Court Opinion

ID: 4421192
Source: CourtListenerOpinion
Date Created: 2019-07-30 16:02:03.109407+00
Date Added: 2024-06-11T14:27:49.906409
License: Public Domain

In the United States Court of Federal Claims
                                 OFFICE OF SPECIAL MASTERS
                                       Filed: June 24, 2019

* * * * * * * * * * * * * * *
LINDA PARKER,                               *       No. 14-979V
                                            *
               Petitioner,                  *       Special Master Sanders
                                            *
 v.                                         *       Entitlement Hearing; Influenza (“Flu”)
                                            *       Vaccine; Rheumatoid Arthritis (“RA”);
SECRETARY OF HEALTH                         *       Polyarticular Inflammation; Althen
AND HUMAN SERVICES,                         *       Causation
                                            *
               Respondent.                  *
* * * * * * * * * * * * * * *
William Cochran, Jr., Black McLaren Jones Ryland & Griffee, PC, Memphis, TN, for Petitioner.
Lisa A. Watts, United States Department of Justice, Washington, D.C., for Respondent.

                                  DECISION ON ENTITLEMENT1

        On October 14, 2014, Linda Parker (“Petitioner”) filed a petition pursuant to the National
Vaccine Injury Compensation Program.2 Petitioner alleged that the influenza (“flu”) vaccine that
she received on October 19, 2013, caused her to develop rheumatoid arthritis (“RA”) and
polyarticular inflammation. Pet. at 1, ECF No. 1

        After carefully analyzing and weighing all of the evidence and testimony presented in
this case in accordance with the applicable legal standards, I find that Petitioner has not met her
legal burden. Petitioner has failed to provide preponderant evidence that the flu vaccine she
received on October 19, 2013, caused her to develop RA or polyarticular inflammation.
Accordingly, Petitioner is not entitled to compensation.

1
  This decision shall 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 note (2012) (Federal Management and Promotion of
Electronic Government Services). This means the Decision will be available to anyone with access to
the Internet. In accordance with Vaccine Rule 18(b), a party has 14 days to identify and move to delete
medical or other information that satisfies the criteria in § 300aa-12(d)(4)(B). Further, consistent with the
rule requirement, a motion for redaction must include a proposed redacted decision. If, upon review, I
agree that the identified material fits within the requirements of that provision, such material will be
deleted from public access.
2
  The Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, 42 U.S.C. §§
300aa-10 et seq. (hereinafter “Vaccine Act,” “the Act,” or “the Program”).

                                                     1
I.     Procedural History

         Petitioner filed her petition on October 14, 2014, ECF No. 1, and the case was then
assigned to Special Master Dorsey. See ECF No. 4. Over the following four months, Petitioner
filed fifteen exhibits consisting of medical records and affidavits, see Pet’r’s Exs. 1–15, ECF
Nos. 7-1–7-6, 8-2–8-6, 10-2–10-6, as well as a statement of completion on March 27, 2015.
ECF No. 12. Respondent filed his Rule 4(c) report and two pieces of medical literature on July
10, 2015. See Resp’t’s Report, ECF No. 22; Resp’t’s Exs. A–B, ECF Nos. 22-1–22-2. Special
Master Dorsey ordered Petitioner to file an expert report by November 30, 2015. ECF No. 26.

        This case was reassigned to Special Master Roth on October 21, 2015. See ECF No. 27.
Over the next eight months, Petitioner filed three motions for extensions of time, extending her
deadline to file an expert report until July 1, 2016. See ECF Nos. 29–31; see also Non-PDF
Orders, docketed Nov. 24, 2015, Feb. 25, 2016, Apr. 28, 2016. On June 10, 2016, Petitioner
filed an expert report authored by Dr. Paul J. Utz and six pieces of supporting medical literature.
Pet’r’s Exs. 17–24, ECF Nos. 32-1–32-8.

         Respondent filed an expert report authored by Dr. Mehdad Matloubian on November 14,
2016. Resp’t’s Exs. C–D, ECF Nos. 34-1–34-2. On January 23, 2017, Respondent filed thirty-
seven pieces of medical literature via compact disk. See Resp’t’s Exs. E–OO, ECF No. 36.
Petitioner filed a supplemental expert report from Dr. Utz and five pieces of supporting medical
literature on March 22, 2017, Pet’r’s Exs. 25–30, ECF Nos. 37-1–37-6, and additional medical
records on June 6, 2016. Pet’r’s Exs. 31–36, ECF Nos. 39-1–39-6.

        This case was reassigned to me on June 20, 2017. See ECF No. 40. On August 10, 2017,
I issued an order scheduling an entitlement hearing for April 16–17, 2018. ECF No. 43. On
January 19, 2018, Petitioner filed her opening prehearing brief. ECF No. 46. Respondent filed
his responsive prehearing brief and one piece of medical literature on February 20, 2018. ECF
No. 48; Resp’t’s Ex. PP, ECF No. 48-1. Petitioner filed her reply prehearing brief on March 23,
2018. ECF No. 54. Petitioner also filed a second supplemental expert report authored by Dr.
Utz and five pieces of supporting medical literature on this date. Pet’r’s Exs. 44–49, ECF Nos.
55-1–55-6.

        On April 2, 2018, Respondent contacted Chambers to request a status conference.
Informal Comm., docketed Apr. 2, 2018. I held a status conference with the parties on April 4,
2018, where Respondent indicated that Petitioner’s expert report filed on March 23, 2018, raised
“several new arguments” and that “his expert w[ould] not be able to respond to the new
arguments prior to the hearing, and w[ould] likely not be prepared to respond to the arguments at
the hearing if it proceed[ed] as scheduled.” ECF No. 57. I agreed with Respondent and
“expressed concern that the hearing may not be productive if Respondent’s expert ha[d] not had
an opportunity to review the newly-raised arguments.” Id. Therefore, I rescheduled the
entitlement hearing for August 16–17, 2018, and ordered Respondent to file a response to
Petitioner’s second supplemental expert report by May 10, 2018. ECF No. 59. On May 9, 2018,
Respondent filed a responsive supplemental expert report authored by Dr. Matloubian and five
pieces of supporting medical literature. Resp’t’s Exs. UU; UU Tabs 1–5, ECF Nos. 62-1–66-5.

                                                 2
         On August 13, 2018, Petitioner filed a motion to admit late-filed medical literature at the
hearing, ECF No. 64, and two additional pieces of medical literature. Pet’r’s Exs. 51–52, ECF
Nos. 63-1–63-2. Respondent filed his response on August 14, 2018, in which he argued that
“Petitioner’s motion fail[ed] to articulate reasonable, much less ‘compelling’ circumstances for
the relief sought . . . and should properly be denied.” ECF No. 65. I granted Petitioner’s motion
on August 14, 2018, because “there [was] good cause to grant [the] motion and admit the
exhibits” and “their admission w[ould] not unfairly prejudice Respondent.” ECF No. 66 at 1–2.
I permitted Respondent to “introduce, if necessary, literature which directly address[ed] the
specific issues addressed by Petitioner’s Exhibits 51 and 52 at any time before his expert
testifie[ed].” Id. at 1. Respondent filed one piece of medical literature in response to this Order
on August 15, 2018. See Resp’t’s Ex. VV, ECF No. 67-1.

       I held an entitlement hearing on August 16–17, 2018. See Min. Entry, docketed Aug. 20,
2018. The parties have not filed any post hearing briefing. See docket. This matter is now ripe
for consideration.

II.    Factual Background

       A.      Pre Vaccination

        Although Petitioner saw several different providers for various conditions unrelated to
this claim, her pre vaccination records reflect no apparent chronic pain complaints. Her medical
records document a few acute pain complaints related to injuries, such as an injury to her hand.
See Pet’r’s Ex. 8 at 21, ECF No. 8-3. She also complained of knee pain prior to her vaccination.
A handwritten note from a March 28, 2012 visit with internist, Dr. Win Thu, reflects that
Petitioner complained of “knee pain” in addition to other issues, some of which are illegible.
Pet’r’s Ex. 15 at 5, ECF No. 10-6. Dr. Thu’s assessment and plan are likewise illegible in the
note. Id.

        Petitioner was also treated by Dr. Kent Wenger during the years prior to her vaccination.
See Pet’r’s Ex. 11, ECF No. 10-2. A note dated March 14, 2012, reflects that Dr. Wenger had
been seeing Petitioner since 2006 for psychological treatment. Id. at 1. There are visit notes
from twelve dates between 2010 and 2013 contained in the record. Id. at 3–6, 10–13. Although
these notes are handwritten and difficult to read, most do not appear to contain any complaints of
physical pain that would be potentially relevant to this case. However, there are two references
to Petitioner’s knees. The March 13, 2012 note reflects that Petitioner “hurt [her] knee.” Id. at
12. The April 5, 2012 note reflects that Petitioner was doing “some walking” but that her “knees
[were] in bad shape.” Id. at 11. The note also contains the following: “need to exercise
[illegible] hurts knees.” Id. On the same date, Dr. Wenger noted that Petitioner “[d]eveloped an
immune sensitivity to” a medication that she had previously taken. Id.

                                                 3
        Petitioner’s medical records reflect that she smoked every day.3 See, e.g., Pet’r’s Ex. 4 at
2, ECF No. 7-4. Petitioner was a lab technician at Putnam Community Medical Center. Pet’r’s
Ex. 6 at 2, ECF No. 7-6.

        B.      Vaccination

        Petitioner received a seasonal flu vaccination in her left deltoid on October 19, 2013.
Pet’r’s Ex. 2. ECF No. 7-2.

        C.      Post Vaccination

                    1. Petitioner’s Affidavits

        Petitioner stated in her first affidavit that she experienced soreness in her left shoulder
one day post vaccination, on October 20, 2013. Pet’r’s Ex. 1 at ¶ 4, ECF No. 7-1. Petitioner
stated that the pain spread to both shoulders, and eventually to her knees, hips, groin, wrists, and
hands. Id.

        In Petitioner’s second affidavit, she further stated that by October 21, 2013, her left
shoulder was weak, and the pain was “severe and interfered with [her] ability to sleep.” Pet’r’s
Ex. 12 at ¶ 4, ECF No. 10-3. Petitioner then explained that “[b]etween October 21, 2013, and
November 1, 2013, the pain and weakness in [her] left shoulder subsided to some extent but did
not go away.” Id. at ¶ 5. Petitioner noted that during that time period, “the type of pain [she]
was experiencing in [her] left shoulder began to appear in [her] right shoulder.” Id. Petitioner
grew “quite distressed” and on November 1, 2013, she left work to go to the emergency room for
evaluation. Id. at ¶ 6. At that time, she “was experiencing pain in both shoulders that seemed to
be radiating from [her] shoulders to [her] chest.” Id. Petitioner then stated that those symptoms
“continued, and [she] also began experiencing intermittent pain in [her] knees and wrists as well
as back pain, swelling in [her] extremities, and muscle aches.” Id. at ¶ 7.

        Petitioner described additional symptoms that she began to experience “[a]fter November
1, 2013.” Id. at ¶¶ 9–10. She stated that she experienced groin pain, which she reported to a
provider on April 3, 2014. Id. at ¶ 9. She further stated that she began to experience pain in her
hips and swelling in her right hand, which she reported to a provider on April 16, 2014. Id. at
¶ 10. Petitioner also asserted in her affidavit that she used a cane to assist with walking during
the visit on April 16, 2014. Id.

                    2. Medical Records

        The first medical record after Petitioner’s vaccination is from November 1, 2013. On that
date, Petitioner presented to the Putnam Community Medical Center Emergency Department.
Pet’r’s Ex. 3, ECF No. 7-3; see also Pet’r’s Ex. 10a at 36–50, ECF No. 8-5. The “Principal

3
 On an intake form dated April 16, 2014, Petitioner confirmed that she smoked one pack of cigarettes per
day. Pet’r’s Ex. 6 at 8. In a December 6, 2017 note, a provider documented that Petitioner had been
smoking one pack of cigarettes per day since 1975. Pet’r’s Ex. 41 at 7, ECF No. 49-5.
                                                   4
Admitting Diagnosis/Reason for Visit” listed on the registration form for that visit is “high blood
pressure.” Pet’r’s Ex. 3 at 1. The nurses’ notes reflect that Petitioner complained of “pain in
[her] left lateral posterior chest and right lateral posterior chest,” as well as nausea upon
presentation. Id. at 19. Notes also reflect that Petitioner complained of “pain in [her] back[,]”
which “radiate[d] to [her] chest” and was “aching.” Id. at 20. Petitioner reported that the pain
began one week prior and was intermittent; at its worst, the pain was a ten out of ten on a pain
scale. Id. Petitioner reported substernal area chest pain at five out of ten on a pain scale. Id.
Petitioner also reported shortness of breath at rest, nausea, and anorexia. Id. The emergency
department physician documented that Petitioner discovered that she had high blood pressure at
a physician’s office and was also complaining of bilateral shoulder pain. Id. at 16. The
physician’s examination revealed “mild pain in both shoulder joints on external rotation” and
anxiety. Id. at 17. Ultimately, Petitioner was discharged the same day in stable condition, with a
diagnosis of hypokalemia4 and weakness. Id. at 18, 22. She was advised to follow up in one
week. Id. at 18.

        On December 18, 2013, Petitioner saw Dr. Wenger for psychiatric therapy. Pet’r’s Ex.
11 at 3. Dr. Wenger documented in the note from that date that Petitioner reported increased
pain since receiving the flu vaccine in October. Id. He also noted that the pain had “spread out
from there (l[eft] arm)” and by this visit was in the right arm and both knees. Id. He wrote that
it was “excruciating (!)” pain. Id. Parts of Dr. Wenger’s notes are difficult to read, but he
appears to have noted Petitioner’s flu shot and pain, accompanied by several “?” notations,
suggesting that he was unsure of a cause or correlation. Id. Under the plan section of the note,
Dr. Wenger circled “support” and wrote “not hypochondriac – see rheum.” Id. A medication list
from this visit indicates that Petitioner was taking Toradol,5 although it is unclear whether Dr.
Wenger prescribed the medication to Petitioner or whether she reported that she was taking the
medication from some other source at that time. Id. at 7.

         On January 12, 2014, Petitioner presented to the Putnam Community Medical Center
Emergency Department with complaints of lower back pain after a fall at work. Pet’r’s Ex. 10 at
24. Petitioner reported that she fell from an upright position six and a half hours before she
presented to the emergency department. Id. at 26. She complained of lower back pain with
movement, and the physician documented that her pain was mild, while range of motion
(“ROM”) was painful and muscle spasm was noted in the left and right lower back. Id. Imaging
showed degenerative disc changes but no acute abnormalities. Id. at 25. The nurses’ notes
reflect that Petitioner also complained of a left knee injury, although only the lower back
complaints were documented by the physician. Id. at 29. Petitioner was discharged home with a
diagnosis of a lumbar spine sprain. Id. at 27. She was prescribed Toradol and instructed to
follow up with a private physician for further care. Id. at 27, 31–32.

4
  Hypokalemia is the “presence of an abnormally low concentration of potassium ions in the circulating
blood.” Hypokalemia, STEDMANS MEDICAL DICTIONARY 429130 (2014).
5
  Toradol (ketorolac tromethamine) is “a nonsteroidal anti-inflammatory drug (NSAID), [which] is
indicated for the ‘short-term’ (up to 5 days in adults), management of moderately severe acute pain that
requires analgesia at the opioid level and only as continuation treatment following IV or IM dosing of
ketorolac tromethamine, if necessary.” Roche Pharmaceuticals, Toradol Oral Medicine Label (2013),
https://www.accessdata.fda.gov/drugsatfda_docs/label/2013/019645s019lbl.pdf.

