopez. Id.
The plan was to follow-up in two weeks. Id.

On June 15, 2018 Petitioner was seen again at MD Healthcare Hollywood for a follow-up
regarding Petitioner’s lab results. Ex. 44 at 223-227. The assessment revealed that Petitioner’s
symptoms, including hypertension, lactose intolerance, and fibromyalgia were all stable on current
treatments and a diet and exercise plan was discussed. Id. at 176. On September 14, 2018,
Petitioner again visited Dr. Nogueiras where they discussed her dyslipidemia. Id. at 171. She was
advised to continue with fish oil 2000 mg and begin Rosuvastatin 500mg with follow-up in three
months. Id.

On January 11, 2019, Petitioner returned to MD Healthcare Hollywood following an acute
illness including a cough and fever. Ex. 44 at 156. She was screened for pneumonia and prescribed
an antibiotic. Id. at 158. A note by Dr. Nogueria indicated that Petitioner had continued taking
Methotrexate to treat her RA symptoms until 2019, when the treatment was discontinued by Dr.
Lopez “because of RA in remission for over 1 year.” Id. at 8. Petitioner continued to follow-up for
her on-going ailments and attend wellness checks with Dr. Nogueiras throughout 2019 and 2020.

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See Id. 132-158.

II. Testimony at Hearing

A. Ms. Monzon

Petitioner provided an affidavit and testified at the hearing with the aid of an interpreter.
See Affidavit, filed on July 9, 2020 as Ex. 41 (ECF No. 38-2) (“Affidavit”); Tr. 5-25. Petitioner
resides in Hallandale, Florida, where she works as a housekeeper, and she received the Tdap
vaccine there in April 2016. Id. at 6; Affidavit at 2. She was healthy prior to receipt of the vaccine,
had not previously experienced arthritic-like pain, and had not been told by any treaters she might
suffer from such a condition. Id. at 7-8. She also was not a smoker in her prior history. Id. at 24.

Ms. Monzon went on to describe her symptoms following the vaccination on April 12,
2016. Tr. at 8. She testified that the day after receiving the vaccination she felt pain in the injection
arm and that two days after receiving the vaccination, she felt the need to rest more frequently and
she began losing her physical strength. Id.; Affidavit at 2. Ms. Monzon explained that she went to
the doctor on April 22, 2016 and she was very worried because she knew what was happening to
her was not normal. Tr. at 10; Affidavit at 2. She explained that she had developed a hematoma on
the injection site and that she also felt pain and weakness in her joints. Id.

Next, Ms. Monzon described a visit to a neurologist on June 23, 2016. Tr. at 10. She
testified that she told the doctor she was experiencing rigidity in her neck, muscular pain, fatigue,
and was having difficulty walking. Id. at 10-11. She also described a previous doctor visit, on June
6, 2016, with Dr. Lopez who prescribed her Prednisone for her symptoms. Id. at 11. Ms. Monzon
indicated that the prescription alleviated her symptoms only slightly. Id. Ms. Monzon continued
to follow up with her rheumatologist, Dr. Lopez, throughout the remainder of 2016, and the
treatment she received was helpful, although her symptoms did not abate totally. Id. at 14. That
fall, Petitioner was prescribed Methotrexate, which helped lessen her pain. Id. at 14-15.

By the summer of 2017, Petitioner learned from Dr. Lopez that if she did not maintain the
medications she would likely see a recurrence of the more severe symptoms. Tr. at 15. She did so,
finding that by the end of 2017 her pain was diminished and symptoms largely controlled, even
though she still consistently felt fatigue. Id. As of 2018, Petitioner’s pain persisted, albeit in a less
intense manner, as she maintained her medicinal course, although she stopped taking Methotrexate
when she left on a trip out of the United States (a pause that was not determined to have impacted
her status, given the other medications she continued to take). Id. at 16-17. Ms. Monzon described
her symptoms for 2019 as comparable to the past—persistent pain but controlled with her
medications. Id. at 17-18.

B. Daniel Wallace, M.D.

Dr. Wallace provided three expert reports on Petitioner’s behalf and provided testimony at

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the hearing. Report, dated June 22, 2018, filed as Ex. 13 (ECF No. 19-2) (“First Wallace Rep.”);
Report, dated December, 21, 2018, filed as Ex. 30 (ECF No. 24-2) (“Second Wallace Rep.”);
Report, dated March 29, 2019, filed as Ex. 36 (ECF No. 25-2) (“Third Wallace Rep.”); Tr. 26-113.
Dr. Wallace maintained that Petitioner’s Tdap vaccine was causally associated with her
development of RA a short time later. First Wallace Rep. at 6.

Dr. Wallace is the Medical Director of the Wallace Rheumatic Study Center in Beverly
Hills, California. See CV, dated December 21, 2018, filed as Ex. 31 (ECF No. 24-3) (“Wallace
CV”). He obtained his medical degree from the University of Southern California and served his
residency at Cedars-Sinai Medical Center in Los Angeles, California. Id. at 1. Dr. Wallace also
completed a rheumatology fellowship at UCLA School of Medicine. Id. Currently, Dr. Wallace is
an attending physician at Cedars Sinai Medical Center, a Clinical Professor of Medicine at David
Geffen School of Medicine at UCLA, and the Associate director of the Rheumatology Fellowship
Program and Professor of Medicine at Cedars-Sinai Medical Center. Id. Dr. Wallace has also
published numerous books and articles and received various grants, including grants specifically
for rheumatoid arthritis research. Id. at 4-6.

Dr. Wallace is board-certified in rheumatology and internal medicine. Tr. at 27. Most of
his time is spent in clinical practice, and he has seen over a thousand patients with RA. Id. at 27-
28. He otherwise teaches and conducts research—specifically in certain RA variants, like lupus,
or Sjogren’s syndrome. Id. at 27-28, 30. Dr. Wallace is not an immunologist or epidemiologist,
however, and has no specific experience writing on or researching the alleged association between
the Tdap vaccine and RA. Id. at 35, 89-90, 107-08.

Dr. Wallace’s first report described RA as a chronic, progressive inflammatory disease
which primarily affects the joints, attacking the synovium, or connective tissue “wrapping” found
in the joints. First Wallace Rep. at 2; Tr. at 36, 45, 74, 84. RA is common in the United States,
affecting upwards of two million people. Tr. at 36. Its clinical manifestations include arthralgia,
swelling, redness, and limited range of motion. Id. Both steroids and non-steroidal inflammatory
drugs are used to control symptoms, but do not stop the underlying progression of the disease. Id.
RA is understood to have an autoimmune mechanism. Id. at 36. It also has a number of risk factors
making it more likely, including family history/genetic susceptibility as well as gender. Id. at 85,
100. Although RA typically evolves over many months, it can present acutely and also go into
remission, but can later be reactivated by infections like trauma, surgery, or comorbidity. Id. at 74,
84. Even though swelling is a common component of RA’s presentation, Dr. Wallace noted that
RA could initially present with simply pain, with swelling manifesting later. Id. at 44-45, 48.

Dr. Wallace differentiated RA from PMR, a separate condition that nevertheless can be
difficult to distinguish from RA due to their overlapping clinical presentations. First Wallace Rep.
at 2. Though both are chronic inflammatory conditions, PMR (which is also likely driven by an

6
autoimmune process) tends to be characterized by pain and stiffness in the shoulder and/or the
pelvic girdle, rather than featuring RA’s symmetric arthralgia in multiple sets of joints. Id.; Tr. at
36-37. Dr. Wallace also noted that RA and PMR differ in their biomarkers. An anti-CCP antibody
test is highly relevant to diagnosing RA, since the presence of those antibodies are very specific to
RA (but not to PMR). First Wallace Rep. at 2 (citing U. Sauerland et al., Clinical Utility of the
Anti-CCP Assay: Experiences with 700 Patients, 1050(1) Ann. N.Y. Acad. Sci. 314-318 (2005),
filed as Ex. 31 on December 21, 2018 (ECF No. 24-4) (“Sauerland”)), 3; Tr. at 37, 39. 3 Dr. Wallace
felt the initial speculation that Petitioner had PMR was not unreasonable, but that her later
diagnosis was properly revised as more evidence for RA came in—in particular the proof provided
by the positive anti-CCP test. Tr. at 37, 41, 43, 82.

The anti-CCP antibody plays a significant role in RA’s pathogenesis, and Dr. Wallace
briefly described how the antibody is scientifically understood to come into being. Certain
individuals possess a genetic mutation that causes a particular protein, arginine, to be incorrectly
converted (via a process called “citrullination”) into citrulline—triggering production of antibodies
against the citrulline that also cross-react against joint tissues, furthering the pathogenesis of RA.
First Wallace Rep. at 3; Tr. at 38. This citrullination process is thought to occur in the oral cavities
or lungs, and can be exacerbated by smoking, poor oral hygiene, or other lung-impacting factors,
like pollutants. Tr. at 85. It is rare for an individual to be diagnosed with RA and not test positive
for the anti-CCP antibodies—although a person can be “seropositive” for the antibodies long
before they develop clinical symptoms of RA. Id. at 39-41.

As noted above, Dr. Wallace opined that Ms. Monzon likely had RA, and was thus
correctly diagnosed with it. Tr. at 37, 38. She tested positive for the anti-CCP antibodies, and in
fact possessed them well before receiving the Tdap vaccine deemed causal in this case. Tr. at 37,
42-43, 66, 86, 103; see also Ex. 6 at 8. Indeed, her clinical presentation would have led Dr. Wallace
to conduct testing for the antibody, since it appeared she might have RA based on her symptoms.
Id. at 41, 82. In addition, Ms. Monzon at one point early in her course tested positive for the
existence of inflammatory biomarkers, further suggesting an RA process was occurring. Id. at 43-
44, 46-47, 49; First Wallace Rep. at 3 (citing N. Shadick et al., C-Reactive Protein in the Prediction
of Rheumatoid Arthritis in Women, 166 Arch. Intern. Med. 2490-2494 (2006), filed as Ex. 22 on
June 22, 2018 (ECF No. 20-2)). 4 Dr. Wallace went so far as to propose that the mere evidence of
the anti-CCP antibodies was itself suggestive of ongoing inflammation. Tr. at 46-47, 50-51.

