Delozier v. Secretary of Health and Human Services

CORRECTED
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 15-124V
(to be published)

************************* Chief Special Master Corcoran
CHRISTINE DELOZIER, *
parent and next friend of L.T., a minor, *
* Filed: December 10, 2019
Petitioner, *
* Alopecia Areata; Autoimmune
v. * Condition; Vaccine as Trigger;
* Chronic Condition; Althen Prong
SECRETARY OF HEALTH AND * One; Genetic Basis for Condition
HUMAN SERVICES, *
*
Respondent. *
*
*************************

Richard Gage, Richard Gage, P.C., Cheyenne, WY, for Petitioner.

Jennifer L. Reynaud, U.S. Dep’t of Justice, Washington, DC, for Respondent.

RULING ON ENTITLEMENT1

On February 9, 2015, Christine DeLozier,2 as parent and next of friend of L.T., a minor,
filed a petition seeking compensation under the National Vaccine and Injury Compensation
Program (the “Vaccine Program”).3 (ECF No. 1) (“Petition”). Petitioner alleged that L.T. suffered

1
This Ruling shall be posted on the Court of Federal Claims’ website in accordance with the E-Government Act of
2002, 44 U.S.C. § 3501 (2012)). This means that the Ruling will be available to anyone with access to the internet.
As provided by 42 U.S.C. § 300aa-12(d)(4)(B), however, the parties may object to the Ruling’s inclusion of certain
kinds of confidential information. Specifically, under Vaccine Rule 18(b), each party has fourteen days within which
to request redaction “of any information furnished by that party: (1) that is a trade secret or commercial or financial
in substance and is privileged or confidential; or (2) that includes medical files or similar files, the disclosure of which
would constitute a clearly unwarranted invasion of privacy.” Vaccine Rule 18(b). Otherwise, the whole Ruling will
be available to the public. Id.
2
Although the Petition was originally filed under the name “Christine Torres,” Petitioner has since changed her last
name to DeLozier, and therefore the case caption has been amended. (ECF No. 58).
3
The Vaccine Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660,
100 Stat. 3758, codified as amended at 42 U.S.C. §§ 300aa-10 through 34 (2012) [hereinafter “Vaccine Act” or “the
Act”]. Individual section references hereafter will be to § 300aa of the Act (but will omit that statutory prefix).

1
from alopecia areata (“AA”) attributable to a hepatitis B vaccine (“HBV vaccine”) L.T. received
on November 6, 2012.

An entitlement hearing was held in this matter on February 4, 2019, and with post-trial
briefing concluded in June the case is now ripe for resolution. Based on the evidence submitted, I
find that Petitioner has preponderantly established that the HBV vaccine could trigger an
autoimmune response resulting in a single AA occurrence—and therefore since the medical record
supports the contention that this occurred in L.T.’s case, Petitioner is entitled to an award of
damages associated with that first occurrence. I do not find, however, that preponderant evidence
supports Petitioner’s broader contention that all subsequent outbreaks of AA Petitioner has
experienced (or may in the future) are also attributable to her 2012 receipt of the HBV
vaccination—and therefore she is not entitled to damages associated with any such subsequent,
unrelated AA occurrences.

I. Factual Background

L.T.’s family health history and pre-vaccination health

L.T. was born on June 29, 2009, largely healthy after a 32-week pregnancy. Ex. 1 at 3; see
also Ex. 4 at 11, 84, 89–90. Significantly for this case, L.T. appears to have a family history of
autoimmune diseases. Ms. DeLozier in particular (who testified at trial) has previously
experienced an unspecified autoimmune connective disorder. See Ex. 1 at 4; Tr. at 26–28. This
condition carried symptoms of diffuse hair loss, a positive ANA,4 and occurred about seven to ten
years before L.T.’s birth. Ex. 1 at 3; see also Ex. 4 at 11. Petitioner specifically reported that she
developed this disorder after being out of the country—and recalled having received the HBV
vaccine prior to travelling. Ex. 4 at 11.

L.T. was growing and developing normally before her receipt of a third HBV dose,
although she did suffer from asthma and eczema. Tr. 19–20 (stating that L.T. had eczema before
her third HBV vaccine); Ex. 3 at 314 (noting diagnosis of asthma in November 2011). She had
received her first and second HBV vaccine doses at two and four months old, respectively, with
no reported reaction. Ex. 4 at 36–37; Tr. at 31; see generally Ex. 5 (vaccination record). Thereafter
there is a gap in medical records—and a deviation from the normal HBV vaccination schedule—
because of a lapse in insurance coverage. Tr. at 30–31.

4
An antinuclear antibody (“ANA”) test is typically used to assess the presence of systemic lupus erythematosus
(“SLE”), as well as other autoimmune diseases (e.g., mixed connective tissue disease, scleroderma, rheumatoid
arthritis, Sjögren’s syndrome, and polymyositis). However, because otherwise-healthy individuals often test positive
for ANA, follow-up testing is necessary to corroborate the diagnosis, although a negative result generally excludes
the diagnosis of some autoimmune diseases. See K. Pagana, et al., Mosby’s: Manual of Diagnostic and Laboratory
Tests 80, 82 (6th ed. 2018).

2
 L.T.’s vaccination and health history to the end of 2013

L.T. was three years old when she received her third dose of the HBV vaccine on November
6, 2012. Not long after, Ms. DeLozier noticed problems with L.T.’s health. Specifically, she
observed that “a couple days after vaccine there was increased hair coming out [of L.T.’s head].”
Tr. at 11. Then, four days after vaccination, she noticed “two prominent bald spots”—about the
size of a quarter—on L.T.’s head. Id. at 11. At the same time, L.T. complained of joint pain in her
hip and wrists, had developed a rash, and appeared to be walking with a limp. See id. at 11–12.

Later that month, Ms. DeLozier took L.T. to a dermatologist, Dr. Elaine Gilmore.5 Ex. 4 at
8–10; see generally Ex. 7 (Records from Dr. Gilmore’s office). At that visit, Dr. Gilmore observed
“widespread . . . alopecic patches on the scalp.” Ex. 4 at 9. In her assessment, Dr. Gilmore noted
that L.T.’s recent hair loss was “possibly stimulated by [her] recent [HBV] vaccine,” although she
expressed the need for further research to evaluate whether such a relationship had scientific
support. Id. Dr. Gilmore also noted that L.T. had symptoms of eczema, and discussed the possible
diagnosis of atopic dermatitis versus irritant contact dermatitis with Petitioner. Id.

After examination, Dr. Gilmore prescribed L.T. a topical steroid to treat her alopecia and
an ointment to treat her eczema. Ex. 4 at 9. Dr. Gilmore recorded L.T.’s family history of eczema,
but noted (erroneously) that L.T. appeared to lack a family history of alopecia or similar conditions.
Ex. 4 at 8, 11 (observing a family history of connective tissue disease in mother characterized by
hair loss during doctor’s appointment a few months later); Tr. at 8–9 (describing family history in
mother of autoimmune connective tissue disorder characterized by hair loss). In December 2012,
L.T. had a series of lab tests done that revealed she had a positive ANA screen. Ex. 4 at 6.

On January 7, 2013, L.T. visited Dr. Gilmore’s practice again and this time was treated by
Kristen Ahern, M.D., a resident/fellow. Ex. 7 at 1. Petitioner reported that L.T.’s dermatitis was
improving, although her bald spots were worsening. Id. Dr. Ahern (consistent with Dr. Gilmore)
also noted that L.T.’s alopecia was “possibly stimulated by recent [HBV] vaccine,” and instructed
Petitioner to continue on the treatment plan previously discussed. Id. at 2. A physical exam showed
a negative hair pull test and small black dots in some of the bald spots indicating hairs that were
present (and thus potentially returning) but had “not yet erupted.” Id. at 1.

On January 22, 2013, L.T. visited Bethany Marston, M.D., a pediatric rheumatologist. See
Ex. 4 at 11. Dr. Marston noted that L.T. was suffering from AA and transient joint pain that had
developed about four days after her third HBV vaccination. Id. Dr. Marston recorded that L.T.’s

5
There is some discrepancy between when Petitioner alleges this visit occurred and what the records establish.
Petitioner asserts that L.T. saw Dr. Gilmore on November 12, 2012. Pet’r’s Post-Hearing Brief at 2 (citing Ex. 4, at
1). But Exhibit 4 at 1 is actually a note from a subsequent March 2013 doctor’s visit at Sunrise Pediatrics, and thus
references the November visit as part of L.T.’s medical history. See Ex. 4 at 1 (“date form completed 3/27/13”). The
date “11/12” (on Ex. 4 at 1) seems to be a generic reference to November 2012. In any event, the evidence does
establish that Petitioner sought some treatment for L.T. in November 2012, and the records reflect her
contemporaneous assertion that L.T. experienced hair loss within a few days of vaccination.