                                                    5
         Three days later, on January 15, 2014, Petitioner presented to the Putnam Community
Medical Center Emergency Department with wrist pain that began two or three days prior. Id. at
15, 21. Petitioner reported decreased ROM and pain in her right wrist due to a fall at work four
days prior. Id. at 17. The physician’s note reflects that Petitioner was previously evaluated for
the fall at work, but she did not mention an issue with her wrist at that time. Id. The physician
observed “injury or acute deformity, swelling, [and] tenderness” in Petitioner’s right wrist. Id.
Imaging reflected no fracture, dislocation, or instability of the wrist. Id. at 16. Petitioner was
discharged with a diagnosis of a contusion. Id. at 19, 22. She was prescribed Tylenol-Codeine
#36 and was advised to follow up with orthopedics in two or three days. Id. at 22–23.

         Two days later, on January 17, 2014, Petitioner saw Physician’s Assistant (“PA”) David
C. Cox at Medical Express (“MedEx”) complaining of joint pain. Pet’r’s Ex. 4 at 1–5. The PA
documented that Petitioner reported intermittent joint pain in both shoulders and knees, as well
as her right wrist. Id. at 2. Petitioner also reported that the pain “started after flu inj[ection]” and
was becoming more frequent. Id. The note reflects Petitioner reported walking as an
aggravating factor for her pain, while Toradol and Tylenol #3 were alleviating factors. Id. The
PA also documented that Petitioner complained of “muscle aches, arthralgias/joint pain, back
pain, and swelling in the extremities.” Id. Upon examination, he found that Petitioner was
anxious and depressed, and documented normal motor strength but with “tenderness and limited
ROM” in “Joints, Bone, and Muscles.” Id. at 2–3. He did not specify to which joints, bones,
and/or muscles those findings applied. Id. Petitioner declined lab studies during the visit. Id. at
3. The PA diagnosed unspecified joint pain and prescribed ketorolac7 intramuscularly, Mobic8
tablets, and prednisone tablets.9 Id. Petitioner was instructed to follow up with another doctor.
Id.

        On January 22, 2014, Petitioner followed up with Dr. Alex M. Pulido at Pulido Internal
Medicine. Pet’r’s Ex. 5, ECF No. 7-5. The visit note from that date reflects that the reason for
the appointment was to establish a new primary care provider. Id. at 3. In the review of
symptoms, Dr. Pulido documented that Petitioner denied carpal tunnel syndrome, joint stiffness,
leg cramps, muscle aches, pain in shoulder(s), painful joints, sciatics, swollen joints, trauma to
arm(s), trauma to hip(s), trauma to knee(s), trauma to ankles(s), and weakness. Id. at 5.
Although there were no abnormal findings documented in the examination portion of the note,
Dr. Pulido assessed hypertension, hyperlipidemia, diverticulitis of colon, obesity, personal
history of tobacco use, and “unspecified polyarthropathy or polyarthritis, multiple sites.” Id. at

6
  Tylenol-Codeine #3 is a “combination of medication . . . used to help relieve mild to moderate pain. It
contains an opioid . . . pain reliever (codeine) and a non-opioid pain reliever (acetaminophen).”
TYLENOL-CODEINE NO.3, https://www.webmd.com/drugs/2/drug-3179/tylenol-codeine-3-oral/details
(last visited June 7, 2019).
7
  Ketorolac tromethamine is “a nonsteroidal anti-inflammatory drug administered intramuscularly,
intravenously, or orally for short-term management of pain[.]” Dorland’s at 984.
8
  Mobic is a brand name for meloxicam, an NSAID used in the treatment of osteoarthritis. Dorland’s at
1126, 1171.
9
  Prednisone is “a synthetic glucocorticoid derived from cortisone, administered orally as an anti-
inflammatory and immunosuppressant in a wide variety of disorders.” Dorland’s at 1509.
                                                    6
3. Dr. Pulido ordered testing, including rheumatoid factor (“RF”),10 erythrocyte sedimentation
rate (“ESR”),11 antinuclear antibodies (“ANA”)12 w/Reflex if Positive,13 and creatine
phosphokinase (“CPK”).14 Id. at 4. Petitioner’s labs were negative for ANA and RF, but she
had a high ESR of 47 and a CPK level of 30. Id. at 8–10; Pet’r’s Ex. 10 at 12–14. A cardio
CRP-high sensitivity test reflected a level of 25.3 mg/L. Pet’r’s Ex. 5 at 10; Pet’r’s Ex. 10 at 11.

        Petitioner cancelled an appointment scheduled with Dr. Pulido for February 5, 2014.
Pet’r’s Ex. 5 at 7.

        On March 25, 2014, Petitioner submitted a report to the Department of Health and
Human Services (“HHS”) Vaccine Adverse Event Reporting System (“VAERS”) regarding the
flu vaccine she received on October 19, 2013. Pet’r’s Ex. 9, ECF No. 8-4. A letter from HHS to
Petitioner reflects that some items were missing from the VAERS report, and HHS asked
Petitioner to submit additional information. Id. However, only one page of the letter is
contained in the record, and it is unclear what information was identified as missing. Id. It is
also unclear whether Petitioner responded to the letter.

        On April 3, 2014, Petitioner returned to MedEx and saw Dr. Shirine S. Gharda. Pet’r’s
Ex. 4 at 6–9. Petitioner’s chief complaint at this visit was a “[r]ight knee problem.” Id. at 6.
She reported one day of constant right knee pain at a level of five out of ten, which was
alleviated with ice. Id. at 7. The doctor noted that Petitioner also had swelling and right
shoulder and right groin pain. Id. Dr. Gharda further documented the following: “migratory
polyarthralgias with swelling since [O]ct[ober] 2013[;] initial[] work up showed elevated [ESR]
and [CRP;] having flare needs prednisone. To go see rheumatologist.” Id. In another section of
the note, Dr. Gharda wrote that Petitioner reported “arthralgias/joint pain (right knee and left
shoulder pain and swelling for 2 days).” Id. Upon exam, Dr. Gharda noted “erythema,15
swelling, and warmth (to right knee).” Id. at 8. However, Dr. Gharda also noted “normal motor
strength . . . normal movement of all extremities and no tenderness,” and no edema. Id.
Petitioner was prescribed prednisone tablets, Solu-Medrol16 for injection, and ketorolac tablets.
Id. She was instructed to follow up with a rheumatologist and return as needed. Id.

10
   Rheumatoid factor tests for “antibodies directed against antigenic determinants . . . in the Fc region of
the IgG class of immunoglobulins.” Dorland’s at 676. These antibodies “are found in the serum of about
80 percent of persons with classical or definite [RA].” Id.
11
   Erythrocyte sedimentation rate measures “the rate at which erythrocytes precipitate out from a well-
mixed specimen of venous blood, measured by the distance the top of the column of erythrocytes falls in
a given time interval under specified conditions[.]” Dorland’s at 1594.
12
   Antinuclear antibodies are “antibodies directed against nuclear antigens; ones against a variety of
different antigens are . . . frequently found in [RA.]” Dorland’s at 101.
13
   A reflex test “occurs when an initial test meets pre-determined criteria . . . and the primary test result is
inconclusive[.]” Reflex Testing, TRIHEALTH LABORATORIES, https://apps.trihealth.com/trihealthlab/
Reflex%20Testing.pdf (last visited June 10, 2019).
14
   Creatine phosphokinase (AKA creatine kinase) is “an Mg2+-activated enzyme of the transferase class
that catalyzes the phosphorylation of creatine by ATP to form phosphocreatine.” Dorland’s at 429.
15
   Erythema is “redness of the skin produced by congestion of the capillaries.” Dorland’s at 643.
16
   Solu-Medrol is the “trademark for preparation of methylprednisolone sodium succinate.” Dorland’s at
1731.
                                                       7
        On April 16, 2014, Petitioner saw Dr. T. Mark Lloyd at the Southeastern Integrated
Medical (“SIMED”) Southeastern Arthritis Center. Pet’r’s Ex. 6 at 1–15. On a medical history
form, Petitioner reported her symptoms as “[p]ain [and] inflam[m]ation in all joints.” Id. at 2.
During the visit, the doctor documented in Petitioner’s history of present illness that she had a
“migratory polyarthritis” since October 2013, which “ha[d] involved shoulders/hips/knees and
most recently swelling in her [right] hand.” Id. at 11. He wrote that Petitioner “to date has a
+CRP only/neg[ative] serologies,” and had responded to high dose steroids. Id. Dr. Lloyd noted
that Petitioner’s “only [history] [wa]s a flu shot the day before this started.” Id. He wrote that
Petitioner’s hips were sore and stiff on that date, but that her hands were “qauiet,” presumably a
typo intended to reflect that Petitioner’s hands were “quiet.” Id.; see id. at 16 (containing a
nearly identical history of present illness note). Dr. Lloyd listed “symmetric polyarticular
inflammation” as an “active problem” for Petitioner. Id. Notes from the physical examination
do not reflect any significant abnormalities. Id. at 12–13. Dr. Lloyd ordered lab work and
prescribed Medrol. Id. at 13–14.

        Petitioner presented to Putnam Community Medical Center for the lab work. Pet’r’s Ex.
6 at 21–28; Pet’r’s Ex. 10 at 3–6. Petitioner’s lab work reflects that she was again negative for
the RF and ANA. Pet’r’s Ex. 6 at 22; Pet’r’s Ex. 10 at 5–6. Her cyclic citrullinated peptides17
(“CCP”) result was 97, and the lab results indicate that any result above 59 represents a “strong
positive.” Pet’r’s Ex. 6 at 22; Pet’r’s Ex. 10 at 6. Petitioner’s ESR was 64. Pet’r’s Ex. 6 at 25;
Pet’r’s Ex. 10 at 4. Her C-reactive protein (“CRP”)18 result was 11. Pet’r’s Ex. 6 at 28; Pet’r’s
Ex. 10 at 3.

        A letter in Petitioner’s file dated April 18, 2014 and authored by Dr. Lloyd reflects that
Petitioner was “having trouble walking and [would] need to be excused from work for at least
[three] days due to her medical condition.” Pet’r’s Ex. 6 at 29.

        Petitioner returned to see Dr. Lloyd on May 7, 2014. Pet’r’s Ex. 6 at 16–20. Dr. Lloyd’s
history of present illness note is essentially the same as the prior visit. Id. at 16. In this note, Dr.
Lloyd listed “drug monitoring of medications” and “[RA]” along with “symmetric polyarticular
inflammation” in Petitioner’s “active problems” list. Id. In a “therapy” portion of the visit note,
Dr. Lloyd documented the results of Petitioner’s CCP, ESR, and CRP results and noted that he
would reduce the Medrol dose and start methotrexate.19 Id. at 19. Dr. Lloyd also documented
that he discussed concerns about tobacco use with Petitioner. Id.

17
   Citrullination is “a posttranslational modification of proteins in which peptideylarginine deiminase
catalyzes the conversion of arginine residues to citrulline residues. . . . [I]t also occurs in a variety of
inflammatory conditions.” Dorland’s at 366. A posttranslational modification is an alteration “to protein
structure that take[s] place after synthesis.” Id. at 1503. In genetics, such modification refers to “the
process by which the series of codons (triplet bases) in a messenger RNA (mRNA) is converted to the
ordered sequence of amino acids that constitutes a specific polypeptide chain.” Id. at 1953.
18
   C-reactive protein is “a globulin that forms a precipitate with the somatic C-polysaccharide of the
pneumococcus in vitro; it is the most predominant of the acute phase proteins.” Dorland’s at 1532.
19
   Methotrexate is “a folic acid antagonist that acts by inhibiting synthesis of DNA, RNA, thymidylate,
and protein; used as an . . . antiarthritic in the treatment of . . . severe rheumatoid and psoriatic arthritis.”
Dorland’s at 1151.
                                                        8
        On July 2, 2014, Petitioner saw Dr. Wenger. Pet’r’s Ex. 11 at 2. Although much of the
note is difficult to read, it appears that Petitioner reported the history of her pain complaints and
treatment with Dr. Lloyd. Id. She reported that she “missed a lot of work” due to pain. Id.
Petitioner also reported problems with stress at work and told Dr. Wenger that she “hit a bear”
and that her car was in the shop. Id.

         On October 22, 2014, Petitioner saw Dr. Gharda. Pet’r’s Ex. 13 at 1–11, ECF No. 10-4.
The note from that visit reflects that Petitioner reported that she had no primary care provider.
Id. Petitioner’s chief complaint was “pain.” Id. Dr. Gharda noted that Petitioner was diagnosed
with RA in August of 201420 and “ha[d] seen [a] rheumatologist for migrating joint pain and
swelling with redness.” Id. Dr. Gharda further noted that Petitioner “[t]ried methotrexate and
could not tolerate it[, and was then] on prednisone[, w]ith frequent flares.” Id. Dr. Gharda
reported that Petitioner was requesting a “referral to Shands [Hospital/University of Florida]
rheumatology.” Id. at 1. Petitioner reported “muscle aches, arthralgias/joint pain, and swelling
in the extremities.” Id. at 2–3. An examination revealed “tenderness (to heel, yesterday to
knee).” Id. at 3. Dr. Gharda provided a referral to rheumatology, with the following “Note to
Provider: long history of po[l]yarthrthra[]lgias, with joint swelling and redness with diagnosis of
RA[;] resistant to methotrexate, on prednisone. Concerned something else might be going on.”
Id. at 3. Dr. Gharda also provided a prescription for Percocet.21 Id. at 3, 7.

         On December 11, 2014, Petitioner had a visit with Dr. Adrian Vazquez at University of
Florida Health. Id. at 13–16; see also Pet’r’s Ex. 14 at 11–14, ECF No. 10-5. At this visit, Dr.
Vazquez included a lengthy summary of the history of present illness. Pet’r’s Ex. 13 at 14. In
that summary, Dr. Vazquez wrote that Petitioner described her lab results and “report[ed] . .
. that in fall 2013 she began having left shoulder pain then it migrated to the right shoulder then
knees, feet and hands became involved. [She also reported] [h]and involvement including
MCPs22/PIPs23 with associated swelling, warmth, erythema, and [morning] stiffness [for about
one] hour. [Petitioner described her] [p]ain as constant, aching, 7/10 pain unless she was on
prednisone or Medrol.” Id. Dr. Vazquez also wrote that Petitioner showed him a picture of her
right hand, which revealed “swelling/erythema of MCPs particularly 2nd-3rd MCPs.” Id. Dr.
Vazquez described the medications that Petitioner had tried, including prednisone and
methotrexate. Id. He noted that Petitioner was taking Medrol 16 mg per day, which “controlled
her joint pain/swelling,” but that she was “self-medicating as she never returned to see Dr.
Lloyd.” Id. The visit note reflects that Petitioner was smoking one and a half packs of cigarettes
per day at this time. Id. at 15. Dr. Vazquez “[s]uspect[ed] [that Petitioner] has [RA] based on
history,24 picture of [her right] hand and reported +CCP Ab.” Pet’r’s Ex. 14 at 13. Differential

20
   The last visit note from Dr. Lloyd was dated May 7, 2014. Pet’r’s Ex. 6 at 16–20. There are no records
reflecting a diagnosis or visit with any medical providers in August of 2014.
21
   Percocet is the “trademark for a combination preparation of oxycodone hydrochloride and
acetaminophen.” Dorland’s at 1409.
22
   Metacarpophalangeal joints (MCPs) are those “pertaining to the metacarpus and phalanges,” or the
hand and fingers. Dorland’s at 1142.
23
   Proximal interphalangeal joints (PIPs) are the joints between the first and second phalanges, or bones in
one’s fingers. See Dorland’s at 950, 973.
24
   There is no mention of the August 2014 diagnosis referenced by Dr. Gharda.
                                                     9
diagnoses included seronegative spondylarthritis (“SpA”),25 crystal arthritides,26 and
osteoarthritis.27 Id. He also noted that Petitioner was at risk for osteopenia28/osteoporosis29
because she had been taking “moderate-high doses of corticosteroids” for more than a year. Id.
Dr. Vazquez documented that Petitioner’s exam was normal but opined that her symptoms were
“likely masked by Medrol 16mg” per day. Id. Dr. Vazquez counseled Petitioner “on the
importance of smoking cessation” and noted that smoking is “likely worsening her arthritis.” Id.
He ordered labs and imaging. Pet’r’s Ex. 13 at 16; Pet’r’s Ex. 14 at 14.

