VICP Registry Case Source Bundle
Canonical URL: https://vicp-registry.org/case/USCOURTS-cofc-1_17-vv-01475
Package ID: USCOURTS-cofc-1_17-vv-01475
Petitioner: Katherine Kelly
Filed: 2017-10-10
Decided: 2022-11-07
Vaccine: influenza
Vaccination date: 2016-09-30
Condition: polymyalgia rheumatica
Outcome: dismissed
Award amount USD: 

AI-assisted case summary:
Katherine Kelly, a 73-year-old woman, filed a petition on October 10, 2017, alleging that an influenza vaccine received on September 30, 2016, caused her to develop polymyalgia rheumatica (PMR). Petitioner's initial symptoms of fever and joint pain appeared approximately two weeks after vaccination. Her treating physician, Dr. Bransdorf, diagnosed her with PMR and noted improvement with prednisone. The case proceeded as an off-Table claim, requiring Ms. Kelly to prove causation-in-fact. Petitioner presented expert testimony from rheumatologist Thomas Zizic, M.D., who proposed molecular mimicry as a theory of causation, suggesting the flu vaccine's hemagglutinin could cross-react with self-antigens like collagen. Dr. Zizic also noted similarities between PMR and giant cell arteritis (GCA) and cited case reports linking PMR and GCA to the flu vaccine. Respondent, the Secretary of Health and Human Services, presented expert testimony from immunologist and rheumatologist Mehrdad Matloubian, M.D., Ph.D. Dr. Matloubian argued that the pathogenesis of PMR is unknown, no specific antigens have been identified, and molecular mimicry is speculative. He critiqued the literature cited by Dr. Zizic, noting that collagen is not a recognized self-antigen in PMR and that the cited studies did not support molecular mimicry. Dr. Matloubian also pointed out that PMR primarily affects the elderly due to aging immune systems and that the case reports cited by Dr. Zizic were either irrelevant due to different types of vasculitis or showed only a temporal association without establishing causality. Special Master Daniel T. Horner found that Ms. Kelly failed to establish a reputable medical theory of causation (Althen prong one), a logical sequence of cause and effect (Althen prong two), or a proximate temporal relationship (Althen prong three). The Special Master concluded that Dr. Zizic's theory of molecular mimicry was not supported by sound and reliable scientific explanation, particularly regarding the link between the flu vaccine, collagen, and PMR, and that the case reports did not establish causality. The Special Master also found that the treating physicians' initial notes suggesting a possible vaccine reaction did not establish causation for PMR, and that the temporal association between the vaccination and the onset of PMR symptoms was likely coincidental given the idiopathic nature of PMR and the petitioner's age. Consequently, the Special Master determined that Ms. Kelly's PMR was idiopathic rather than vaccine-induced. The petition was denied and dismissed.

Theory of causation field:
Petitioner Katherine Kelly, age 73, received an influenza vaccine on September 30, 2016, and subsequently developed polymyalgia rheumatica (PMR). Petitioner's expert, Thomas Zizic, M.D., proposed molecular mimicry as the causation theory, suggesting influenza vaccine antigens (hemagglutinin) could cross-react with self-antigens (collagen) in genetically susceptible individuals, leading to cell-mediated autoimmune disease. Dr. Zizic also posited PMR and GCA are manifestations of the same disease process and cited case reports linking flu vaccines to PMR/GCA. Respondent's expert, Mehrdad Matloubian, M.D., Ph.D., argued PMR's pathogenesis is unknown, lacks identified antigens, and molecular mimicry is speculative. Dr. Matloubian critiqued Dr. Zizic's reliance on specific studies (Dessen et al., Sun et al.), stating they did not support molecular mimicry or a structural similarity between hemagglutinin and collagen, and that collagen is not a recognized PMR self-antigen. Dr. Matloubian also noted PMR primarily affects the elderly due to aging immune systems and that case reports showed only temporal association or were irrelevant (ANCA-associated vasculitis). Special Master Daniel T. Horner found petitioner failed all three Althen prongs: (1) no reputable medical theory linking flu vaccine to PMR, as Dr. Zizic's molecular mimicry theory was speculative and lacked scientific support, and the GCA comparison was unpersuasive; (2) no logical sequence of cause and effect, as treating physicians' initial notes were insufficient and the temporal association was likely coincidental; (3) no proximate temporal relationship, as causation was not established. The petition was denied. Attorneys: Diana Stadelnikas for petitioner, Kyle Pozza for respondent. Decision Date: November 7, 2022.

Public staged source text:

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DOCUMENT 1: USCOURTS-cofc-1_17-vv-01475-0
Date issued/filed: 2022-11-07
Pages: 16
Docket text: PUBLIC DECISION (Originally filed: 10/12/2022) regarding 56 DECISION of Special Master. Signed by Special Master Daniel T. Horner. (amb) Service on parties made.
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Case 1:17-vv-01475-UNJ Document 60 Filed 11/07/22 Page 1 of 16
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 17-1475V
Filed: October 12, 2022
PUBLISHED
Special Master Horner
KATHERINE KELLY,
Petitioner,
Entitlement; influenza (“flu”)
v.
vaccine; polymyalgia
rheumatica (“PMR”); denial.
SECRETARY OF HEALTH AND
HUMAN SERVICES,
Respondent.
Diana Stadelnikas, Maglio Christopher and Toale, Sarasota, FL, for petitioner.
Kyle Pozza, U.S. Department of Justice, Washington, DC, for respondent.
DECISION1
On October 10, 2017, petitioner filed a petition under the National Childhood
Vaccine Injury Act, 42 U.S.C. § 300aa-10-34 (2012),2 alleging that the influenza (“flu”)
vaccine she received on September 30, 2016, caused her to develop polymyalgia
rheumatica (“PMR”). (ECF No. 1.) For the reasons set forth below, I conclude that
petitioner is not entitled to compensation for her PMR.
I. Applicable Statutory Scheme
Under the National Vaccine Injury Compensation Program, compensation
awards are made to individuals who have suffered injuries after receiving vaccines. In
general, to gain an award, a petitioner must make a number of factual demonstrations,
including showing that an individual received a vaccination covered by the statute;
1 Because this decision contains a reasoned explanation for the special master’s action in this case, it will
be posted on the United States Court of Federal Claims’ website in accordance with the E-Government
Act of 2002. See 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), petitioner has 14 days to identify and move to redact
medical or other information the disclosure of which would constitute an unwarranted invasion of privacy.
If the special master, upon review, agrees that the identified material fits within this definition, it will be
redacted from public access.
2 Within this decision, all citations to § 300aa will be the relevant sections of the Vaccine Act at 42 U.S.C.
§ 300aa-10-34.