3
joint pain was not associated with swelling, erythema, or functional disability and that L.T.’s
symptoms were responding to the ointments and steroids she was earlier prescribed. See id. Other
testing revealed negative inflammatory markers and rheumatoid factor, and, “despite a
questionable family [history] of unspecified [mixed connective disease] in her mom and some
other autoimmune-induced syndromes in her extended family,” L.T.’s positive ANA was deemed
by Dr. Marston most likely the result of her then-resolving AA. Id.

L.T. returned to Dr. Gilmore’s practice again in March 2013. Ex. 7 at 4. L.T. was seen at
this time by Kimberly Brady, M.D., a resident. Ex. 7 at 4. Dr. Brady recorded that L.T.’s parents
had not noticed any improvement in her condition since their last visit. Id. She also noted that
L.T.’s HBV vaccine appeared temporally related to her AA, but “because this is not a widely seen
association, and [AA] is a relatively common disorder, it is difficult to say that the hepatitis vaccine
was responsible for the onset of [AA].” Id. at 4–5. Dr. Brady’s physical exam also revealed a
negative hair pull test and small black dots in some bald areas. Id. at 4–5. To address the lack of
improvement in L.T.’s AA symptoms, Dr. Brady changed L.T.’s steroid cream and ointment
prescription. Id. Other than her AA, L.T. had a normal physical exam. Id.

L.T. visited Dr. Gilmore’s practice three months later in June 2013 (now more than six
months since the onset of her AA symptoms) and was seen by Rachel Garner, M.D., a resident.
Ex. 7 at 7. Dr. Garner noted that L.T. still had some lingering AA symptoms, but there was
evidence of recovery as well—some short hairs in the bald areas that appeared to be new. Id. at 7–
8. L.T.’s rash had also returned, but it was found to be negative for fungus, leading Dr. Garner to
characterize it as atopic dermatitis (eczema), treatable with ointments and creams. Id. at 8. Dr.
Garner also performed a hair pull test which was negative and observed short hairs that appeared
new. Id. at 8.

Later, in August 2013, Petitioner took L.T. to Rochester General Hospital. Ex. 11 at 1.
There, L.T. was seen by Tracy Henderson, M.D. Id. at 4. Dr. Henderson observed that L.T. had
patchy AA and had been diagnosed with AA in November 2012, four days after her third HBV
vaccine. Id.at 4–5. Dr. Henderson also recorded a family history of an autoimmune disease in
L.T.’s mother. Id. at 3. Notes from the visit also show that Petitioner brought several articles into
the visit that mentioned an association between AA and the HBV vaccine. Id. at 4.

L.T.’s health history from 2014 to 2016

There are several subsequent gaps in the medical record. L.T. appears to have had her next
doctor’s visit in April 2014 for behavioral concerns at Rochester General Hospital. Ex. 11 at 12–
17. During this visit Dr. Henderson did not note any AA symptoms in the physical exam section
of the visit records. Id. at 16 (“Well-appearing, alert, very active.”). No mention was made at this
visit of L.T.’s AA, although it also appears the visit (besides behavioral concerns) was occasioned
by Ms. DeLozier’s wish to inquire about L.T.’s dietary issues.

4
 In August 2014, L.T. had a five-year well-child visit at Rochester General Hospital. Ex.
10. at 1-10. There, Andrew Sherman, M.D., observed that L.T. suffered from chronic eczema. Id.
at 4. Dr. Sherman also logged that L.T. had previously experienced AA because of an adverse
reaction to the HBV vaccine in November 2012. Id. Regarding L.T.’s initial hair loss, Dr. Sherman
recorded that L.T. lost her hair for “about a year,” and also suffered from worsening eczema around
the same time. Id. Dr. Sherman’s objective physical examination did not note any AA symptoms,
but did note some eczema behind L.T.’s knees. See id. at 5–6. Only eczema was listed in the current
concerns section. Id. at 6. Accordingly, this record does not suggest that L.T. was at this point still
experiencing sequelae from her November 2012 onset of AA.

L.T. returned to Rochester General Hospital nine months later, on May 22, 2015, because
she developed chicken pox and a sore throat. Ex. 10 at 11–19. Dr. Sherman noted that she had run
a fever for four days after likely exposure to the varicella virus from her brother and father. Id. at
17. At this visit, AA was recorded in the current problem list, but is not mentioned in her in her
physical exam, assessment, and diagnoses (thus strongly suggesting she was not experiencing any
active symptoms from it). Id. 11, 17–18. L.T. was treated for her sore throat and chicken pox and
discharged. Id. at 18. A few months later, on July 1, 2015, L.T. had another visit at Rochester
General Hospital because of possible insect bites and a swollen eye. Id. at 20. AA is mentioned
nowhere but her medical history. See id.

The next filed record is from August 2015, when L.T. returned to Rochester General
Hospital for a sore throat. Ex. 11 at 18–24 (visit on August 10, 2015). L.T. was tested for a sore
throat, treated for her sore throat, and discharged. Id. She was seen by Julia Stein, M.D., who noted
a medical history of AA but did not record any other information about AA at that time. See
generally id. Later that same month, L.T. visited Rochester General Hospital for a routine child
exam. Ex. 10 at 28 (visit on August 19, 2015). L.T.’s weight was noted as being low and weight
management was discussed. Id. at 35. Dr. Sherman did not list any current concerns, active issues,
or chronic issues. Id. No notes of AA were made except in the health history section. See id. (noting
that L.T. was visiting the dermatologist later that day).

The same day, August 19, 2015, L.T. visited Universal Dermatology PLLC—Dr.
Gilmore’s practice. Ex. 9 at 1. Petitioner’s reason for bringing L.T. in was for “hair loss that is
multifocal and mild in severity,” that had manifested two weeks prior. Id. A physical exam
revealed some hair loss patches on L.T.’s central forehead and right inferior occipital scalp, along
with thin eyebrows and “coin-like eczematous patches” on her arms and left thigh. Id. Dr. Gilmore
recommended that her AA could be treated using topical steroids, and that Petitioner should
contact his office if symptoms plateaued or worsened despite treatment. Id.

L.T. had a follow-up visit with Dr. Gilmore on September 25, 2015. Ex. 9 at 5. There, Dr.
Gilmore noted that L.T.’s AA was improving with treatment and improved overall. Id. Dr. Gilmore
observed “minimal alopecic patches on the anterior scalp and thin eyebrows throughout.” Id. Dr.
Gilmore advised Petitioner to reduce the amount of steroid being taken and that L.T. could apply

5
ointment to her face to stimulate eyebrow growth. Id. L.T. was scheduled to follow-up in one-
month for a “focused visit.” Id.

L.T.’s health history from 2016 to present

L.T. next returned to Dr. Gilmore more than six months later, in April 2016. Ex. 28 at 1.
At this time, Dr. Gilmore observed discrete non-scarring patches of hair loss on the “right superior
temple and left occipital scalp.” Id. Dr. Gilmore discussed with Petitioner the natural history of
AA, which can be associated with flares and remissions. Id. Dr. Gilmore also noted that L.T.’s hair
loss, at that time, was not severe enough to warrant systemic therapy. Id.

In November 2016, L.T. presented to Dr. Gilmore again for further evaluation. Ex. 28 at 2.
During the visit Dr. Gilmore observed AA on L.T.’s “right superior central forehead, left superior
central forehead, and left lateral eyebrow.” Id. This distribution of AA was notably different than
what had been reported in August 2015. Compare Ex. 9 at 3 (showing AA patches in August 2015
behind the right ear and on the left superior forehead), with Ex. 28 at 3 (showing AA patches in
November 2016 on the left eyebrow and on two locations on the forehead). Dr. Gilmore discussed
new possible therapies for L.T.’s condition, but explained that it would be difficult to predict her
future hair growth. Id. The next month, L.T. went into Rochester Regional Health for a well-child
visit. Ex. 29 at 6. Dr. Sherman observed that L.T. had AA symptoms, and was also complaining
of knee, wrist, and elbow pain at times, consistent with complaints from the previous month. Id.

L.T. went to the doctor again in December 16, 2016, for a well-child visit at Rochester
Regional Health. Ex. 29 at 1. There, in the subjective notes section, Dr. Sherman recorded that
L.T. “[s]till has [a] patch of alopecia behind right ear and near midline of mid occipital area.” Id.
at 6. The AA patch behind her right ear was also noted in the objective section of the visit record.
Id. at 6–7. L.T. was scheduled for another well-child visit next year and informed Dr. Sherman
that she would follow-up on her AA with a dermatologist and rheumatologist. Id. at 6–8.

L.T. presented to Rochester Regional again in late June 2017 for a cough and sore throat.
Ex. 29 at 17. No notes on AA or eczema were made other than in the health history section. See
id. Then, L.T. visited Rochester Regional again in August 2017 for her eight-year well-child visit.
Ex. 29 at 27. In the subjective notes section of the visit Dr. Sherman recorded that L.T. had no
current concerns and was “doing well.” Id. at 32. Dr. Sherman also did not mention any AA in his
objective examination of L.T. Id. at 33. L.T. declined immunizations citing a prior medical history
of AA after vaccination. Id.