         Imaging was completed on the same day. An x-ray of the cervical spine showed “[n]o
specific evidence for inflammatory arthritis.” Pet’r’s Ex. 14 at 2. X-rays of the right and left
hands and feet revealed “[n]o specific radiographic evidence for inflammatory arthritis” but did
show “mild osteoarthritis of the bilateral hands and feet.” Id. at 2–8. Additionally, the x-rays
showed a “[s]mall radiopaque foreign body in the left foot on the plantar surface of the distal
first phalanx.” Id.

        On January 8, 2014, Petitioner presented to the Putnam Community Medical Center for
additional diagnostic testing. Pet’r’s Ex. 31 at 52, ECF No. 39-1. The order reflects that
Petitioner was to be evaluated for “inflammatory arthritis, atlantoaxial30 instability, crowned
dens syndrome,31 and osteoarthritis.” Id. at 56. A bone densitometry scan (“DEXA”)32 was
performed. Id. at 58–59. The report indicates that the test was compared with a prior test from
October 27, 2010. Id. at 58. The report reflects the following impressions: “(1) The patient has
osteopenic bone mineral density; (2) When compared to the young adult population, the patient’s
fracture category is: moderate; (3) Compared to the prior study the patient’s bone mineral density
has decreased significantly in the hips and mildly in the lumbar spine.” Id.

        On January 13, 2015, Petitioner followed up with Dr. Vazquez. Pet’r’s Ex. 14 at 8–11.
Dr. Vazquez noted that Petitioner’s bilateral hand pain had “improved.” Id. at 8. Petitioner’s
main complaint on this date was “bilateral knee pain worse with ambulation but improved with
rest and diffuse muscle pain that lasts all day.” Id. Dr. Vazquez noted that he did not yet have

25
   Spondylarthritis is “arthritis of the spine.” Dorland’s at 1753.
26
   Crystal arthritides (AKA crystal-induced arthritis) is “arthritis due to the deposition of inorganic
crystalline material within the joints[.]” Dorland’s at 150.
27
   Osteoarthritis is “a noninflammatory degenerative joint disease seen mainly in older persons,
characterized by degeneration of the articular cartilage, hypertrophy of bone at the margins, and changes
in the synovial membrane.” Dorland’s at 1344.
28
   Osteopenia is “1. [A]ny decrease in bone mass below normal. 2. [R]educed bone mass due to decrease
in the rate of osteogenesis to the extent that there is insufficient compensation for normal bone lysis.”
Dorland’s at 1347–48.
29
   Osteoporosis is “reduction in bone mineral density, leading to fractures after minimal trauma.”
Dorland’s at 1348.
30
   Atlantoaxial means “pertaining to the atlas and the axis.” Dorland’s at 173. The atlas is “the first
cervical vertebra, which articulates above the occipital bone and below with the axis.” Id. The axis is
“the second cervical vertebra[.]” Id. at 185.
31
   Crowned dens syndrome is “crystal-induced arthritis around the dens axis, often accompanied by fever
and neck pain.” Dorland’s at 1826.
32
   A bone densitometry scan determines one’s “bone mineral density,” and is “used in the diagnosis and
management of conditions such as osteogenesis imperfecta and osteoporosis.” Dorland’s at 487.
                                                   10
the results of the DEXA scan. Id. In the physical examination portion of the note, Dr. Vazquez
documented that there was synovial33 thickening over the right second MCP joint, bilateral
patellar crepitus,34 and diffuse myofascial tenderness to light touch. Id. at 9. Dr. Vazquez
diagnosed Petitioner with uncontrolled seropositive RA and stable osteoarthritis. Id. at 10–11.
He also diagnosed diffuse myofascial pain syndrome,35 which he noted was “likely secondary to
chronic depression/anxiety and sleep issues.” Id. at 10. He noted that “[f]ibromyalgia is often
caused [and] exacerbated by untreated depression and/or sleep disorders” and suggested that
Petitioner might benefit from a change in certain medications prescribed by her psychiatrist or
primary care physician. Id. at 11. Dr. Vazquez also discussed the risks and potential benefits of
Enbrel,36 and Petitioner agreed to initiate therapy with that medication to treat her seropositive
RA. Id. at 10–11.

        Petitioner had a visit with Dr. Wenger on January 21, 2015. Pet’r’s Ex. 33 at 6, ECF No.
39-3. Dr. Wenger noted that Petitioner was “still on steroids,” which helped her walk and use
her hands but also caused hair loss and weight gain. Id. Dr. Wenger documented that Petitioner
saw Dr. Vazquez, who suggested a medication change to Enbrel and a different psychiatric
medication. Id. Dr. Wenger wrote that he had some concern with the proposed substitute in
Petitioner’s psychiatric medication due to Petitioner’s history but still planned to add it to
Petitioner’s regimen. Id.

       Petitioner saw Dr. Wenger again on February 25, 2015. Id. at 5. Dr. Wenger
documented in his note that Petitioner had not yet started Enbrel due to “insurance barriers.” Id.
He noted that Petitioner had “pain chronic (RA),” which was not helped by the change of
medicine suggested by Dr. Vazquez. Id. Petitioner also had a visit note dated March 12, 2015 in
Dr. Wenger’s records, but the note only reflects “n/s.” Id. at 4. Petitioner saw Dr. Wenger again
on April 1, 2015, and April 22, 2015. Id. at 3–4. It does not appear from the notes that Dr.
Wenger documented anything related to pain or movement difficulties on either date. Id.

        Petitioner presented to the Putnam Community Medical Center for lab work on July 3,
2015. Pet’r’s Ex. 16, ECF No. 23-1; see also Pet’r’s Ex. 31 at 31–51. On that date, Petitioner’s
RA factor result was flagged as high. Pet’r’s Ex. 16 at 1. The report lists the reference interval
for the test as 0.0–13.9 IU/ml, and Petitioner’s result was 184.4 IU/ml. Id. at 1, 10. CCP

33
   Synovial is defined as “pertaining to the synovium . . . or secreting synovia.” Dorland’s at 1855. The
synovium is “membrana synovalis capsulae articularis.” Id. at 1856. Synovia is “a transparent alkaline
viscid fluid, resembling the white of an egg, secreted by the synovial membrane, and contained in joint
cavities, bursae, and tendon sheaths.” Id. at 1855.
34
   Joint crepitus is “the grating sensation caused by the rubbing together of the dry synovial surfaces of
the joints.” Dorland’s at 429. The patella is “a triangular sesamoid bone . . . situated at the front of the
knee in the tendon of insertion of the quadriceps extensor femoris muscle.” Id. at 1395.
35
   Myofascial pain syndrome “is a chronic pain condition affecting the musculoskeletal system.” What is
Myofascial Pain Syndrome?, HEALTHLINE, https://www.healthline.com/health/myofascial-pain (last
visited June 10, 2019).
36
   Enbrel is a brand name for etanercept, “a soluble tumor necrosis factor receptor that inactivates tumor
necrosis factor,” which “is used in the treatment of [RA].” Dorland’s at 612, 650.
                                                     11
Antibodies immunoglobulin G (“IgG”)/immunoglobulin A (“IgA”)37 were high, at 80 units. Id.
at 1. Anything higher than 59 in that test is considered to be a “strong positive.” Id. Petitioner’s
complement38 C3 and C439 serum were within the reference intervals, but her total complement
(CH50) was high at 65 U/mL, where the reference interval is 42–62. Id. Petitioner tested
negative for ANA. Id. at 1, 10. A serum protein electrophoresis was “essentially unremarkable.”
Id. at 2. Myeloma (“M-spike”) protein40 was flagged as high at 0.1 g/dL, and the reference
interval indicates “not observed.” Id. at 3. Petitioner had high hemoglobulin (“HGB”),41
hematocrit (“HCT”),42 and mean corpuscular hemoglobulin (“MCH”)43 in her complete blood
count (“CBC”)44 panel. Id. at 6. Her ESR was also high, at 33 mm/hr. Id. at 7.

        Petitioner presented to the Putnam County Medical Center Emergency Department late in
the evening on October 30, 2015. Pet’r’s Ex. 31 at 1–30. On the admission form, the “principal
admitting diagnosis/reason for visit” is listed as “back pain.” Id. at 1. An “attestation statement”
from the same admission reveals that the diagnosis at admission was “cough,” the principal
diagnosis was “bronchitis, not specified as acute or chronic,” and secondary diagnoses were
“essential (primary) hypertension” and “nicotine dependence, unspecified, uncomplicated.” Id.
at 9. The nurse who initially assessed Petitioner reported that she had “pain below the left
shoulder blade [and a] nonproductive cough [for three] days with wheezing.” Id. at 11.
Petitioner reported her pain at a level seven intensity, and the nurse documented “back pain” as
her chief complaint. Id. A chest x-ray was ordered due to the cough. Id. at 10. It revealed “no
radiographic evidence of acute cardiopulmonary disease,” but among the “findings” the report
notes the following: “Bony thorax: Mild osteopenia with degenerative changes of the spine and
shoulders.” Id. Petitioner was discharged early the next day. Id. at 16. Clinical impressions at
the time of discharge were primary, “bronchitis with bronchospasm” and secondary, “back pain.”

37
   IgG is “the principal class of antibody in the blood and extracellular fluid” that “opsonizes pathogens
for engulfment by phagocytes and activates the compliment system[.]” KENNETH MURPHY & CASEY
WEAVER, JANEWAY’S IMMUNOBIOLOGY 424 (9th ed. 2017). IgA “is the principal class [of antibody] in
secretions” and “functions chiefly as a neutralizing agent.” Id.
38
   Complement refers to “the entire functionally related system comprising at least [twenty] distinct serum
proteins, their cellular receptors, and related regulatory that is the effector not only of immune cytolysis
but also of other biologic functions[.]” Dorland’s at 393.
39
   C3 is “a component of both the classical and alternative complement pathways[.]” Dorland’s at 393.
C4 is a “component of the classical complement pathway[.]” Id. at 394.
40
   Myeloma protein refers to “any of the pathological immunoglobulin proteins or fragments . . . secreted
by myeloma cells.” Dorland’s at 1533.
41
   Hemoglobulin is “the red oxygen-carrying pigment of erythrocytes, formed by developing erythrocytes
in bone marrow.” Dorland’s at 839.
42
   Hematocrit level measures “the proportion of the volume of a blood sample that is red blood cells . . .
measured in mL per dL of whole blood or a percent.” Dorland’s at 832.
43
   Mean corpuscular hemoglobulin measures “the average hemoglobulin content of an erythrocyte[.]”
Dorland’s at 840.
44
   Complete blood count is “a series of tests of the peripheral blood that provide[s] a tremendous amount
of information about the hematologic system and many other organ systems.” KATHLEEN DESKA
PAGANA & TIMOTHY J. PAGANA, MOSBY’S MANUAL OF DIAGNOSTIC AND LABORATORY TESTS 174 (5th
ed. 2014).
                                                    12
Id. at 21. Petitioner was prescribed an albuterol45 inhaler, ketorolac thromethamine46 tablets, and
prednisone tablets. Id. at 20.

        Petitioner saw Dr. Wenger on November 10, 2015. Pet’r’s Ex. 33 at 2. He documented
in the visit note that Petitioner was “still on steroids” for “flares of R.A.” Id.

         On March 16, 2016, Petitioner presented to Dr. Myriame Vastey at Azalea Health to
establish care for “[a]rthralgias and hypertension.” Pet’r’s Ex. 32, ECF No. 39-2. Petitioner
reported the onset of arthralgias as two years prior, specifically identifying the location of the
arthralgias in the bilateral hips. Id. at 1. Dr. Vastey noted that Petitioner was diagnosed with RA
two years prior and was told that she may also have fibromyalgia. Id. She also noted that
Petitioner had been treated with methylprednisolone47 but was “out of med[ication].” Id. Dr.
Vastey documented that Petitioner’s hypertension was stable, and she only needed a medication
refill. Id. Petitioner reported at this visit that she continued to smoke a pack of cigarettes per
day and had done so for the last forty-one years. Id. Upon physical examination, Dr. Vastey
noted bilateral knee crepitus, but no significant joint abnormalities. Id. at 3.

       There are also blood test results in the record from March 16, 2016. Pet’r’s Ex. 37 at 17–
19, ECF No. 49-1. Petitioner’s ANA screen was negative, whereas her RF result was 161
IU/mL, which was flagged as high. Id. at 17–18. Her ESR was 22 m/hr, which is within the
range provided in the test of less than or equal to 30 mm/hr. Id. at 18.

       On April 11, 2016, Petitioner presented to the Putnam Community Medical Center
Emergency Department with pain in her right arm. Pet’r’s Ex. 36 at 1, ECF No. 39-6. DO48
Mark Sbarro documented that her chief complaint was an “exacerbation of ra” beginning that
day. Id. at 2. In the physical exam portion of the note, the provider documented that tenderness
was present in both the right and left hands. Id. at 4. He prescribed prednisone, ketorolac
thromethamine, and acetaminophen/hydrocodone. Id. Petitioner was discharged after less than
an hour. Id. at 9, 12.

        Petitioner saw Dr. Vastey again on May 18, 2016. Pet’r’s Ex. 34, ECF No. 39-4. At that
visit, Dr. Vastey noted that Petitioner’s hyperlipidemia started in 2010, and is associated with
“joint pain and myalgia.” Id. at 1. Dr. Vastey reported that Petitioner exhibited bilateral wrist
arthralgias that were constant and fluctuated. Id. Dr. Vastey noted that Petitioner “had two RA
flare up[s] since [her] last visit [two months prior] [and was] scheduled to see [a] rheumatologist
[on] June 14.” Id. Petitioner was instructed to follow up with her rheumatologist but was

45
   Albuterol is “a β-adrenergic agonist, specific for β2-adrenergic receptors; administered by inhalation as
a bronchodilator for the treatment and prophylaxis of bronchospasm associated with bronchitis . . . or
other chronic obstructive airway disease[.]” Dorland’s at 45.
46
   Thromethamine is another name for Toradol. See Toradol, RXLIST, https://www.rxlist.com/toradol-
drug.htm (last visited June 10, 2019).
47
   Methylprednisolone is “a synthetic glucocorticoid derived from progesterone, used in replacement
therapy for adrenocortical insufficiency and as an anti-inflammatory and immunosuppressant in a wide
variety of disorders; administered orally.” Dorland’s at 1154.
48
   DO is an abbreviation for “Doctor of Osteopathy.” See NEIL M. DAVIS, MEDICAL ABBREVIATIONS:
26,000 118 (12th ed. 2005).
                                                     13
prescribed methylprednisolone “in case of flare.” Id. at 4. There are no records indicating that
Petitioner followed up with a rheumatologist in June or any other time between this May 18,
2016 appointment and her next appointment with Dr. Vastey in July of 2017. See Pet’r’s Ex. 34;
Pet’r’s Ex. 37.

        Petitioner saw Dr. Wenger on May 24, 2016. Pet’r’s Ex. 33 at 1. Much of the note is
difficult to read, but he did note the “legal issue of flu shot related to R.A.” in her record on that
date. Id. It appears to be a note regarding releasing records to Petitioner’s attorney, rather than
an opinion regarding the merits of Petitioner’s suit. Id. The record contains the results of a
blood test from May 9, 2017. Petitioner’s ANA screen was negative, and her RF was flagged as
high at 161 IU/mL. Id. at 17–18.

        On July 11, 2017, Petitioner saw Dr. Vastey. Id. at 1. Petitioner reported “acute
symptoms of RA” and noted that symptoms had “progressed and she want[ed] to establish with
rheumatology.” Id. Dr. Vastey noted that steroids “work well with flares” but that Petitioner
had “not taken [disease modifying antirheumatic drugs] DMARDS49 due to concerns of side
effects.” Id. Petitioner reported that she continued to smoke a pack of cigarettes per day. Id.
Dr. Vastey noted the use of a cane at this visit. Id. at 4. A note reflects that the plan was to refill
the Medrol prescription, and that a referral to rheumatology was made on July 6, 2017. Id. at 4.
Dr. Vastey noted that Petitioner “still ha[d fifteen] tabs of [P]ercocet.” Id.