Case 1:17-vv-01475-UNJ Document 60 Filed 11/07/22 Page 2 of 16
received it in the United States; suffered a serious, long-standing injury; and has
received no previous award or settlement on account of the injury. Finally – and the key
question in most cases under the Program – the petitioner must also establish a causal
link between the vaccination and the injury. In some cases, the petitioner may simply
demonstrate the occurrence of what has been called a “Table Injury.” That is, it may be
shown that the vaccine recipient suffered an injury of the type enumerated in the
“Vaccine Injury Table,” corresponding to the vaccination in question, within an
applicable time period following the vaccination also specified in the Table. If so, the
Table Injury is presumed to have been caused by the vaccination, and the petitioner is
automatically entitled to compensation, unless it is affirmatively shown that the injury
was caused by some factor other than the vaccination. § 300aa-13(a)(1)(A); § 300 aa-
11(c)(1)(C)(i); § 300aa-14(a); § 300aa-13(a)(1)(B).
In many cases, however, the vaccine recipient may have suffered an injury not of
the type covered in the Vaccine Injury Table. In such instances, an alternative means
exists to demonstrate entitlement to a Program award. That is, the petitioner may gain
an award by showing that the recipient’s injury was “caused-in-fact” by the vaccination
in question. § 300aa-13(a)(1)(B); § 300aa-11(c)(1)(C)(ii). In such a situation the
presumptions available under the Vaccine Injury Table are inoperative. The burden is
on the petitioner to introduce evidence demonstrating that the vaccination actually
caused the injury in question. Althen v. Sec’y of Health & Human Servs., 418 F.3d
1274, 1278 (Fed. Cir. 2005); Hines v. Sec’y of Health & Human Servs., 940 F.2d 1518,
1525 (Fed. Cir. 1991). Because PMR is not listed as an injury on the Vaccine Injury
Table, petitioner must satisfy this burden of proof.
The showing of “causation-in-fact” must satisfy the “preponderance of the
evidence” standard, the same standard ordinarily used in tort litigation. § 300aa-
13(a)(1)(A); see also Althen, 418 F.3d at 1279; Hines, 940 F.2d at 1525. Under that
standard, the petitioner must show that it is “more probable than not” that the
vaccination was the cause of the injury. Althen, 418 F.3d at 1279. The petitioner need
not show that the vaccination was the sole cause of the injury or condition, but must
demonstrate that the vaccination was at least a “substantial factor” in causing the
condition, and was a “but for” cause. Shyface v. Sec’y of Health & Human Servs., 165
F.3d 1344, 1352 (Fed. Cir. 1999). Thus, the petitioner must supply “proof of a logical
sequence of cause and effect showing that the vaccination was the reason for the
injury;” the logical sequence must be supported by “reputable medical or scientific
explanation, i.e., evidence in the form of scientific studies or expert medical testimony.”
Althen, 418 F.3d at 1278; Grant v. Sec’y of Health & Human Servs., 956 F.2d 1144,
1148 (Fed. Cir. 1992). A petitioner may not receive a Vaccine Program award based
solely on his or her assertions; rather, the petition must be supported by either medical
records or by the opinion of a competent physician. § 300aa-13(a)(1).
In what has become the predominant framing of this burden of proof, the Althen
court described the “causation-in-fact” standard, as follows:
2

Case 1:17-vv-01475-UNJ Document 60 Filed 11/07/22 Page 3 of 16
Concisely stated, Althen’s burden is to show by preponderant evidence
that the vaccination brought about her injury by providing: (1) a medical
theory causally connecting the vaccination and the injury; (2) a logical
sequence of cause and effect showing that the vaccination was the reason
for the injury; and (3) a showing of proximate temporal relationship
between vaccination and injury. If Althen satisfies this burden, she is
entitled to recover unless the [government] shows, also by a
preponderance of the evidence, that the injury was in fact caused by
factors unrelated to the vaccine.
Althen, 418 F.3d at 1278 (citations omitted). The Althen court noted that a petitioner
need not necessarily supply evidence from medical literature supporting petitioner’s
causation contention, so long as the petitioner supplies the medical opinion of an
expert. Id. at 1279-80. That expert’s opinion must be based upon “sound and reliable”
scientific explanation. Boatmon v. Sec’y of Health & Human Servs., 941 F.3d 1351,
1359 (Fed. Cir. 2019) (quoting Knudsen v. Sec’y of Health & Human Servs., 35 F.3d
543, 548-49 (Fed. Cir. 1994)). The Althen court also indicated that, in finding causation,
a Program factfinder may rely upon “circumstantial evidence,” which the court found to
be consistent with the “system created by Congress, in which close calls regarding
causation are resolved in favor of injured claimants.” 418 F.3d at 1280.
II. Procedural History
On October 10, 2017, petitioner filed her petition, alleging that the flu vaccine she
received on September 30, 2016, caused her to develop PMR. (ECF No. 1.) This case
was initially assigned to Special Master Millman. (ECF No. 6.) Petitioner subsequently
filed medical records in support of her claim on October 10, 2017, and March 16, 2018,
followed by a Statement of Completion on May 16, 2018. (ECF Nos. 7, 12, 14.) After
reviewing petitioner’s materials, respondent filed his Rule 4(c) report contesting
entitlement on July 25, 2018. (ECF No. 19.) Respondent argued that petitioner failed to
substantiate that her flu vaccine was the cause-in-fact of her PMR. (Id. at 5.)
In response to respondent’s Rule 4(c) report recommending against
compensation, petitioner filed a report from rheumatologist Thomas Zizic, M.D., on May
24, 2019. (ECF No. 28; Ex. 10.) The case was subsequently reassigned to my docket
on June 4, 2019. (ECF No. 32.) On September 3, 2019, respondent filed a responsive
report from immunologist and rheumatologist Mehrdad Matloubian, M.D., Ph.D. (ECF
No. 34; Ex. A.) Petitioner then submitted a supplemental report from Dr. Zizic on May 6,
2020. (ECF No. 42; Ex. 40.) The expert report stage concluded with respondent’s filing
of an additional report from Dr. Matloubian on August 17, 2020. (ECF No. 44; Ex. C.)
On November 17, 2020, the parties indicated that the case was ripe for an
entitlement determination. (ECF No. 47.) Petitioner proposed filing a motion for a ruling
on the written record. (Id.) On May 3, 2021, petitioner filed her motion for a ruling on
the written record and accompanying memorandum. (ECF No. 50.) Respondent filed
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his responsive memorandum on September 29, 2021. (ECF No. 54.) Petitioner filed a
reply on October 6, 2021. (ECF No. 55.)
Special masters “must determine that the record is comprehensive and fully
developed before ruling on the record.” Kreizenbeck v. Sec’y of Health & Human
Servs., 945 F.3d 1362, 1366 (Fed. Cir. 2020); see also Vaccine Rule 8(d); Vaccine Rule
3(b)(2). The parties must have a full and fair opportunity to present their case and
develop a record sufficient for review. Id. In light of all of the above, and upon review of
the entire record, I conclude that petitioner has had a full and fair opportunity to develop
the record of this case and that the case is ripe for resolution on the existing record.
III. Factual History
a. As Reflected in the Medical Records
Petitioner’s pre-vaccination medical history included hyperkalemia and attention
deficit hyperactivity disorder (“ADHD”), for which she took Adderall. (See, e.g., Ex. 3,
pp. 6-7, 13, 17.) Before vaccination, petitioner exercised regularly and ran two
marathons in 2013. (Id. at 17, 21.) Petitioner was seventy-three years old when she
received the high dose flu vaccine on September 30, 2016. (Ex. 1, p. 1; see also Ex. 3,
p. 7.)