L.T. returned to Rochester Regional in October 2018 for her nine-year well-child visit. Ex.
29 at 42. In the subjective notes section Dr. Sherman recorded that there were no current concerns,
L.T. was doing well, and there were “no current hair changes.” Id. at 47–48 (assessing no active
or chronic issues and stating that L.T. was doing well). In the objective physical assessment Dr.
Sherman did not note any AA. Id. at 48. No records were filed for the period after the end of 2018
setting forth any concerns about new AA flares.

6
II. Witness Testimony

A. Petitioner’s expert: Dr. David Norris

Dr. Norris filed a single report and testified at hearing. See Ex. 16, filed June 7, 2017 (ECF
No. 40-1) (“Norris Report”). He opined largely that L.T.’s third HBV vaccine “was the trigger that
caused [her] to develop [AA].” Norris Report at 2.

Dr. Norris obtained a B.A. from Johns Hopkins University in 1969. Ex. 17, filed on June
7, 2017 (ECF No. 40-2) (“Norris CV”). He earned his M.D. from Duke University Medical School
in 1972. Id. at 1. After completing his formal education, Dr. Norris held a sub-fellowship in
Hematology and Oncology during 1973 at Duke University; an internship in Internal Medicine
during 1973–1974 at Ohio State University; and a Dermatology Residency during 1974–1977 at
the University of Colorado School of Medicine. Id. Additionally, Dr. Norris is board certified in
Dermatology, Dermatologic Immunology and Diagnostic and Laboratory Immunology. Id.

Dr. Norris is presently the chairman of the Department of Dermatology at the University
of Colorado School of Medicine, where he has also been a professor. Norris CV at 1. Dr. Norris
has received research funding for several topics relating to immunodermatology and the “Alopecia
Areata Registry.” Id. at 3. Dr. Norris is also published and has conducted research related to AA,
dermatology, and immunodermatology. See generally id.

Dr. Norris provided an overall description of AA. Norris Report at 1. AA is a clinical hair
loss disease that is “at its root an immunologic disease controlled by genes.” Tr. 41–42. In
particular, AA is a polygenic autoimmune disease, with “other autoimmune components that go
along with it.” Id. at 42. The most common of such comorbid conditions is hypothyroidism, “[b]ut
another important immunologic disease that goes along with [AA] is atopy.” Tr. at 42–43 (noting
that L.T. has atopic dermatitis). He also described the waxing and waning nature of the disease,
and how a patient’s long-term prognosis is ultimately affected by her genetic profile. Id. at 51–52
(“the current thinking is that the patients that have the worst genetic profile will get the worst
disease and early on and the . . . baldness on the scalp will remain”).

From this, Dr. Norris proposed a theory of how vaccines generally (and more specifically,
the HBV vaccine) could cause AA. Norris Report at 2. Dr. Norris submitted that because it is an
autoimmune disease, AA’s onset may follow events such as “infections, periods of stress, and
immunostimulation, including vaccination.” Id. (citing Y. Zafrir, et al., Vaccines, Infections, and
Alopecia Areata, in Vaccines & Autoimmunity (Yehuda Shoenfeld et al. eds., 2015), filed as Ex.
27 on Jan. 30, 2019 (ECF No. 55-2) (“Zafrir”)); Tr. at 43–44. Dr. Norris, referring to Zafrir,
explained that that these events can cause a change in the “immune privilege” of hair follicles
(meaning the capacity to tolerate antigen presentation without an inflammatory, immune-driven
response), which in turn causes the hair loss associated with AA. Tr. at 44–45. Dr. Norris added
that in his understanding, the dermatologic medical community accepts the existence of triggers
as significant in causing AA, with 25 percent of AA patients able to identify a likely trigger after

7
symptoms occur. Id. at 48. However, as Respondent has correctly observed, Zafrir considered
mouse studies that “suggest[ed] that there was no association between vaccination and AA
development.” Zafrir at 3 (emphasis added).6

Dr. Norris offered some other specific items of medical literature that he maintained
supported the contention that the HBV vaccine could trigger AA. Tr. at 57; Norris Report at 2
(citing R. Wise, et al., Hair Loss After Routine Immunizations, 278 JAMA 1176 (1997), filed as
Ex. 26 on Jan. 30, 2019 (ECF No. 55-1) (“Wise”) (concluding that “we believe that immunizations
warrant consideration among potential causes of hair loss”); Tr. at 49–51. Wise analyzed reports
from the Vaccine Adverse Event Reporting System (“VAERS”), plus reports made to the FDA
that predated VAERS, of instances in which AA following vaccination was alleged. See Wise at
1. The study yielded 60 evaluable reports of hair loss following immunization since 1984 and
coded for alopecia, with 46 of the instant cases involving the HBV vaccine. Id. In addition, 16 of
the 60 cases involved a positive rechallenge7—meaning the individual had previously been
vaccinated, but saw new symptoms in a shorter timeframe after receipt of a follow-up dose. Id.
Although only four of the sixteen were confirmed as definite rechallenges, three of the four
rechallenges involved the administration of the HBV vaccine. Id. at 1–2.

Dr. Norris deemed such evidence to strongly support causation. Tr. at 51. But he did
acknowledge some limitations with Wise. He conceded that Wise was published more than 20
years ago (and hence had not been followed up with any corroborative studies), and also that the
study’s authors had only discussed hair loss in general terms. Id. at 50. However, he maintained
his opinion that the cases discussed in Wise mostly involved AA. Id. Overall, Dr. Norris deemed
Wise his best evidence for the proposition that the HBV vaccine could cause AA. See Tr. at 89.

Petitioner also relied on a more recent article, although it was filed shortly after the hearing
(and not otherwise mentioned by Dr. Norris in his testimony). See C. Richardson, et al., Evaluation
of the Relationship Between Alopecia Areata and Viral Antigen Exposure, 9 Am. J. Clinical

6
Zafrir has other issues that limit the weight it should receive. It was co-authored by Dr. Yehuda Shoenfeld, a
frequently-seen medical expert in Vaccine Program cases who takes an expansive (but frequently unpersuasive and/or
unreliable) view of the capacity of vaccines generally to cause autoimmunity. See, e.g., Yalacki v. Sec’y of Health &
Human Servs., No. 14-278V, 2019 WL 1061429, at *33 (Fed. Cl. Spec. Mstr. Jan. 31, 2019) (finding that Dr.
Shoenfeld’s blanket assertions regarding vaccines and autoimmunity “harm his overall credibility”). Zafrir also relied
on another article not filed in this case that—as Dr. Norris conceded—says nothing about AA triggers. Zafrir at 2,
citing D. Bogdanos, et al., Tracing Environmental Markers if Autoimmunity: Introducing the Infectome, 56
Immunologic Research 220 (2013). Respondent’s Post-Hearing Brief at 6, filed on June 3, 2019, (ECF No. 65); Tr. at
97–98.
7
Other special masters have described “rechallenge” as follows: “[c]hallenge-rechallenge happens when a person (1)
is exposed to one antigen, (2) reacts to that antigen in a particular way, (3) is given the same antigen again, and (4)
reacts to that antigen similarly. Typically, the second reaction is faster and more severe.” Nussman v. Sec’y of Health
& Human Servs., 83 Fed. Cl. 111, 119 (Fed. Cl. 2008) (internal citations omitted) (quoting Nussman v. Sec’y of Health
& Human Servs., No. 99-500V, 2008 WL 449656, at *9 (Fed. Cl. Spec. Mstr. Jan. 31, 2008)).

8
Dermatology 119 (2018), filed on February 28, 2019, as Ex. 30 (ECF No. 60) (“Richardson”).8
Richardson’s findings are based on a larger sample of patients—nearly 250,000 cases of HBV
vaccination and 656 cases of AA—derived from the electronic medical record database at the
University of Rochester Medical Center. See Richardson at 1. The query sought “to identify
patients with AA, coexisting viral infections, vaccinations, or interferon therapy [ ] to determine if
the presence of AA and these conditions was higher than in AA patients without the associated
conditions or therapy.” Id.

Accounting for different types of alopecia and hair loss, Richardson’s authors observed an
increased frequency of AA among those who had received the HBV surface antigen, whether from
vaccination or wild virus infection. See Richardson at 4, 6 (finding support for the conclusion “that
exposure to hepatitis B antigens, through either infection or vaccination, are associated with AA
in a subset of patients”). Specifically, they observed AA to be two times more prevalent in
individuals exposed to the HBV vaccine than the total population, and 2.73 times more likely to
occur in a person exposed to the HBV vaccine. Id. at 4 (showing increased prevalence and odds
ratio of AA after exposure to the HBV vaccine).9 Richardson discussed two possible mechanisms
that could explain how HBV vaccination could trigger AA: (1) the induction of interferon (a
cytokine whose upregulation could be instigated by the immune process stimulated by
vaccination);10 or (2) molecular mimicry. Id. at 5. Richardson supports the plausibility of each of
these causative theories, although it admits more research is needed to determine if either is the
responsible biologic mechanism causing the increased prevalence and odds reported earlier. See
id. at 5–7.