3
A review of 700 patients revealed a sensitivity to RA in 74 percent of subjects with the anti-CCP antibody, and a
specificity for RA in over 90 percent. Anti-CCP reactivity can be seen in other conditions, but at lower rates: systemic
lupus (12.7%), Sjogren’s syndrome (3.3%), polymyalgia rheumatica (<5%). First Wallace Rep. at 2 (citing Sauerland).
4
Dr. Wallace deemed this evidence more significant than observations by Dr. Lopez at the time that there was “no
evidence of [RA] disease activity” otherwise. Tr. at 49

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 By contrast, Dr. Wallace did not accept Respondent’s proposed counter-diagnosis of
preclinical RA. Tr. at 72. He allowed that the preclinical classification (which he defined as the
possession of anti-CCP antibodies without other clinical symptoms characteristic of RA) had
medical acceptability. Id.; K. Mankia et al., Preclinical Rheumatoid Arthritis: Progress Toward
Prevention, 68(4) Arthritis & Rheumatology 779-788 (2016), filed as Ex. 37 on March 29, 2019
(ECF No. 25-3). However, he concluded that Petitioner’s course was not consistent with it. First
Wallace Rep. at 4. Even though Petitioner never went on to exhibit certain classic RA features,
such as swollen joints, RA is a progressive disease—and therefore patients do not always display
these symptoms right away. Tr. at 45. Moreover, prompt treatment with steroids and Methotrexate
can limit or suppress swelling symptoms, so that they do not become clinically apparent until years
after onset, if ever. Id. at 45-46. And Dr. Wallace emphasized his conclusion that the temporal
association of Petitioner’s post-vaccination onset was diagnostically-meaningful. Id. at 72. 5

Dr. Wallace similarly rejected the suggestion that Petitioner might be better understood as
suffering from fibromyalgia (which was in effect mistaken, early on, by Petitioner’s treaters to be
RA). Fibromyalgia, he explained, is a “central desensitization syndrome” characterized by muscle
aches and pain when touched, and not itself a disease, making it possible for Ms. Monzon to have
had it and RA concurrently. Tr. at 50. In the absence of an alternative explanation for the anti-CCP
results (which would have no bearing on fibromyalgia), Dr. Wallace concluded that the most
medically sound explanation was that she did in fact have RA (with fibromyalgia only a secondary
condition). Second Wallace Rep. at 3.

Next, Dr. Wallace addressed his primary causal contention: that the Tdap vaccine was the
“inciting event” for the initiation of Petitioner’s RA. Tr. at 37. He began with what is known
generally about potential associations between vaccines and RA, which he characterized as
“obvious.” Id. at 58; First Wallace Rep. at 3. Though rare, stimulation of the immune system with
vaccinations has been associated with flares of preexisting autoimmune disease, like RA, and
causing new autoimmune reactions. First Wallace Rep. at 3, citing L. Calabrese et al., Checkpoint
Immunotherapy: Good for Cancer Therapy, Bad for Rheumatic Diseases, 76(1) Ann. Rheum. Dis.
1-3 (2017), filed as Ex. 26 on June 22, 2018 (ECF No. 20-6); Y. Segal et al., Vaccine-Induced
Autoimmunity: the Role of Molecular Mimicry and Immune Crossreaction, 14 Cellular & Molec.
Immun. 1-9 (2018), filed as Ex 27 on June 22, 2018 (ECF No. 20-7)). A vaccine could thus
theoretically “light up somebody who is predisposed to RA.” Tr. at 52, 62-63.

Dr. Wallace placed particular emphasis on a recent meta-analysis of the risk of RA after

5
Dr. Wallace also took issue with a contention in one of Dr. Oddis’s reports that the positive anti-CCP antibody
findings could have been incorrect, arguing that the testing was sensitive enough to render this extremely unlikely.
Second Wallace Report at 2. However, Dr. Oddis acknowledged at hearing that it was only a possibility that
Petitioner’s anti-CCP antibody test was a false positive, and he seemed to some extent to abandon this argument at
trial. Tr. at 187. I find it more likely than not that the positive anti-CCP antibody testing results received for Petitioner
in the summer of 2014 were accurate.

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vaccinations. First Wallace Rep. at 4 (citing B. Wang et al., Vaccinations and Risk of Systemic
Lupus Erythematosus and Rheumatoid Arthritis: A Systemic Review and Meta-Analysis, 16
Autoimmunity Rev. 756-765 (2017), filed as Ex. 25 on June 22, 2018 (ECF No. 20-5) (“Wang”)).
Based on an aggregated overview of sixteen observational studies, Wang noted an “obvious
association between vaccination and increased risk of RA.” First Wallace Rep. at 5; Wang at 762.
Dr. Wallace deemed Wang’s findings to have statistical significance, although he admitted that
they did not amount to a scientific certainty. Tr. at 57, 86.

Importantly, Wang was not restricted to evaluation of the impact of Tdap or other vaccines
with a tetanus component. Wang at 759. Indeed, Dr. Wallace specifically acknowledged that only
three of the sixteen studies cited in Wang clearly, or even arguably, included the Tdap vaccine in
their analysis (one of which was one of the primary items of literature relied upon by Respondent,
as discussed below). Tr. at 105-06; Wang at 759. Petitioner filed those studies after the hearing,
and subsequent close review confirmed they said little about a Tdap-RA association. See generally
P. Ray et al., Risk of Rheumatoid Arthritis Following Vaccination with Tetanus, Influenza and
Hepatitis B Vaccines Among Persons 15-59 Years of Age, 29 Vaccine 6592-6597, at 6592 (2011),
filed as Ex. 47 on Feb. 8, 2021 (ECF No. 48-3) (“Ray”); T. Verstraeten, et al., Analysis of Adverse
Events of Potential Autoimmune Etiology in a Large Integrated Safety Database of AS04
Adjuvanted Vaccines, 26 Vaccine 6630-6638 at 6637 (2008), filed as Ex. 48 on Feb. 8, 2021 (ECF
No. 48-4) (“Verstraeten”).

Ray, for example, was a large retrospective study involving a cohort analysis of nearly 400
cases of new-onset RA in vaccinated and unvaccinated people, as well as a case-control study of
37 cases of new-onset RA. Ray at 6592. Ray’s authors found no statistically significant association
between exposure to tetanus vaccine and development of RA. Id. at 6592, 6595. Verstraeten was
an integrated analysis aimed at assessing the safety of AS04-adjuvanted vaccines, like the human
papillomavirus vaccine (“HPV”), with regard to adverse events of potential autoimmune etiology.
Verstraeten at 6630. Tdap does not contain this adjuvant. In randomized controlled trials including
over 68,000 subjects, HPV, hepatitis B, and genital herpes simplex virus vaccines (AS04
adjuvanted) were analyzed in an integrated analysis of individual data. Id. Verstraeten’s authors
actually found no evidence of an increase in relative risk associated with AS04-adjuvanted
vaccines. Id. Thus, Verstraeten not only did not evaluate the alleged RA-Tdap association, but
found no association for the vaccines it did consider.

Dr. Wallace’s discussion of specific items of literature referenced in Wang also included
an article relied upon by Respondent to rebut any Tdap-RA association. See C. Bengtsson et al.,
Common Vaccinations Among Adults do not Increase the Risk of Developing RA: Results from the
Swedish EIRA Study, 69 Ann. Rheum. Dis. 1831-1833 (2010), filed as Ex. D on October 1, 2018
(ECF No. 22-2) (“Bengtsson”). Bengtsson looked at a possible association between vaccination in
adults and the risk of developing RA, analyzing data from a Swedish population-based RA case-

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control study encompassing 1,998 incident cases of RA. Bengtsson at 1831. Bengtsson found no
increased risk of RA following vaccination in general or for any specific vaccination studied. Id.

Dr. Wallace criticized Bengtsson, however, as under-powered in an epidemiologic sense,
given its relatively-small sample size, especially when compared to some of the studies referenced
in Wang, and also observed that the study relied on a subject sample that was arbitrary in defining
a relevant timeframe for purposes of assessing post-vaccination risk. Tr. at 53-55, 62. Indeed, Dr.
Wallace pointed out that Wang was not only the more recent item of literature, but had expressly
included Bengtsson’s findings, while still concluding overall that vaccines could be associated
with RA. Id. at 56; Wang at 759, 763. And overall, although Dr. Wallace could not identify an
epidemiological association between immunization and RA, he did not consider this to undermine
his theory, since the absence of a statistically significant risk did not mean zero risk. Second
Wallace Rep. at 3.

Besides Wang, Dr. Wallace discussed some case reports. The first involved a recurrence
of reactive arthritis after a booster dose of tetanus toxoid. A. Kaul et al., Recurrence of Reactive
Arthritis after a Booster Dose of Tetanus Toxoid, 61 Ann. Rheum. Dis. 185 (2002), filed as Ex. 19
on June 22, 2018 (ECF No. 19-8) (“Kaul”). The patient, a 24-year old male, presented with acute
swelling of the right ankle two weeks after receiving the immunization. Kaul at 1. The second case
report involved a 34-year old woman in 1986 who developed a severe local reaction three weeks
after receiving the second dose of the tetanus toxoid. A. Jawad, et al., Immunization Triggering
Rheumatoid Arthritis?, 48 Annals of the Rheumatic Disease 185 (1989), filed as Ex. 18 on June
22, 2018 (ECF No. 19-7) (“Jawad”). The patient’s RA was almost completely resolved in one year.
Id. at 185. The third case report involved two patients who developed RA following immunization
against diphtheria, poliomyelitis and tetanus toxoid. J. Maillefert et al., Arthritis Following
Combined Vaccine against Diphtheria, Poliomyelitis, and Tetanus Toxoid, 18 Clinical &
Experimental Rheumatology 255-56 (2000), filed as Ex. 21 on June 22, 2018 (ECF No. 19-10)
(“Maillefert”). One patient developed post-immunization mono-arthritis of the knee that regressed
following synovectomy. Maillefert at 255. Five years later, the arthritis recurred after a booster
vaccine injection. Id. The other patient developed arthritis of the ankle one day following
immunization that persisted for three days. Id.