On October 14, 2016, petitioner left a phone message for her primary care
provider, Richard Bransdorf, M.D. (Ex. 4, p. 8.) She reported that she had a fever for
two days following the flu shot and subsequently developed joint and bone pain in her
shoulder, hips, and back. (Id.) A handwritten reply noted that petitioner’s complaints
were “likely d/t [due to] shot,” and recommended that petitioner treat her symptoms with
Tylenol or Aleve and schedule an appointment if they did not resolve within a few days.3
(Id.) Petitioner left another phone message on October 17, 2016, reporting that her pain
was gradually improving but remained persistent. (Id. at 6.) The physician’s assistant
(“PA”), David Burns, noted that it “sounds like [a] flu like reaction to [the] vaccine” and
stated that if petitioner was improving, there was no need for concern. (Id.)
Petitioner visited Dr. Bransdorf on November 18, 2016. (Ex. 3, pp. 6-7.) Dr.
Bransdorf documented that petitioner received the flu vaccine on September 30, 2016,
and later developed myalgias and fever. (Id. at 7.) Petitioner reported that her
symptoms continued to wax and wane and that the pain was primarily in her shoulder
and groin. (Id.) She noted that she was exhausted because her pain prevented her
from resting and that she had difficulty lifting her arms above her head and pulling on a
shirt. (Id.) During the visit, petitioner was afebrile and exhibited no neurological
symptoms. (Id.) Upon examination, Dr. Bransdorf observed tenderness of the
shoulders and groin bilaterally. (Id.) Dr. Bransdorf’s impression was myalgia/myositis.
(Id.) Dr. Bransdorf prescribed 20 mg of prednisone and ordered laboratory tests. (Id.)
3 The signature below the handwritten note is illegible, and it is unclear who authored the note. (See Ex.
4, p. 8.) Petitioner asserts that Dr. Bransdorf is presumably the author of the handwritten note because
he was petitioner’s covering physician. (See ECF No. 50, pp. 2, 17; ECF No. 55, p. 6.)
4

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Petitioner’s erythrocyte sedimentation rate (“ESR”) was normal, but her C-reactive
protein (“CRP”), an inflammatory marker, was elevated. (Id. at 35.)
On November 28, 2016, petitioner returned to Dr. Bransdorf for a follow-up visit.
(Ex. 3, pp. 8-9.) Dr. Bransdorf noted that petitioner began prednisone due to possible
PMR. (Id. at 9.) Petitioner reported that the prednisone provided “almost immediate
relief.” (Id.) Dr. Bransdorf’s diagnosis at this visit was PMR. (Id.) He instructed
petitioner to continue taking prednisone and tapered her dose to 10 mg per day. (Id.)
Petitioner returned to Dr. Bransdorf on January 10, 2017. (Id. at 10-11.) She
reported that she remained on 10 mg of prednisone and was doing well. (Id. at 11.)
However, she noted that she suffered a flare in symptoms after running five miles. (Id.)
The plan was for her to continue 10 mg of prednisone for three months and limit her
exercise. (Id.)
At a follow-up visit with Dr. Bransdorf on May 15, 2017, petitioner reported that
she had been doing well but recently experienced neck pain. (Ex. 5, pp. 6-7.)
Petitioner was having difficulty sleeping due to the neck pain. (Id. at 7.) Dr. Bransdorf
noted that it was unclear whether petitioner’s neck pain was due to a PMR flare or a
mechanical injury. (Id.) At the time of the visit, she was taking 10 mg of prednisone
daily. (Id.) A neck examination revealed tender paraspinal muscles with normal range
of motion. (Id.) Dr. Bransdorf increased petitioner’s prednisone dose to 20 mg daily,
prescribed a muscle relaxer, and ordered an x-ray. (Id.) The cervical spine x-ray
showed mild degenerative spondylosis and diffuse bony demineralization. (Id. at 14.)
Petitioner emailed Dr. Bransdorf on May 28, 2017, to clarify that she believed her
neck pain began in late April after a long car ride. (Id. at 16.) She explained that it
started in the right side of her neck and extended behind her ear and that it was tender
when she pushed on it. (Id.) She stated that the pain then increased, progressed to her
back, and radiated to her head and throat. (Id.) Petitioner also noted that the muscle
relaxer did not help at first but provided some pain relief after multiple doses. (Id.)
Given the headache she experienced, she was concerned for possible giant cell arteritis
(“GCA”). (Id.)
During a visit with Dr. Bransdorf on August 8, 2017, petitioner reported that she
had been taking 20 mg of prednisone, that her neck and shoulder pain had improved,
and that she had some muscle aches. (Ex. 6, p. 7.) Petitioner’s blood pressure was
elevated, which was likely due to her steroid use. (Id.) Her physical examination was
normal. (Id. at 8.) Dr. Bransdorf directed petitioner to taper the prednisone and begin
anti-hypertensive medication. (Id.) A subsequent bone density study to screen for
osteoporosis on August 17, 2017, showed petitioner’s bone density had worsened since
a previous study on July 25, 2011. (Id. at 11.)
On November 28, 2017, petitioner returned to Dr. Bransdorf. (Ex. 7, pp. 2-6.)
Petitioner reported that she was taking 15 mg of prednisone and that she had arthralgia
and joint pains but no muscle aches. (Id. at 5.) Her CRP was elevated, but her physical
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examination was normal. (Id. at 4-5.) Dr. Bransdorf directed petitioner to remain on her
medications. (Id. at 5.) Petitioner continued to follow up with Dr. Bransdorf routinely.
(See, e.g., Ex. 8 pp. 11-14 (2/28/2018 visit); id. at 7-11 (8/9/2018 visit); id. at 4-7
(11/21/2018 visit).
Petitioner returned to Dr. Bransdorf on February 21, 2019, to follow up on her
current medications. (Ex. 42, p. 9.) Petitioner reported that she was doing well but still
had shoulder and hip aches. (Id. at 11.) At the time of this visit, petitioner was on 5 mg
of prednisone per day. (Id.) Dr. Bransdorf increased petitioner’s prednisone dose to 10
mg per day with instructions to begin tapering after two weeks to help with her myalgias.
(Id.)
On March 21, 2019, petitioner saw PA Burns for complaints of a vision disruption
in her right eye. (Id. at 6.) Petitioner reported that she experienced a sudden change in
vision in her right eye with images “appearing shattered” and brighter and more vibrant.
(Id. at 8.) The episode lasted about twenty minutes and then resolved on its own. (Id.)
Petitioner denied experiencing any migraines but reported frequent visual scotomas.
(Id.) Petitioner was concerned for possible GCA. (Id.) PA Burns referred petitioner to
an ophthalmologist for further evaluation. (Id. at 8-9.) PA Burns’s referral order noted
“hx PMR/GCA.” (Id. at 17.)
Petitioner did not submit any records documenting her treatment beyond March
21, 2019.
IV. Expert Opinions
a. Petitioner’s Expert, Thomas Zizic, M.D.
