(18.5%) had subclinical hypothyroidism with negative autoanti-
Alopecia areata (AA) is an autoimmune process involving a
Th1 reaction directed against an unknown antigen, most proba-
bly located in the bulb area of the anagen hair follicle.
often associated with other autoimmune phenomena, particu-
larly autoimmune thyroiditis and vitiligo. In AA, pigmented hair is
affected more that lighter or graying hair, and hair often regrows
nonpigmented. On this basis, melanocyte-related proteins have
been investigated as potential autoantigens. Trautman et al.
assessed the melanocyte density and the presence or absence
of dendrites in samples of lesional scalp obtained from
18 patients with AA and compared them to that of ﬁve healthy
Of the patients, 13 (72%) had trace to +1 MART-1
staining for melanocytes, usually with limited dendritic pro-
cesses; three had +2 staining; and two had +3 staining. All con-
trols showed a +3 staining for melanocytes. The authors
concluded that AA shows a decreased number of follicular mel-
anocytes, but it is unclear if this results from an autoimmune
attack or is because of rapid hair cycling.
In conclusion, there are indications that the melanocyte of the
hair follicle might be an antigenic target in FFA, in a similar way to
what it has been suggested for AA. AA and FFA share in common
a perifollicular lymphocytic inﬂammatory inﬁltrate, as well as fre-
quent association with autoimmune thyroiditis and vitiligo.
anagen hair follicle, melanotic dopa-positive melanocytes are
readily detectable in the basal layer of the infundibulum, around
the upper dermal papilla, and they may also be detected in the
basal layer of the sebaceous gland.
Therefore, it can be specu-
lated that AA may be triggered by antigens expressed by the mel-
anocytes of the bulb, whereas FFA may be triggered by antigenic
stimuli originating from the melanocytes of the upper hair follicle,
especially the infundibulum. This difference may explain why AA
and FFA result in nonscarring alopecia and scarring alopecia,
respectively. Also, this may be the reason why in FFA hair color
is not affected by the supposed destruction of melanocytes in the
upper follicle, as the pigment is acquired by the hair shaft in the
area of the bulb. Nevertheless, the role of the melanocyte as an
antigenic target in FFA appears to be not as strong and not as
clear as in AA. Further studies are necessary to verify this tempt-
Alexander C. Katoulis
Aikaterini I. Liakou
2nd Department of Dermatology and Venereology, National
and Kapodistrian University of Athens, Medical School,
“Attikon” University General Hospital, Athens, Greece
2nd Department of Pathology, National and Kapodistrian
University of Athens, Medical School, “Attikon” University
General Hospital, Athens, Greece
Funding sources: None.
Conﬂicts of interest: None declared.
The IRB of “ATTIKON” hospital has approved the study.
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Eruptive pseudoangiomatosis in two children with acute
Eruptive pseudoangiomatosis (EPA) is an acute, benign, self-
limited, asymptomatic exanthema of unknown cause affecting
characterized by angioma-like papules due to transi-
tory dermal blood vessel dilatation.
We present two pediatric
patients with acute lymphoblastic leukemia (ALL) and EPA.
A 7-year-old female presented with a 7-day history of an asymp-
tomatic skin rash. She had received chemotherapy for ALL with
methotrexate, 6-mercaptopurine, and doxorubicin 4 weeks before.
Multiple small, bright red papules surrounded by a white halo
(Fig. 1) were observed on the head, limbs, and trunk. She had no
history of recent infections. EPA was diagnosed, no treatment was
prescribed, and complete resolution occurred in 12 days.
A 5-year-old female presented an asymptomatic exanthema of
4 days duration. She had received chemotherapy for ALL with
methotrexate and 6-mercaptopurine 20 days before symptom
International Journal of Dermatology 2018, 57, e30–e43 ª 2018 The International Society of Dermatology