Dr. Wallace proffered the mechanism of molecular mimicry in a genetically-predisposed
individual as a plausible mechanism by which one or more vaccine components could cause an
autoimmune response. Tr. at 95. He described molecular mimicry as a process in which antibodies
formed in response to stimulation of the immune system by a pathogen or vaccine attack the body’s
own tissues. First Wallace Rep. at 3 (citing M. Van Gemeren et al., Vaccine-Related Autoimmune
Hepatitis: The Same Disease as Idiopathic Autoimmune Hepatitis? Two Clinical Reports and
Review, 52:1 Scandinavian J. of Gastroenterology 18-22 (2017), filed as Ex. 24 on June 22, 2018
(ECF No. 20-4)). This cross-reaction is mediated by similarities in amino acid structure between

10
the body’s own proteins and those of the vaccine. Id. Dr. Wallace maintained that such an
autoimmune process mediated by molecular mimicry could occur in response to any antigen
component of a vaccine—and thus in the case of the Tdap vaccine, the tetanus, diphtheria, or
pertussis antigen components might have prompted this cross- reaction. First Wallace Rep. at 4.
He did, however, note that certain case reports placed particular emphasis on the tetanus toxoid
component. Id. at 5 (citing Maillefert).

Adjuvants contained in vaccines could also, in Dr. Wallace’s view, play a role in adverse
autoimmune reactions. First Wallace Rep. at 4. Adjuvants are purposely used as immunogenicity-
enhancing agents which can help prompt an adaptive immune response (in which the body “learns”
how to manufacture antibodies specific to the vaccine’s antigens, so that it will know how to fight
a wild infection in the future). Id. However, adjuvants might also trigger undesired autoimmune
reactions in individuals with a genetic susceptibility (specifically those carrying certain HLA-
DRB1 alleles highly associated with RA), leading to an abnormal immune response and
development of full-blown autoimmune disorders. Id. (citing Y. Shoenfeld et al., “ASIA” –
Autoimmune/Inflammatory Syndrome Induced by Adjuvants, 36(1) J. of Autoimmunity 4-8 (2011),
filed as Ex 23 on June 22, 2018 (ECF No. 20-3). 6 Some of the HLA-DRB1 alleles implicated in
autoimmune reactions to adjuvants are also important markers for RA, with more than 80 percent
of RA patients carrying at least one of these alleles. Id. (citing S. Kerlan-Kandon et al., HLA-DRB1
Transcripts in Rheumatoid Arthritis, 124 Clinical & Experimental Immun. 142-9 (2001), filed as
Ex. 20 on June 22, 2018 (ECF No. 19-9)).

A third, less well-developed mechanistic explanation considered by Dr. Wallace was an
anamnestic immune response. Tr. at 69. This can occur when an individual has had some prior
exposure to an antigen (whether in vaccination, an infectious incident, or some other
environmental factor), resulting in a greater autoimmune response to a subsequent exposure. Id. at
70-71. But Dr. Wallace offered little corroborative support for this contention, and acknowledged
he lacked the expertise to assign this proposed mechanism much evidentiary significance. Id. at
77.

Dr. Wallace found support for his causation theory in Ms. Monzon’s medical record.
Petitioner had experienced no pre-existing conditions that could have caused RA-like symptoms,
and around the time of her vaccination she was not subject to any infections or trauma that could
have possibly induced RA. First Wallace Rep. at 6. In addition, two of Petitioner’s treating

6 The ASIA theory for adjuvant-induced autoimmunity has never been deemed medically reliable in any prior Program

cases. See generally Morris v. Sec'y of Health & Human Servs., No. 12-415V, 2016 WL 3022141, at *12 (Fed. Cl.
Spec. Mstr. Apr. 1, 2016) (discussing lack of reliability of ASIA theory); Rowan v. Sec'y of Health & Human Servs.,
No. 10-272V, 2014 WL 7465661, at *16 (Fed. Cl. Spec. Mstr. Dec. 8, 2014), mot. for review den'd, 2015 WL 3562409
(Fed. Cl. May 18, 2015); D'Angiolini v. Sec'y of Health & Human Servs., No. 99-578V, 2014 WL 1678145, at *60
(Fed. Cl. Spect. Mstr. Mar. 27, 2014), mot. for review den'd, 122 Fed. Cl. 86 (2015), aff'd, 645 F. App'x 1002 (Fed.
Cir. 2016).

11
physicians stated in their notes that her Tdap immunization had some connection to her RA-like
symptom. Id. And testing results (which revealed the presence of the anti-CCP antibodies plus
some inflammation biomarkers) were all consistent with an ongoing course of RA, as well as her
symptoms and response to treatment. Id. Overall, in Dr. Wallace’s view a patient in whom a
systemic inflammatory process is already underway would, all other things being equal, be more
likely to experience an adverse autoimmune-mediated reaction to vaccination. Second Wallace
Rep. at 2. Here, he maintained, Petitioner’s possession of anti-CCP antibodies reflected the
presence of systemic inflammation. Tr. at 38.

Finally, Dr. Wallace addressed the temporal association between Petitioner’s vaccination
and clinical onset of her RA. First Wallace Rep. at 5; Second Wallace Rep. at 5. An autoimmune
process mediated by molecular mimicry could commence rapidly following vaccination, although
the exact time when such a process becomes symptomatic would vary considerably from one
patient to the next. First Wallace Rep. at 5. Thus, Petitioner’s asserted two-day post-vaccination
onset was medically acceptable. Tr. at 96. In support, Dr. Wallace cited one case report in which
he claimed the patient developed arthritis approximately 24 hours after tetanus/diphtheria/polio
immunization. Id. (citing Jawad). However, the Jawad subject in fact developed RA three weeks
after a second dose of tetanus toxoid. Id. at 1.

Responding to Dr. Oddis’s opinion that there is no evidence in the literature that a specific
RA autoantibody like anti-CCP can develop so quickly (i.e. just over two months) after a vaccine,
Dr. Wallace restated his opinion that an autoimmune process mediated by molecular mimicry
could commence rapidly following vaccination, with specific timeframes varying depending on
the patient. Second Wallace Rep. at 5. Therefore, in his view the close temporal association of
vaccination and symptom onset in Petitioner’s case further strengthened the hypothesis that the
former caused the latter. Id.; Tr. at 72-73.

C. Chester V. Oddis, M.D.

Dr. Oddis, a rheumatologist, prepared one report on behalf of Respondent and provided
testimony at the hearing. Report, dated September 28, 2018, filed as Ex. A (ECF No. 21-1) (“Oddis
Rep.”); Tr. at 114-210. Dr. Oddis opined that Petitioner’s presentation, clinical descriptions, and
immediate onset of symptoms were most consistent with “preclinical” RA, and that the Tdap
vaccine could not otherwise cause this to occur. Wallace Rep. at 5.

Dr. Oddis received his bachelor’s degree in biochemistry from the University of Pittsburg.
Dr. Oddis Curriculum Vitae, filed as Ex. B-1 on Sept. 28, 2018 (ECF No. 21-2) (“Oddis CV”) at
1. He then obtained his medical degree from Pennsylvania State University College of Medicine
where he also completed his residency in internal medicine. Oddis CV at 1. He then completed a
fellowship in rheumatology at the University of Pittsburg School of Medicine. Id. He is board
certified in internal medicine and rheumatology. Id. at 3. Dr. Oddis is currently Professor of

12
Medicine in the Division of Rheumatology and Clinical Immunology and Director of the Myositis
Center in the School of Medicine at the University of Pittsburg. Id. at 2. His primary area of
research and clinical care is in the clinical, epidemiologic, serologic and treatment aspects of the
idiopathic inflammatory myopathies (myositis) and autoimmune interstitial lung disease. Id. Dr.
Oddis has also published numerous journal articles on these subjects. Id. at 2, 4-15. Although his
focus is different, Dr. Oddis also regularly sees patients with RA, and he would deem a handful to
be properly diagnosed with preclinical RA. Tr. at 116, 117. He does not have epidemiologic
expertise. Id. at 166.

Dr. Oddis began his testimony with a review of the same RA concepts discussed by Dr.
Wallace. He acknowledged RA to be autoimmune in pathogenesis, featuring small joint
inflammatory arthropathy and usually “synovitis,” or inflammation of the joint lining. Tr. at 120-
21. The classic clinical signs and symptoms of RA include objective inflammation of the joints,
stiffness and pain in the small joints of the hands and feet predominantly, and evidence of abnormal
autoantibodies in laboratory tests. Id. at 121-22. Dr. Oddis acknowledged that the presence of anti-
CCP antibodies is an important criterion for RA’s diagnosis, adding that these particular antibodies
can long predate clinical symptoms. Id. at 122, 174. However, despite the specificity of the anti-
CCP antibody for RA, Dr. Oddis would not exclusively rely on their presence to diagnose RA in
an individual. Id. at 153, 185-86. RA’s true cause remains unknown, and although it has many risk
factors, Dr. Oddis disputed vaccines are among them, stressing that rheumatologists readily
encourage their patients to be vaccinated. Id. at 154-55, 56, 190.

Dr. Oddis also outlined the concept of preclinical RA, which he defined as a period in time
for a patient where there is detectable autoimmunity, plus or minus inflammation, that otherwise
predates the onset of clinically apparent or classic rheumatic disease. Tr. at 123; Oddis Rep. at 4
(quoting K. Deane et al., Pathogenesis and Prevention of Rheumatic Disease: Focus on Preclinical
RA and SLE, 10 Nat. Rev. Rheumatol. 212-214 (2014) at 212, filed as Ex. C on October 1, 2018
(ECF No. 22-1) (“Deane”)). Preclinical RA is a relatively new diagnostic classification, and can
be applied both where a person presents with nonspecific RA-like symptoms, or tests positive for
anti-CCP antibodies in the absence of confirming clinical symptoms. Tr. at 123, 126; Deane at 213
(“the measure of tissue injury that should be used to define the onset of clinically apparent
disease…is an important consideration in characterizing the preclinical period”).