        Petitioner presented to the Putnam Community Medical Center Emergency Department
on August 28, 2017, for arthritis pain. Pet’r’s Ex. 38 at 102–32, ECF No. 49-2. Dr. Gerry Meta
documented that Petitioner complained of severe right and left wrist pain, which he described as
an “RA FLARE.” Id. at 112. The onset of pain was the same day and was rated as nine out of
ten on a pain scale. Id. at 112, 117. Ketorolac tromethamine was administered intramuscularly.
Id. at 122. Petitioner was also prescribed Percocet. Id. at 129.

         On August 31, 2017, Petitioner saw PA Joseph Altamirando at Azela Health to follow up
after the emergency room visit, which he noted was due to “another RA flare [involving] severe
swelling of [her] right wrist.” Pet’r’s Ex. 37 at 1. PA Altamirando noted that Petitioner made an
appointment with rheumatology for December and was unable to get an earlier appointment. Id.
at 1, 9. PA Altamirando also documented that Petitioner reported that Toradol and prednisone
“do help but she knows she cannot take [them] constantly.” Id. PA Altamirando advised
Petitioner to take steroids and Toradol “in brief regimens [of three to four] days, then remain off
for as long as possible.” Id. at 9.

        On October 25, 2017, Petitioner presented to St. John’s Family Care for left hip pain that
started two weeks prior. Pet’r’s Ex. 42 at 9, ECF No. 49-6. Petitioner reported that the pain was
achy, moderate, and aggravated by movement. Id. Another portion of the note reflects that
Petitioner “fe[lt] like [the hip] [wa]s broken.” Id. at 11. An x-ray revealed no fractures or
degenerative changes but did reveal “mild joint space narrowing.” Id. at 10. Petitioner was
prescribed Percocet for the pain. Id.

49
  Disease-modifying antirheumatic drugs “act on the immune system to slow the progression of [RA].”
Treating Rheumatoid Arthritis with Disease-Modifying Drugs (DMARDs), WEBMD, https://www.web
md.com/rheumatoid-arthritis/guide/dmard-rheumatoid-arthritis-treatment#1 (last visited June 10, 2019).
                                                  14
         Petitioner reported back to Dr. Vastey on November 2, 2017 with complaints of back
pain that started one week prior. Pet’r’s Ex. 37 at 11. Petitioner also complained of left hip pain
which had persisted for three weeks. Id. Petitioner reported that she had an x-ray the previous
week but was told that the results were normal so “she would like an order for an MRI.” Id.
Petitioner reported that her pain was at a level of three out of ten. Id. at 13. Dr. Vastey ordered
an x-ray of the lumbar spine and a urine drug screen.50 Id. at 14. She also prescribed Percocet
tablets to be taken twice daily “as needed for severe pain” and instructed Petitioner to follow up
in two weeks. Id. The x-ray report impression was “[m]ild compression fracture at the superior
endplate of L3. The age [was] uncertain. Bilateral facet joint arthropathy at L4-5 and L5-S1
with suspected neural foraminal stenosis.”51 Id. at 20; Pet’r’s Ex. 38 at 6.

        On November 14, 2017, Petitioner saw a nurse practitioner at Florida Neurosurgical
Associates. Pet’r’s Ex. 43 at 16–18, ECF No. 50-1. She complained of lumbar and left lower
extremity pain that began approximately four weeks prior. Id. at 16. Petitioner told the provider
that “she was sitting on the floor at work . . . and when she got up she felt a twing in her back.”
Id. Petitioner reported that she thought the pain was related to her RA, so she took a dose of
steroids, but the pain did not improve. Id. The provider ordered an MRI. Id. at 17. A note
authored by Dr. Eric W. Scott at Florida Neurosurgical Associates on November 15, 2017,
reflects that x-rays and an MRI revealed an old fracture at L3, facet arthropathy, and a disc
bulge, but no disc herniation or stenosis. Id. at 11, 14–15, 18. Dr. Scott documented that
Petitioner’s symptoms were “highly suggestive of primary hip joint disease and/or sacroiliitis,52”
and he ordered an MRI of the left hip. Id.

       An MRI of the left hip obtained on November 21, 2017, revealed “[m]oderately severe
changes of femoral neck stress fracture;” “[m]oderately severe degenerative joint changes and
associated synovitis;53” and “[m]ild insertional tendinosis54 of the gluteus minimus/medius55 and
hamstring tendons.” Id. at 8. Dr. Scott referred Petitioner to Dr. Timothy Lane for her left hip
pain. Pet’r’s Ex. 40 at 4–7, ECF No. 49-4; see also Pet’r’s Ex. 43 at 2–4.

50
   Petitioner’s urine drug screen was positive for benzodiazepines. Pet’r Ex. 37 at 16. Alprazolam, which
Petitioner had been prescribed by Dr. Wenger, is a benzodiazepine.
51
   Neural foraminal stenosis “is a type of spinal stenosis . . . [which] occurs when the small openings
between the bones in [the] spine, called the neural foramina, narrow or tighten.” Neural Foraminal
Stenosis, HEALTHLINE, https://www.healthline.com/health/neural-foraminal-stenosis (last visited June 10,
2019).
52
   Sacroiliitis is “inflammation (arthritis) in the sacroiliac joint.” Dorland’s at 1662.
53
   Synovitis is “inflammation of a synovium; it is usually painful, particularly on motion, and is
characterized by a fluctuating swelling due to effusion within a synovial sac.” Dorland’s at 1856.
54
   Insertional tendinopathy “is a common disorder caused by repetitive tendon strain and subsequent poor
tendon healing.” Insertional Tendinopathy, AMBOSS, https://www.amboss.com/us/knowledge/Insert
ional_tendinopathy (last visited June 10, 2019).
55
   The gluteus minimus muscle is located in the “lateral surface of [the] ilium between [the] anterior and
inferior gluteus lines.” The gluteus medius muscle is located in the “lateral surface of [the] ilium between
[the] anterior and posterior gluteus lines.” Both muscles “abduct[] and rotate[ the] thigh medially.”
Dorland’s at 1205.
                                                    15
        Dr. Lane noted on November 28, 2017, that Petitioner “ha[d] had pain involving her left
hip for six months to a year,” which was “moderate in severity.” Pet’r’s Ex. 40 at 4. Dr. Lane
further documented that around November 2, 2017, Petitioner had increased pain which caused
difficulty at work and at home. Id. Dr. Lane ordered x-rays, which “reveal[ed] bone-on-bone
changes present in the left hip and osteopenia.” Id. at 6. He also reviewed the November 21,
2017 MRI, along with a Dr. Vogler, and determined that “the findings [were] consistent with
avascular necrosis56 of the femoral head57 with an insufficiency fracture and bone edema
extending into the intertrochanteric area58 and femoral neck.” Id. Dr. Lane documented that he
discussed surgery with Petitioner, and she elected to proceed with total hip replacement. Id.

       Petitioner was seen for a preoperative exam on December 1, 2017. Id. at 2. A CT scan
and lab tests were completed. Id. at 8–9, 18. Petitioner had a total left hip replacement on
December 6, 2017. Id. at 10–17; see Pet’r’s Ex. 41 at 47. The surgical records reflect several
diagnoses underlying the need for the surgery. Pet’r’s Ex. 41 at 4 (“[r]heumatoid and
osteoarthritis” and a “stress fracture” in the hip), 6 (“degenerative arthritis/avascular necrosis”).

        Kindred at Home (“KAH”) provided in-home surgery aftercare starting on December 9,
2017. See Pet’r’s Ex. 39, ECF No. 49-3. Petitioner followed up with Dr. Lane at The
Orthopedic Institute on January 2, 2018. Pet’r’s Ex. 40 at 1, 19. Although he noted that
Petitioner was “walking well with and without her walker,” he recommended continued use of
the walker for another month. Id. The note reflects that Petitioner planned to return to work in
March. Id.

        On February 19, 2018, Petitioner had a rheumatology consultation with Dr. Annabelle
Lee at Baptist Primary Care – South Rheumatology. Pet’r’s Ex. 50 at 1–13, ECF No. 61-1. The
note from that date reflects that Petitioner was referred by Dr. Lane “for consultation regarding
elevated [RF].” Id. at 1. The history of present illness portion of the note reflects the following:

        [Petitioner] reportedly had symptoms as early as October 2013 [which] started
        [twenty-four] hours after she received a flu shot. She reportedly had [an]
        “extreme immune response” with pain on left shoulder associated with limited
        [ROM]. She took over-the-counter NSAIDs with symptoms resolving within a
        week. After that, she had migratory polyarthralgia involving right shoulder, left
        knee, right knee, both hands, ankles, and both hips. She ha[d] noted MCP
        swelling, redness, and warmth. She was empirically treated with prednisone
        which significantly helped. She had been tested for [RF] which was reportedly
        negative in the past.

Id. That section then reviews Petitioner’s treatment history. Id. The note contains
“Results/Data,” but the formatting makes the data difficult to interpret. Id. at 3–11. Dr. Lee

56
   Avascular necrosis “is the death of bone tissue due to a lack of blood supply.” Avascular Necrosis,
MAYO CLINIC, https://www.mayoclinic.org/diseases-conditions/avascular-necrosis/symptoms-causes/syc-
20369859 (last visited June 10, 2019).
57
   Femoral head (AKA caput femoris) is the “head of [the] femur.” Dorland’s at 286.
58
   The intertrochanteric area is “situated in or pertaining to the space between the greater and the lesser
trochanter.” Dorland’s at 951.
                                                    16
assessed osteoarthritis and RA of the foot and hand. Id. at 11. Dr. Lee planned to check labs,
obtain x-rays, continue with prednisone prescriptions, and follow up as indicated or necessary.
Id. at 13.

        Petitioner had x-rays taken on February 21, 2018. Knee x-rays reflected degenerative
arthropathy, more pronounced on the left than the right. Id. at 14–16, 21–23. A hip x-ray taken
on the same day reflected “[e]vidence of some chronic inflammation of the right psoas59 in
insertion upon the lesser trochanter60 [but] no arthritic changes identified on the right.” Id. at 17,
24. X-rays of the hands reflected degenerative arthropathy. Id. at 18, 25–26. An x-ray of the
left foot reflected “[d]emineralization61 consistent with osteoporosis or osteopenia, but with no
complication identified [and] [n]o arthritic changes seen.” Id. at 19, 27. An x-ray of the right
foot reflected “demineralization consistent with osteoporosis or osteopenia [but] [n]o further
abnormalit[ies].” Id. at 20, 28.

        Petitioner also had blood tests on February 21, 2018. Petitioner’s 14-3-3η (eta) protein62
test was high with more than 20 ng/mL, where the reference range is less than 0.2. Id. at 29.
Petitioner’s CCP test had a result of 65 units, indicated as a strong positive. Id. Her RF was 153
IU/mL. Id. at 31. The modified ESR was 36 mm/hr. C-reactive protein was also high, at 32.4
mg/L, where the reference range is less than 8.0. Id. at 32. At the end of the blood tests results,
there is a note that the “[b]lood work confirm[ed RA].” Id.

                    3. Petitioner’s Testimony

         Petitioner testified at the entitlement hearing in this case. See Tr. 9:8–54:8. Petitioner
explained that she received a flu vaccine every year due to her employment at a hospital, and that
she had never had any issues with the vaccine prior to 2013. Tr. 12:14–13:2. She testified that
she was “a very healthy and active person,” and that she experienced no regular morning
stiffness, persistent swelling in her joints, or persistent pain. Tr. 11:9–11, 11:25–12:7. Petitioner
testified that she smoked a pack of cigarettes per day for a long time but has since “tried to cut
that down because [she] knows it is not good for [her] condition.” Tr. 30:12–21.

        Petitioner described receiving the vaccine on a Friday evening while at work and testified
that she “wasn’t feeling quite right” the next day. Tr. 13:16–19. She explained that her
symptoms were more “exaggerated” than normal post vaccination symptoms, which she
described as “soreness in the injection site” or “aches for a couple of days.” Tr. 13:21–22, 28:8–
10. Petitioner testified that when she went home after her shift, she could not sleep due to a
“deep ache” in her left shoulder, that was “so bad [that she] couldn’t sleep and [she] couldn’t

59
   The psoas muscles are defined as “muscles of [the] lower back.” They are divided into the psoas minor
and psoas major. The former “flexes [the] trunk,” while the latter “flexes [the] thigh or trunk.”
Dorland’s at 1209, 1547.
60
   Trochanter refers to “either of the two processes below the neck of the femur.” Dorland’s at 1970.
61
   Demineralization refers to “excessive elimination of mineral or inorganic salt[.]” Dorland’s at 485.
62
   The 14-3-3η (eta) protein “is the newest blood test to be used in the diagnosis of RA. People with RA
seem to have elevated levels of the 14-3-3η protein in their blood.” Blood Tests to Help Diagnose
Rheumatoid Arthritis (RA), ARTHRITIS-HEALTH, https://www.arthritis-health.com/types/rheumatoid/
blood-tests-help-diagnose-rheumatoid-arthritis-ra (last visited June 11, 2019).
                                                  17
move literally without helping [her]self turn over.” Tr. 14:4–7, 14:14–15. She explained that the
pain involved her entire shoulder, not just the site of the vaccination. Tr. 14:6. She testified that
she attempted to treat the pain with over the counter medications, but “nothing helped.” Tr.
14:16–17.

        Petitioner testified that she “joked” with the nurse who administered the vaccine
regarding what she perceived to be unusual symptoms. Tr. 13:22–14:3. She explained that she
did not report the pain that she was experiencing because she was “not aware at that time” that
there was a way to report such a problem. Tr. 29:10–18. Petitioner testified that she is not aware
of a way to report issues with the flu vaccine to her employer’s workers’ compensation provider.
Tr. 30:5–11.

        Petitioner testified that the pain “subsided somewhat” after approximately three days, and
she thought that the problem was resolved. Tr. 14:18. However, three days later the same pain
began again in the right shoulder. Tr. 14:21–23. Petitioner stated that the pain was to the point
where she was unable to lift her arms above her head to put on a shirt. Tr. 14:23–25. Her
shoulders “were red and warm” during this time, and that those symptoms began two to three
days after she received the vaccine. Tr. 15:3–4. Petitioner testified that she sometimes required
the help of her niece, who would come from about five miles away, to help her get dressed. Tr.
53:1–12.

        On November 1, 2013, Petitioner “went to get checked out due to pain in both
shoulders.” 15:13–20. She testified that it was unusual for her to go to the emergency room,
noting that “nobody in healthcare really utilizes the ER unless they really think there is a
problem.” Tr. 16:2–5. Petitioner’s medical record noted that her blood pressure was high due to
anxiety related to her pain symptoms. Pet’r’s Ex. 3 at 16.

         Petitioner described her symptoms between November 1, 2013 and the end of 2013 as
“deep, aching” pain. Tr. 16:10–18. She testified that she “never knew where [the pain] was
go[ing to] show up,” and that it was “sometimes to the point [she] felt [she] couldn’t bear it.” Tr.
16:19, 16:24. Petitioner explained that she experienced pain in her left knee, then right knee, and
that in “one episode [her] hand was very swollen[,] huge and red and hot.” Tr. 16:21–23. She
testified that the pain “was debilitating and [she] would have to call out of work” when it
appeared in her legs. Tr. 16:24–17:1. She testified that she was given a written reprimand at
work for absences. Tr. 41:15–23.

        Petitioner testified that at her January 2014 MedEx visit several days later, she was
unable to walk without a cane due to joint pain. Tr. 18:19–20. She testified that she did not go
back to the emergency room because she did not go for routine injury or pain. Tr. 33:1.
Petitioner could not recall when she began to use the cane, which belonged to her father, before
that visit. Tr. 35:11–20.

