Declaration of Helsinki.
The patient reported in this study
Copyright © 2024 JLE. Téléchargé par UNIVERSITE PARIS CITE le 08/04/2024.
losartan, furosemide, acenocoumarol, bisoprolol, allop-
provided written informed consent for surgery.
Consent for publication: Written consent to publish this
case report and accompanying images was obtained from
the patient.
1
Guangdong Medical University, Xiao-huan LONG1
Zhanjiang, Guangdong, China Zhen-ju Tang1
2
Department of Dermatology, Yu-teng Huang1
Hui-shan JIANG2
Yangjiang People’s Hospital
Wei-liang WANG2
affiliated to Guangdong Medical
University, Yangjiang,
Guangdong, China
<13751641793@163.com>
<xiaohuanlong_1998@163.com>
References
1. Vaiman M, Lazarovitch T, Heller L, Lotan G. Ecthyma gangrenosum
and ecthyma-like lesions: review article. Eur J Clin Microbiol Infect
Dis 2015 ; 34 : 633-9.
2. Jamal A, Saleem A, Rezwan F, Sheikh A, Shamsi T. Successful
management of colistin- and carbapenem-resistant Klebsiella
pneumoniae-associated ecthyma gangrenosum in acute myeloid
leukemia: a rare complication. SAGE Open Med Case Rep 2022 :
10 : 2050313X221102113.
3. Yamout BI, Alroughani R. Multiple sclerosis. Semin Neurol 2018 ;
38 : 212-25.
4. Vaiman M, Lasarovitch T, Heller L, et al. Ecthyma gangrenosum
versus ecthyma-like lesions: should we separate these conditions. Acta
Dermatovenerol Alp Pannonica Adriat 2015 ; 24 : 69-72.
5. Koumaki D, Koumaki V, Katoulis AC, et al. Ecthyma gangrenosum
caused by Klebsiella pneumoniae and Streptococcus vestibularis
in a patient with acute myeloid leukemia: an emerging pathogen.
Int J Dermatol 2019 ; 58 : E83-5.
6. Jackson S, Gilchrist H, Nesbitt LT Jr. Update on the dermatologic
use of systemic glucocorticosteroids. Dermatol Ther 2007 ; 20 : 187-
205.
7. Stuck AE, Minder CE, Frey FJ. Risk of infectious complications in pa-
tients taking glucocorticosteroids. Rev Infect Dis 1989 ; 11 : 954-63.
doi:10.1684/ejd.2024.4612
Silodosin-induced leukocytoclastic
vasculitis: a first case report
Silodosin is an α1-adrenergic receptor antagonist which
causes smooth muscle relaxation in the lower urinary tract
by antagonizing α1A-adrenergic receptors in the prostate
and urethra [1]. The most common side effects of silodosin
include retrograde or abnormal ejaculation and orthos-
tatic hypotension [1]. Leukocytoclastic vasculitis (LCV)
is a cutaneous small vessel vasculitis (CSVV) which is not
commonly associated with silodosin. Herein, we describe
a patient with LCV probably induced by silodosin.
A 68-year-old male patient had a medical history of
valvular replacement (aortic and mitral), gout, and benign
prostatic hypertrophy (BPH). He was treated with
92
urinol and tamsulosin. In August 2022, in view of the
worsening of BPH symptoms, he started treatment with
silodosin. Ten days later, he noticed an onset of palpable
and non-blanchable purpuric spots, mainly on the lower
limbs (figure 1A). Physical examination performed by his
dermatologist revealed no fever, mucous membrane
involvement or lymphadenopathy. A painful, symmetri-
cally-distributed purpura was seen on the lower limbs. No
evidence of infection, collagen-vascular diseases, haema-
tological disorders, or malignancy was found. No new
medication had been introduced during the previous
period, except for silodosin. The diagnosis of cutaneous
adverse drug reaction related to silodosin was suspected
by his dermatologist, and a skin biopsy was obtained.
Laboratory work-up, including haemogram, prothrombin
time, and liver and renal function tests, was normal.
Silodosin was withdrawn and the other long-term medi-
cations were maintained. Treatment with topical corti-
costeroids and cetirizine per os led to rapid resolution of
the skin lesions. Results of microbiological and autoim-
munity tests ruled out other causes of LCV: Antinuclear
antibodies (ANA), dsDNA autoantibodies, antiphospho-
lipid antibodies, lupus anticoagulant, anti-cyclical citrul-
linated peptide antibodies (anti-CCP), antineutrophil
cytoplasmic antibodies (ANCA), cryoglobulins, myelop-
eroxidase (MPO) antibodies and rheumatoid factor were
negative. PCR results for hepatitis B and C, HIV, syphilis,
cytomegalovirus, EBV and SARS-CoV-2 were negative.
Erythrocyte sedimentation rate, protein electrophoresis,
and C3 and C4 complement levels were normal. Urinalysis
was negative for proteinuria and haematuria. The skin
biopsy revealed fibrinoid necrosis, erythrocyte extravasa-
tion and pycnotic neutrophils, admixed with eosinophils
and lymphocytes, consistent with LCV (figure 1B). No
deposits of IgG, IgM, IgA or C3 were detected by direct
immunofluorescence. Drug-induced LCV was considered
according to the Naranjo probability scale; the causality
of silodosin was probable (Naranjo’s score: 5) [2].
Leukocytoclastic vasculitis (LCV), formerly known as
hypersensitivity vasculitis, is a CSVV manifesting with
palpable purpura, and its severity ranges from benign
and self-limiting to life-threatening with multiple organ
failure. It can occur in association with drugs, infections,
collagen-vascular diseases, haematological disorders and
malignancy [3]. Drug-induced LCV accounts for about
10% of all LCV cases [4]. The pathogenic mechanism of
LCV is unclear, but studies suggest that it is related to
a type III immune complex-mediated reaction [5].
Confirming drug imputability is an important step in the
management of cutaneous adverse drug reactions,
however, the literature on the utility of skin testing for
drug-induced LCV is sparse. Rare reports of patch-test
positivity for drugs (pylthiouracil and topical non-steroid
anti-inflammatory drugs) have been reported.
Considering the dearth of evidence regarding sensitivity,
specificity and safety of patch testing for drug imputa-
bility in the setting of LCV, skin tests appears to be of
limited utility and are not recommended [6]. In our
patient, a diagnosis of silodosin-induced LCV was
retained considering the temporal correlation between
drug intake and the onset of skin eruption, improvement
of symptoms after suspected drug withdrawal, skin
biopsy findings, and exclusion of other causes of
EJD, vol. 34, n° 1, January-February 2024
 A B