Petitioner presented an expert opinion from rheumatologist Thomas Zizic, M.D.,
in support of her claim. Dr. Zizic is a physician and Associate Professor of Medicine at
Johns Hopkins Hospital and Johns Hopkins University School of Medicine in Baltimore,
Maryland. (Ex. 10, p. 1; Ex. 11, p. 1.) He received his medical degree from Johns
Hopkins University School of Medicine and completed an internship and residency in
internal medicine at Johns Hopkins University Hospital Center. (Ex. 10, p. 1; Ex. 11, p.
1.) He later completed a post-doctoral fellowship in rheumatology at Johns Hopkins.
(Ex. 10, p. 1.) From approximately 1973 to 1982, Dr, Zizic served as the Associate
Director for the Rheumatic Disease Unit for Johns Hopkins at the Good Samaritan
Hospital. (Ex. 10, p. 1; Ex. 11, p. 4.) He is a founding fellow of the American College of
Rheumatology and previously served as President of the Maryland Society of
Rheumatic Disease. (Ex. 10, pp. 1-2; Ex. 11, p. 3.) His research focuses on
osteoarthritis, osteoporosis, and connective tissue diseases, including systemic lupus
erythematosus, PMR, rheumatoid arthritis, and polymyositis. (Ex. 10, p. 2.)
Additionally, Dr. Zizic has published approximately 100 articles and abstracts in peer-
reviewed journals and various chapters in medical textbooks. (Id.; Ex. 11, pp. 7-18.)
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Regarding petitioner’s diagnosis, Dr. Zizic explained that PMR is an inflammatory
condition that generally manifests in persons over fifty years of age. (Ex. 10, p. 20.) He
stated that there are no laboratory tests used to diagnose the condition. (Id. at 21.)
Instead, the diagnosis is made based on clinical presentation, inflammatory markers,
and response to treatment. (Id.) While the cause of PMR is unknown, Dr. Zizic stated
that it is widely understood in the medical community to be a cell-mediated autoimmune
disease. (Id.) He elaborated that the disease manifests as an inflammatory reaction
impacting the lining of a joint, often in the shoulders and hips, and occasionally the
arteries. (Id.) Given that it is a cell-mediated autoimmune disease, Dr. Zizic asserted
that patients with PMR are not expected to have autoantibodies. (Ex. 40, p. 3.)
Dr. Zizic agreed with petitioner’s diagnosis of PMR but also suggested that
petitioner also exhibited symptoms indicative of GCA, including neck pain and
headache. (Ex. 40, p. 2.) However, Dr. Zizic acknowledged that petitioner “did not
have sufficient clinical manifestations to diagnose giant cell arteritis.” (Id. at 4.)
Although petitioner was not diagnosed with GCA, Dr. Zizic opined that both diseases
are types of vasculitis. (Ex. 10, p. 21.) He elaborated that PMR and GCA are “different
manifestations of the same disease process.” (Id. at 21-22; see also Ex. 40, p. 3
(discussing how PMR is on the mild spectrum of GCA).) Dr. Zizic emphasized that 40%
of patients with GCA also have PMR, while 10% of PMR patients develop GCA in the
course of their disease. (Ex. 10, p. 25; Ex. 40, p. 8.) He further noted that there is
“evidence for the presence of identical vasculitis in both polymyalgia rheumatica and
giant cell arteritis.” (Ex. 40, p. 5 (citing D. Blockmans et al., New Arguments for a
Vasculitic Nature of Polymyalgia Rheumatica Using Positron Emission Tomography, 38
RHEUMATOLOGY 444 (1999) (Ex. 14).) To Dr. Zizic, this suggests that like GCA, PMR is
part of a vascular process. (Id. (citing Cornelia M. Weyand et al., Tissue Cytokine
Patterns in Patients with Polymyalgia Rheumatica and Giant Cell Arteritis, 121 ANNALS
INTERNAL MED. 484 (1994) (Ex. 36); Cornelia M. Weyand et al., Disease Patterns and
Tissue Cytokine Profiles in Giant Cell Arteritis, 40 ARTHRITIS & RHEUMATISM 19 (1997)
(Ex. 38).) Dr. Zizic added that it is significant that PMR is a type of vasculitis because
dendritic cells in the adventitia-media border of the artery play a key role in causing
vasculitis. (Id. at 4-5 (citing Cornelia M. Weyand & Jörg J. Goronzy, Medium- and
Large-Vessel Vasculitis, 349 NEW ENGLAND J. MED. 160 (2003) (Ex. 41); Cornelia M.
Weyand et al., Vascular Dendritic Cells in Giant Cell Arteritis, 1062 ANNALS NEW YORK
ACAD. SCI. 195 (2005) (Ex. 37)).) Therefore, Dr. Zizic challenged Dr. Matloubian’s
assertion that there is no understanding of the pathogenesis of PMR. (See id. at 8
(reiterating that PMR and GCA “are at opposite ends of the severity spectrum of the
same cell-mediated autoimmune vasculitis”).)
Dr. Zizic offered molecular mimicry as a theory for causation. He opined that
several environmental factors, including the flu vaccine, can “activate the immune
system, leading to the development of antigen-specific T and B lymphocytes that can be
activated as naïve cells or as memory cells.” (Ex. 10, pp. 28-29.) He elaborated that
the molecules contained in vaccines can cross-react with self-molecules and cause a
cell-mediated autoimmune disease in genetically susceptible individuals. (Id. at 29-30.)
Dr. Zizic relied on articles by Dessen et al. and Sun et al. to show that the “influenza
7

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virus hemagglutinin 308-317 peptide shares a similar 3-dimensional structure with
CII256-271 and can bind HLA-DR4/1 molecules with higher affinity.” (Id. at 29 (citing
Andréa Dessen et al., X-Ray Crystal Structure of HLA-DR4 (DRA*0101, DRB1*0401)
Complexed with a Peptide from Human Collagen II, 7 IMMUNITY 473 (1997) (Ex. 18);
Jian Sun et al., Superior Molecularly Altered Influenza Virus Hemagglutinin Peptide 308-
317 Inhibits Collagen-Induced Arthritis by Inducing CD4+ Treg Cell Expansion, 64
ARTHRITIS & RHEUMATISM 2158 (2012) (Ex. 32)).) Dr. Zizic further explained that
identifying the specific self-antigen in petitioner is impossible due to the variety of
different peptides recognized by autoreactive T cell receptors. He added that the
antigens in cell-mediated immunity are in the inflamed tissue and are therefore often
unidentifiable. (Ex. 40, pp. 8-9.) However, Dr. Zizic opined that both self-reactive T
cells and B cells can result from epitope mimicry and cause autoimmune disease. (Id.
at 9.) He noted that the Rose article cited by Dr. Matloubian acknowledges this fact.
(See id. (citing Noel R. Rose, Negative Selection, Epitope Mimicry and Autoimmunity,
49 CURRENT OPINION IN IMMUNOLOGY 51 (2017) (Ex. A, Tab 12)).) Dr. Zizic also opined
that in addition to the flu vaccine petitioner received, other factors, such as history of
earlier flu vaccines and effects of aging, can predispose an individual to autoimmunity
and cause the breakdown of tolerance to self via molecular mimicry. (Ex. 10, pp. 27-29;
Ex. 40, pp. 6-8.)