8
Richardson was not identified or discussed during the hearing, despite it being published almost a full year prior. It
was also co-authored by one of L.T.’s treaters, Dr. Elaine Gilmore. Richardson at 1. In addition, it focuses on only
two cases—one of which is likely L.T. herself. See Richardson at 2 (describing “patient 1” as a “3-year-old female
with hair loss of several weeks’ duration []. [AA] began 4 days after receiving the third dose of the hepatitis B vaccine.
The patient also developed transient joint pain of the wrists, arms, and right knee without associated swelling. She had
a positive antinuclear antibody (ANA) (1:320 speckled/homogenous pattern) . . . . , and she had no significant medical
history. Her family history included a mother with positive ANA and AA, and a sister with positive thyroid antibodies.
Physical examination revealed widespread and well-demarcated alopecic patches on the scalp without scarring,
erythema, or scale.”). Such references actually undercut Petitioner’s assertion that “nobody in [L.T.’s] family had ever
been diagnosed with alopecia.” See Petitioner’s Post-hearing Brief at 1, filed on June 3, 2019, (ECF No. 64).
9
The authors also observed that the enhanced possibility of AA after vaccination was statistically reliable. See
Richardson at 4 fig. 2 (reporting a p-value of <0.0005 for HBV and AA association). A low p-value helps establish
“statistical significance,” because it shows “something other than chance must be involved.” Federal Judicial Center
& National Research Council, Reference Manual on Scientific Evidence 250 (3d ed. 2011). By contrast, a large p-
value “indicate[s] that disparity can easily be explained by the play of chance.” Id. Generally, a p-value of 5 percent
or less (p<0.05) is considered the starting point—indicating that random error is not at work. Id. at 251–52; see also
id. at 251 n.101 (citing Castaneda v. Partilda, 430 U.S. 482, 496 n.17 (1977); Hazelwood School District v. United
States, 433 U.S. 299, 311 n.17 (1977)).
10
Interferons are “any family of glycoproteins that exert virus non-specific but host specific antiviral activity by
inducing the transcription of cellular genes coding for antiviral proteins that selectively inhibit the synthesis of viral
RNA and proteins.” Dorland’s Illustrated Medical Dictionary 948 (32 ed. 2012) (hereinafter “Dorland’s”).

9
 In addition to proposing that the HBV vaccine could trigger AA, Dr. Norris testified about
L.T.’s individual circumstances, opining that the vaccine had likely done so in this case (and in a
reasonable timeframe as well). Norris Report at 2; Tr. at 55–56. In support, he identified four cases
from Wise in which the studied individual reported hair loss as early as one day after vaccination.
Norris Report at 2; Tr. at 55–56 (“[i]n the case here, though, it’s . . . . [onset is in] several days,
and there are plenty of cases like that in the literature”); Wise at 1–2. He also emphasized that in
the cases reported in Wise, onset of hair loss after vaccination was “usually more rapid after
subsequent revaccination with HBV vaccine.” Norris Report at 2. Thus, he reasoned, because L.T.
had previously received the HBV vaccine, her immune response in November 2012 (and its
purported damaging impact, in the form of AA) was likely faster than it would have been. Tr. at
84 (disagreeing with Dr. Tollefson’s opinion).

On cross examination Dr. Norris defended Wise and its applicability to this case. See Tr. at
108–32. Respondent’s counsel questioned Dr. Norris about several issues with Wise—e.g., the
small sample size of clear rechallenge cases, the lack of specificity in Wise when describing the
type of hair loss, and whether any of the clear rechallenge cases were similar enough to L.T.’s case
to be helpful. Id. On each of these points Dr. Norris maintained that Wise was persuasive. Id.

B. Respondent’s expert: Dr. Megha Tollefson

Dr. Tollefson served as Respondent’s expert, and offered a single report as well as
testimony at hearing. Ex. A, filed Sept. 15, 2017 (ECF No. 43-1) (“Tollefson Report”). Dr.
Tollefson disputed Dr. Norris’s opinion that L.T.’s injuries were caused by her receipt of the HBV
vaccine in February 2012, maintaining instead that her genetic risk factors played more of a role
in causing her symptoms. See generally Tollefson Report.

Dr. Tollefson graduated with a BA from Stanford University in 1999. Ex. B, filed on Jan.
28, 2019 (ECF No. 54-1) (“Tollefson CV”). She went on to earn her M.D. from Mayo Medical
School in 2003. Tollefson CV at 1. She subsequently completed a pediatric residency at the Mayo
Clinic College of Medicine from 2003–2006; a dermatology residency at the Mayo Clinic College
of Medicine from 2007–2010; and a pediatric dermatology fellowship at Stanford University from
2010–2011. Id. Dr. Tollefson is board certified in dermatology and pediatric dermatology. Id. She
has been an attending pediatric dermatologist at the Mayo Clinic since 2010. Id. at 2. She has also
served as an assistant professor in pediatrics at the Mayo Clinic College of Medicine and Science.
Id. Outside of her clinical practice Dr. Tollefson has a few publications and research projects on
AA in children. Id. at 11, 19–20, 31.

Like Dr. Norris, Dr. Tollefson took some time at hearing to review AA (which she agreed
L.T. experienced). Tollefson Report at 4; Tr. at 150. She accepted Dr. Norris’s contention that AA
is rightly understood to be an autoimmune disorder with a possible genetic basis. Tollefson Report
at 2–3; Tr. at 150–51. However, in her view susceptibility to AA stems mostly from genetic

10
factors—particularly mutations in the filaggrin11 gene. See Tollefson Report at 3 (“[p]atients with
[AA] have a strong underlying genetic susceptibility profile . . . more likely to be associated with
more severe disease and strong risk among family members.”) (citing R. Betz, et al., Loss-of-
function Mutations in the filaggrin gene and Alopecia Areata: Strong Risk Factor for a Severe
Course of Disease in Patients Comorbid for Atopic Disease, 127(11) J. Investigative Dermatology
2539–43 (2007)); see also Tr. at 151. Dr. Tollefson also noted that certain gene mutations have
been associated with a “more severe disease course, and also with atopic dermatitis (AD), or
eczema.” Id. Dr. Tollefson allowed, however, that some environmental triggers (for example,
stressful events) could also produce AA, but that no one trigger has been identified as a primary
cause. Id.

Based on review of the relevant medical records, Dr. Tollefson opined that L.T. possessed
several of the risk factors necessary for the development of AA. Tollefson Report at 3. In
particular, she identified L.T.’s family history, as well as her eczema and respiratory problems. Id.
at 3–4. To support her assertion that L.T. had a strong family history of autoimmune disease, Dr.
Tollefson referenced Ms. DeLozier’s unspecified autoimmune connective tissue disorder, with
hair loss and a positive ANA; L.T.’s third cousin having vitiligo; and L.T.’s older sister having
positive thyroid antibodies. Id. This, Dr. Tollefson maintained, opened the door to the possibility
that L.T. would have a positive ANA if tested (and in fact L.T. did so on some occasions). Id.
(noting that a positive ANA can develop even in the absence of other symptoms). At a minimum,
such facts allowed for the conclusion that L.T. was at an increased risk of autoimmune disease and
AA. Id. (citing N. Barahmani, et al., History of Atopy or Autoimmunity Increases Risk of Alopecia
Areata, 61 J. Am. Acad. Dermatology 581–91 (2009), filed as Ex. C (ECF No. 54-2)
(“Barahmani”)).

Dr. Tollefson also discussed some other risk factors, like L.T.’s eczema and “episodes of
wheezing responsive to albuterol and steroids.” Tollefson Report at 4. As she explained, eczema
in many patients has been linked to mutations “in the filaggrin gene and other innate immune
factors.” Id. (citing T. Miyagaki, et al., Lifetime Incidence Risk of Alopecia Areata Estimated at
2.1% by Rochester Epidemiology Project, 1990–2009, 134(4) J. Investigative Dermatology1141–
42 (2014), filed as Ex. G (ECF No. 54-6)) (noting also that “vaccines do not cause eczema).
Respiratory problems are also common in patients who have a family history of eczema. Id. Based
upon these factors, Dr. Tollefson proposed that L.T. might have “atopic diathesis,” with a genetic
risk for atopic disorders “none of which are caused by any vaccines.” Id. The presence of such
atopic diseases increased L.T.’s risk for AA. Id. (citing Barahmani).

Besides offering her own reading of the record, Dr. Tollefson disputed the reliability of
some of the primary literature relied upon by Dr. Norris to associate the HBV vaccine specifically

11
Filaggrin is “a protein that is synthesized in the granular level of the epidermis and aggregates intermediate filaments
of keratin by promoting formation of disulfide bonds.” Dorland’s at 706.