         Petitioner testified that she continued to have intermittent joint pain between January and
April 2014. Tr. 21:11–14. She explained that an ER physician with whom she worked told her
that it “sounded as if [she] had something going on that would be best addressed by a
rheumatologist,” and that the colleague recommended that she visit Dr. Lloyd. Tr. 21:17–21.

                                                 18
Petitioner testified that during her first visit with Dr. Lloyd, he “never touched [her]” and “barely
looked at [her]” even though she was “using a cane and crying.” Tr. 43:11–15.

         Petitioner testified that she saw another rheumatologist on one occasion, but that he was
“rude, disrespectful,” and “spent most of his time going over the reasons that he would drop [her]
as a patient,” such as “if [she] was late or missed an appointment.” Tr. 44:20–45:3. Petitioner
testified that she “never went back because [she] felt that was enough time spent with that
doctor.” Tr. 45:3–4.

        Petitioner testified that prednisone is the “only thing that has kept [her] working.” Tr.
19:23–20:1. She testified that she continues to take prednisone “when [she] has flares,” but that
it “has a lot of side effects.” Tr. 25:7–11. Petitioner testified that she continues to have
symptoms which she associates with RA, including pain which rises to the point where she uses
a wheelchair on occasion. Tr. 25:20–24. She testified that she is scheduled to discuss future
treatment options with Dr. Lee at an upcoming appointment. Tr. 26:16–19.

        Petitioner testified that none of her treating physicians have opined that the flu vaccine
was the cause of her RA. Tr. 44:9–12. She testified that she has discussed the potential
connection with Dr. Lee, but that Dr. Lee has not given an opinion either way. Tr. 44:12.
Petitioner testified that she submitted a VAERS report because she “felt that [she] had an adverse
reaction” to the vaccine. She also contacted an attorney, because she thought “maybe they’[d]
heard” about a connection between the flu vaccine and her injuries. Tr. 47:3–4.

III.   Expert Review

       A.      Petitioner’s Expert, Dr. Paul J. Utz

        Dr. Utz authored three expert reports and testified at the hearing for Petitioner. Pet’r’s
Exs. 17, 25, 44, ECF Nos. 32-1, 37-1, 55-1. Dr. Utz graduated from Stanford University
Medical School in 1991. Pet’r’s Ex. 17 at 1. He was board certified in internal medicine from
1994 to 2004 and in rheumatology from 1996 to either 2016 or 2017. Id. at 1; Pet’r’s Ex. 18 at 1;
Tr. 57:1–3. He is a professor of medicine at Stanford University and serves as the Director of
Stanford’s Medical Scientist Training Program. Pet’r’s Ex. 17 at 1. He previously served as
Acting Chief of the University of Medicine’s Division of Immunology and Rheumatology and as
Director of the Center for Clinical Immunology. Id. at 2. Dr. Utz has published “probably
somewhere between 100 and 150 [publications].” Tr. 59:9–10. That literature does not directly
address the causation theory discussed in this case, but it does “include papers on [RA and]
autoantibodies.” Tr. 59:11–12. He also has experience working with vaccines, as he “was
actively involved in vaccine development” with Bayhill Therapeutics for “over a decade” and
has “started a new company (Tolerion, Inc in Palo Alto) to pursue vaccine development.” Pet’r’s
Ex. 17 at 1. Dr. Utz testified that he currently runs a research laboratory that studies autoimmune
diseases “exclusively [in] humans,” although the laboratory “used to also do mouse studies.” Tr.
56:4–7.

        Since 2010, Dr. Utz has provided expert opinions in nineteen Vaccine Program cases.
Pet’r’s Ex. 17 at 2. He previously testified twice in the last several years and has authored

                                                 19
approximately twenty reports. Tr. 63:3. He has also reviewed approximately ten to fifteen cases
where he has given a preliminary opinion that there was likely no relation between a person’s
injuries and a vaccine. Tr. 63:8–10. Dr. Utz testified that approximately ten percent of his
income derives from litigation, although it varies. Tr. 63:20–21. He testified that he is in the
research lab three out of five workdays per week and does administrative work the other two
days. Tr. 61:16–21. Dr. Utz stated that his clinical time is inconsistent due to his other
responsibilities, but he does volunteer to see patients at the VA hospital, “largely just to cover the
other doctors.” Tr. 62:2–3. Dr. Utz has treated “hundreds” of patients with RA and recommends
they receive vaccines, including the influenza vaccine. Tr. 62:9–22. Respondent had no
objection to Dr. Utz’s admission as an “expert of medicine in the areas of immunology and
rheumatology,” and he was so admitted. Tr. 64:11–16.

       B.      Causation Theory

        Dr. Utz opined that, based on Petitioner’s “well[]documented history, it is [his] opinion,
with a reasonable degree of medical and scientific certainty, that [Petitioner] developed
seropositive RA as a direct result of receiving an influenza vaccine.” Pet’r’s Ex. 17 at 6. He
wrote that a review of her medical record “failed to identify any triggering events such as
infection or new drug,” which left “only her influenza vaccine emerging as the most likely
trigger of her disease.” Id.

        Dr. Utz testified that the “etiology of RA is not known,” but it is clearly inflammatory
and “autoimmune in nature.” Tr. 69:23–70:2. He testified that a “variety of different
mechanisms” have been discussed in the literature. Tr. 70:5. During his testimony, Dr. Utz
stated, “in terms of the mechanism I put forward, molecular mimicry as the primary, although
others that could have also been involved included things such as bystander activation of T cells
and B cells.” Tr. 66:9–12.

       Dr. Utz wrote in his first report that “[w]hen an immune response to a non-self-antigen
such as components of an influenza vaccine cross reacts with self molecules, the process is
termed ‘molecular mimicry.’” Pet’r’s Ex. 17 at 8. Dr. Utz testified “molecular mimicry is an
accepted proposed mechanism in [RA]” that “most rheumatologists would accept.” Tr. 71:7–9.

        Dr. Utz wrote that “[m]olecular mimicry has been very well[]described in several
situations.” Pet’r’s Ex. 17 at 10. He continued that “[t]he best example” of molecular mimicry
“is acute rheumatic fever, in which antigens from beta streptococcus cross react with antigens in
the joints, brain, skin and heart, causing acute rheumatic fever.” Id. Dr. Utz also described “two
particularly interesting examples [that] are noteworthy [in the area of vaccines], although there
are many others.” Id. First, Dr. Utz explained that a vaccine was developed for Lyme disease,
but was later “withdrawn from the market due to published reports of arthritis induction by the
vaccine.” Id. Dr. Utz wrote that molecular studies demonstrated that arthritis resulted from
cross-reactivity between a Lyme protein and a cell surface self-antigen which is critical for
immune cells to stick to one other. Id. He noted that “[t]he discovery of molecular mimicry
caused by the organism itself, and probably also the vaccine, led to [the vaccine’s]
discontinuation in humans.” Id. Second, Dr. Utz explained that a vaccine for Hepatitis B was
“developed as a conjugate between a hepatitis B antigen and a TLR9 activating DNA

                                                 20
oligonucleotide.” Id. However, he noted that trials for the vaccine were stopped after two
subjects developed an autoimmune condition associated with Hepatitis B, which was thought by
the FDA to be related to the vaccine. Id.

          Dr. Utz opined that “[i]t is plausible, and [he] would argue very likely, that similar
molecular mechanisms are at play in [Petitioner’s] case.” Id. The mechanism Dr. Utz proposed
is that “influenza antigen(s) in the vaccine are delivered to the immune system, leading to cross[-
]reactivity and molecular mimicry to self-antigens that then break tolerance to self, causing RA.”
Id. at 10–11. Dr. Utz elaborated that “[m]any arthritides . . . are postulated to be . . . or known to
be . . . caused by exposure to an infectious antigen or foreign antigen.” Id. at 11. He listed
systemic lupus erythematosus63 (“SLE”) and RA as conditions “postulated to be” caused by
infectious antigens or foreign antigens, while he listed Lyme arthritis, serum sickness, and
parvovirus infection as conditions “known to be” caused by those antigens. Id. Dr. Utz wrote
that in all of those diseases with a known cause, “ample literature documents that immune
complexes can be found early in the disease course[, but] immune complexes may not be present
later when patients come to medical attention, suggesting a ‘hit-and-run’ etiology.” Id. Dr. Utz
opined that RA can be triggered in a similar manner. Id.

        Dr. Utz wrote that “[i]t is likely in [Petitioner’s] case that this is a classic example of a
memory immune response in which preexisting memory B and T cells were activated by the
vaccine.” Id. He stated that when compared with primary responses, “memory responses are
rapid, and can be orders of magnitude stronger.” Id. He noted that it is “likely” that “Petitioner
would have been exposed to influenza viruses and related antigens during her lifetime.” Id.
Therefore, Dr. Utz explained, “[t]he induction of the cross-reactivity does not require a
replicating agent.” Tr. 95:5–6. He continued that Petitioner “had a nonreplicating agent, the
vaccine, that broke tolerance, even after the vaccine was gone months later, and that was the hit
and run event that triggered the immune response.” Tr. 95:13–16. Dr. Utz asserted that in this
case, Petitioner’s arthritis may have been triggered “secondary to formation of immune
complexes containing influenza antigens from the vaccine and antibodies produced in response
to previous influenza infections or vaccines; activation of T cells from the vaccine; cross-priming
to a new antigen; or a combination thereof.” Pet’r’s Ex. 17 at 11.

         Dr. Utz wrote that “[a] number of different RA protein antigens have been described” in
the literature, with “the most prominent being Type II collagen, a constituent of joint synovium.”
Id. at 13. He wrote that “[i]njection of Type II collagen in combination with adjuvant into mice
leads to the development of B and T cell autoreactivity, associated with severe synovial
inflammation (as was observed in [Petitioner] after her vaccination).” Id. Dr. Utz stated that
Type II collagen is one of the major proteins found in joints and he wrote that “[i]t is well
accepted in the field of rheumatology that Type II collagen is an autoantigen in RA.” Id. at 14.
The “collagen molecule, . . . a peptide derived from human collagen, can complex with the HLA-
DR464 molecule and be presented to lymphocytes.” Tr. 98:14–16. Dr. Utz made clear he is not

63
   Systemic lupus erythematosus is “a chronic, inflammatory, often febrile multisystemic disorder of
connective tissue that proceeds through remissions and relapses; it may be either acute or insidious in
onset and is characterized principally by involvement of the skin, joint, kidneys, and serosal membranes.”
Dorland’s at 1080.
64
   Dr. Utz explained in his testimony that HLA-DR4 is a “human leukocyte antigen.” Tr. 78:8–10.
                                                   21
stating that “anyone has demonstrated that a T cell receptor is recognizing the collagen and
influenza peptides.” Tr. 101:18–20. He clarified that “the peptides, when they’re in the MHC
groove, are structurally similar and, . . . there’s a good possibility that collagen peptides and
influenza peptides could cross react when they’re presented in the context of the DR4 molecule.”
Tr. 101:22–102:2. Dr. Utz explained by way of analogy. He likened the antigen peptides to
hotdogs and the MHC molecule to a hotdog bun. Tr. 77:2–3. He noted that “MHC molecules
can see more than one peptide, but not all of them,” and an MHC “molecule with the peptide can
present that to a T cell, which will then recognize the peptide together with components of
[MHC].” Id. at 5–9. Under my questioning, Dr. Utz stated that “collagen is by far the antigen
where the most evidence exists,” but “there could be other antigens besides collagen, including
other things that might be citrullinated.65” Tr. 358:15–18.

        Dr. Utz also referenced an article authored by Sun, et al.,66 which he wrote “demonstrated
that hemagglutinin peptides can activate T cells that can cause synovitis.” Pet’r’s Ex. 17 at 13
(citing Pet’r’s Ex. 17, Ref. 6, ECF No. 32-8). Dr. Utz testified that hemagglutinin, a protein
found in the influenza vaccine, “might cross-react or have a similar amino acid sequence [with
self-proteins].” Tr. 91:17–21. Dr. Utz stated that several of the articles filed in this case
identified peptides present in the influenza vaccine that could cause a cross reactive immune
response that triggers RA. Therefore, Dr. Utz concluded that the literature supports his
“mechanistic theory that an influenza vaccine constituent can cause RA in a genetically
susceptible individual.” Pet’r’s Ex. 17 at 14.

        Dr. Utz acknowledged that he found “no epidemiologic link between RA and influenza
vaccination” in the literature that he searched but stated that it was unsurprising that he found no
such link,67 and that such a link is not required to support his theory. Id. at 11.

        C.      Petitioner’s Diagnosis and Current Health

        Dr. Utz reviewed and summarized Petitioner’s medical history and affidavit in his reports
and again during his testimony. Pet’r’s Ex. 17 at 2–6; Tr. 55–216. He explained that RA is an
autoimmune disease that can be diagnosed following an examination of the patient’s joints and
laboratory testing, including tests for RF and CCP. Tr. 69:9–20. He opined that Petitioner “had
no preexisting evidence that she had any systemic rheumatic disease or any arthralgia or other
joint problems that would have predisposed her to [RA] . . . .” Tr. 65:19–22. Dr. Utz did note
that Petitioner “had an important risk factor (tobacco use) that is strongly believed to play an
additional role in the development of CCP-positive RA.” Pet’r’s Ex. 17 at 7. In his report, Dr.
Utz wrote that although “smoking is believed to be an environmental contributor to the
development of RA[, it] is not associated with acute triggering of rheumatic disease as has been

65
   Citrullination is “a posttranslational modification of proteins in which peptideylarginine deiminase
catalyzes the conversion of arginine residues to citrulline residues. . . . [I]t also occurs in a variety of
inflammatory conditions.” Dorland’s at 366.
66
   Jian Sun et al., Superior Molecularly Altered Influenza Virus Hemagglutinin Peptide 308–317 Inhibits
Collagen-Induced Arthritis by Inducing CD4+ Treg Cell Expansion, ARTHRITIS & RHEUMATOLOGY
(2012) 64:2158–68.
67
   Dr. Utz noted that “even large epidemiologic studies will not have the power to capture rare, patient-
specific events such as occurred in [Petitioner’s] case.” Pet’r’s Ex. 17 at 12.
                                                     22
overserved with vaccines, certain drugs, and infections.” Id. at 6–7. Dr. Utz later wrote that
“Petitioner has a genetic predisposition to develop RA and that tobacco use over 40 years
increased her likelihood of developing seropositive RA if she encountered the ‘right’, or in this
case ‘wrong/bad’, environmental trigger.” Pet’r’s Ex. 25 at 3. He followed that assertion with
testimony that Petitioner “was probably DR4 positive. We don’t know that for sure.” Tr. 137:7–
8.

        Dr. Utz noted in his report that there are researchers that have studied “a ‘preclinical’
period of disease” that “is characterized by abnormalities in disease-related biomarkers before
the onset of the clinically apparent signs and symptoms.” See Pet’r’s Ex. 25 at 4–7 (citing
Resp’t’s Ex. Q68 at 1–4). Dr. Utz wrote that this research is developed with the hope that
biomarkers of autoimmunity present during this period can be used to reverse or prevent tissue
damage and the future development of clinically apparent disease, and is not focused on
identifying potential triggers for the development of RA. Dr. Utz asserted that the categorization
of an individual as preclinical is controversial because all individuals who exhibit these
biomarkers do not always go on to develop RA. In fact, one of these researchers, Dr. Kevin
Deane, noted that “we don’t know . . . what drives the initial development of autoantibodies . . .
what triggers the expansion of autoimmunity . . . or what leads to the transition . . . to clinically
apparent synovitis.” Pet’r’s Ex. 25 at 4 (citing Resp’t’s Ex. C at 7 (citing Resp’t’s Ex. R69 at 1.))
Dr. Utz cautioned against designation of a patient as preclinical because the authors themselves
stated “this relationship has largely been studied retrospectively in patients with established
disease [and] whether smoking is an initial trigger for autoimmunity . . . remains unclear.”
Pet’r’s Ex. 25 at 6 (citing Resp’t’s Ex. Q at 3).