Dr. Zizic offered several case reports to support his opinion, noting that forms of
vasculitis, including PMR and GCA, have been reported after the flu vaccination. (Ex.
10, pp. 19-20 (citing Rainer Birck et al., ANCA-Associated Vasculitis Following Influenza
Vaccination, 15 J. CLINICAL RHEUMATOLOGY 289 (2009) (Ex. 12); Caterina Bonetto et al.,
Vasculitis as an Adverse Event Following Immunization – Systematic Literature Review,
34 VACCINE 6641 (2016) (Ex. 15); Eric Liozon et al., Polymyalgia Rheumatica Following
Influenza Vaccination, 48 J. AM. GERIATRICS SOC’Y 1553 (2000) (Ex. 25); Juan Marti &
Enrique Anton, Polymyalgia Rheumatica Complicating Influenza Vaccination, 52 J. AM.
GERIATRICS SOC’Y 1412 (2004) (Ex. 26); Carlos Perez & Elias Maravi, Polymyalgia
Rheumatica Following Influenza Vaccination, 23 MUSCLE & NERVE 824 (2000) (Ex. 27);
A. Soriano et al., Giant Cell Arteritis and Polymyalgia Rheumatica After Influenza
Vaccination: Report of 10 Cases and Review of the Literature, 21 LUPUS 153 (2012) (Ex.
31); Makoto Wada et al., Giant Cell Arteritis with Polymyalgia Rheumatica Associated
with Influenza Vaccination, 38 J. DERMATOLOGY 1099 (2011) (Ex. 33)).)
While Dr. Zizic did not extensively address the issue of timing in his reports, he
noted that petitioner first experienced symptoms of PMR two weeks after receiving the
flu vaccine. (See Ex. 40, p. 1.) Additionally, Dr. Zizic offered a case report that found
that a range of 12 to 21 days was an appropriate temporal relationship for onset of
vasculitis following the flu vaccine. (Yaron Zafrir, Nancy Agmon-Levin, & Yehuda
Shoenfeld, Post-Influenza Vasculitides: A Possible New Entity, 15 J. CLINICAL
RHEUMATOLOGY 269, 270 (2009) (Ex. 39)).
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b. Respondent’s Expert, Mehrdad Matloubian, M.D., Ph.D.
Respondent offered an expert opinion from immunologist and rheumatologist
Mehrdad Matloubian, M.D., Ph.D. Dr. Matloubian is board-certified in rheumatology and
has a Ph.D. in virology and immunology. (Ex. A, p. 1; Ex. B, pp. 1-2.) He is currently a
physician and Associate Professor of Medicine in the rheumatology division at the
University of California, San Francisco. (Ex. A, p. 1; Ex. B, p. 2.) He has expertise in T
and B cell responses to viruses and factors that regulate lymphocyte circulation and
trafficking. (Ex. A, p. 1.) His research primarily focuses on innate and adaptive immune
responses of T and B cells to acute and chronic viral infections. (Id.) Additionally, Dr.
Matloubian has published several peer-reviewed articles on these topics. (Id.; Ex. B,
pp. 10-14.)
Dr. Matloubian explained that PMR is an inflammatory disease of unknown
etiology. (Ex. A, p. 3.) He noted that symptoms of PMR include aching and morning
stiffness in the shoulders, hip girdle, and neck. (Id.) Given that MRI or ultrasound
imaging have shown bursitis or synovitis in patients with PMR, Dr. Matloubian explained
that PMR is understood to be a disease of the joints underlying the muscle groups. (Id.
at 3-4.) He discussed that it is usually a systemic inflammatory disease characterized
by elevated inflammatory markers such as ESR and/or CRP. (Id.) He further stated
that there is no known trigger for the disease. (Id.) Dr. Matloubian opined that
petitioner’s course of PMR was typical for the disease given her occasional flares and
responsiveness to prednisone. (Id. at 4.) He added that it is not unusual for a
previously healthy person to experience an abrupt onset of PMR as petitioner
experienced. (Id. at 3; Ex. C, p. 3.)
In response to Dr. Zizic’s discussion of the similarities between PMR and GCA,
Dr. Matloubian noted that while petitioner had some neck symptoms and a headache,
petitioner did not have any other symptoms suggestive of GCA and was never
diagnosed with the disease. (Ex. A, p. 4.) He also discussed some differences
between the two diseases. He noted that GCA often requires treatment with higher
doses of prednisone than PMR. (Id.) While petitioner was treated with 5-20 mg of
prednisone daily throughout the course of her disease, Dr. Matloubian noted that
treatment of GCA requires prednisone in the 40-60 mg per day range. (Id.) He added
that GCA is diagnosed based on a temporal artery biopsy, which petitioner never had
done. (Ex. C, p. 2.) Dr. Matloubian elaborated that there was insufficient evidence in
the medical records to diagnose petitioner with GCA. (Id.) Therefore, Dr. Matloubian
concluded that it was unlikely petitioner had GCA.
Dr. Matloubian challenged molecular mimicry as a plausible mechanism by which
the flu vaccine can cause PMR. Given that the medical community’s understanding of
PMR’s pathogenesis is “primitive” and its mechanism is unknown, Dr. Matloubian
opined that “the sequence of events that leads to development of inflammation and
secretion of inflammatory cytokines, such as IL-6, is not known.” (Ex. A, p. 4.) He
added that the “absence of autoantibodies in PMR to a specific component of the
musculoskeletal system suggests that this disease may not be antigen-specific, and
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most likely not induced through processes such as molecular mimicry.” (Id.)
Additionally, since most PMR patients quickly respond to low doses of prednisone, Dr.
Matloubian explained that this suggests that unlike other autoimmune diseases such as
rheumatoid arthritis, PMR is not antigen-driven or characterized by persistent
inflammation. (Id.) He further explained that that “no foreign or self-antigens have been
identified as the target of the immune response that leads to the development of PMR.”
(Id. at 6; see also Ex. C, p. 3.) Given that PMR primarily affects the elderly population,
Dr. Matloubian opined that PMR is most likely caused by aging immune systems and
“change[s] in balance towards pro-inflammatory pathways.” (Ex. A, pp. 5-6.) He
concluded that without “an understanding of the basic pathogenesis of PMR, any
medical theory set forth linking [the] influenza vaccination and development of PMR is
purely speculative and unreliable.” (Id. at 6.)
Additionally, for molecular mimicry to be a plausible mechanism by which the flu
vaccine can cause a disease, Dr. Matloubian explained that the flu infection should also
be capable of triggering the disease. (Ex. A, p. 9; Ex. C, p. 2 (citing Rose, supra, at Ex.
A, Tab 12).) However, as noted by Dr. Matloubian, researchers have not identified an
infectious cause for PMR. (Ex. A, p. 10; Ex. C, pp. 2-3.) Dr. Matloubian cited data from
the World Health Organization, which showed no higher incidence of PMR following
influenza outbreaks. (Ex. A, p. 10.) Therefore, Dr. Matloubian opined that molecular
mimicry is an unlikely mechanism by which the flu vaccine could cause PMR. (Id.)