11
with AA. See Tollefson Report at 3; Tr. 151–56. Wise, for example, did not appear to differentiate
among the various types of alopecia. Tollefson Report at 3; Tr. at 155–56. This made it “impossible
to say how many, if any of [those] cases, were associated with [AA].” Tollefson Report at 3. In
addition, the four “clear examples” of hair loss from Wise offered to support proof of rechallenge
after a subsequent HBV vaccination were either distinguishable from L.T.’s case or not probative
of causation. Tr. at 153 (noting only a purely temporal relationship in patient 1 between vaccination
and hair loss), 154–55 (stating that the facts given about patient 2 only show that patient was
susceptible to hair loss and there was multiple triggers), 155 (stating that patient 3 likely suffered
from telogen effluvium12 rather than from AA). As a result, Wise at best established a pure
temporal association between vaccination and AA. Tollefson Report at 3.

Dr. Tollefson similarly contested the degree to which the concept of challenge-rechallenge
supported Petitioner’s causation arguments in light of L.T.’s own history. Many of the studied
individuals referenced in Wise had experienced hair loss in the process of receiving multiple doses
of HBV. Tr. at 151–55; Tollefson Report at 3; see also Wise at 1–2 (Patient 1 developing hair loss
after second and third HPV vaccine; Patient 2 developing hair loss after first, second, and third
HPV vaccine; Patient 3 developing hair loss after first and second HPV vaccine). By contrast,
although L.T. received HPV twice prior to the vaccination at issue, she never previously
experienced any adverse effects. Tollefson Report at 3.

Dr. Tollefson also responded to questions on a number of related issues. See generally Tr.
166–72. Some of these questions were directed to the role of genetics in developing AA. Tr. at
168. She admitted that in some children, genetics played a more important role in the development
of AA than a triggering event. Tr. at 168. Other questions were directed to a hypothetical: whether,
in an individual who had AA, multiple relapses (separated by years) could be attributed to different
triggers. Tr. at 171. To that, Dr. Tollefson answered yes. Id.

Finally, Dr. Tollefson questioned whether onset of L.T.’s AA symptoms occurred in a
medically acceptable timeframe. Tollefson Report at 3. In so maintaining, she noted that L.T.’s
onset did not in fact closely match the cases reported in Wise, who received the same vaccine but
experienced symptoms each time. Id. Dr. Tollefson proposed that onset of AA after a trigger could
occur as much as a few weeks to a couple of months thereafter, although she was unable to identify
a minimum time that it would take for symptoms to manifest, without more evidence of an
autoimmune reaction. Tr. at 158. (stating that she would need to know “as Dr. Norris said, if there
was any subclinical inflammation there”).

C. Christine DeLozier

12
Telogen effluvium is “the early, excessive, temporary loss of club hairs from normal resting follicles in the scalp as
a result of traumatization by some stimulus (e.g., after surgery or childbirth; with starvation, side effects of drugs,
traction on hair, high fever, or certain diseases; or with psychogenic stress). The normal hair cycle is changed and the
anagen phase ends prematurely, moving into the catagen and telogen phases.” Dorland’s at 595.

12
 Ms. DeLozier testified at hearing about L.T.’s health history and family medical history.
See Tr. at 5–31. She explained that she had a history of hair loss herself. Tr. at 8, 27. She had
experienced such hair loss after a trip to Nicaragua, several years before L.T. was born, and
recalled that she had received the HBV vaccine shortly before this trip. Tr. at 27–28. Ms.
DeLozier’s hair loss was diagnosed as a mixed connective tissue disorder, and testing revealed a
positive ANA. Tr. at 8–9.

Petitioner also described L.T.’s experience with AA over time. Tr. at 12–22. As she
admitted, L.T. had experienced a partial recovery from her AA about a year after onset. Tr. at 19–
20 (describing L.T.’s hairline as receded and thinner). Thereafter, L.T. would experience
recurrences of hair loss if she had an illness or infection. Tr. 20–22. Petitioner did not testify to
another post-vaccination AA recurrence.

III. Procedural History

After filing this action, Petitioner continued to file relevant medical records. Respondent
then filed his Rule 4(c) Report on February 28, 2017 (ECF No. 36), contesting whether Petitioner
had established an evidentiary basis for entitlement. Rule 4(c) Report at 4–5. Over the next few
years, the parties continued to litigate this case, and even engaged in a period of settlement
discussions that were ultimately unfruitful. (ECF No. 44). They filed expert reports, pre-hearing
briefs, and then presented evidence at an entitlement hearing held in February of 2019. Post-trial
briefs were filed in June 2019. (ECF Nos. 64, 65).

IV. Applicable Law

A. Standards for Vaccine Claims

To receive compensation in the Vaccine Program, a petitioner must prove that: (1) they
suffered an injury falling within the Vaccine Injury Table (i.e., a “Table Injury”); or (2) they
suffered an injury actually caused by a vaccine (i.e., a “Non-Table Injury.) See Sections
13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3; § 11(c)(1)(C)(ii)(I); see also
Moberly v. Sec'y of Health & Human Servs., 592 F.3d 1315, 1321 (Fed. Cir. 2010); Capizzano v.
Sec'y of Health & Human Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006). In this case, Petitioner
does not assert a Table claim.

For both Table and Non–Table claims, Vaccine Program petitioners bear a “preponderance
of the evidence” burden of proof. Section 13(1)(a). That is, a petitioner must offer evidence that
leads the “trier of fact to believe that the existence of a fact is more probable than its nonexistence
before [he] may find in favor of the party who has the burden to persuade the judge of the fact's
existence.” Moberly, 592 F.3d at 1322 n.2; see also Snowbank Enter. v. United States, 6 Cl. Ct.
476, 486 (1984) (explaining that mere conjecture or speculation is insufficient under a
preponderance standard). On one hand, proof of medical certainty is not required. Bunting v. Sec'y
of Health & Human Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). But on the other hand, a petitioner

13
must demonstrate that the vaccine was “not only [the] but-for cause of the injury but also a
substantial factor in bringing about the injury.” Moberly, 592 F.3d at 1321 (quoting Shyface v.
Sec'y of Health & Human Servs., 165 F.3d 1344, 1352–53 (Fed. Cir. 1999)); Pafford v. Sec'y of
Health & Human Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). A petitioner may not receive a
Vaccine Program award based solely on his assertions; rather, the petition must be supported by
either medical records or by the opinion of a competent physician. Section 13(a)(1).

In attempting to establish entitlement to a Vaccine Program award of compensation for a
Non–Table claim, a petitioner must satisfy all three of the elements established by the Federal
Circuit in Althen v. Sec'y of Health & Human Servs., 418 F.3d 1274 (Fed. Cir. 2005): “(1) a medical
theory causally connecting the vaccination and the injury; (2) a logical sequence of cause and
effect showing that the vaccination was the reason for the injury; and (3) a showing of proximate
temporal relationship between vaccination and injury.” Althen, 418 F.3d at 1278. Each Althen
prong requires a different showing and is discussed in turn along with the parties’ arguments and
my findings.

Under Althen prong one, petitioners must provide a “reputable medical theory,”
demonstrating that the vaccine received can cause the type of injury alleged. Pafford, 451 F.3d at
1355–56 (citations omitted). To satisfy this prong, a petitioner's theory must be based on a “sound
and reliable medical or scientific explanation.” Knudsen v. Sec'y of Health & Human Servs., 35
F.3d 543, 548 (Fed. Cir. 1994). Such a theory must only be “legally probable, not medically or
scientifically certain.” Id. at 549. This standard was recently clarified by the Federal Circuit. See
Boatmon v. Sec'y of Health & Human Servs., 941 F.3d 1351, 1359–60 (Fed. Cir. 2019) (stating
that the correct standard for Althen prong one is “reputable,” and “sound and reliable” not a “lower
reasonable standard” (internal quotations omitted)).

Petitioners may satisfy the first Althen prong without resort to medical literature,
epidemiological studies, demonstration of a specific mechanism, or a generally accepted medical
theory. Andreu v. Sec'y of Health & Human Servs., 569 F.3d 1367, 1378–79 (Fed. Cir. 2009) (citing
Capizzano, 440 F.3d at 1325–26). Special masters, despite their expertise, are not empowered by
statute to conclusively resolve what are essentially thorny scientific and medical questions, and
thus scientific evidence offered to establish Althen prong one is viewed “not through the lens of
the laboratorian, but instead from the vantage point of the Vaccine Act's preponderant evidence
standard.” Id. at 1380. This is consistent with the 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).13

13
Although there has been some confusion in the past as to whether the first Althen prong is itself subject to a
preponderant standard, ample controlling authority stands for the more straightforward proposition that the first Althen
prong is subject to a preponderance standard. Broekelschen v. Sec'y of Health & Human Servs., 618 F.3d 1339, 1350
(Fed. Cir. 2010).

14
 The second Althen prong requires proof of a logical sequence of cause and effect, usually
supported by facts derived from a petitioner's medical records. Althen, 418 F.3d at 1278; Andreu,
569 F.3d at 1375–77; Capizzano, 440 F.3d at 1326; Grant v. Sec'y of Health & Human Servs., 956
F.2d 1144, 1148 (Fed. Cir. 1992). In establishing that a vaccine “did cause” injury, the opinions
and views of the injured party's treating physicians are entitled to some weight. Andreu, 569 F.3d
at 1367; Capizzano, 440 F.3d at 1326 (“medical records and medical opinion testimony are favored
in vaccine cases, as treating physicians are likely to be in the best position to determine whether a
‘logical sequence of cause and effect show[s] that the vaccination was the reason for the injury’”)
(quoting Althen, 418 F.3d at 1280). Medical records are generally viewed as particularly
trustworthy evidence, since they are created contemporaneously with the treatment of the patient.
Cucuras v. Sec'y of Health & Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).

