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Livedoid vasculopathy and high levels
of lipoprotein (a): response to danazol
Paulo Ricardo Criado*, Danielle Priscilia de Souza Espinel†,
Neusa Yuriko Sakai Valente†, Afsaneh Alavi‡&
Robert S. Kirsner§
*Dermatology, Dermatology Sao Paulo, Hospital das Clínicas da Faculdade
de Medicina da USP, †Dermatology Department, São Paulo University, São
Paulo, Brazil, ‡Medicine (Dermatology), University of Toronto, Toronto,
Ontario, Canada and §Dermatology and Cutaneous Surgery, University of
Miami, Miami, Florida
ABSTRACT: Livedoid vasculopathy (LV) is a thrombo occlusive disorder presenting with recurrent
painful ulcers of lower extremities. Association of LV with increased level of lipoprotein (a) (LP(a) ), a
risk factor for cardiovascular disease, has been reported. Danazol has been used with success in the
management of LV, but none of the previous studies looked at the correlation between response to the
treatment and level of LP(a). The aim of this study was to demonstrate the efficacy of low-dose danazol
in the treatment of LV and its effects on LP(a).We present four cases with LV who were successfully
treated with low-dose danazol, assessing the clinical characteristics and laboratory tests including the
level of LP(a). The average age of the patients was 45 years and the mean duration of the disease was 19
years. The treatment regime of danazol 200 mg daily led to complete healing of ulcers and reduction in
pain and a 70% (ranging from 52 to 87%) reduction in the level of LP(a). The limitation of this study is
“small sample size.” In our patients with LV, low-dose danazol led to clinical improvement along with
significant reduction in the level of LP(a).
KEYWORDS: pharmacology, skin signs of systemic disease, therapy-systemic
Introduction
Livedoid vasculopathy (LV) is an occlusive cutane-
ous disease of the dermal vessels with scant inflam-
mation on histopathology examination. LV is
characterized by the presence of painful recurrent
ulcerations of lower extremities, especially in the
ankles and feet, livedo reticularis and ivory-white
atrophic scars, called atrophie blanche (1).
The main pathophysiologic mechanism consid-
ered is a vaso-occlusive phenomenon as a result of
intraluminal thrombosis of the dermis venules (2).
However, the etiopathogenesis is not completely
established, and so many cases remain idiopathic.
Disorders related to hypercoagulable states,
impaired of fibrinolysis and/or autoimmune
diseases are the conditions most frequently
Address correspondence and reprint requests to: Afsaneh
Alavi, MD, dermatologist, Wound Care Centre, Women’s
College Hospital (Main Building), 76 Grenville Street 10th
floor. Toronto, ON M5S 1B2, Canada or email:
afsaneh.alavi@utoronto.ca.
1
Dermatologic Therapy, Vol. ••, 2015, ••–••
Printed in the United States · All rights reserved
© 2015 Wiley Periodicals, Inc.
DERMATOLOGIC THERAPY
ISSN 1396-0296