        In his report, Dr. Utz relied on Petitioner’s statements to identify the onset of her
symptoms. He noted that “[a]ccording to [Petitioner’s] affidavit, on October 20, 2013, [one day
post vaccination, Petitioner’s] left shoulder was sore.” Id. at 3. Dr. Utz later wrote in his report
that “Petitioner developed severe pain in the shoulders and other joints within hours to days of
vaccination, followed by polyarticular arthralgia and ultimately inflammatory arthritis.” Id. at
15. During his testimony, Dr. Utz stated that “[he] now think[s] more about three to six days
were more around the time where–she was really struggling the first three days, but then the
three to six days.” Tr. 65:25–66:3.

        Dr. Utz highlighted that Petitioner “was negative for RF and [CCP] soon after
vaccination, but then went on to develop positive tests for both factors over time.” Pet’r’s Ex. 17
at 7. Dr. Utz noted that RA onset can be acute or subacute, as in Petitioner’s case. Id. at 11. Dr.
Utz testified that Petitioner detailed symptoms within days after the vaccination that were very
compelling, such as her inability to dress herself. Tr. 53:1–5; Tr. 197:9. He testified that based
on her account, “the trigger for her RA was the vaccine” within three to six days. Tr. 138:10.

        Dr. Utz wrote that Petitioner’s “ongoing treatment with moderately high doses of
corticosteroids very likely contributed to her stuttering course and delay in meeting

68
   Kevin D. Deane & Hani El-Gabalawy, Pathogenesis and Prevention of Rheumatic Disease: Focus on
Preclinical RA and SLE, NAT. REV. RHEUMATOL. (2014) 10:212–28.
69
   Kevin D. Deane, Autoantibodies, Citrullinated Histones and Initiation of Synovitis, NATURE REV.
RHEUMATOLOGY (2015) 11:688–89.
                                                 23
Classification Criteria for [RA].” Pet’r’s Ex. 17 at 7. Dr. Utz wrote that Petitioner currently
meets the criteria for the diagnosis of RA. Id.

       D.      Respondent’s Expert, Dr. Mehrdad Matloubian

       Dr. Matloubian authored two expert reports and testified at the hearing on behalf of
Respondent. Resp’t’s Exs. C, UU, ECF Nos. 34-1, 62-1; Tr. 224–337. Dr. Matloubian
graduated from the University of California, Los Angeles School of Medicine in 1996. Resp’t’s
Ex. D at 2, ECF No. 34-2. While in medical school, Dr. Matloubian also received a Ph.D. in
virology in the Department of Microbiology and Immunology. Id. Dr. Matloubian is currently
board certified in rheumatology and was previously certified in internal medicine. Tr. 225:16–
18. Dr. Matloubian is an associate professor at the University of California, San Francisco
School of Medicine, Rheumatology Division. Tr. 225:21–23. Dr. Matloubian’s other roles at
the University of California, San Francisco include Director of the Rheumatology Precision
Medicine Corps. and Co-Director of the Molecular Medicine Consult Service. Tr. 226:9–10, 22–
23.

         Dr. Matloubian has engaged in virology- and immunology-based research for over twenty
years. Resp’t’s Ex. C at 2. He has published peer-reviewed articles focused on “innate and
adaptive immune responses, including those of T and B cells, to acute and chronic viral
infections.” Id. In addition to teaching, Dr. Matloubian is a practicing rheumatologist and sees
patients once a week. Tr. 228:2–3. He treats patients with autoimmune rheumatologic diseases,
including RA, and he has diagnosed patients with RA. Tr. 228:16–229:8. Dr. Matloubian
testified that he has seen approximately one hundred RA patients in a given year. Tr. 229:14–15.
He has appeared as an expert witness for Respondent approximately thirty times and testified at
hearing seven times beginning in 2015. Tr. 231:17–24. Dr. Matloubian stated that about fifteen
percent of his annual income comes from his participation in the program. Tr. 232:5. Dr.
Matloubian was admitted to testify as an expert in rheumatology and immunology with no
objection from Petitioner.

       E.      Dr. Matloubian’s Reports and Testimony

       Dr. Matloubian began his expert report with a recount of Petitioner’s medical history.
Resp’t’s Ex. C at 1–4. The report identifies two major questions with respect to Petitioner’s
case: “1) What is the rheumatologic diagnosis for the [P]etitioner’s musculoskeletal complaints;
and 2) Was her condition caused by her influenza vaccination?” Id. at 4.

        Dr. Matloubian did not dispute that Petitioner suffers from RA. Dr. Matloubian agreed
that the “diagnosis of seropositive RA is quite reasonable in [Petitioner’s] case.” Id. at 5. He
also agreed “with Dr. Vazquez[] . . . that a chronic pain syndrome influence by [P]etitioner’s
history of anxiety and depression as well as osteoarthritis of her knees . . . were most likely
contributing to her musculoskeletal symptomatology.” Id.

                                                24
         Dr. Matloubian described RA as “a systemic inflammatory disease whose major
manifestation is peripheral arthritis, mainly in the small joints of the hands and feet.” Id. Dr.
Matloubian noted that RA is “quite common,” particularly “between the ages of 50 and 75.” Id.
He added that about one percent of the Caucasian population is affected and there is a “lifetime
risk of . . . 3.6% (1 in 29) for women.” Id. Dr. Matloubian described presentations of RA
ranging from “fulminant” to “insidious” and detailed an “established [] set of validated criteria”
for diagnosis. Id. These criteria include the number and site of involved joints with synovitis
and serological abnormalities. Id. During his testimony, Dr. Matloubian distinguished between
seronegative and seropositive RA, stating that the latter, “which is about two-thirds of the cases,
is characterized by having either anti-CCP antibodies or [RF] or both.” Tr. 233:1–3.

        Dr. Matloubian explained that “autoantibodies that are specific for [RA] are directed
against [] citrullinated protein epitopes,” but “[RF] has an unfortunate name because it is not
unique to [RA] and occurs in many other diseases . . . [involving] chronic stimulation of the
immune system.” Tr. 235:22–25. Dr. Matloubian also cautioned that “when patients present
with [RA] clinically, [e.g.,] with joint inflammation[,] . . . the disease actually started years
before and what supports that is that many of the patients have positive anti-CCP antibodies . . .”
Tr. 236:13–16. He stated this chronology “is not something that is disputed in the rheumatology
community, and there is a lot of effort to identify the different stages of preclinical [RA].” Tr.
236:22–24.

         Dr. Matloubian wrote in his report that “[t]he pathogenesis of RA is quite complex and
not completely understood.” Resp’t’s Ex. C at 4. Dr. Matloubian’s report also included Figure 2
taken from the van Steenbergen et al.70 article illustrating the “six phases of RA development.”
Id. at 6 (citing Resp’t’s Ex. O at 2221). The figure is comprised of six stick figures that
correspond to each phase and help to explain the progression of the disease. Id. Dr. Matloubian
also used this figure during his testimony. Tr. 237:7–239:9. Phases A and B highlight the
impact of genetic factors, such as HLA-DRB1 shared epitope, and environmental factors, such as
smoking and antibiotics. Resp’t’s Ex. C at 6. Dr. Matloubian stated that “about 50 percent of
the risk for RA comes from the genes, and half of that comes from the HLA-DR4 that Dr. Utz
discussed.” Tr. 237:14–15. Dr. Matloubian continued to explain that phase B is “a person who
has a genetic risk, and then they get exposed to an environmental risk factor . . . –the major risk
factor [being] smoking.” Tr. 237:17–20. Ultimately the genetics and the environment “lead[] to
the production of anti-CCP antibodies, and this [is] phase C.” Tr. 237:24–25. Dr. Matloubian
noted that the illustration for phase C in the figure is shaped like an antibody to denote
autoimmunity and to underscore that this phase is “defined by breakdown of tolerance to self-
antigens[ that] happens when a person becomes anti-CCP positive.” Tr. 238:2–4. The remaining
phases D, E, and F illustrate the development of clinical symptoms that are then categorized first
as generalized symptoms, then undifferentiated arthritis, and ultimately diagnosed as RA with
the onset of joint inflammation. Resp’t’s Ex. C at 6. Dr. Matloubian noted during his testimony

70
  H.W. van Steenbergen et al., The Preclinical Phase of Rheumatoid Arthritis: What is Acknowledged
and What Needs to be Assessed?, ARTHRITIS RHEUMATISM 65(9):2219–32 (2013).
                                                 25
that it is unknown “how long it will take an individual to go from development of anti-CCP to
development of [RA], and not everybody goes through all phases.” Tr. 239:5–8. Dr. Matloubian
cited the Deane papers to assert that despite the largely unknown pathogenesis of RA,
“[e]stablished and emerging data demonstrate that [there is] a preclinical period.” Resp’t’s Ex. Q
at 1. He continued that “[n]umerous genetic and environmental risk factors for [autoimmune
rheumatoid diseases] have also been identified, and many of these factors are likely to act before
the clinical appearance of tissue injury to initiate and/or propagate autoimmunity and
autoimmune disease.” Id. In his report, Dr. Matloubian also stated that there is a “lag of many
years” between autoantibody development and clinical symptoms of RA. Resp’t’s Ex. C at 7.
And, because of this delay, “it is extremely difficult to establish a causal link to a specific
environmental exposure, and one cannot completely rule out stochastic (e.g., random)
immunologic events.” Id.

        Dr. Matloubian was asked how the phases of RA development applied in Petitioner’s
case. Dr. Matloubian stated that prior to Petitioner’s vaccination in October 2013, Petitioner did
not suffer from stiffness, persistent swelling or pain, or inflammatory arthritis. Tr. 314:2–8. Dr.
Matloubian wrote in his report that “[P]etitioner did not have either a personal history or a family
history of autoimmune diseases, suggesting unlikelihood of a genetic predisposition.” Resp’t’s
Ex. C at 9. He testified that, at the time of the vaccination, Petitioner had environmental risk
factors for several years and, “[b]ased on what we know about the natural history of [RA] . . .
[Petitioner] was most likely in Phase C, because there’s a strong link between smoking, genetics,
and development of anti-CCP.” Tr. 321:7–11. He noted that he could not find where Petitioner
suffered from joint pain in her knuckles or her feet and stated that he was “not sure she even
went through Phase D.” Tr. 321:17–24. Dr. Matloubian identified Petitioner’s “swollen, red, hot
knee” treated on April 3, 2014 as the first evidence of her inflammatory arthritis and asserted that
“chances were high that [Petitioner] was anti-CCP positive before she developed her
inflammatory arthritis.” Tr. 314:17–19. These symptoms, Dr. Matloubian argued, were
evidence of Phase E. Tr. 322:23. Dr. Matloubian stated that Petitioner was into Phase F when
she presented to Dr. Lloyd with inflammation of the small joints and hands on April 27, 2014.
Tr. 323:9–18. He noted that Petitioner’s blood test that identified the presence of anti-CCP
occurred at her April 16, 2014 visit. Tr. 323:24–25.

        Dr. Matloubian was then asked how these phases can be applied to any specific patient if
phases can be experienced out of order or skipped altogether. He stated the figure illustrates
“proposed preclinical phases” to “identify people and put in an intervention.” Tr. 335:8, 23–24.
He clarified that the point of the paper is to help the Court understand and not necessarily to
apply each phase to Petitioner’s case. Tr. 334:16–20. Although each patient can proceed
through the phases differently, Dr. Matloubian testified that he is “not aware that somebody
[could] present[] with . . . symmetric arthritis and then develop [RF], [despite the fact that] most
people, at the time of diagnosis, are anti-CCP positive.” Tr. 336:14–17. Dr. Matloubian could
not see how the clinical presentation could appear prior to the development of RF. Tr. 336:12–
17.

                                                 26
         Dr. Matloubian then turned to whether Petitioner’s condition was caused by the flu
vaccine. In his report, he concluded that “[P]etitioner’s major risk factor for development of RA
is her long history of smoking.” Resp’t’s Ex. C at 7. Dr. Matloubian also concluded that
“[P]etitioner had most likely developed positive anti-CCP antibodies years before her
presentation with inflammatory arthritis, and thus had a silent autoimmune disease.” Id. To
determine whether vaccination can act as a trigger for symptoms of RA and cause a patient to
move from phase C to phase D in the progression, Dr. Matloubian returned to a discussion of the
filed literature. His report cited to Ray et. al.,71 a small case-control study, and Bengtsson et.
al.,72 a “much larger and more extensive study. Id. The authors of the smaller study “did not
find any association between influenza vaccination and development of RA.” Id. The authors of
the larger study found “vaccinations neither increased the risk of RA overall nor the risk of two
major subgroups of RA [CCP positive or negative] . . . . Furthermore, vaccinations did not
increase the risk of RA in smokers or carriers of HLA-DRBi shared epitope alleles, two groups
with established risk factors for RA.” Id. Dr. Matloubian noted in his report one article73 that
stated case reports and case series suggest a link between RA and vaccination, but the authors
cautioned that “establishing a causal association requires a comparative group who have not been
immunized.” Id. at 8 (quoting Resp’t’s Ex. W at 2).

        Dr. Matloubian also discussed three arguments from the Schattner study74 to rebut Dr.
Utz. Resp’t’s Ex. C at 8 (citing Resp’t’s Ex. X at 3881). “First, [specific] virus infections
should be linked to [specific] autoimmunity. Second, a mechanism or mechanisms whereby
exposure to viral antigens (be it during infection or vaccination) lead to autoimmunity must be
established. Third, evidence must be obtained that patients who have been vaccinated against
specific viruses developed a specific autoimmune disease, bearing in mind that association alone
does not necessarily indicate causality.” Id. (emphasis in original).

        Dr. Matloubian testified that it is significant that RA patients are still encouraged to get
flu vaccines. Tr. 288:1. He explained that “people who have [RA] are generally on
immunosuppressive medication, so if they get the actual [flu] infection, they have a higher risk
of having really bad outcomes.” Tr. 288:5–8. Dr. Matloubian concluded that “the rheumatology
community and the medical community [do] not think that influenza vaccine is a risk for RA
patients.” Tr. 288:11–13.

       During his testimony, Dr. Matloubian also opined that “most autoimmune diseases are
not associated with infections.” Tr. 255:1–2. He explained that some autoimmune diseases are

71
   Paula Ray et al., Risk of Rheumatoid Arthritis Following Vaccination with Tetanus, Influenza, and
Hepatitis B Vaccines Among Persons 15–59 Years of Age, VACCINE 29:6592–97 (2011).
72
   Camilla Bengtsson et al., Common Vaccinations Among Adults Do Not Increase the Risk of Developing
Rheumatoid Arthritis: Results From the Swedish EIRA Study, ANN. RHEUM. DIS. 69:1831–33 (2010).
73
   D.P.M. Symmons & K. Chakravarty, Can Immunization Trigger Rheumatoid Arthritis?, ANNALS OF
THE RHEUMATIC DISEASES 52:843–44 (1993).
74
   Ami Schattner, Consequence or Coincidence? The Occurrence, Pathogenesis and Significance of
Autoimmune Manifestations After Viral Vaccines, VACCINE 23:3879–86 (2005).
                                                27
“single-gene mutation” diseases that do not need a trigger and “tend to happen earlier in life.”
Tr. 255:3–5. He also provided examples of autoimmune diseases “associated with infection,
such as psoriasis.” Tr. 255:6–7. RA is not considered to be a post infectious disease, although
Dr. Matloubian clarified that there is such a thing as post infectious inflammatory arthritis. Tr.
255:20–256:1. He testified that these “disappear after two-four weeks, and they don’t go on to
become autoimmune arthritis . . . in the most part.” Tr. 256:12–14.
         Dr. Matloubian discussed case reports of RA following an influenza vaccination. He
stated that the relationship is entirely based on timing. “They don’t really talk about causation or
mechanistic relationships.” Tr. 292:14–15. Dr. Matloubian strongly objected to Dr. Utz’s
molecular mimicry causation theory. He conceded that molecular mimicry has been established
as mechanism for other autoimmune diseases such as “rheumatic fever happening after Group A
streptococcus infection and for Guillain-Barré, happening after campylobacter jejuni.” Tr.
258:21–23. In both those cases, Dr. Matloubian explained, “the same T cells see the pathogen-
specific peptide and the self-peptide, then that T cell is called cross-reactive, because it can
cross-react between those two, and that’s the basis of molecular mimicry is that the T cell sees
them as the same.” Tr. 259:21–25. Dr. Matloubian emphasized that it is not enough for the T
cell to see them both; the T cell must see them as the same thing. Tr. 260:7–22. He stated there
have been many examples of “sequence homology, but when they test it out, it do[es not] pan out
as either activating the T cells being cross-reactive or causing disease.” Tr. 260:18–20.