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 they must be
considered and carefully evaluated. Section 13(b)(1) (providing that “[a]ny such diagnosis,
conclusion, judgment, test result, report, or summary shall not be binding on the special master or
court”); Snyder v. Sec'y of Health & Human Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“there is
nothing . . . that mandates that the testimony of a treating physician is sacrosanct—that it must be
accepted in its entirety and cannot be rebutted”). As with expert testimony offered to establish a
theory of causation, the opinions or diagnoses of treating physicians are only as trustworthy as the
reasonableness of their suppositions or bases. The views of treating physicians should also be
weighed against other, contrary evidence also present in the record—including conflicting
opinions among such individuals. Hibbard v. Sec'y of Health & Human Servs., 100 Fed. Cl. 742,
749 (2011) (not arbitrary or capricious for special master to weigh competing treating physicians'
conclusions against each other), aff'd, 698 F.3d 1355 (Fed. Cir. 2012); Veryzer v. Sec'y of Dept. of
Health & Human Servs., No. 06–522V, 2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr. Apr. 29,
2011), mot. for review den'd, 100 Fed. Cl. 344, 356–57 (2011), aff'd without opinion, 475 F. App’x.
765 (Fed. Cir. 2012).

The third Althen prong requires establishing a “proximate temporal relationship” between
the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to the
phrase “medically-acceptable temporal relationship.” Id. 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).

15
 B. Law Governing Analysis of Fact Evidence

The process for making determinations in Vaccine Program cases regarding factual issues
begins with consideration of the medical records. Section 11(c)(2). The special master is required
to consider “all [ ] relevant medical and scientific evidence contained in the record,” including
“any diagnosis, conclusion, medical judgment, or autopsy or coroner's report which is contained
in the record regarding the nature, causation, and aggravation of the petitioner's illness, disability,
injury, condition, or death,” as well as the “results of any diagnostic or evaluative test which are
contained in the record and the summaries and conclusions.” Section 13(b)(1)(A). The special
master is then required to weigh the evidence presented, including contemporaneous medical
records and testimony. See Burns v. Sec'y of Health & Human Servs., 3 F.3d 415, 417 (Fed. Cir.
1993) (determining that it is within the special master's discretion to determine whether to afford
greater weight to contemporaneous medical records than to other evidence, such as oral testimony
surrounding the events in question that was given at a later date, provided that such determination
is evidenced by a rational determination).

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

Accordingly, if the medical records are clear, consistent, and complete, then they should
be afforded substantial weight. Lowrie v. Sec'y of Health & Human Servs., No. 03–1585V, 2005
WL 6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical
records are generally found to be deserving of greater evidentiary weight than oral testimony—
especially where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528;
see also Murphy v. Sec'y of Health & Human Servs., 23 Cl. Ct. 726, 733 (1991), aff'd per curiam,
968 F.2d 1226 (Fed. Cir. 1992), cert. den'd, Murphy v. Sullivan, 506 U.S. 974 (1992) (citing United
States v. United States Gypsum Co., 333 U.S. 364, 396 (1947) (“[i]t has generally been held that
oral testimony which is in conflict with contemporaneous documents is entitled to little evidentiary
weight.”)).

16
 However, there are situations in which compelling oral testimony may be more persuasive
than written records, such as where records are deemed to be incomplete or inaccurate. Campbell
v. Sec'y of Health & Human Servs., 69 Fed. Cl. 775, 779 (2006) (“like any norm based upon
common sense and experience, this rule should not be treated as an absolute and must yield where
the factual predicates for its application are weak or lacking”); Lowrie, 2005 WL 6117475, at *19
(“[w]ritten records which are, themselves, inconsistent, should be accorded less deference than
those which are internally consistent”) (quoting Murphy, 23 Cl. Ct. at 733)). Ultimately, a
determination regarding a witness's credibility is needed when determining the weight that such
testimony should be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec'y of Health & Human
Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).

When witness testimony is offered to overcome the presumption of accuracy afforded to
contemporaneous medical records, such testimony must be “consistent, clear, cogent, and
compelling.” Sanchez, 2013 WL 1880825, at *3 (citing Blutstein v. Sec'y of Health & Human
Servs., No. 90–2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30, 1998)). In
determining the accuracy and completeness of medical records, the Court of Federal Claims has
listed four possible explanations for inconsistencies between contemporaneously created medical
records and later testimony: (1) a person's failure to recount to the medical professional everything
that happened during the relevant time period; (2) the medical professional's failure to document
everything reported to her or him; (3) a person's faulty recollection of the events when presenting
testimony; or (4) a person's purposeful recounting of symptoms that did not exist. La Londe v.
Sec'y of Health & Human Servs., 110 Fed. Cl. 184, 203–04 (2013), aff'd, 746 F.3d 1334 (Fed. Cir.
2014). In making a determination regarding whether to afford greater weight to contemporaneous
medical records or other evidence, such as testimony at hearing, there must be evidence that this
decision was the result of a rational determination. Burns, 3 F.3d at 417.

C. Analysis of Expert Testimony

Establishing a sound and reliable medical theory often requires a petitioner to present
expert testimony in support of his claim. Lampe v. Sec'y of Health & Human Servs., 219 F.3d 1357,
1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to the
factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharm., Inc., 509
U.S. 579, 594–96 (1993). See Cedillo v. Sec'y of Health & Human Servs., 617 F.3d 1328, 1339
(Fed. Cir. 2010) (citing Terran v. Sec'y of Health & Human Servs., 195 F.3d 1302, 1316 (Fed. Cir.
1999). Under Daubert, the factors for analyzing the reliability of testimony are:

(1) whether a theory or technique can be (and has been) tested; (2) whether the
theory or technique has been subjected to peer review and publication; (3) whether
there is a known or potential rate of error and whether there are standards for
controlling the error; and (4) whether the theory or technique enjoys general
acceptance within a relevant scientific community.

17
Terran, 195 F.3d at 1316 n.2 (citing Daubert, 509 U.S. at 592–95).

However, in the Vaccine Program the Daubert factors play a slightly different role than
they do when applied in other federal judicial settings—e.g., the district courts. Typically, Daubert
factors are employed by judges (in the performance of their evidentiary gatekeeper roles) to
exclude evidence that is unreliable or could confuse a jury. By contrast, in Vaccine Program cases
these factors are used in the weighing of the reliability of scientific evidence proffered. Davis v.
Sec'y of Health & Human Servs., 94 Fed. Cl. 53, 66–67 (2010) (“uniquely in this Circuit, the
Daubert factors have been employed also as an acceptable evidentiary-gauging tool with respect
to persuasiveness of expert testimony already admitted”). The flexible use of the Daubert factors
to evaluate the persuasiveness and reliability of expert testimony has routinely been upheld. See,
e.g., Snyder, 88 Fed. Cl. at 742–45. In this matter (as in numerous other Vaccine Program cases),
Daubert has not been employed at the threshold, to determine what evidence should be admitted,
but instead to determine whether expert testimony offered is reliable and/or persuasive.

Respondent frequently offers one or more experts of her own in order to rebut a petitioner's
case. Where both sides offer expert testimony, a special master's decision may be “based on the
credibility of the experts and the relative persuasiveness of their competing theories.”
Broekelschen v. Sec'y of Health & Human Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing
Lampe, 219 F.3d at 1362). However, nothing requires the acceptance of an expert's conclusion
“connected to existing data only by the ipse dixit of the expert,” especially if “there is simply too
great an analytical gap between the data and the opinion proffered.” Snyder, 88 Fed. Cl. at 743
(quoting Gen. Elec. Co. v. Joiner, 522 U.S. 146 91997)); see also Isaac v. Sec'y of Health & Human
Servs., No. 08–601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012), mot. for
review den'd, 108 Fed. Cl. 743 (2013), aff'd, 540 F. App’x. 999 (Fed. Cir. 2013) (citing Cedillo,
617 F.3d at 1339). Weighing the relative persuasiveness of competing expert testimony, based on
a particular expert's credibility, is part of the overall reliability analysis to which special masters
must subject expert testimony in Vaccine Program cases. Moberly, 592 F.3d at 1325–26
(“[a]ssessments as to the reliability of expert testimony often turn on credibility determinations”);
see also Porter v. Sec'y of Health & 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”).

D. Consideration of Medical Literature

Both parties filed medical and scientific literature in this case, but not all such items factor
into the outcome of this decision. While I have reviewed all the medical literature submitted in this
case, I discuss only those articles that are most relevant to my determination and/or are central to
Petitioner's case—just as I have not exhaustively discussed every individual medical record filed.
Moriarty v. Sec'y of Health & Human Servs., No. 2015–5072, 2016 WL 1358616, at *5 (Fed. Cir.
Apr. 6, 2016) (“[w]e generally presume that a special master considered the relevant record
evidence even though he does not explicitly reference such evidence in his decision”) (citation

18
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”).