Because preclinical RA overlaps to some extent with full RA, it would be easy in treatment
to confuse the two. Thus, a patient might receive common RA treatment based on a few clinical
indicia plus a positive anti-CCP antibody test, even though all criteria for the disease itself had not
been met. Oddis Rep. at 4. Dr. Oddis admitted, however, that in his experience the antibodies
would not be looked for absent some strong clinical hint that RA might exist. Tr. at 124. The best
treatment course for persons thought to have preclinical RA would be to follow them over time,
watching to see whether their presentation evolved into the more classic form of RA. Id. Dr. Oddis
could only speculate how often preclinical RA does so evolve (and he has personally only observed
20 to 25 patients to whom he would apply the new diagnostic classification). Id. at 125, 127-28.

13
 Petitioner, Dr. Oddis maintained, was best diagnosed with preclinical RA that had (to date)
never actually evolved into classic RA. Tr. at 161, 180-81, 183-84. To support this contention, Dr.
Oddis conducted a painstakingly-specific review of Petitioner’s medical history. Oddis Rep. at 2;
Tr. at 132-48. Her initial post-vaccination treater visits (in late-April and early-May 2016) featured
non-specific complaints that allowed no definitive diagnosis, as she presented only with joint pain
not also accompanied by RA’s characteristic swelling. Tr. at 132-33.

By Petitioner’s first rheumatology visit with Dr. Lopez on June 16, 2016 (Ex. 3 at 4), the
clinical impression was that Petitioner had low back pain, cervicalgia (neck pain), and myalgia.
Oddis Rep. at 2; Tr. at 137. No likelihood of RA is mentioned. Oddis Rep. at 2. She also had full
range of motion of all her joints, and no synovitis and or tender points of fibromyalgia, but focal
tenderness of the trapezius muscles was noted. Id. (citing Ex. 3 at 4). Dr. Oddis discounted the
possibility that Ms. Monzon had initially experienced some form of vaccine-induced reactive
arthritis, arguing that the sole evidence to support anything inflammatory was occurring was her
high ESR rate from the May 21, 2016 doctor’s visit (Tr. at 134, 207), followed by a high CRP in
June (Tr. at 137), but ultimately he could not opine what the etiology of her initial symptoms
represented. Tr. at 209.

Dr. Oddis also highlighted a lack of treater support for an RA diagnosis overall (although
he could not dispute the existence of some evidence supporting it). Petitioner’s managing
rheumatologist, Dr. Lopez, initially did not believe that Ms. Monzon had RA. Oddis Rep. at 2. Dr.
Lopez had only embraced RA after the positive anti-CCP antibody test results. Tr at 138-39, 184.
But thereafter, in all subsequent medical record notes, Dr. Lopez never observed any of the
characteristic features of RA, or other laboratory or clinical evidence of RA disease activity in
many of her clinical notes. Id. Other treaters also made no note of clinical findings consistent with
RA. Id. at 123-38. Indeed, after the June and July 2016 visits, PMR appeared to be the preferred
diagnosis, and it remained so until the positive anti-CCP test results were obtained. Id. at 138; Ex.
6 at 2-3. And by October 2016, when Petitioner was being treated for RA (mainly on account of
the anti-CCP antibody findings), fibromyalgia had entered the differential (a significant
development in Dr. Oddis’s view). Tr. at 140; Ex. 6 at 2-3.

By the fall of 2016, Ms. Monzon was receiving RA-specific medications like Methotrexate
(again, without her symptoms having begun to include classic indicia such as swelling). Tr. at 140-
41. But she also began to receive treatments specific for fibromyalgia and chronic pain, like
Cyclobenzaprine and Duloxetine. Id. at 141-42; Ex. 10 at 173-175. Several months into 2017,
however, there was no change in her clinical presentation, with no manifestation of previously-
absent RA symptoms, and she ceased taking an anti-inflammatory drug. Tr. at 142; Ex. 10 at 176-
178. Then, by June of 2017, Petitioner’s treater notes record “no disease activity” and “[t]he
fibromyalgia was better on the combination of Cyclobenzaprine and Duloxetine.” Tr. at 143
(quoting Ex. 10 at 179-182). Dr. Oddis deemed these records to establish “a classic scenario of
preclinical [RA],” since Petitioner’s presentation was still mostly characterized by the existence
of the anti-CCP antibodies but without fully-corroborating clinical indicia of RA. Tr. at 144-45.

14
 At hearing, Dr. Oddis also discussed the updated medical records for 2018 that had been
filed after he had prepared his written report, and in his view they strongly supported the
conclusion that Petitioner suffered from preclinical RA. Tr. at 146. Thus, by the spring and summer
of 2018, it was evident that Petitioner had full range of motion of all of the joints, no evidence of
any RA disease activity, and also showed marked improvements in her fibromyalgia symptoms
given the disease-specific treatments she had been receiving. Tr. at 146; Ex. 39 at 2; Ex. 42 at 22.
Then, by October 2018 Petitioner was taken off Methotrexate, while continuing to receive the
fibromyalgia medications. Tr. at 147; Ex. 38 at 8. But even six months later she displayed “no
clinical or lab evidence of [RA] disease activity.” Id. Her presentation was similarly consistent
even by October 2020. Tr. at 148; Ex. 43 at 2. Thus, additional evidence from Petitioner’s medical
treatment history did not reveal disease progression or symptoms recurrence.

Dr. Oddis made a point of discussing Petitioner’s suggestion that the absence of certain
commonly-associated RA symptoms in her history, such as swelling, could be attributed to the
success of RA-specific treatments in suppression expression of such symptoms. Tr. at 149, 154.
Although he allowed for the possibility that RA-specific medication, like Methotrexate, might
ameliorate some RA symptoms, he pointed out (based on the totality of Petitioner’s record) that
even after Petitioner later ceased these medications, she experienced no “documented joint
inflammation . . . or an abnormal physical examination consistent with rheumatoid arthritis.” Id.
at 149, citing Ex 8 at 4. As a result, Dr. Oddis remained convinced Petitioner had never progressed
out of preclinical RA. Tr. at 153-54.

Turning to Dr. Wallace’s causation theory, Dr. Oddis denied that reliable evidence existed
to suggest RA could be caused or triggered by the Tdap vaccine. Tr. at 161-62; Oddis Rep. at 5.
Patients with established autoimmune rheumatic disorders were encouraged to receive appropriate
vaccination, suggesting as an overall matter that the risk of adverse reaction was low. Oddis Rep.
at 5; Bengtsson at 1833. Dr. Oddis acknowledged that molecular mimicry was a medically-
acceptable mechanistic explanation for many autoimmune disease processes, as well as the fact
that the Tdap vaccine amounts to an antigenic stimulus that, in the setting of a genetic tendency to
develop an autoimmune disorder, could theoretically play a triggering role. Id.; Tr. at 194. But
Bengtsson, a case-controlled 7 study, had observed no increased RA risk post-vaccination (for any
vaccine), including in a subset of patients with anti-CCP positivity. Id. (citing Bengtsson at 1831);
Tr. at 156. While Dr. Oddis agreed that (as argued more extensively by Dr. Wallace) Bengtsson
had some methodologic flaws, he felt those same kinds of critiques could also be applied to the
single-patient case studies relied upon by Petitioner, and overall that Bengtsson still had persuasive
force. Id. at 156-59, 199.

Dr. Oddis also spent some time discussing the Wang meta-analysis cited by Dr. Wallace
in support of the proposition that vaccines can cause RA. Tr. at 163. Although he deemed Wang

7
A case-control study compares a group with a disease or condition to a control group without the condition. Snyder
v. Sec’y of Health & Hum. Servs., No. 01-162V, 2009 WL 332044 at *199 (Fed. Cl. Spec. Mstr. Feb. 12, 2009).

15
helpful in generating hypotheses regarding association between vaccines and RA, he felt the article
was not sufficient to establish causality. Id. at 164. Wang in his view made broad generalizations,
relying on findings involving different kinds of vaccines (with a minority of its referenced articles
even involving the Tdap vaccine), and therefore its conclusions were more of an intriguing
hypothesis than reliable causal evidence. Id. at 163-65.

Dr. Oddis similarly discounted some of the case reports cited by Dr. Wallace in his expert
report. Kaul, for example, involved a diagnosis (reactive arthritis) not at issue, while Jawad was
over 30 years old, and thus relied on somewhat outdated criteria for defining RA, and also involved
a longer onset timeframe. Tr. at 168-71, 177. Overall, Dr. Oddis characterized case reports as
“interesting” but of limited value with respect to causation. Id. at 167-68, 205.

Regarding the timeframe for onset, Dr. Oddis indicated his openness to the theory that in
some cases RA symptoms could follow closely after an inciting occurrence. Tr. at 191. But he
deemed an “explosive” presentation of symptoms to be uncommon with classic RA, which usually
was progressive and insidious, developing “over weeks to months.” Id. at 123. Dr. Oddis also
emphasized that it was highly likely Petitioner possessed the anti-CCP antibodies (which have not
otherwise been alleged to have been vaccine-caused) long before vaccination. Oddis Rep. at 4-5.
And he did not accept Dr. Wallace’s contention that the mere possession of these antibodies placed
a person in an elevated inflammatory state, such that the impact of vaccination would increase the
likelihood of symptoms onset. Tr. at 173, 176.

Besides disputing RA as the proper diagnosis, Dr. Oddis provided his opinion about some
of the other competing or co-diagnoses at issue. He noted that as of July 2016 (and before her RA
diagnosis), Ms. Monzon had been diagnosed with PMR (Ex. 3 at 2), but he questioned the validity
of the diagnosis. Oddis Rep. at 2. At best, her initial symptoms of neck and leg pain, plus the
subsequent one-time ESR elevation, initially appeared consistent with PMR, but Petitioner’s age
combined with the subsequent finding of a positive anti-CCP ruled that diagnosis out. Id. However,
he deemed the fibromyalgia diagnosis far more evidentiarily-supported. Oddis Rep. at 5.
Petitioner’s overall course of symptoms, the physical examination findings, the impression of her
treating rheumatologist, and the effectiveness of the fibromyalgia treatments Petitioner received
all corroborated its likelihood as an appropriate diagnosis. Id.; Tr. at 209.