        Dr. Matloubian described Dr. Utz’s theory of “molecular mimicry between the influenza
hemagglutinin, or HA and collagen, which is an antigen in [RA], [stating] the vaccine-activated
influenza-specific T cells, [] then cross reacted with self-collagen and caused, allegedly, [RA].”
Tr. 266:25–267:4. Dr. Matloubian identified this as an oversimplification of molecular mimicry
and testified about the “Characteristics of Peptide-MHC Molecule Interactions”75 to describe
“how a peptide binds to an MHC or HLA molecule.” Tr. 268:21–23. Dr. Matloubian testified
that “each of us have six MHCs, and they’re different from each other.” Tr. 269:16–17. He
explained that when an individual is infected with influenza, MHCs will present peptides derived
from the pathogen so they can bind to them. Every person’s immune system creates their own
peptides, and although “the peptides that bind to MHC molecules share structural features that
promote this interaction,” each person has different peptides created by that person’s immune
system. Tr. 270:3–5. Furthermore, “[t]he residues of a peptide that bind to the MHC molecules
are distinct from those recognized by T cells.” Tr. 270:15–16. Ultimately, Dr. Matloubian
explained that “the peptide has these anchor residues that fit in the pocket of MHC.” Tr. 271:1–
2. He continued, “they bind to the MHC, but what the T cell sees . . . is on top of the peptide and
very different from the contact residues that allow the peptide to bind to the MHC.” Tr. 271:2–5.

       Using Dr. Utz’s analogy, Dr. Matloubian stated that all the peptides have the same
hotdog structure to sit in the MHC molecule bun, but the T cells only care about what
condiments are on the hot dog and not the hotdog or the bun. Tr. 272:10–17. Dr. Matloubian

75
 A.K. ABBAS ET AL., Chapter 6: Antigen Presentation to T Lymphocytes and the Functions of Major
Histocompatibility Complex Molecules, in CELLULAR AND MOLECULAR IMMUNOLOGY (9th ed. 2018).
                                                28
criticized the literature that Dr. Utz filed stating there are no data to suggest “that just because the
peptides have the same conformation, meaning that they bind, they fit in that peptide groove, that
means that the same T cell receptor can see them both.” Tr. 277:20–24. Dr. Matloubian asserted
that “in vitro phenomena do[ ] not necessarily translate to causing a disease in a human.” Tr.
261:24–25. He continued, that cross-reacting antibodies in tissue culture does not mean that
inside the body those cells “cause tissue damage and cause disease.” Tr. 262:4–6. Dr.
Matloubian concluded that “[t]he only thing that Dr. Utz showed in those papers is that collagen
and hemagglutinin [ ] can bind to DR4, and that by itself doesn’t mean that the same T cell
receptor can see both antigens.” Tr. 273:7–11

        Dr. Matloubian admitted on cross-examination that other individuals who are considered
experts in this field have hypothesized that molecular mimicry could be the basis of a causal
relationship between infectious agents and RA. Tr. 304:20.

        Dr. Matloubian was also asked about his assertion that Petitioner did not exhibit any
evidence of inflammatory arthritis prior to her swollen knee. Tr. 315:12–13. He conceded that
she complained of swelling in her extremities but categorized the complaint as an isolated wrist
injury attributed to acute trauma. Tr. 316:3–6. When asked whether the prednisone treatment is
evidence that her treater was concerned about inflammation, Dr. Matloubian stated, “whoever is
prescribing it thought that the person must have had inflammation at one point.” Tr. 318:6–8.

IV.    The Applicable Legal Standard

        To receive compensation under the Vaccine Act, Petitioner must demonstrate either that:
(1) she suffered a “Table Injury” – i.e., an injury falling within the Vaccine Injury Table –
corresponding to the vaccine in question within the time frame prescribed by the Vaccine Injury
Table set forth at § 14, as amended by 42 C.F.R. § 100.3; or (2) that her illness is an “off-Table
Injury,” one not listed on the Table, that resulted from her receipt of a covered vaccine. See §
11(c)(1)(C); Moberly v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1321 (Fed. Cir. 2010);
Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1319–20 (Fed. Cir. 2006).
Petitioner does not assert a Table claim. Thus, it must be proven that her vaccine was the cause-
in-fact of her injury.

        To establish causation-in-fact, Petitioner must demonstrate by a preponderance of the
evidence that the vaccines were the cause of her injury. § 13(a)(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
& Human Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). 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 1321–22 (quoting Shyface v. Sec’y of Health & Human
Servs., 165 F.3d 1344, 1352–53 (Fed. Cir. 1999)). The vaccine received, however, need not be
the predominant cause of the injury. Shyface, 165 F.3d at 1351.

                                                  29
         A petitioner may not receive a Vaccine Program award based solely on her assertions;
rather, the petition must be supported by either medical records or by the opinion of a competent
physician. Section 13(a)(1). In Althen v. Sec’y of Health & Human Servs., the Federal Circuit set
forth a three-pronged test used to determine whether a petitioner has established a causal link
between a vaccine and the claimed injury. See 418 F.3d 1274, 1278 (Fed. Cir. 2005). The
Althen test requires a petitioner to set forth: “(1) a medical theory causally connecting the
vaccination and the injury; (2) a logical sequence of cause and effect showing that the
vaccination was the reason for the injury; and (3) a showing of a proximate temporal relationship
between vaccination and injury.” Id. To establish entitlement to compensation under the
Program, a petitioner is required to establish each of the three prongs of Althen by a
preponderance of the evidence. See id. (internal citations omitted).

         Specifically, under the first prong of Althen, a petitioner must offer a scientific or medical
theory that answers in the affirmative the question “can [the] vaccine(s) at issue cause the type of
injury alleged?” See Pafford v. Sec’y of Health & Human Servs., No. 01-0165V, 2004 WL
1717359, at *4 (Fed. Cl. Spec. Mstr. July 16, 2004), aff’d, 64 Fed. Cl. 19 (2005), aff’d, 451 F.3d
1352 (Fed. Cir. 2006). This may be accomplished in a number of ways. “Reliability and
plausibility of . . . pathogenesis can be bolstered by providing evidence that at least a sufficient
minority in the medical community has accepted the theory, so as to render it credible.” Id.
Additionally, “epidemiological studies and an expert’s experience, while not dispositive, lend
significant credence to the claim of plausibility.” Id. Medical literature published in respected
medical journals is also persuasive. Id. “However, publication ‘does not necessarily correlate
with reliability,’ because ‘in some instances well-grounded but innovative theories will not have
been published.’” Id. (quoting Daubert v. Merrell Dow Pharm., Inc., 509 U.S. 579, 593–94
(1993) (emphasis in original)). Furthermore, a petitioner is not required to present medical
literature or epidemiological studies to prove her burden. Grant v. Sec’y of Health and Human
Servs., 956 F.2d 1144, 1149 (Fed. Cir. 1992); Andreu v. Sec’y Health & Human Servs., 569 F.3d
1367, 1380 (Fed. Cir. 2009). However, to the extent medical literature and epidemiological
studies are provided, these are subject to critique by Respondent’s experts, and the special master
will consider them when deciding whether the petitioner has met her burden of proof. 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. But this
does not negate or reduce a petitioner’s ultimate burden to establish his overall entitlement to
damages by preponderant evidence. W.C. v. Sec’y of Health & Human Servs., 704 F.3d 1352,
1356 (Fed. Cir. 2013) (citations omitted).

        In addition to showing that the vaccine at issue can cause a particular injury, a petitioner
must also, under Althen’s second prong, prove that the vaccine actually did cause the alleged
injury in her particular case. See Pafford, 2004 WL 1717359, at *4; Althen, 418 F.3d at 1278. A
petitioner does not meet this obligation by showing only a temporal association between the
vaccination and the injury; the petitioner “must explain how and why the injury occurred.”
Pafford, 2004 WL 1717359, at *4 (emphasis in original) (internal citations omitted). Ruling out
other potential causes is an important element but does not itself establish causation. Id.
Additionally, conjecture or speculation does not meet the preponderance standard. Id.

                                                  30
        Although a temporal association alone is insufficient to establish causation, under the
third prong of Althen, a petitioner must show that the timing of the injury fits with the causal
theory. See Althen, 418 F.3d at 1278. The special master cannot infer causation from temporal
proximity alone. See Thibaudeau v. Sec’y of Health & Human Servs., 24 Cl. Ct. 400, 403–04
(Fed. Cl. Oct. 23, 1991); see also Grant, 956 F.2d at 1148 (“‘[T]he inoculation is not the cause of
every event that occurs within the ten[-]day period. . . . Without more, this proximate temporal
relationship will not support a finding of causation.’” (quoting Hasler v. United States, 718 F.2d
202, 205 (6th Cir. 1983))). 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 & Human
Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what is a medically acceptable
timeframe must also coincide 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 & Human Servs., 101
Fed. Cl. 532, 542 (2011), recons. den’d after remand, 105 Fed. Cl. 353 (2012), aff’d mem., 2013
WL 1896173 (Fed. Cir. 2013); Koehn v. Sec’y of Health & Human Servs., No. 11-355V, 2013
WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for review den’d (Fed. Cl. Dec. 3, 2013),
aff’d, 773 F.3d 1239 (Fed. Cir. 2014).

        Petitioners who demonstrate by a preponderance of the evidence that they suffered an
injury caused by vaccination are entitled to compensation, unless Respondent can demonstrate
by a preponderance of the evidence that the injury was caused by factors unrelated to the
vaccination. See Althen, 418 F.3d at 1278; Paluck v. Sec’y of Health & Human Servs., 786 F.3d
1373, 1386 (Fed. Cir. 2015) (citing de Bazan v. Sec’y of Health & Human Servs., 539 F.3d 1347,
1352 (Fed. Cir. 2008) (holding that it is not a petitioner’s burden “to rule out possible alternative
causes” (internal citations omitted))); Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543,
547 (Fed. Cir. 1994).

         Respondent frequently offers experts 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 &
Human Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (internal citations omitted). 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 &
Human 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”).

       Both parties filed medical and scientific literature in this case, but not every filed item
was probative to the outcome of this decision. While I have reviewed all of 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 & Human Servs., 844 F.3d 1322, 1328 (Fed.
Cir. Apr. 6, 2016) (“[w]e generally presume that a special master considered the relevant record

                                                 31
evidence even though he does not explicitly reference such evidence in his decision”) (citation
omitted); see also Paterek v. Sec’y of Health & Human Servs., 527 F. App'x 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”).

V.     Analysis

       A.      Experts

        Petitioner’s expert Dr. Utz and Respondent’s expert Dr. Matloubian both have a
background in rheumatology. Dr. Utz was board certified for many years up until recently,
whereas Dr. Matloubian maintains his certification. Although Dr. Utz does not regularly see
patients, it is clear from his testimony that he is well versed in the symptomology and diagnostics
of RA.

       Drs. Utz and Matloubian were also admitted as experts in immunology due to work each
has done in academic and research settings. Dr. Utz articulated a molecular mimicry causation
theory. His work in vaccine development qualifies him to assert such a theory. Dr.
Matloubian’s research on the innate and adaptive responses of the immune system to acute and
chronic infections provides credibility to his criticisms of Dr. Utz’s theory. Despite their
uncontested qualifications, there is little that the experts agree on outside of Petitioner’s ultimate
diagnosis.

       B.      Althen prong one

        In his report, Dr. Utz initially identified several different mechanisms, one or more of
which could be a contributor to his proposed causation theory. This is problematic because to
satisfy prong two of Althen, there must be a medical theory presented that can be applied to
Petitioner’s case to show a logical sequence of cause and effect between Petitioner’s vaccination
and injury. Practically, it is difficult to apply a theory to a fact pattern if the theory is non-
specific. Dr. Utz wrote that Petitioner’s injury may have occurred “through molecular mimicry,
formation of immune complexes, cross-priming, or a combination of these.” Pet’r’s Ex. 17 at 14.
Dr. Utz testified that molecular mimicry was the primary mechanism that he put forward,
although he added that “others that could have also been involved included things such as
bystander activation of T cells and B cells.” Tr. 66:9–12. Alternatives notwithstanding, Dr. Utz
focused almost exclusively on molecular mimicry in his writings and testimony. Consequently,
that was also the focus of Dr. Matloubian’s response. Dr. Utz did not explain how any of these
additional mechanisms could combine with molecular mimicry in a case involving the flu
vaccine and RA. He also did not explain how it would be possible to determine which, if any, of
these various mechanisms would be applicable to Petitioner’s case. Dr. Utz’s inability to
unequivocally identify his theory of causation (with or without identifying the specifics of the
mechanism) undercuts his assertation that his opinion meets the more likely than not standard.
This kitchen-sink approach is overbroad and vague. Because of the lack of evidence provided
with respect to the other theories, I find that there has not been persuasive evidence to support
any of them by a more likely than not standard. Therefore, I will focus solely on his theory of
molecular mimicry.

                                                  32
         Drs. Utz and Matloubian agreed that RA is an autoimmune, anti-inflammatory disease.
They also agreed that molecular mimicry can be a reliable causation theory for some
autoimmune diseases. They disagree whether RA could have a molecular mimicry pathogenesis
if the etiology is not infectious. Dr. Utz never directly addressed whether he believes a disease
has to be post infectious for molecular mimicry to apply. He did, however, state in his
supplemental report that he has “taken the position repeatedly, in all non-adjuvanted vaccine
cases in which [he] ha[s] served as an expert, that molecular mimicry is a valid hypothesis,
noting that [it] cannot be proven in humans.” Pet’r’s Ex. 44 at 6. This suggests that the etiology
of a condition is irrelevant to his assessment of whether molecular mimicry can apply. Dr. Utz
asserted that in RA cases, a susceptible individual can be triggered by the immune system’s
repeated exposure to certain influenza peptides, whether from the wild virus or vaccinations. He
does not clarify if exposure to the wild virus is needed, or if multiple vaccinations will suffice.
This argument implies that RA could be post infectious, because the HA peptide at the heart of
his theory is present in the virus and the vaccine. It is unclear how Dr. Utz would articulate his
molecular mimicry theory in a case that clearly involves a non-infectious disease, but that
question need not be answered here. Dr. Utz argued that in a case such as Petitioner’s,
vaccination could cause the immune response necessary to trigger autoimmunity without
infection because most adults have been exposed previously to the flu several times through prior
vaccinations or infection. Dr. Matloubian was more definitive. He testified that molecular
mimicry is “not necessarily an explanation for all kinds of autoimmune disease, especially those
that are not associated with infection.” Tr. 259:8–10. Furthermore, Dr. Matloubian testified that
RA is not post infectious, and the flu virus has not been identified as a trigger for RA. Dr.
Matloubian asserted that Dr. Utz could not provide any literature that RA has been linked to
influenza, however, there is evidence that other rheumatological conditions and autoimmune
diseases have been linked, in rare cases, to influenza. Dr. Matloubian embraced this evidence to
argue that these same links should be seen in RA cases but are not. Dr. Matloubian wrote, “[t]he
fact that development of an autoimmune inflammatory arthritis after an influenza infection has
not been described strongly argues against Dr. Utz’s molecular mimicry theory,” particularly
when this same condition “has been described to occur after much rarer viral infections, such as
Chikungunya virus.” Resp’t’s Ex. UU at 8.