ANALYSIS

I. Overview of Alopecia Areata

As both testifying experts agreed, AA is widely understood to be an autoimmune disease
characterized by hair loss. Norris Report at 1; Tollefson Report at 2–3. Such hair loss appears in
patches, typically on the scalp. S. Birela, et al., Chapter 66: Non-bulbous Skin Diseases: Alopecia
Areata, Vitiligo, Psoriasis, and Urticaria, in The Autoimmune Diseases 971, 971–74 (N. Rose &
I. Mackay Eds., 2014) (co-authored by Dr. Norris) (“Autoimmune Diseases”).14 AA is relatively
common, with around two percent of people experiencing it at some point in their lives. Id. at 971;
Norris Report at 1. This translates to roughly 5.3–6.5 million people in the United States. See
Autoimmune Diseases at 971; Norris Report at 1.

AA is associated with a number of other diseases and conditions, such as vitiligo, atopic
dermatitis (eczema), hyper and hypothryoidism, and, less commonly, other autoimmune diseases
like connective tissue disease. Autoimmune Diseases at 972. Other conditions like nail loss or
abnormalities may precede or follow AA. See Zafrir at 2. The disease also unquestionably has a
genetic aspect. Norris Report at 1; Tollefson Report at 2–3. Indeed, literature suggests that “genetic
control of innate and acquired immunity is the most powerful factor in determining the
susceptibility to all variants of AA.” Autoimmune Diseases at 973 (emphasis added).

AA occurs when a “mononuclear cell inflammatory infiltrate attacks the hair follicle (HF)
bulb.” Autoimmune Diseases at 971. The HF is responsible for producing the hair shaft. See id.
Thereafter, T cell cytokines and cytotoxic T cells produce cytotoxic damage. See id. This disrupts
the normal function of the HF, resulting in thin, fragile hairs that easily detach or break off. See id.
However, because immune damage is localized to the hair bulb, regrowth of the hair can occur
after total hair loss, although the process can be slow. Id. at 972.

The triggers for AA are not well understood. See Richardson at 2. “Potential triggers
include emotional stress, metabolic or endocrine disorders, infections, drugs, and vaccines.” Id.
Several potential pathogenic mechanisms by which AA might occur have been proposed, including
molecular mimicry15, the induction of the cytokine interferon (type 1 IFN), or a “cytokine storm,”

14
AA is only one type of alopecia. Other types include alopecia totalis (loss of all hair on the scalp) and alopecia
universialis (loss of all scalp and body hair). See Zafrir at 1–2. Additionally, there is another type of alopecia called
telogen effluvium that is known to occur in response to stress on the body. Tollefson Report at 3.
15
Molecular mimicry is of course a commonly-invoked mechanism in the Vaccine Program for explaining how the
immune system might aberrantly cause disease, and proposes that foreign antigens presenting to immune system cells
might be confused with self-structures, causing the immune system to mistakenly attack both the antigens and self-

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in which cytokines upregulated after some instigating event greatly increase in number for a period
of time, causing harm simply through their proliferation. Richardson at 5–6; Tr. at 115; Pet’r’s
Brief at 7. Once AA is triggered, its clinical course is variable and not monophasic in progression.
Tr. at 51–52; Resp.’s Post-Hearing Brief at 7. As Dr. Norris elaborated in his testimony, some
patients experience recurring loss and regrowth, other patients experience one episode, and some
will experience “everything in between.” Tr. at 51–52.

II. Petitioner Has Carried Her Althen Burden With Respect to Her First Instance of AA
in November 2012
Petitioner has barely met her preponderant burden with respect to L.T.’s initial outbreak of
AA. The evidence is close, and almost in equipoise, on most of the Althen prongs in this case. But
well-reasoned and controlling precedent in the Vaccine Program requires me in such close cases
to decide the matter for the petitioner. See Walther v. Sec’y of Health & Human Servs., 485 F.3d,
1146, 1150 (Fed. Cir. 2007) (“[u]nder our case law, ‘close calls regarding causation are resolved
in favor of injured claimants.’”) (quoting Althen, 418 F.3d at 1280). I find that is appropriate here.

First, there is just enough evidence to support Petitioner’s contention under the “can cause”
prong that AA could be triggered by vaccination - and the HBV vaccine in particular. It was largely
agreed-upon by the experts in this case that AA is likely an autoimmune process, thereby “opening
the door” to a determination that something impacting the immune response could be implicated
as causal. In addition, Petitioner offered some reasonable items of literature, like Wise, supporting
the association between the HBV vaccine and hair loss generally, if not AA specifically. See Wise
at 1–2.

Wise also demonstrated some instances of challenge–rechallenge. While this aspect of Wise
did not aid Petitioner specifically on the second Althen prong (since the record in this case does
not establish that L.T. ever experienced AA or hair loss following her earlier HBV doses),16 it does
lend some support for the contended HBV-AA association. Respondent is also correct about
Wise’s limitations as strong proof of the association (indeed, its authors acknowledge the tentative
scope of its determinations (Wise at 1)), and this item of literature has not been updated with
corroborative research since its publication twenty years before (although it has not been rebutted
either). Wise nevertheless is deserving of some weight, and does go directly to the issue in
contention.

structures (with the latter constituting the damaging autoimmune response). Lauren Sompayrac, How the Immune
System Works 122 (5th ed. 2016).
16
Rechallenge is commonly understood to have this dichotomous effect when asserted by a Vaccine Act petitioner.
Cases relying on rechallenge to prove Althen prong I have sometimes failed under Althen prong II. See Nussman v.
Sec’y of Health & Human Servs., 83 Fed. Cl. 111, 119 (Fed. Cl. 2008) (“[t]here can only be rechallenge if there was
an initial challenge and associated adverse reaction”).

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 Richardson also assists Petitioner’s theory to a degree. Richardson involved a significantly
larger sample size than Wise, and statistical analysis of this sample showed a reliable correlation
of increased rates of AA in individuals who also had the HBV vaccine. Richardson by its own
admission is not definitive on the point (especially to the extent it did not account for the possibility
of a mere temporal association of AA to HBV vaccination). See Richardson at 5. In addition,
Richardson’s post-hearing filing (and the fact that it was not discussed by Dr. Norris) causes me
to give it a little less weight than I might otherwise. See McClellan v. Sec’y of Health & Human
Servs., No. 14-714V, 2019 WL 4072130, at *30 n.28 (Fed. Cl. Spec. Mstr. July 2019, 2019) (“I
typically give late-filed items less weight where a party has not demonstrated a justification for
their dilatoriness—for example, because the item in question was only published after hearing.”).17
It nevertheless was credible evidence favoring Petitioner’s claim—and was not refuted by
Respondent, let alone addressed in his post-hearing briefing.

Respondent’s failure to rebut Petitioner’s case went beyond not addressing the late-filed
Richardson. Certainly he pointed out some deficiencies in Petitioner’s causation theory, such as
the lack of a reliable mechanistic explanation for how a vaccine would induce the breaking of
immune tolerance (although it is well recognized in the Program that petitioners can prevail even
in the absence of proof of mechanism). Dr. Tollefson was also a credible and competent expert
witness, and her points about the genetic basis for AA were effectively established. But in this case
(unlike others) Respondent was unable to offer evidence casting doubt on Petitioner’s theory (e.g.,
an epidemiologic study that discounted the purported association between the HBV vaccine and
AA).18 I also found Dr. Norris to be a qualified and persuasive expert witness, and his embrace of
Petitioner’s theory gave it a little added heft.

Second, the record does support (again, just barely) the conclusion that the HBV vaccine
in this case likely triggered L.T.’s AA onset in November 2012. Petitioner has offered treater
support for this contention, such as Dr. Gilmore’s notes from an appointment in January 2013. Ex.
7 at 1–2. While Respondent correctly observes that the record also includes some more ambiguous
statements about an association (especially since not all treaters signed on to this reasoning), or
may simply evidence overreliance on the temporal association (which is recognized as an
insufficient basis to ascertain causation), I nevertheless discern sufficient, reliable treater support
connecting L.T.’s AA to her HBV vaccination to deem it evidentiarily significant. Dr. Norris also

17
The fact that one of L.T.’s own treaters co-authored Richardson (and even appears to discuss L.T.) is also somewhat
problematic—although in other cases articles written about an injured party have been deemed deserving of
evidentiary weight (and in Respondent’s favor) if only for their discussion of a condition. See McClellan, 2019 WL
4072130, at *4 (discussing article addressing mutation in petitioner’s daughter, the allegedly injured party).

18
In many prior cases, I have found the existence of strong and reliable epidemiologic evidence to tip the scales in
Respondent’s favor—even though it is unquestionably the case that this kind of proof need not be offered by a
petitioner. See, e.g., Maciel v. Sec’y of Health & Human Servs., No. 15-362V, 2018 WL 6259230, at *27 (Fed. Cl.
Spec. Mstr. Oct. 12, 2018). The converse must also be true: where Respondent does not offer such evidence, arguments
a Petitioner may make on causation will stand a little more unscathed.

