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showed superﬁcial and deep perivascular and dermal inﬁltrates
of neutrophils and eosinophils. Both biopsies were consistent
with LCV with signiﬁcant tissue eosinophilia.
Against the patient's rheumatologist's recommendations, the
patient stopped taking CZP and began a 3-week prednisone
taper, which entailed taking 60 mg by mouth for week 1, 40 mg
by mouth for week 2, and 20 mg by mouth for week 3. The
patient additionally received 50 mg of dapsone once daily for
1 month. The rash cleared completely approximately 3 months
after cessation of CZP.

inﬁltrate to a mononuclear-predominant inﬁltrate (7). Furthermore, drug-induced LCV is often characterized as having an
eosinophilic-predominant inﬁltrate (8).
CZP is approved for treatment of psoriatic arthritis in many
countries, including the US (1). With the increasing use of CZP,
physicians should be aware of this side eﬀect and consider drug
cessation if indicated.

DISCUSSION
LCV may have a multitude of presentations, making it difﬁcult to diagnose. While the initial presentation is often cutaneous, LCV may cause a variety of other problems including
myopathy, gastrointestinal bleeding, and renal insuﬃciency
(3, 4). It can also result in permanent scarring (5). Common
presentations of LCV include palpable purpura, urticaria, ulcers,
or nodules (3, 6). These lesions may be exquisitely painful or
pruritic, and lower leg edema and myalgias are frequently present (3). Histopathologically, LCV is described as ﬁbrinoid necrosis of dermal small vessels, hemorrhage, thrombosis, and
perivascular polymorphonuclear leukocytes (3, 6). However, the
histologic variability of LCV has been reported to morph over
the course of 24 to 48 hours from a neutrophilic-predominant

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1.
2.

Hansen RB, Kavanaugh A. Certolizumab pegol for the treatment of psoriatic arthritis. Expert Rev Clin Immunol 2015;11(3):307-318.
Jinesh S. Pharmaceutical aspects of anti-inﬂammatory TNF-blocking
drugs. Inﬂammopharmacology 2015;23(2-3):71-77.
Sams WM Jr, Thorne EG, Small P, Mass MF, McIntosh RM, Stanford
RE. Leukocytoclastic vasculitis. Arch Dermatol 1976;112(2):219-226.
Tsai MH, Yang JH, Kung SL, Hsiao YP. Levamisole-induced myopathy
and leukocytoclastic vasculitis: a case report and literature review. Dermatol
Ther (Heidelb) 2013;26(6):476-480.
Butts GT, Bishop PR, Wyatt JP, Nowicki MJ. Leukocytoclastic vasculitis
in an adolescent with ulcerative colitis: report of a case and review of the
literature. Sage Open Med Case Rep 2014;2:2050313X14547609.
Ekenstam EAF, Callen JP. Cutaneous leukocytoclastic vasculitis: clinical and laboratory features of 82 patients seen in private practice. Arch
Dermatol 1984;120(4):484-489.
Zax RH, Hodge SJ, Callen JP. Cutaneous leukocytoclastic vasculitis: serial histopathologic evaluation demonstrates the dynamic nature of the
inﬁltrate. Arch Dermatol 1990;126(1):69-72.
Bahrami S, Malone JC, Webb KG, Callen JP. Tissue eosinophilia as an
indicator of drug-induced cutaneous small-vessel vasculitis. Arch Dermatol
2006;142(2):155-161.

Baylor University Medical Center Proceedings

Volume 30, Number 2

Table of Contents for the Digital Edition of Baylor University Medical Center Proceedings April 2017