        Dr. Matloubian is correct that Petitioner has not presented any publications to support his
contention. However, in the vaccine program, the lack of studies is not probative evidence that a
theory should be discounted. This is largely due to the rare nature of most of the alleged vaccine
injuries and the improbability or impossibility that properly controlled studies could be
conducted. Dr. Matloubian’s reliance on the Chikungunya virus does identify an instance
wherein the actual increase in the occurrence of such a rare disease generates statistical
abnormalities sufficient to infer causation. However, RA is not quite as rare. In cases where the
alleged condition is rare, but not unheard of, a small absolute increase in the number of patients
may not generate a statistically significant percentage increase for researches. This does not
disprove causation for the rare case.

        Furthermore, Respondent has provided no study that definitively disproves Dr. Utz’s
assertion. There have been some large-scale studies that resulted from researchers and experts
identifying multiple case reports linking a particular vaccine to a type of illness. These studies

                                                 33
have been used to establish causation in some cases and negate it in others. Dr. Matloubian
conceded that the flu vaccine has been causally linked to other autoimmune diseases and
arthralgias. Tr. 258:21–23; Tr. 306:11. He also noted that case reports have linked
inflammatory arthritis to the flu. Tr. 308:16–18. Dr. Matloubian went further on cross-
examination, “[activation of the immune system through vaccination] was postulated as a
mechanism, a risk factor in contributing to – on top of the other risk factors to RA . . .” Tr.
305:23–306:8. Dr. Utz has identified molecular mimicry as a potential mechanism for the flu
vaccine to cause RA that has been considered in the field, but not sufficiently tested for the
literature to be dispositive.

        The experts agreed that RA patients should be vaccinated against the flu, and Dr.
Matloubian argued that this is further evidence that the vaccine is not a factor in the development
or progression of RA. The recommendation that RA patients are vaccinated is also consistent
with the Bengtsson et al. study’s conclusions that “it is unlikely that vaccinations in general
should be considered as a major risk factor for RA” and “active immunisation does not increase
the risk of RA in individuals with major risk factors.” Resp’t’s Ex. C at 9; Resp’t’s Ex. B at 5.
Although the lack of corroborative studies cannot be the basis to discount a proposed theory,
Respondent has relied on a persuasive study that shows the greater rheumatology community
found no increased risk for development of RA in individuals with risk factors post vaccination.
That does not mean, however, that Petitioner’s theory could not occur in a given case. Vaccine-
caused injuries are rare by definition, and usually the exception to the rule.

        Respondent’s main argument attacks the specific peptides that Dr. Utz identified for
cross-reactivity. In the spirit of the program, “to require identification and proof of specific
biological mechanisms would be inconsistent with the purpose and nature of the vaccine
compensation program.” Knudsen, 35 F.3d at 549. Petitioners are tasked, however, with
presenting a “sequence of cause and effect [that] is logical and legally probable.” Id. at 548–59.
In other words, to the extent that petitioners do present a specific biological mechanism, it must
make sense. Other cases in the program where petitioners’ expert unsuccessfully identified the
relevant proteins and affected body systems have failed because the disease pathogenesis was not
consistent with the identified immune response. See Jewell v. Sec’y of Health and Human
Servs., No. 11-138V, 2016 WL 5404165 (Fed. Cl. Spec. Mstr. Aug. 29, 2015) (petitioners failed
to prove that cytokine activity is capable of impacting the brain’s 5-HT system in the ways
proposed by petitioners’ experts); see also Dougherty v. Sec’y of Health and Human Servs., No.
15-1333V, 2018 WL 3989519 (Fed. Cl. Spec. Mstr. July 5, 2018) (petitioner failed to provide
evidence that antibodies reacting to hypocretin-2 receptors would only damage these receptors if
located in a limited region in the brain, despite their widespread presence in other regions of the
body).

        In the present case, Dr. Utz identified a specific viral antigen that is present in the flu
vaccine, HA, and explained how it can bind to DR4. He then identified the human autoantigen
collagen that can also bind to DR4 with a similar structure to HA. Dr. Matloubian agreed that
both peptides bind to DR4 but did not agree that cross-reactivity would occur or that disease
would be the result. Drs. Utz and Matloubian both explained how the T cell receptors reacted to
peptides with similar homology. Dr. Utz provided literature in an attempt to show that despite an
inability to definitively prove it, other experts believed the similarity between the two peptides

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suggested that the peptide found in the vaccine could be misinterpreted as the autoantigen found
in RA patients. Dr. Matloubian countered that Dr. Utz’s theory is improbable without evidence
“that the T cells that can cause [RA] can recognize and be activated by both antigen that is
derived from that vaccine, as well as antigens that are . . . related to that disease.” Tr. 309:5–7
(emphasis added). Dr. Matloubian stated that one of the papers Dr. Utz relied on undercut his
theory because the authors found “when HA binds to HLA-DR4, because of the interactions with
it, the whole molecule looks different than when collagen binds to HLA-DR4.” Tr. 275:15–17.

          Dr. Utz’s assertion that this cross-reaction occurs and induces RA has not been
established by medical literature, but again, that is not the standard in the vaccine program. The
difficulty in determining the viability of a theory that is novel or rarely applicable highlights the
unknown etiology of many conditions seen in the program. Dr. Utz has been able to identify a
peptide that is an autoantigen in RA and similar in composition to another peptide that is found
in the flu virus and vaccine. Because of his specificity, it is possible to better understand that the
respective roles of these peptides during immune system response and in the pathogenesis of RA
are consistent with cross-reactivation. Whether Dr. Utz’s theory is applicable to Petitioner’s case
turns on his assertions that: (1) she was not preclinical, (2) vaccination is a necessary trigger, and
(3) the timeframe for symptom onset was appropriate. That analysis will be done pursuant to
prong two. Generally, Dr. Utz has presented a theory that explains how seropositive RA could
develop in an individual with environmental and genetic risk factors, who was otherwise
asymptomatic.

        It should be noted that Petitioner did not submit a significant aggravation claim in this
case. Dr. Utz did not argue that Petitioner’s vaccination hastened her development of RA. In
fact, Dr. Utz took issue with Dr. Matloubian’s assertion that Petitioner suffered from preclinical
RA. He stated, “[i]t is misleading to think that all asymptomatic individuals with abnormal
cytokines levels or positive CCP antibodies develop RA.” Pet’r’s Ex. 25 at 4. Dr. Utz asserted
that Dr. Matloubian took Dr. Deane’s study out of context and noted that “the EULAR
recommendations also noted that an individual should not be classified as having ‘preclinical’
RA unless they later develop clinical disease.” Id. at 6. Dr. Utz stated that Dr. Deanne also
“note[d] that the naming of different stages of disease development is also controversial.” Id.
Dr. Utz quoted the authors’ inability to conclude “whether smoking is an initial trigger for
autoimmunity and/or a propagating factor, or even perhaps a permissive factor for some other
aetiologic agent such as a bacterial organism.” Id. He wrote, “experts . . . are actively
contemplating the possibility that bacterial triggers, and by inference vaccines, viruses, drugs,
and other environmental triggers, play a role in RA. Id. Dr. Utz’s theory is considered in the
context of someone “free from any sort of persistent or recurring polyarticular joint symptoms”
that post vaccination, “developed new onset, seropositive, RA.” Pet’r’s Ex. 17 at 14–15. By a
preponderance of the evidence, Petitioner’s theory of molecular mimicry does explain how the
flu vaccine could in fact cause the development of RA.

       C.      Althen prong two

        Although Dr. Utz set out a detailed causation theory, he provided no evidence to link his
theory to Petitioner’s case. Dr. Utz set out in the conclusion of his final report to apply the facts
in Petitioner’s case to his causation theory. He wrote, “Petitioner was free from any sort of . . .

                                                 35
symptoms.” Pet’r’s Ex. 44 at 12. He continued that “[a]lthough she was a smoker, this is not a
trigger;” therefore, “[t]he only environmental trigger [he] could identify was the influenza
vaccine.” Id. Dr. Utz wrote in his report that “Dr. Matloubian’s argument supports [his]
argument that Petitioner had a genetic predisposition to develop RA.” Pet’r’s Ex. 25 at 3. He
later testified that Petitioner was probably DR4 positive. However, he did not discuss what
evidence there is of such in her family’s history or her medical record. Instead, it appears that he
begins with that conclusion and then argues there is no other explanation. Additionally, Dr. Utz
did not discuss any evidence that Petitioner was suffering from an acute immune system
response to the flu vaccine. He noted that she suffered from immediate shoulder pain, but he
was unclear whether her pain resulted from the mechanics of the vaccine administration; and, it
is unlikely given the timing that her pain resulted from the onset of her autoimmunity. Dr. Utz
agreed with Dr. Matloubian’s assertion that “seminal studies [have shown] that autoantibodies
and abnormal levels of cytokines are found in blood of patients months or years before they
develop clinical RA.” Id. at 4. He continued, “[h]owever, it is misleading to think that all
asymptomatic individuals with abnormal cytokine levels or positive CCP antibodies develop
RA.” Id. Dr. Utz failed to mention at this point that Petitioner did develop RA. In fact, Dr. Utz
failed to provide a single example of an instance where clinical symptoms preceded the
development of CCP antibodies. He did admit, however, that “Petitioner’s course is not
atypical.” Id.

        Petitioner’s age, race, and gender placed her in a category of individuals with an
increased risk for RA. Her years of heavy smoking greatly exacerbated that risk and provided an
environmental trigger that both experts agreed is universally accepted in the rheumatological
community. Dr. Matloubian testified that it is also universally accepted in the rheumatology
community that patients present with clinical symptoms and are diagnosed with RA after a
significant amount of time with asymptomatic autoimmunity. Dr. Utz agreed. Furthermore, Dr.
Utz presented no evidence that Petitioner experienced symptoms consistent with an immune
system reaction to a trigger after years of environmental factors and previous exposure to the flu
virus or vaccine. Dr. Utz did not present evidence that other “triggers” had been identified to
analogize to Petitioner’s vaccination. In fact, both experts agreed that the etiology of RA was
unknown. Petitioner’s expert focused on her antibody testing to establish the vaccine as a
trigger; however, he admitted there is no way to know whether Petitioner became anti-CCP
positive before or after vaccination. He also admitted that Petitioner’s RF test was not the best
indicator of RA autoimmunity.

         As a final note to be discussed more thoroughly pursuant to prong three, Petitioner’s
self-described timing of symptom onset supports Respondent’s contention that Petitioner was
anti-CCP positive before vaccination. Also, Dr. Utz did not provide a persuasive explanation for
how Petitioner’s clinical symptoms could manifest one day after her vaccination if molecular
mimicry had to occur following the body’s recognition of the relevant peptide in the vaccine. In
contrast, if Respondent’s expert correctly identified Petitioner’s symptom onset, Petitioner would
not have experienced her first sign of inflammation until six months post vaccination. Either
way, the development of Petitioner’s symptoms does not support the application of molecular
mimicry to Petitioner’s case.

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       D.      Althen prong three

        In his report, Dr. Utz stated that Petitioner’s symptoms began one day post vaccination,
on October 20, 2013, with soreness in her shoulders. Pet’r’s Ex. 17 at 3. He later testified that
she “was really struggling the first three days, but then the three to six days.” Tr. 66:2. On
cross-examination, Dr. Utz committed to onset at day three. Tr. 155:12. During re-direct, Dr.
Utz stated that Petitioner “had her first evidence of inflammatory arthritis within the first
[thirteen] or so days after her vaccination.” Tr. 338:17–19. When I asked Dr. Utz about the
onset of Petitioner’s symptoms after all his previously quoted testimony, Dr. Utz stated that
Petitioner’s symptoms began with shoulder pain on the day of vaccination. Tr. 361:23–24. Dr.
Utz was then asked whether the shoulder pain was due to the administration of the vaccine or the
beginning of autoimmunity. His answer was unclear. Tr. 363:2–364:11. Ultimately, Dr. Utz
stated that he [did not] remember if it’s within one day or three days, but it’s – it’s pretty quick.”
Tr. 364:9–10. When asked whether a three-day onset is significant for his causation theory when
compared to a one-day onset, Dr. Utz answered that it is not. Tr. 365:7.

        On every occasion that Dr. Utz was asked to clarify Petitioner’s onset of symptoms, his
response changed. A causation theory that is based on molecular mimicry requires the
involvement of the adaptive immune process. There was no literature filed or testimony
provided to suggest that cross-reactivity can occur and autoimmunity can develop within twenty-
four hours of exposure to the foreign antigen. Dr. Utz attempted to address varying onset dates
in his report, stating, “[i]t is likely in [Petitioner’s] case that this is a classic example of memory
immune response, in which preexisting memory B and T cell were activated by the vaccine.”
Pet’r’s Ex. 17 at 11. He goes on to describe this as “[d]isease triggering [that] may have
occurred secondary to formation of immune complexes . . . .” Id. Dr. Utz introduced several
new mechanisms at this point in his report, but they are not further explained in subsequent
writing or testimony. The connection, if any, between molecular mimicry and these immune
complexes is never made. Furthermore, Dr. Utz described these phenomena as “scientifically
plausible,” which is not the standard for the vaccine program. This secondary explanation for
the timing of Petitioner’s symptom onset lacks development and is inconsistent with Petitioner’s
main theory of molecular mimicry.

        Dr. Matloubian testified that Petitioner first exhibited symptoms of RA “when she saw
Dr. Gharda on April 3, 2014, and she documented right knee was swollen and warm.” Tr.
248:6–9. He explained that RA is an autoinflammatory disease, meaning the inflammation
results from the autoantibody production. Both experts agree that there is no way to know
whether Petitioner was anti-CCP positive prior to her test in April of 2014. They agree that in
clinical practice, patients often test anti-CCP positive prior to testing positive for RF. Tr.
154:20–21; Tr. 235:18–21. They also agree that anti-CCP testing is more specific for RA than
RF. Tr. 154:5–8; Tr. 233:23–24.

         Based on the testimony of both experts regarding the development of RA, as well as the
literature filed, it is more likely than not that Petitioner’s symptoms could have only developed
after she experienced autoimmunity. Although Petitioner was not tested for autoantibodies prior
to her vaccination, the testimony and literature illustrate her progression from genetic risk at
birth, to smoking for several years, to the development of autoimmunity over time, and finally to

                                                  37
the manifestation of symptoms. The timing proposed by Petitioner’s expert was inconsistent and
too short to reflect an appropriate temporal relationship for Petitioner’s RA to be caused by
molecular mimicry. Furthermore, Dr. Matloubian’s assertion that Petitioner’s symptoms
manifested six months post vaccination is too long for molecular mimicry to be the cause.
Petitioner does not meet her burden under either reading of the facts.

VI.     Conclusion

        After a review of the record, including Petitioner’s medical records, personal statements,
expert reports, accompanying literature, and testimony, Petitioner has not proven it is more likely
than not that she suffered from a vaccine-caused injury. Petitioner’s expert focused on molecular
mimicry but identified bystander activation, immune complexes, and others as plausible
explanations. Petitioner failed to establish it is more likely than not that her flu vaccination
triggered any autoimmune response that lead to her development of RA. Additionally, the onset
of her symptoms was muddled by her expert, and his last attempt at clarification under my
questioning revealed a temporal relationship that would not be appropriate based on a molecular
mimicry theory. Therefore, Petitioner has not satisfied her burden under Althen. There is no
question about Petitioner’s diagnosis of RA, and I reviewed the entire record in order to make a
determination whether Petitioner’s condition was a result of her vaccination. I could not
conclude that it was. Petitioner’s claim is hereby DENIED.

       In the absence of a timely filed motion for review filed pursuant to Vaccine Rule 23, the
Clerk of Court is directed to ENTER JUDGMENT consistent with this decision.76

        IT IS SO ORDERED.

                                                  s/Herbrina D. Sanders
                                                  Herbrina D. Sanders
                                                  Special Master

76
  Pursuant to Vaccine Rule 11(a), entry of judgment is expedited by the parties’ joint filing of a notice
renouncing the right to seek review.
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