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provided a persuasive interpretation of the record, and what factors specific to L.T. would
implicate the vaccine as triggering her genetically-associated AA. See generally Tr. at 66–69.19

Finally, the timeframe in which L.T.’s AA began—two to four days post-vaccination—
was established to be a medically acceptable temporal relationship for an autoimmune response.
Petitioner claims this timeframe is supported by Wise and Dr. Norris’s expert opinion. Dr. Norris’s
opinion as to timing, in his report and testimony, relied mostly on Wise. Tr. at 56; Norris Report
at 2. Although Respondent’s criticisms of Wise are reasonable, I find overall that the concept that
the autoimmune response to the HBV vaccine could begin in that timeframe is reasonable,
especially given Dr. Norris’s acceptance of it.

I again emphasize that Petitioner’s showing was not particularly robust. Other evidence
could have rebutted it. But the record in this case establishes that, at least with respect to the first
occasion of L.T.’s AA, Petitioner carried her preponderant burden.

III. Petitioner Has Not Carried her Burden of Proof with Respect to Any Subsequent
Occurrences of AA
Although Petitioner has established entitlement to damages stemming from her first
occurrence of AA after the November 2012 vaccination, I do not find that she persuasively
established that any subsequent recurrences (the first of which appears to have happened around
the time of her August 2015 return visit to Dr. Gilmore, reporting new-onset AA symptoms) can
also be attributed to that same initial vaccine event. The thinness of Petitioner’s overall evidentiary
showing may have been just enough to be preponderant in determining causation with respect to
the first occurrence of AA, but that same slim showing shifts against Petitioner when the larger
picture (including what the experts agreed about AA) is taken into account.

Determination of this aspect of Petitioner’s claim turns almost wholly on the first Althen
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prong. Although I have found that Petitioner was successful in establishing that a vaccine might
be a sufficient environmental trigger to produce an occurrence of AA, the context of that
occurrence is significant. Both experts agreed that AA is known to have a significant genetic
component that serves as a baseline “requirement” for AA to manifest. Tr. at 41–42, 150–51; see
also A. Alkhalifah, et al., Alopecia Areata Update: Part I. Clinical Picture, Histopathology, and
Pathogensis, 62 J. Am. Acad. Dermatology, no. 2, 177, 184–85 (2010) , filed on July 18, 2017, as

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As already noted, however, this case does not support the conclusion that L.T.’s vaccine reaction was associated
with her prior receipt of the HBV vaccine, under a challenge-rechallenge theory. The record does not establish she
ever reacted to those prior vaccinations, nor did she experience AA after them. The general concept that a person who
has received a vaccine before without incident will nevertheless inherently (or likely) have a faster response later, as
reflected in the injury asserted in a Vaccine Act claim, is speculative and conclusory.
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I note as well that Petitioner’s subsequent recurrences of AA (the first of which appears to have happened no earlier
than August 2015) have not been shown to have happened post-vaccination. Accordingly, Petitioner would still in this
case not be entitled to damages for those occurrences even if she had not maintained that the first vaccination explained
all subsequent AA recurrences.

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Ex. 18 (ECF No. 42) (family history of AA increases chances of developing the condition); A.
Gilhar, et al., Alopecia Areata, 336:16 New Eng. J. Med. 1514, 1521–22 (2012), filed on July 18,
2017, as Ex. 19 (ECF No. 42-1) (patients with AA often have a family history of atopy and
autoimmune disorders). Here, there was ample circumstantial evidence that L.T. was just such a
person. Indeed, as Petitioner herself testified, she had experienced hair loss in association with a
likely autoimmune event even before L.T. did. Tr. at 8–9.

Given the above, can it be concluded that the same initial trigger—here, the November
2012 vaccination—could reliably be deemed responsible for all future AA recurrences? The
evidence offered in this case does not support that assertion. AA is clearly viewed as non-
monophasic and inherently subject to recurrence. Moreover, vaccines are not the sole possible
trigger. Ms. DeLozier admitted as much, when she recounted the fact that L.T. had experienced
recurrences under other circumstances, such as when L.T. had an infection or fever. Tr. at 20–22.

The scientific and expert evidence filed in this case otherwise did not stand for the
proposition that response to an initial vaccine trigger could explain every subsequent occurrence
of AA in a susceptible individual. None of the literature offered by Petitioner so states, or
establishes what a vaccine like HBV would do to alter a person’s subsequent immune privilege in
future triggering events. At best, Dr. Norris attempted to outline how a vaccine could theoretically
create a “smoldering immune response,” consistent with the condition’s relapsing nature, and thus
even separate subsequent triggers would be linked to the initial event, but such assertions were
(unlike most of his testimony) conclusory and unpersuasive. Tr. at 175–77. At bottom, nothing
that is known about AA (at least as reflected in the filings in this case) suggests that the first
instance of AA in a person (likely to occur in childhood) is the linchpin explanation for all
subsequent recurrences.

The capacity of a vaccine to trigger a pathologic response must be placed in the context of
the overall disease’s expected course. In other cases in the Vaccine Program, petitioners have
demonstrated that the “trigger effect” of vaccination can not only cause an initial reaction but lead
to permanent progressive harm, with the initial injury beginning a progressive process of
worsening symptoms. For example, vaccines have in some cases been shown to cause direct,
catastrophic injury to the brain, such as an encephalopathy that has significant follow-on health
impacts. See, e.g., Estep v. Sec’y of Health & Human Servs., 28 Fed. Cl. 664, 669 (Fed. Cl. 1993)
(affirming special master’s finding that a “DPT vaccination can cause an acute encephalopathy,
and that anything that can cause an acute encephalopathy can [subsequently] cause permanent
neurologic damage”). A comparable theory that has found success involves circumstances where
petitioners demonstrate that a seizure triggered by vaccination (sometimes merely due to the fever
associated with the body’s innate immune response) will set up conditions for future, more harmful
seizures in the future. Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1375–76 (Fed.
Cir. 2009) (reversing special master, and finding that petitioners had shown that the vaccine in
question could trigger seizures).

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 The “trigger” effect of the vaccine in this case, by contrast, is different – more isolated and
discrete in scope. Both sides’ experts agreed that AA has a significant genetic underpinning, and
thus a person who likely possesses that predisposition (a conclusion that can be made about L.T.
based on preponderant evidence) is more susceptible to experiencing AA on a lifelong basis. While
it may have been established in this case that the HBV vaccine could trigger one instance of AA,
it has not been similarly shown that any trigger (vaccine or not) would so alter a person’s immune
response that all AA recurrences would invariably be associated with the first, made worse due to
the first, etc. None of the medical literature filed in this case stands for this proposition, and in fact
(in stressing the importance of the genetic susceptibility to AA) actually undermines it.

It is more likely that an individual’s subsequent recurrences are attributable to the genetic
susceptibility underlying AA. See McClellan, 2019 WL 4072130, at *35–36 (finding that
petitioner “did not establish that a vaccine could, under the circumstances, trigger a non-febrile
seizure sufficient to significantly worsen a preexisting seizure disorder with an unmistakable
genetic origin”); Sharpe v. Sec’y of Health & Human Servs., No. 14-65V, 2018 WL 7625360 (Fed.
Cl. Spec. Mstr. Nov. 5, 2018) (finding that neither the record supported “[p]etitioner’s contention
that the vaccines [] received could, or did, injure [their daughter] as alleged,” nor did petitioners
establish a significant aggravation claim given their daughter’s existing “DYNC [gene]
mutation”), aff’d, 142 Fed. Cl. 630 (2019), appeal docketed, No. 19-1951 (Fed. Cir. May 31,
2019). And Dr. Norris did not otherwise credibly establish with reliable evidence that AA can be
thought of as a “smoldering” condition, in which the instigating trigger for an outbreak is a spark
that is never extinguished.

The implication of my ruling is that Petitioner’s recoverable damages in this case are
circumscribed in several respects. Clearly she is entitled to costs associated with L.T.’s treatment
from November 2012 until any initial AA symptoms associated with the triggering abated (and a
preliminary review of the record suggests that had occurred by no later than August 2014). She
can also seek an award of pain and suffering associated with her initial November 2012 symptoms.
But she cannot recover damages associated with any new, discrete AA recurrences that L.T.
experienced post-vaccination, beginning no later than August 2015.

CONCLUSION

Ms. DeLozier has carried her burden in establishing that the HBV vaccine could trigger
AA, and did so in L.T.’s case in November 2012. She should therefore receive a damages award
reflecting the costs of treatment of that first occurrence, plus any other damages flowing therefrom.
However, she has not established an entitlement to damages associated with any subsequent AA
recurrences, which have not preponderantly been shown to be attributable to the earlier HBV
vaccine.

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 In order to guide the parties through the damages phase of the action, a separate damages
order will issue.

IT IS SO ORDERED.
/s/ Brian H. Corcoran
Brian H. Corcoran
Chief Special Master

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