On cross-examination, Dr. Oddis acknowledged that Ms. Monzon displayed no real RA
symptoms pre-vaccination. Tr. at 180-81. He also allowed that there was a possibility that the Tdap
vaccine could trigger RA, but he unquestionably did not concede the medical reliability of the
contention. Id. at 171, 196.

III. Procedural History

This matter commenced with the filing of the Petition on August 4, 2017. On March 15,
2018, Respondent filed a Rule 4(c) report asserting that Petitioner had not established a prima
facie case and that compensation was not appropriate. Petitioner subsequently filed an expert

16
report from Dr. Wallace and Respondent filed an expert report from Dr. Oddis. On December 21,
2018, Petitioner filed a supplemental report from Dr. Wallace, and on March 29, 2019, Petitioner
filed an additional supplemental report from Dr. Wallace in response to a specific inquiry from the
Court regarding the possibility that Petitioner’s RA was pre-clinical at the time of vaccination. An
entitlement hearing was set for August 21, 2020 and a schedule was set for prehearing briefing.
Petitioner filed her prehearing submission on May 5, 2019 and after an unopposed motion for an
extension of time was granted, Respondent filed his prehearing submission on July 9, 2020. The
July 9, 2020, the entitlement hearing was also rescheduled to February 4, 2021. Some medical
records were subsequently filed and then a one-day hearing entitlement hearing took place on
February 4, 2021. Petitioner was ordered to file various items of medical literature that were
discussed during the hearing and she did so on February 8, 2021. The parties did not elect to file
post-hearing briefs, and the matter is now fully ripe for resolution.

IV. Applicable Legal Standards

A. Petitioner’s Overall Burden in Vaccine Program Cases

To receive compensation in the Vaccine Program, a petitioner must prove either: (1) that
he suffered a “Table Injury”—i.e., an injury falling within the Vaccine Injury Table—
corresponding to one of the vaccinations in question within a statutorily prescribed period of time
or, in the alternative, (2) that his illnesses were actually caused by a vaccine (a “Non-Table
Injury”). See Sections 13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3; §
11(c)(1)(C)(ii)(I); see also Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1321 (Fed.
Cir. 2010); Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006).8
In this case, Petitioner does not assert a Table claim.

For both Table and Non-Table claims, Vaccine Program petitioners bear a “preponderance
of the evidence” burden of proof. Section 13(1)(a). 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, 592 F.3d at 1322 n.2; see also Snowbank Enter. v. United States, 6 Cl. Ct.
476, 486 (1984) (mere conjecture or speculation is insufficient under a preponderance standard).
Proof of medical certainty is not required. Bunting v. Sec’y of Health & Hum. Servs., 931 F.2d
867, 873 (Fed. Cir. 1991). In particular, a 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,

8 Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding authority.

Hanlon v. Sec’y of Health & Hum. Servs., 40 Fed. Cl. 625, 630 (1998). By contrast, Federal Circuit rulings concerning
legal issues are binding on special masters. Guillory v. Sec’y of Health & Hum. Servs., 59 Fed. Cl. 121, 124 (2003),
aff’d 104 F. Appx. 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Hum. Servs., No. 13-159V, 2014 WL
504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).

17
1352–53 (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 by the opinion of a competent
physician. Section 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. Sec’y of Health & Hum. Servs., 418 F.3d 1274, 1278 (2005): “(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 proximate
temporal relationship between vaccination and injury.”

Each of the Althen prongs requires a different showing. Under Althen prong one, petitioners
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 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 549.

Petitioners 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). Special masters, despite their expertise, are not empowered by
statute to conclusively resolve what are essentially thorny 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. Accordingly, special masters must take care not to increase the burden
placed on petitioners in offering a scientific theory linking vaccine to injury.

In discussing the evidentiary standard applicable to the first Althen prong, the Federal
Circuit has consistently rejected the contention that it can be satisfied merely by establishing the
proposed causal theory’s scientific or medical plausibility. See Boatmon v. Sec’y of Health & Hum.
Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019); see also LaLonde v. Sec’y of Health & Hum. Servs.,
746 F.3d 1334, 1339 (Fed. Cir. 2014) (“[h]owever, in the past we have made clear that simply
identifying a ‘plausible’ theory of causation is insufficient for a petitioner to meet her burden of
proof.” (citing Moberly, 592 F.3d at 1322)). Petitioners otherwise always have the ultimate burden
of establishing their overall Vaccine Act claim with preponderant evidence, regardless of what
evidentiary level of evidence on the “can cause” prong is required. W.C. v. Sec’y of Health & Hum.
Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013) (citations omitted); Tarsell v. United States, 133 Fed.

18
Cl. 782, 793 (2017) (noting that Moberly “addresses the petitioner’s overall burden of proving
causation-in-fact under the Vaccine Act” by a preponderance standard).

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; Grant v. Sec’y of Health & Hum. Servs., 956
F.2d 1144, 1148 (Fed. Cir. 1992). In establishing that a vaccine “did cause” injury, the opinions
and views of the injured party’s treating physicians are entitled to some weight. Andreu, 569 F.3d
at 1367; Capizzano, 440 F.3d at 1326 (“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, since 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).

Medical records and statements of a treating physician, however, do not per se bind the
special master to adopt the conclusions of such an individual, even if they must be considered and
carefully evaluated. Section 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) (“there 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 be weighed against other, contrary
evidence also present in the record—including conflicting opinions among such individuals.
Hibbard v. Sec’y of Health & Hum. Servs., 100 Fed. Cl. 742, 749 (2011) (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); Veryzer v. Sec’y of Dept. of Health & Hum. Servs., No. 06-522V,
2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr. Apr. 29, 2011), mot. for review denied, 100 Fed.
Cl. 344, 356 (2011), aff’d without opinion, 475 F. Appx. 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. 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 for what
is a medically acceptable timeframe must align with the theory of how the relevant vaccine can
cause an 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, 105 Fed. Cl. 353 (2012), aff’d

19
mem., 503 F. Appx. 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), mot. for rev. denied (Fed. Cl. Dec. 3,
2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).

B. Legal Standards Governing Factual Determinations

The process for making determinations in Vaccine Program cases regarding factual issues
begins with consideration of the medical records. Section 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.” Section 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 415, 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 evidenced by
a rational determination).

Medical records that are created contemporaneously with the events they describe are
presumed to be accurate and “complete” (i.e., presenting all relevant information on a patient’s
health problems as of the time of their creation). Cucuras, 993 F.2d at 1528; Doe/70 v. Sec’y of
Health & Hum. Servs., 95 Fed. Cl. 598, 608 (2010) (“[g]iven the inconsistencies between
petitioner’s testimony and his contemporaneous medical records, the special master’s decision to
rely on petitioner’s medical records was rational and consistent with applicable law”), aff’d sub
nom. Rickett v. Sec’y of Health & Hum. Servs., 468 F. Appx. 952 (Fed. Cir. 2011) (non-
precedential opinion). This presumption is based on the linked propositions that (i) sick people
visit medical professionals; (ii) sick people honestly report their health problems to those
professionals; and (iii) medical professionals record what they are told or observe when examining
their patients in as accurate a manner as possible, so that they are aware of enough relevant facts
to make appropriate treatment decisions. Sanchez v. Sec’y of Health & Hum. Servs., No. 11-685V,
2013 WL 1880825, at *2 (Fed. Cl. Spec. Mstr. Apr. 10, 2013); Cucuras v. Sec’y of Health & Hum.
Servs., 26 Cl. Ct. 537, 543 (1992), aff’d, 993 F.2d at 1525 (Fed. Cir. 1993) (“[i]t strains reason to
conclude that petitioners would fail to accurately report the onset of their daughter’s symptoms”).

Accordingly, if the medical records are clear, consistent, and complete, then they should
be afforded substantial weight. Lowrie v. Sec’y of Health & Hum. Servs., No. 03-1585V, 2005 WL
6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical records
are generally 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

20
Murphy v. Sec’y of Dep’t of Health & Hum. Servs., 23 Cl. Ct. 726, 733 (1991) (citing United States
v. United States 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.”)).

There are, however, situations in which compelling oral testimony may be more persuasive
than written records, such as where records are deemed to be incomplete or inaccurate. Campbell
v. Sec’y of Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“like 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 (“’[w]ritten
records which are, themselves, inconsistent, should be accorded less deference than those which
are internally consistent’”) (quoting Murphy, 23 Cl. Ct. at 733)). Ultimately, a determination
regarding a witness’s credibility is needed when determining the weight that such testimony should
be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec’y of Health & Hum. Servs., 991 F.2d 1570,
1575 (Fed. Cir. 1993).

When witness testimony is offered to overcome the presumption of accuracy afforded to
contemporaneous medical records, such testimony must be “consistent, clear, cogent, and
compelling.” Sanchez, 2013 WL 1880825, at *3 (citing Blutstein v. Sec’y of Health & Hum. Servs.,
No. 90-2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30, 1998)). 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 making
a determination regarding whether to afford greater weight to contemporaneous medical records
or other evidence, such as testimony at hearing, there must be evidence that this decision was the
result of a rational determination. Burns, 3 F.3d at 417.

C. Analysis of Expert Testimony

Establishing a sound and reliable medical theory often requires a petitioner to present
expert testimony in support of his 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 Pharmaceuticals,
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

21
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
when applied in other federal judicial fora (such as the district courts). Daubert factors are usually
employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence
that is unreliable and/or could confuse a jury. In Vaccine Program cases, by contrast, these factors
are used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec’y of Health
& Hum. Servs., 94 Fed. Cl. 53, 66–67 (2010) (“uniquely 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 the
persuasiveness and reliability of expert testimony has routinely been upheld. See, e.g., Snyder, 88
Fed. Cl. at 742–45. In this matter (as in numerous other Vaccine Program cases), Daubert has not
been employed at the threshold, to determine what evidence should be admitted, but instead to
determine whether expert testimony offered is reliable and/or persuasive.