Dr. Matloubian identified several flaws in Dr. Zizic’s opinion. He asserted that Dr.
Zizic’s theory is unsound because although Dr. Zizic identified collagen as a self-antigen
in PMR, collagen is a T cell antigen associated with rheumatoid arthritis, type I diabetes,
and multiple sclerosis, but has not been recognized as a self-antigen in PMR. (Ex. A, p.
10; Ex. C, p. 3.) Further, Dr. Matloubian challenged the literature Dr. Zizic relied on to
support his theory that the hemagglutinin contained in the flu vaccine cross-reacts with
collagen to trigger PMR. Regarding the Dessen et al. article (Ex. 18), Dr. Matloubian
noted that the authors do not discuss molecular mimicry or recognize hemagglutinin and
collagen as structurally similar. (Ex. A, p. 11.) Additionally, Dr. Matloubian noted that
the Sun et al. article (Ex. 32) merely shows that an altered hemagglutinin peptide can
inhibit T cell responses to a collagen-derived peptide in mice and rheumatoid arthritis
patients. (Id. at 13.) However, the Sun et al. authors do not discuss molecular mimicry.
(Id.)
Further, Dr. Matloubian disputed the relevance of the case reports Dr. Zizic relied
on to bolster his theory. In the Liozon et al. case report, the subject’s symptoms
appeared two days after receiving the flu vaccination; however, she also had a urinary
tract infection requiring intravenous steroids. (Liozon et al., supra, at Ex. 25.) Dr.
Matloubian explained that the patient’s urinary tract infection complicated any alleged
vaccine association. (Ex. A, p. 7.) Additionally, in the Soriano et al. and Wada et al.
case reports, which both explore reports of PMR and/or GCA, the subjects’ onset of
symptoms ranged from one day to three months post-vaccination. (Soriano et al.,
supra, at Ex. 31; Wada et al., supra, at Ex. 33.) Dr. Matloubian opined, “[s]uch a large
difference in the timing of onset of symptoms is not compatible with a unifying
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immunological mechanism and is more suggestive of a coincidental rather than a causal
association between vaccination and disease.” (Ex. A, p. 7.) Regarding the Soriano et
al. case report, Dr. Matloubian noted that many of the vaccines examined contained
adjuvants; conversely, the vaccine petitioner received did not contain adjuvants. (Id.)
Dr. Matloubian also explained that several of the case reports Dr. Zizic referenced
examined types of vasculitis associated with antineutrophil cytoplasmic antibodies
(“ANCA”) and are therefore irrelevant to the case as petitioner did not suffer an ANCA-
associated disease. (Id. (citing Birck et al., supra, at Ex. 12; Bonetto et al., supra, at Ex.
15; Zafrir, Agmon-Levin, & Shoenfeld, supra, at Ex. 39).) Dr. Matloubian also asserted
that the case reports show only a temporal association between vaccination and
disease but do not support causality. (Id.)
Regarding timing, Dr. Matloubian agreed that petitioner’s PMR symptoms
“became apparent” after receiving her flu vaccine. (Ex. A, p. 6.) However, Dr.
Matloubian appeared to suggest that petitioner’s PMR may have been dormant before it
manifested clinically. (Id.) He explained that autoimmune diseases are often “years in
the making and only diagnosed when they become clinically apparent.” (Id.) He
therefore cautioned against inferring causation due to a temporal association between
vaccination and clinical manifestation of symptoms. (See id. at 5-6.) Given Dr.
Matloubian’s opinion that the pathogenesis of PMR is unknown, Dr, Matloubian
suggested that there is no scientifically appropriate timeframe for which to infer vaccine-
causation. (Id.)
V. Discussion
As explained above, petitioner’s burden is to demonstrate by preponderant
evidence, each of the three Althen prongs used to determine actual causation (i.e., an
acceptable medical theory, a logical sequence of cause and effect, and a proximate
temporal relationship). Althen, 418 F.3d at 1278.
a. Althen Prong One
Under Althen prong one, petitioner must provide a “reputable medical theory,”
demonstrating that the vaccine received can cause the type of injury alleged. Pafford v.
Sec’y of Health & Human Servs., 451 F.3d 1352, 1355-56 (Fed. Cir. 2006) (citations
omitted). Such a theory must only be “legally probable, not medically or scientifically
certain.” Knudsen, 35 F.3d at 549. Petitioner may satisfy the first Althen prong without
resort to medical literature, epidemiological studies, demonstration of a specific
mechanism, or a generally accepted medical theory. Andreu v. Sec’y of Health &
Human Servs., 569 F.3d 1367, 1378-79 (Fed. Cir. 2009) (citing Capizzano v. Sec’y of
Health & Human Servs., 440 F.3d 1317, 1325-26 (Fed. Cir. 2006)). However, “[a]
petitioner must provide a ‘reputable medical or scientific explanation’ for [her] theory.
While it does not require medical or scientific certainty, it must still be ‘sound and
reliable.’” Boatmon, 941 F.3d at 1359 (quoting Knudsen, 35 F.3d at 548-49).
Dr. Zizic summarizes his theory of causation as follows:
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Inflammation and damage involving the walls of blood vessels in the
vascular syndromes have been attributed to immunologic mechanisms.
Although immune-complex mediated mechanisms appear to be operative
in some vasculitides, cellular immune mechanisms are more likely to be
important in the initiation and perpetuation of lesions in patients with
polymyalgia rheumatica and giant cell arteritis. As discussed above, in
genetically susceptible individuals, influenza antigens in the vaccine lead to
cross-reactivity and molecular mimicry to self-antigens that then break
tolerance to self. Some individuals develop humoral autoimmune diseases
such as rheumatoid arthritis and others develop cell-mediated autoimmune
diseases such as polymyalgia rheumatica and giant cell arteritis.
(Ex. 10, p. 30.)
Petitioner’s causation theory has several shortcomings. First, Dr. Zizic opined
that the hemagglutinin contained in the flu vaccine can cross react with type II collagen,
thus triggering activation of B and/or T lymphocytes through molecular mimicry based
largely upon articles by Dessen et al. and Sun et al. (Ex. 10, p. 29 (citing Dessen et al.,
supra, at Ex. 18; Sun et al., supra, at Ex. 32).) However, Dr. Matloubian explained that
neither the Dessen et al. article nor the Sun et al. article discussed molecular mimicry or
identified hemagglutinin and collagen as structurally similar. (Ex. A, pp. 11-13.)
Further, Dr. Matloubian persuasively explained that while collagen is a self-antigen
associated with rheumatoid arthritis, it had not been identified as a self-antigen in PMR.
(Id. at 10.) In fact, Dr. Matloubian asserted that “no foreign or self-antigens have been
identified as the target of the immune response that leads to the development of PMR.”
