CASE
TA 50-year-old Caucasian male with a history of type II diabetes
mellitus, gout, psoriasis and psoriatic arthritis
presented for patchy hair loss during treatment with
etanercept. Prior to etanercept therapy, trials of sulfasalazine,
methotrexate, and oral prednisone in conjunction with topical
corticosteroids yielded suboptimal therapeutic control.
Although his psoriasis improved with etanercept, localized
and sharply demarcated, circular patches of hair loss involving
his frontal and parietal scalp along with midline beard
began occurring nine months following the initiation of etanercept.
The base of these lesions was smooth, and showed
no signs of scarring or atrophy. Despite changing to another
tumor necrosis factor- α (TNF- α ) inhibitor, adalimumab, for
better psoriatic arthritis management and topical application
of 0.05% fluocinonide gel and 0.05% desonide cream to
the scalp and beard, respectively, his hair loss continued to
progressively enlarge to near-complete alopecia universalis
(Figure 1, 2). Four months following the discontinuation of
all TNF- α inhibitors, his alopecia persists. The patient has no
personal or family history of alopecia areata. His other medications
include liraglutide, insulin glargine, glipizide, metformin,
fenofibrate, and simvastatin.
DISCUSSION
Alopecia areata (AA) is a non-scarring alopecia that typically
presents as well-circumscribed, circular patches of hair loss
primarily distributed on scalp. It commonly arises in association
with other autoimmune conditions. Histologically, AA
is characterized by perifollicular lymphocytic, macrophage,
and Langerhan cell infiltrate, primarily devoid of eosinophils,
amidst a background of degenerative hair follicles.1 Although
the underlying pathophysiology of is unknown, AA’s development
is postulated to be an autoimmune response of CD4+
and CD8+ to bulbar auto-antigens, which results in the destruction
of hair follicles.2
Despite being very effective in the treatment of several autoimmune
diseases such as inflammatory bowel disease,
psoriasis, and rheumatoid arthritis, TNF-α antagonists have
yielded dismal results in the management of AA. While the
proinflammatory cytokine, TNF-α, inhibits hair growth in-vitro,3
clinical trials employing a TNF-α inhibitor, etanercept, failed to demonstrate a beneficial role in the course of alopecia areata.4
A few of these patients even experienced further escalation of
AA during treatment.
With the addition of our patient, approximately thirty-four cases
of TNF-α linked AA are documented in the literature. These
cases involve all four TNF-α antagonists (adalimumab, certolizumab
pegol, etanercept, and infliximab) and eruptions in both
patients with and without a previous personal or family history
of AA.5-8 To our knowledge, this report is the first case of TNF-α
antagonist induced AA continuing and progressing beyond the