Respondent frequently offers one or more experts in order 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). However, 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 Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)); see also Isaac v. Sec’y of Health &
Hum. Servs., No. 08-601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012), mot.
for rev. denied, 108 Fed. Cl. 743 (2013), aff’d, 540 F. Appx. 999 (Fed. Cir. 2013) (citing Cedillo,
617 F.3d at 1339). Weighing the relative persuasiveness of competing expert testimony, based on
a particular expert’s credibility, is part of the overall reliability analysis to which special masters
must subject expert testimony in Vaccine Program cases. Moberly, 592 F.3d 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) (“this
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”).

Expert opinions based on unsupported facts may be given relatively little weight. See
Dobrydnev v. Sec’y of Health & Hum. Servs., 556 F. Appx. 976, 992–93 (Fed. Cir. 2014) (“[a]
doctor’s conclusion is only as good as the facts upon which it is based”) (citing Brooke Group Ltd.
v. Brown & Williamson Tobacco Corp., 509 U.S. 209, 242 (1993) (“[w]hen an expert assumes

22
facts that are not supported by a preponderance of the evidence, a finder of fact may properly reject
the expert’s opinion”)). Expert opinions that fail to address or are at odds with contemporaneous
medical records may therefore be less persuasive than those which correspond to such records. See
Gerami v. Sec’y of Health & Hum. Servs., No. 12-442V, 2013 WL 5998109, at *4 (Fed. Cl. Spec.
Mstr. Oct. 11, 2013), aff’d, 127 Fed. Cl. 299 (2014).

D. Consideration of Medical Literature

Both parties filed medical and scientific literature in this case, but not every filed item
factors into the outcome of this decision. While I have reviewed all the medical literature submitted
in this case, I discuss only those articles that are most relevant to my determination and/or are
central to Petitioner’s case—just as I have not exhaustively discussed every individual medical
record filed. Moriarty v. Sec’y of Health & Hum. Servs., 844 F.3d 1322, 1328 (Fed. Cir. 2016)
(“[w]e generally presume that a special master considered the relevant record evidence even
though he does not explicitly reference such evidence in his decision”) (citation omitted); see also
Paterek v. Sec’y of Health & Hum. Servs., 527 F. Appx. 875, 884 (Fed. Cir. 2013) (“[f]inding
certain information not relevant does not lead to—and likely undermines—the conclusion that it
was not considered”).

E. Consideration of Comparable Special Master Decisions

In reaching a decision in this case, I have considered other decisions issued by special
masters (including my own) involving similar injuries, vaccines, or circumstances. I also reference
some of those cases in this Decision, in an effort to establish common themes, as well as
demonstrate how prior determinations impact my thinking on the present case.

There is no error in doing so. It is certainly correct that prior decisions from different cases
do not control the outcome herein. 9 Boatmon v. Sec’y of Health & Hum. Servs., 941 F.3d 1351,
1358–59 (Fed. Cir. 2019); Hanlon v. Sec’y of Health & Hum. Servs., 40 Fed. Cl. 625, 630 (1998).
Thus, the fact that another special master reasonably determined elsewhere, on the basis of facts
not in evidence in this case, that preponderant evidence supported the conclusion that vaccine X
caused petitioner’s injury Y does not compel me to reach the same conclusion in this case.
Different actions present different background medical histories, different experts, and different
items of medical literature, and therefore can reasonably result in contrary determinations.

However, it is equally the case that special masters reasonably draw upon their experience
in resolving Vaccine Act claims. Doe v. Sec’y of Health & Hum. Servs., 76 Fed. Cl. 328, 338–39

9 By contrast, Federal Circuit rulings concerning legal issues are binding on special masters. Guillory v. Sec’y of Health

& Hum. Servs., 59 Fed. Cl. 121, 124 (2003), aff’d 104 F. Appx. 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of
Health & Hum. Servs., No. 13-159V, 2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014). Special masters
are also bound within a specific case by determinations made by judges of the Court of Federal Claims after a motion
for review is resolved.

23
(2007) (“[o]ne reason that proceedings are more expeditious in the hands of special masters is that
the special masters have the expertise and experience to know the type of information that is most
probative of a claim”) (emphasis added). They would therefore be remiss in ignoring prior cases
presenting similar theories or factual circumstances, along with the reasoning employed in
reaching such decisions. This is especially so given that special masters not only routinely hear
from the same experts in comparable cases but are also repeatedly offered the same items of
medical literature regarding certain common causation theories. It defies reason and logic to
obligate special masters to “reinvent the wheel”, so to speak, in each new case before them, paying
no heed at all to how their colleagues past and present have addressed similar causation theories
or fact patterns. It is for this reason that prior decisions can have high persuasive value—and why
special masters often explain how a new determination relates to such past decisions. 10 Even if the
Federal Circuit does not require special masters to distinguish other relevant cases (Boatmon, 941
F.3d at 1358), it is still wise to do so.

ANALYSIS

I. Overview of RA’s Treatment in Vaccine Program

Since both testifying experts are rheumatologists with demonstrated experience in
diagnosing and treating RA, and both spoke at length about its characteristics (and largely
concurred in so doing), little more needs to be said about it herein. Overall, RA is “a chronic
systemic disease primarily of the joints, usually polyarticular, marked by inflammatory changes in
the synovial membranes and articular structures and by muscle atrophy and rarefaction of the
bones. In late stages deformity and ankylosis develop. The cause is unknown, but autoimmune
mechanisms and virus infection have been postulated.” Dorland’s Illustrated Medical Dictionary,
157 (32nd. ed. 2012); Q. Guo et al., Rheumatoid Arthritis: Pathological Mechanisms and Modern
Pharmacologic Therapies, 6 Bone Research 15 (2018), filed as Ex. 17 on June 22, 2018 (ECF No.
19-6) (“Guo”). Clinical manifestations include arthralgia, swelling, redness, and limited range of
motion. Guo at 1.

Program petitioners asserting RA as a vaccine injury have in a few circumstances obtained
entitlement awards. See, e.g., H.J. v. Sec’y of Health & Hum. Servs., No. 11-301V, 2015 WL
6848357 (Fed. Cl. Spec. Mstr. Nov. 6, 2015) (petitioner established that her immune system was
predisposed to autoimmune diseases such as RA, and that the Tdap vaccine significantly

10
Consideration of prior determinations is a two-way street that does not only inure to the benefit of one party. Thus,
I would likely take into account the numerous decisions finding no association between vaccination and autism when
confronted with a new claim asserting autism as an injury and have informed such claimants early in the life of their
case that the claim was not viable for just that reason. But I would also deem a non-Table claim asserting GBS after
receipt of the flu vaccine as not requiring extensive proof on Althen prong one “can cause” matters, for the simple
reason that the Program has repeatedly litigated the issue in favor of petitioners.

24
aggravated her pre-existing RA); Campbell v. Sec’y of Health & Hum. Servs., 97 Fed. Cl. 650
(2011) (petitioner successfully demonstrated that the flu vaccine could cause RA). However, it is
not a class of claim that is guaranteed to succeed. See, e.g., Suliman v. Sec’y of Health & Hum.
Servs., No. 13-993V, 2018 WL 6803697 (Fed. Cl. Spec. Mstr. Nov. 27, 2018) (dismissing petition
and denying entitlement for claim alleging Tdap vaccination caused Petitioner to develop
polymyalgia rheumatica and/or myositis); Bean-Sasser v. Sec’y of Health & Hum. Servs., No. 13-
326V, 2016 WL 1649355 (Fed. Cl. Spec. Mstr. April 5, 2016) (denying entitlement to Petitioner
alleging hepatitis B vaccine caused her to manifest symptoms of rheumatoid arthritis
approximately 11 hours later).

Indeed, I recently denied entitlement in a case where a petitioner alleged that he developed
RA following receipt of the flu vaccine. Hock v. Sec’y of Health & Hum. Servs., No. 17-168V,
2020 WL 6392770 (Fed. Cl. Spec. Mstr. Sept. 30, 2020). As I explained in Hock, other than the
Campbell decision noted above I could identify no cases finding that any vaccine could cause
either the development of rheumatoid factor or anti-CCP antibodies associated with RA’s
chronicity. 11 Indeed, given what is known about RA (and in particular the fact that the presence of
the antibodies closely associated with it often long precede onset of RA symptoms), it is highly
unlikely a vaccine could either cause these autoantibodies to develop in a medically-reasonable
timeframe, or spark an autoimmune process dependent upon them, such that a vaccine
administered close in time to appearance of RA symptoms could be deemed causal. See also Olson
v. Sec’y of Health & Hum. Servs., No.13-439V, 2017 WL 3624085 at *5 (Fed. Cl. Spec. Mstr. July
14, 2017 (HPV vaccine not causal of RA), mot. for review den’d, 2017 WL 6809589 (Fed. Cl.
Dec. 14, 2017), aff’d, 758 Fed. App’x. 919 (Fed. Cir. 2018).

II. The Evidence Best Supports Preclinical RA as the Proper Diagnosis

The Vaccine Act provides a framework permitting petitioners to seek compensation for a
vaccine-related “illness, disability, injury, or condition.” 42 U.S.C. §§ 300aa-11(c)(1)(C),
(c)(1)(D)(i). In many cases, determining the nature of the alleged injury is critical to the claim’s
resolution (especially if causation theories depend on the alleged injury having occurred).
Broekelschen, 618 F.3d at 1346 (“identifying the injury is a prerequisite to the [causation]
analysis”). Here, I must determine as a preliminary matter whether Petitioner’s preferred diagnosis
of RA is preponderantly established, or if (as Respondent maintains) the evidence supports the
conclusion that she more likely suffered from preclinical RA.

Petitioner was able to offer a number of reliable evidentiary items supportive of the RA
diagnosis. In particular, she had some common (if nonspecific) presenting symptoms, like joint
pain. She could point to a positive anti-CCP antibody test result, as well as the fact that this result
encouraged her primary rheumatologic treater to embrace RA as the proper diagnosis, and to
prescribe RA-oriented medical treatments that had some efficacy. And some of Petitioner’s other

11
H.J. involved a claim of significant aggravation, which has not been asserted herein.

25
initial treaters—i.e., those who saw her in the first two to three months post-onset—allowed for
the possibility that her RA-like symptoms were in reaction to vaccination (although I do not see
compelling treater support associating vaccination with RA specifically).