(Id. at 6.) Dr. Matloubian further opined that for molecular mimicry to be a viable
mechanism by which the flu vaccine can trigger PMR, the flu infection must be capable
of causing the disease. (Id. at 9.) However, since PMR is a disease of unknown cause,
an infectious etiology has not been identified, and neither the flu vaccine nor the flu
infection has been associated with the disease. (Id. at 9-10.) In fact, Dr. Matloubian
indicates that no trigger of any kind has been identified in the development of PMR.4
(Id. at 4.)
In response to Dr. Matloubian’s criticism, Dr. Zizic acknowledged that self-
antigens specific to PMR are unidentifiable. (See Ex. 40, pp. 8-9.) However, Dr. Zizic
was critical of Dr. Matloubian’s suggestion that identifiable autoantibodies are
necessary, stressing instead that the condition at issue is a cell-mediated autoimmune
disease. (Id. at 3.) In that regard, Dr. Zizic stresses a hypothesis of GCA development,
contending that GCA and PMR are “different manifestations of the same disease
4 In a previous Vaccine Program case, a special master rejected molecular mimicry as a mechanism by
which the flu vaccine can cause PMR. C.P. v. Sec’y of Health & Human Servs., No. 14-917V, 2019 WL
5483621, at *28 (Fed. Cl. Spec. Mstr. Aug. 21, 2019). In C.P., the special master found it significant that
there are no autoantibodies or identifiable antigens in patients with PMR and that as a result, no
sequence of amino acids can be compared to those in the flu vaccine. Id. at *26, 28. The special master
in C.P. also credited Dr. Matloubian’s opinion that the pathogenesis of PMR is unknown and there is no
established association between the flu virus or vaccine and PMR. Id. at *28.
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process.” (Ex. 10, p. 22; Ex. 40, p. 7.) Dr. Zizic suggests that a number of reports have
linked PMR to the flu vaccine in connection with GCA. (Ex. 10, p. 20.) He further
suggests that GCA is “considered by many people to be the best example of a TH1
vasculitis.” (Id. at 21.)
Specifically, he quotes the following:
The cause of GCA is unknown, but the vessel wall inflammation is believed
to be predominantly cell-mediated, rather than autoantibody-induced.
Dendritic cells residing in the adventitia become activated by an unknown
antigen, and signal for T lymphocytes to enter the vessel wall via the vasa
vasorum. Activated T cells differentiate and clonally expand, producing IFN-
gamma, which results in macrophage infiltration. Macrophages infiltrate all
layers of the arterial wall, secreting a broad range of inflammatory
cytokines . . . .
(Ex. 40, p. 7.) However, even if GCA and PMR have some relation,5 application of this
particular theory to PMR is unpersuasive.
One study cited by Dr. Zizic reviewed patients with either GCA or PMR who were
tested by temporal artery biopsy. (Weyand et al., supra, at Ex. 36, p. 484.) While the
study found similarities in inflammatory cytokine profiles (most notably IL-2) between
GCA and PMR patients, the biopsy results showed that none of the subjects
experiencing PMR alone had evidence of arterial inflammatory infiltrate.6 (Id. at 487.)
The authors hypothesized that PMR may include subclinical vascular involvement, but
also noted that there may be important differences between PMR and GCA patients. In
particular, they proposed that INF-gamma, which was not found among PMR patients,
may be essential for the development of vasculitis. (Id. at 489-90.) A follow up study
further explored the relationship between inflammatory cytokines and disease
expression among GCA patients. (Weyand et al., supra, at Ex. 38.) That study
indicated that INF-gamma is likely “a critical cytokine in GCA” given its documented
5 The comorbidity of PMR and GCA and the fact that they are both age-related inflammatory conditions
has led some to propose that PMR may also be a vasculitis and that the two conditions may exist on a
spectrum. (E.g., Blockmans et al., supra, at Ex. 14; Weyand et al., supra, at Ex. 36.) Despite this
hypothesis, researchers have acknowledged that the relationship between the two syndromes remains
“unclear.” (Weyand et al., supra, at Ex. 38, p. 20.) In fact, only 15% of PMR patients later develop
vasculitis. (Weyand et al., supra, at Ex. 36, p. 490.) Conversely, “only a fraction” of GCA patients
develop symptoms characteristic of PMR. (Weyand et al., supra, at Ex. 38, p. 24.) For his part, Dr.
Matloubian does not dispute that there is overlap between GCA and PMR or that PMR may involve
subclinical vascular inflammation, but stresses that the cause of neither condition is known, let alone
having any causal relationship related to influenza antigen. (Ex. C, p. 2.) Dr. Zizic likewise acknowledges
that ultimately the cause of GCA remains unknown. (Ex. 40, p. 7.) In another case involving PMR
(relative to the Tdap vaccine), the same special master presiding in C.P. discussed the comparison
between PMR and GCA in more detail. See Suliman v. Sec’y of Health & Human Servs., No. 13-993V,
2018 WL 6803697, at *25, 28 (Fed. Cl. Spec. Mstr. Nov. 27, 2018). In Suliman, the special master
emphasized that PMR is distinguishable from GCA, and that the petitioner did not have GCA. Id.
6 Dr. Zizic suggests that the temporal artery biopsy is not dispositive of whether vasculitis exists (Ex. 10,
pp 22-23), though he does agree that it is the “gold standard” for detecting GCA (Id. at 21).
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absence from patients without overt vasculitis. (Id. at 24.) Citing back to the prior
study, the authors explained that while the IL-2 demonstrated among PMR patients and
the INF-gamma seen among GCA patients may both be secreted by Th1 helper cells,
“several lines of evidence indicate that production of both cytokines is not necessarily
linked.” (Id. at 25.) Further, they observed that in the follow-up study there was no
correlation between IL-2 and INF-gamma in individual patients. (Id.) Despite
acknowledging this distinction (Ex. 10, p. 24), Dr. Zizic specifically invokes INF-gamma
production as part of his explanation of GCA as a cell-mediated autoimmune process
(Id. at 25). Yet, extension of that mechanism to PMR does not appear to be reliable
based on the above-discussed literature. In that regard, Dr. Matloubian emphasized
that because the medical community’s understanding of PMR’s pathogenesis is
“primitive,” it is impossible to identify “the sequence of events that leads to development
of inflammation and secretion of inflammatory cytokines.” (Ex. A, p. 4.)
The case reports Dr. Zizic relied on cannot remedy the deficiencies in his theory.
While case reports are not wholly without evidentiary value, the case reports show only
a temporal association and do not establish causality. (See Ex. A, p. 7.) Additionally,
many of the case reports Dr. Zizic relied on document ANCA-associated vasculitis
following the flu vaccine, further diminishing their value. (See Birck et al., supra, at Ex.
12; Bonetto et al., supra, at Ex. 15; Zafrir, Agmon-Levin, & Shoenfeld, supra, at Ex. 39.)
Dr. Matloubian opines that the ANCA-associated vasculitis case reports are entirely
irrelevant, because it is a different condition and petitioner was never diagnosed as
having it. (Ex. A, p. 7.)
A petitioner must provide a “‘reputable medical or scientific explanation’ for [her]
theory.” Boatmon, 941 F.3d at 1359 (quoting Knudsen, 35 F.3d at 548-49). Here, Dr.