At the same time, however, the record when reviewed in its totality casts doubt on the
accuracy of the initial RA diagnosis (which I note was arrived at within four months of Petitioner’s
first post-vaccination symptoms complaints). As Dr. Oddis points out, Petitioner’s RA never fully
manifested—in particular because she never experienced any progression in symptoms or swelling
of joints (a symptom particularly significant to RA’s diagnosis, as Dr. Wallace admitted). First
Wallace Rep. at 2. Dr. Wallace’s attempts to downplay the absence of swelling by attributing it to
effective treatment were not persuasive either, as he (i) admitted that these treatments only control
symptoms but “do not stop the underlying progression of the disease” (Wallace Rep. at 2), and (ii)
Dr. Oddis convincingly established through a total record review (including many medical records
he had not possessed at the time of his written report) that even after cessation of all RA-specific
treatment, Petitioner’s RA-like symptoms did not recur or progress. Tr. at 147; Ex. 38 at 3 (six
months after stopping all RA related medication Petitioner still had no clinical or lab evidence of
disease activity).

Dr. Oddis also persuasively noted that at no point in Petitioner’s 15-month care by Dr.
Lopez (from June 2016 through August 2017), was “there ever a description of any clinical features
of RA” (i.e., descriptions of clinical symptoms of any joint swelling or synovitis). Oddis Rep. at
3. And Dr. Lopez’s diagnosis seems to have relied heavily on the positive anti-CCP antibody test.
Oddis Rep. at 3-4; Ex. 6 at 4, 7-10; Ex. 10 at 171-72. The fact that these antibodies are highly
associated with RA does not mean, as Dr. Oddis explained, that an RA diagnosis can be based
primarily upon a positive antibody test result—especially in light of the newer classification of
preclinical RA.

Overall, although Petitioner’s diagnosis contentions have some evidentiary support, I find
the evidence preponderates in favor of the preclinical RA diagnosis favored by Respondent. The
presence of the anti-CCP antibodies is a significant factor in diagnosing RA, but it is alone not
enough. And while Dr. Lopez (relying on Petitioner’s presenting symptoms and the antibody test
results) might reasonably have initially thought that an RA diagnosis was appropriate, the longer
medical history—which shows not only no swelling or synovitis ever developing, but also an
eventual cessation of Petitioner’s initial symptoms despite stopping treatment—is more consistent
with preclinical RA. It is not uncommon in the Program to find that initial treater views as to the
nature of a disease or its cause are later supplanted as more medical evidence comes in. See Deshler
v. Sec’y of Health & Hum. Servs., No. 16-1070V, 2020 WL 4593162, at *21 (Fed. Cl. Spec. Mstr.
July 1, 2020) (treater speculation that petitioner’s GBS was caused by vaccine not corroborated by
subsequent record evidence); Harrington v. Sec’y of Health & Hum. Servs., No. 15-572, 2018 WL
1125831, at *11 (Fed. Cl. Spec. Mstr. Jan. 19, 2018) (entire record did not corroborate initial treater
suspicions that petitioner had experienced GBS).

26
 As a result, and although I have attempted to give Dr. Lopez’s diagnosis as much credence
as possible, Petitioner’s complete presentation as reflected by the record is less consistent with full
RA than the preclinical version outlined by Dr. Oddis.12

III. Petitioner Did Not Preponderantly Show the Tdap Vaccine Can Cause RA

Because I have determined that Petitioner more likely than not never experienced classic
RA as alleged, the matter could be dismissed due to Petitioner’s failure to prove her alleged
injury. 13 However, even if in fact she had suffered from RA as contended, Petitioner’s claim would
still falter on her Althen prong one showing. While she was able to offer some reliable general
evidence about a possible association between other vaccines and RA, or links between the Tdap
vaccine and parallel conditions such as reactive arthritis, the evidence was not sufficiently
preponderant in linking the Tdap vaccine to RA itself.

Petitioner’s expert has not argued that her anti-CCP antibodies came into being as a result
of vaccination (and reliable science does not support such a contention). Tr. at 104-05. 14 Instead,
Dr. Wallace posited that the initial, innate response to the vaccine had sparked Petitioner’s
presenting joint pain. Thus, he specifically maintains that her RA was in some form already
occurring as of the time of vaccination, and that “once an autoimmune process as a result of
vaccination is underway, it is entirely possible for it to manifest as RA, since RA is characterized
by systemic inflammation[.]” Wallace First Rep. at 4. In effect, something about vaccination’s
immune-stimulative role prompted a pathologic setting that would encourage a person’s other RA
risk factors, like the preexisting anti-CCP antibody, to begin to cause the synovial damage
associated with RA. Tr. at 52, 62-63.

Because the record shows Petitioner experienced pain so close in time to vaccination, the
innate immune response by definition would have to be implicated, since it is understood that the

12
By contrast, the record in this case does support the finding that Petitioner suffers from fibromyalgia, as admitted
by Respondent’s expert. Petitioner does not, however, allege that her fibromyalgia was vaccine-cased—and even if
she had, such a claim would not succeed, since she has offered no expert support for the “can cause” aspect of such a
putative claim. See also Morris v. Sec’y of Health & Hum. Servs., No. 12-415V, 2016 WL 3022141, at *12-13 (Fed.
Cl. Spec. Mstr. April 1, 2016) (petitioner’s expert did not establish that myositis/fibromyalgia could be caused by the
Tdap vaccine). I have located no other reasoned Vaccine Program decisions finding that the Tdap vaccine caused
fibromyalgia. In addition, Petitioner was not diagnosed with fibromyalgia until October 3, 2016, but it has not been
demonstrated that her course from vaccination to that point (with an onset two days post-vaccination) was reflective
of what a person experiencing vaccine-caused fibromyalgia would likely encounter. Certainly, the initial symptoms
she encountered that were possibly vaccine-related were deemed more representative of RA than fibromyalgia, further
diminishing any possible association between her later fibromyalgia diagnosis and her vaccination.

13
Petitioner has not alleged preclinical RA could be or was vaccine-caused, and Dr. Wallace did not argue or
demonstrate that the Tdap vaccine could cause a person to enter into such a preclinical state.
14At most, Dr. Wallace allowed that it the timing of development of the anti-CCP antibodies could not be ascertained
one way or another, since no pre-vaccination testing for them ever occurred. Third Wallace Rep. at 2.

27
secondary, adaptive response does not occur in such a short timeframe. See, e.g., Hock, 2020 WL
6392770, at *5 (discussing difference in timing for innate versus adaptive response). But this
theory was under-substantiated, with little reliable evidence offered that would corroborate it. How
would the limited inflammation that vaccination is expected to cause, as part of its inherent
immune-stimulative purpose, interact with those factors known to be pathogenic in RA, like the
anti-CCP antibodies, to produce symptoms? How would the process in turn become chronic? Such
questions were hardly answered by Petitioner’s causation theory.

Dr. Wallace invested heavily in Wang, maintaining that it established a scientifically-
reliable connection between vaccines and RA. Wang at 756. However, as discussed above, only
two of the studies included in Wang bear on the Tdap vaccine—Bengtsson and Ray—with a third,
Verstraeten, turning out not to involve tetanus-containing vaccines at all. See Wang at 765. And
review of these articles revealed no statistically significant association between exposure to the
vaccine and development of RA. Ray at 6592, 6595; see also Verstraeten at 6637 (finding nothing
to suggest unusual patters of autoimmune disorder following exposure to AS04 adjuvanted
vaccines). Thus, although I credit Petitioner’s arguments about weaknesses in Respondent’s
preferred article Bengtsson (which at least facially rebuts the alleged Tdap-RA association), this
does not change the fact that Petitioner’s own literature offered for the opposite contention was
no more persuasive. And Dr. Wallace’s expertise did not extend to the field of epidemiology or
immunology, such that his personal testimony could fill holes that literature (which is of course
not required to prevail) did not.

Dr. Wallace has also placed great weight on individual case reports—and even ignoring
the fact that this class of evidence generally receives less weight in the Program, 15 the case reports
filed herein were similarly unhelpful because they were factually distinguishable. Kaul, for
example, involved a recurrence of reactive arthritis after a booster dose of tetanus toxoid. As Dr.
Oddis explained at hearing, however, reactive arthritis is not the same as RA, and the patient in
Kaul actually had demonstrated preexisting arthritis that was worsened by a vaccine. Tr. at 169.
The Maillefert case report also involved reactive arthritis—not RA—with no long-term evidence
of persistent synovitis. Tr. at 171. And Jawad, which was written more than thirty years ago (before
the significance of anti-CCP antibodies was understood), relied on outdated RA criteria. Tr. at 170.

Dr. Wallace’s proposed mechanisms were similarly not preponderantly substantiated.16
First, he referenced molecular mimicry (a perennial concept in Vaccine Program cases), arguing
that an autoimmune disorder like RA could be mediated by a cross reaction between antibodies

15See, e.g., Campbell, 97 Fed. Cl. at 668 (case reports “do not purport to establish causation definitively, and this
deficiency does indeed reduce their evidentiary value”).

16The concept that an anamnestic immune response explained Petitioner’s alleged autoimmune vaccine reaction was
insufficiently substantiated to any degree in light of Petitioner’s own circumstances, and too vaguely-supported to
assist Petitioner’s causation theory.

28
produced in response to a vaccine’s antigens and self tissue structures that resemble or “mimic”
those same antigens. First Wallace Rep. at 3, 4. But the vagueness and omissions in the
presentation of this aspect of his opinion were too numerous to count. What about the Tdap
antigens would cross-react with the relevant joint tissues, and where? What evidence establishes
that an intercurrent inflammatory process of any kind (brought on by a wild infection or vaccine)
might interact with separate RA risk factors, and how might this happen? And was there some
other cross-reactive antibody created by the vaccine that would contribute to the pathologic
development of RA, in addition to the anti-CCP antibodies?