Zizic was unpersuasive in either seeking to identify components of the flu vaccine that
could be mimicked to cause PMR or in alternatively invoking GCA to circumstantially
identify a mechanism of cell-mediated autoimmunity. And, although petitioner is not
required to prove an exact biological mechanism, she has not otherwise provided any
sound and reliable theory of causation. Therefore, petitioner has failed to meet her
burden to show that the flu vaccine can cause PMR.
b. Althen Prong Two
The second Althen prong requires proof of a logical sequence of cause and
effect, usually supported by facts derived from a petitioner’s medical records. Althen,
418 F.3d at 1278; Andreu, 569 F.3d at 1375-77; Capizzano, 440 F.3d at 1326; Grant,
956 F.2d at 1148. In establishing that a vaccine “did cause” injury, the opinions and
views of the injured party’s treating physicians are entitled to some weight. Andreu, 569
F.3d at 1367; Capizzano, 440 F.3d at 1326 (quoting Althen, 418 F.3d at 1280) (stating
that “medical records and medical opinion testimony are favored in vaccine cases, as
treating physicians are likely to be in the best position to determine whether a ‘logical
sequence of cause and effect show[s] that the vaccination was the reason for the
injury’”). However, medical records and/or statements of a treating physician’s views do
not per se bind the special master to adopt the conclusions of such an individual, even if
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they must be considered and carefully evaluated. See Section 13(b)(1) (providing that
“[a]ny such diagnosis, conclusion, judgment, test result, report, or summary shall not be
binding on the special master or court”); Snyder v. Sec’y of Health & Human Servs., 88
Fed. Cl. 706, 746 n.67 (2009) (stating that “there is nothing . . . that mandates that the
testimony of a treating physician is sacrosanct—that it must be accepted in its entirety
and cannot be rebutted”).
To support a logical sequence of cause and effect, petitioner primarily relies on
statements from Dr. Bransdorf and PA Burns. Petitioner argues that both Dr. Bransdorf
and PA Burns noted that petitioner’s symptoms of joint pain two weeks post-vaccination
may have been due to her flu vaccine. (See ECF No. 50, p. 17; ECF No. 55, p. 6.)
However, these statements do not carry petitioner’s burden under Althen prong two. PA
Burns suggested that petitioner was having a “flu like” reaction to the vaccine (id. at 6);
however, petitioner was not diagnosed with PMR until several weeks later and neither
PA Burns nor Dr. Bransdorf ever attributed petitioner’s PMR to the flu vaccine. Nor, in
any event, do these statements bind a special master to adopt their conclusions.
Snyder, 88 Fed. Cl. at 746, n.67. Further, in light of my finding that petitioner has not
satisfied Althen prong one, the statements from her treating physicians carry little
weight. See Langland v. Sec’y of Health & Human Servs., 109 Fed. Cl. 421, 438 (2013)
(stating that “in the absence of a theory showing a vaccine could cause a particular
injury, a doctor's belief that it did will not prove causation) (emphasis in original); see
e.g., Deshler v. Sec’y of Health & Human Servs., No. 16-1070V, 2020 WL 4593162, at
*21 (Fed. Cl. Spec. Mstr. July 1, 2020).
Although Dr. Zizic suggested that the temporal association between petitioner’s
flu vaccine and onset of PMR indicated a logical sequence of cause and effect, both Dr.
Zizic and Dr. Matloubian agreed that onset of PMR is typical in individuals over fifty
years of age. (Ex. 10, p. 20; Ex. A, p. 5.) Because PMR generally occurs in the elderly
population, Dr. Matloubian indicated that the disease is likely the result of an aging
immune system. (Ex. A, p. 5.) Though generally active and healthy, petitioner was 73
years old at the time of vaccination. (Ex. 1, p. 1; Ex. 3, p. 7.) Further, Dr. Matloubian
asserted that PMR can be dormant for years before individuals experience clinical
manifestations. (Ex. A, p. 6.) Thus, the temporal association between petitioner’s flu
vaccine appears to be merely coincidental. Additionally, temporal association alone
cannot satisfy a petitioner’s burden under Althen prong two. See C.P., 2019 WL
5483621, at *29 (citing Grant, 956 F.2d at 1148).
Dr. Zizic also attempted to show that the flu vaccine can cause PMR based on
PMR’s similarities to GCA. However, as Dr. Zizic acknowledged, GCA accompanies
only a subset of PMR cases. (Ex. 10, p. 25; Ex. 40, p. 8.) Further, although petitioner
expressed concern for GCA (Ex. 5, p. 16; Ex. 42, p. 8), neither Dr. Bransdorf nor PA
Burns ever diagnosed petitioner with GCA. As discussed above, Dr. Matloubian’s
opinion that PMR is a disease of unknown etiology is persuasive. Thus, Dr. Zizic’s
suggestion that petitioner’s PMR indicates vaccine-causation based on a GCA
comorbidity does not establish a logical sequence of cause and effect. The evidence
supports a finding that petitioner’s PMR was idiopathic rather than vaccine induced.
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Accordingly, petitioner has failed to satisfy Althen prong two.
c. Althen Prong Three
The third Althen prong requires establishing a “proximate temporal relationship”
between the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term
has been equated to the phrase “medically-acceptable temporal relationship.” Id. A
petitioner must offer “preponderant proof that the onset of symptoms occurred within a
timeframe which, given the medical understanding of the disorder’s etiology, it is
medically acceptable to infer causation.” de Bazan v. Sec’y of Health & Human Servs.,
539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what is a medically
acceptable timeframe must 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., 503 Fed. Appx. 952 (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).
The parties do not dispute that petitioner manifested symptoms of PMR two
weeks after receiving the flu vaccine; however, Dr. Matloubian persuasively explained
that because petitioner has not shown that the flu vaccine can cause PMR, there is no
appropriate temporal association. (See Ex. A, pp. 5-6.) Thus, petitioner cannot satisfy
her burden under Althen prong three. See Langland, 109 Fed. Cl. at 443 (“[T]o satisfy
the ‘proximate temporal relationship’ prong of the Althen test, petitioners must
demonstrate, by a preponderance of the evidence, that the onset of symptoms occurred
within a time frame for which it is medically acceptable to infer causation-in-fact . . .With
no reputable theory as to how the vaccination could cause the injury, this exercise is not
possible.”) (citing de Bazan, 539 F.3d at 1352); see also Suliman v. Sec’y of Health &
Human Servs., No. 13-993V, 2018 WL 6803697, at *30 (Fed. Cl. Spec. Mstr. Nov. 27,
2018) (finding that petitioner could not satisfy burden under Althen prong three because
petitioner failed to show that the Tdap vaccine could cause PMR and/or myositis.)
VI. Conclusion
Accordingly, for all the reasons described above, petitioner is not entitled to
compensation for her PMR. Therefore, this case is dismissed.7
IT IS SO ORDERED.
s/Daniel T. Horner
Daniel T. Horner
Special Master
7 In the absence of a timely-filed motion for review of this Decision, the Clerk of the Court shall enter
judgment accordingly.
16