I have repeatedly noted in other cases that petitioners cannot simply refer to molecular
mimicry as a mechanistic explanation for certain autoimmune disease processes and expect that to
suffice as preponderant support for their “can cause” showing. See, e.g., McKown v. Sec’y of
Health & Hum. Servs., No. 15-1451V, 2019 WL 4072113 at *50 (Fed. Cl. Spec. Mstr. July 15,
2019) (citing Devonshire v. Sec'y of Health & Hum. Servs., No. 99-031V, 2006 WL 2970418, at
*15 (Fed. Cl. Spec. Mstr. Sept. 2006), aff'd, 76 Fed. Cl. 452 (2007) (“[b]ut merely chanting the
magic words “molecular mimicry” in a Vaccine Act case does not render a causation theory
scientifically reliable, absent additional evidence specifically tying the mechanism to the injury
and/or vaccine in question.”) (emphasis in original)). Dr. Wallace’s embrace of this mechanism,
without support from reliable evidence or his own personal experience in studying the concept,
amounted to just such an insufficient showing.

Dr. Wallace also suggested that an adjuvant contained in the Tdap vaccine to boost its
immunogenicity could have instigated Petitioner’s immune response. Wallace Rep. at 5. The risk
of an abnormal response, he argued, was heightened for individuals with certain genetic
predispositions. Id. Dr. Wallace thus embraced what has been deemed the “ASIA” theory—a
mechanistic concept that has never been deemed medically reliable in prior decisions. Id. at 3;
Pearson v. Sec’y of Health & Hum. Servs., No. 17-489, 2019 WL 1150044 at *11 (Fed. Cl. Spec.
Mstr. Feb. 7, 2019) (discussing lack of reliability of ASIA theory); Morris v. Sec'y of Health &
Hum. Servs., No. 12-415V, 2016 WL 3022141, at *12 (Fed. Cl. Spec. Mstr. Apr. 1, 2016) (same).
When asked about the ASIA theory at hearing, Dr. Wallace was unable to do more than personally
vouch for its persuasiveness. Tr. at 107. Given Dr. Wallace’s lack of immunologic expertise, plus
the insufficiently-reliable proof offered herein to establish that a vaccine adjuvant could spark a
pathologic autoimmune process, I do not find that this mechanism was preponderantly established
as an alternative reasonable explanation for how the Tdap vaccine produced RA for Petitioner.

IV. The Remaining Althen Prongs Have Not Been Satisfied

Besides the above, Petitioner has not presented preponderant evidence to satisfy the second
Althen prong, which requires a Vaccine Act claimant to establish a logical explanation of how the
vaccine actually caused injury under the relevant facts. Althen, 418 F.3d at 1278; Andreu, 569 F.3d
at 1375–77; Capizzano, 440 F.3d at 1326; Grant v. Sec'y of Health & Hum. Servs., 956 F.2d 1144,
1148 (Fed. Cir. 1992).

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 First, and as already discussed, the medical record does not reflect RA disease progression
instigated by vaccination—particularly because that record best supports a preclinical RA
diagnosis. Petitioner’s overall course of symptoms does not reveal the movement toward classic
RA (i.e., from initial pain to swelling and synovitis later) that would be expected for an RA
diagnosis. And as Dr. Oddis persuasively established, the proposed RA diagnosis was undercut
significantly by the fact that Petitioner’s symptoms did not recur even after being taken off RA-
oriented treatments. Indeed (and although I make no finding in this regard), Respondent’s expert
made compelling and unrebutted points about the extent to which Petitioner’s course could be
better understood as associated with her later-diagnosed fibromyalgia—a condition Petitioner has
not alleged to be vaccine-caused in this case.

Second, I cannot conclude from this record that (outside of the temporal relationship
discussed below) the Tdap vaccine played anything more than a transient role in Petitioner’s post-
vaccination symptoms, however they might be understood. Unquestionably, preponderant
evidence supports the conclusion that Petitioner experienced a number of nonspecific symptoms
close-in-time to vaccination that were reasonably thought by some treaters potentially to be
associated with her prior vaccination. 17 But that same record also establishes that (a) Petitioner’s
subsequent RA diagnosis predominantly turned on the anti-CCP antibody findings (which are not
vaccine-attributable), and (b) her subsequent course was ultimately inconsistent with classic RA.
There is also limited evidence of ongoing, measurable inflammation consistent with Dr. Wallace’s
theory. At best, Petitioner did possess certain biomarkers revealing inflammation in the summer
of 2016 – but she the record does not reveal their persistence or recurrence, even after she was
taken off RA-specific medication.

What remains is a temporal association between receipt of the Tdap vaccine and some
immediate, transient symptoms. But an acute and monophasic serum-sickness type-reaction
attributable to vaccination is not equivalent to the chronic vaccine-induced injury alleged in this
case. Ex. 2 at 52-54 (Petitioner diagnosed with a mild reaction to Tdap, cervicalgia and lumbago
that “[s]tarted after recent daily [sic] vaccination, likely adverse effect, flu like reaction”); Hock,
2020 WL 6392770, at *25 (petitioner did not preponderantly establish he had RA beginning a day
after vaccination; his symptoms were instead far more consistent with a transient, reactive arthritis
brought on by serum sickness that, even if vaccine-induced, resolved within two months). Nor is
it compelling that Ms. Monzon’s symptoms had not manifested pre-vaccination, or that no other
explanations exist for her symptoms, as Dr. Wallace seems to assume. First Wallace Rep. at 4. It
is well established Program precedent that “evidence showing an absence of other causes does not
meet petitioners’ affirmative duty to show actual or legal causation.” Grant, 956 F.2d at 1149.

17Although the records do in some places indicate that Petitioner’s primary treater, Dr. Lopez, also associated the
Tdap vaccine with her subsequent symptoms, many appear simply to document Petitioner’s own statements attributing
her symptoms to the vaccine based on the temporal relationship, rather than Dr. Lopez’s independent conclusion. See,
e.g., Ex. 2 at 35-38, 53-55, 74-77; Ex. 10 at 171; Ex. 11 at 10.

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 Finally, Petitioner has not established that a two-day onset for vaccine-caused RA was
medically acceptable. As is often the case, concurrent consideration of the proof offered in support
of the first and third Althen prongs may be required in assessing if this prong is satisfied, given the
close relationship between the two. See, e.g., de Bazan, 539 F.3d at 1352 (the explanation for what
is a medically acceptable timeframe for injury onset must also coincide with the theory of how the
relevant vaccine can cause an injury (Althen prong one's requirement)); Shapiro v. Sec'y of Health
& Hum. Servs., 101 Fed. Cl. 532, 542 (2011), recons. den'd after remand, 105 Fed. Cl. 353 (2012),
aff'd mem., 503 Fed. App’x. 952 (Fed. Cir. 2013).

As previously discussed, Petitioner’s prong one showing has not been preponderantly
established—and this greatly diminishes the likelihood she could demonstrate that a two-day onset
based on such a theory is also medically acceptable. Moreover, Dr. Wallace’s contentions about a
rapid autoimmune process brought on by a vaccine, thereby encouraging other pathologic
contributors to RA (specifically the anti-CCP antibodies) to swing into action, was not
corroborated with sufficient independent evidence to even conclude this would occur at all, let
alone within 48 hours of vaccination. Indeed, it is contrary to what is known about RA’s disease
course generally to find that it would more often than not progress so rapidly after trigger, even if
the possibility is there (for the plausibility of fast onset is not equivalent to a preponderant
showing). Thus, although Dr. Oddis conceded RA might present acutely, it has not been shown in
this case that the Tdap vaccine could trigger initial clinical manifestations of RA in so short a
timeframe.

I again note that the record does support the conclusion that Petitioner experienced some
kind of post-vaccination reaction. A two-day timeframe for such a non-specific reaction is
medically acceptable. Keja v. Sec.’y of Health & Hum. Servs., No. 17-1511, 2021 WL 1736816,
at *20 (Fed. Cl. Spec. Mstr. Apr. 2, 2021) (serum sickness reaction to vaccine could manifest
within a day of vaccination); Hock, 2020 WL 6392770, at *25 (one-day post-vaccination transient
reaction). But Petitioner does not claim to have experienced an unspecified reaction as her injury—
she asserts that it was the onset of classic RA, that persisted thereafter for a year or more (and
could one day recur). 18 Onset of RA in such a short timeframe has not been demonstrated to be
medically reasonable.

18 Even if Petitioner’s claim had been narrowed to the allegation that she experienced a nonspecific vaccine reaction,

manifesting as pain in her joints and elsewhere, that persisted over time but turned out to be distinct from RA or
fibromyalgia, I would not be able to conclude on this record that the vaccine was responsible for the chronicity of
Petitioner’s symptoms. Dr. Wallace for his part did not so contend either, or devote any of his testimony or reports to
this alternative possible claim.

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 CONCLUSION

The Vaccine Act permits me to award compensation only if a petitioner alleging a “non-
Table Injury” can show by medical records or competent medical opinion that the injury was more
likely than not vaccine-caused. Petitioner was unable to offer a scientific theory supported by
sufficient proof of how the Tdap vaccine specifically could trigger RA or a preclinical version of
it, nor did she establish it did so in her case.

I greatly sympathize with Petitioner’s medical suffering, and deem it beyond question that
post-vaccination she experienced a medical turn for the worse. Moreover, she reasonably and in
good faith has questioned whether the Tdap vaccination could have played a role in her health
problems. And the record does support the conclusion that she experienced some post-vaccine
reaction—I simply cannot conclude that this reaction was RA. There is insufficient evidence to
support an award of compensation, and I must therefore DISMISS this claim.

In the absence of a timely-filed motion for review (see Appendix B to the Rules of the
Court), the Clerk shall enter judgment in accordance with this decision. 19

IT IS SO ORDERED.

s/Brian H. Corcoran
Brian H. Corcoran
Chief Special Master

19
Pursuant to Vaccine Rule 11(a), the parties may expedite entry of judgment by filing a joint notice renouncing
their right to seek review.

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