Figure 1. A) Palpable and non-blanchable purpuric spots on the lower limb. B) Skin biopsy showing fibrinoid necrosis,
erythrocyte extravasation and pycnotic neutrophils, admixed with eosinophils and lymphocytes, consistent with LCV.

v­ asculitis. To our knowledge, and based on a review of 2. Naranjo CA, Busto U, Sellers EM, et al. A method for estimating
Copyright © 2024 JLE. Téléchargé par UNIVERSITE PARIS CITE le 08/04/2024.

the literature in the PubMed database (MeSH terms:
silodosin, vasculitis), this is the first report of
­silodosin-induced LCV.
LCV is a rare but serious side effect, and clinicians
should be aware of the possibility of LCV associated
with silodosin. ■
Conflicts of interest: none.
Funding: none.
Consent: written informed consent was obtained from the
patient to publish this report in accordance with the jour-
nal’s patient consent policy.
the probability of adverse drug reactions. Clin Pharmacol Ther 1981 ;
30 : 239-45.
3. Lotti T, Ghersetich I, Comacchi C, Jorizzo JL. Cutaneous small-vessel
vasculitis. J Am Acad Dermatol 1998 ; 39 : 667-90.
4. Ha YJ, Han YJ, Choi YW, Myung KB, Choi HY. Sibutramine
(reductil®)-induced cutaneous leukocytoclastic vasculitis: a case
report. Ann Dermatol 2011 ; 23 : 544-7.
5. Gupta M. Levetiracetam-induced leukocytoclastic vasculitis. Indian
J Pharm 2017 ; 49 : 124-6
6. Woodruff CM, Botto N. The role of patch testing in evaluating
delayed hypersensitivity reactions to medications. Clin Rev Allerg
Immunol 2022 ; 62 : 548-61.
doi:10.1684/ejd.2024.4613

Acknowledgements: none.
1
Department of Pharmacology. Bouraoui OUNI1
Faculty of Medicine, Khadija MANSOUR2 Nagashima-type palmoplantar keratosis
University of Sousse, Tunisia Malek SASSI3 associated with Tc17 cells in a patient with
Badereddine SRIHA4
2
Department of Pharmacology,
Nesrine BENSAYED5
rheumatoid arthritis
EPS Fattouma Bourguiba,
Neila FATHALLAH1
Faculty of Medicine,
Raoudha SLIM1
University of Monastir, Tunisia
3
Faculty of pharmacy, Nagashima-type palmoplantar keratosis (NPPK) is an
University of Monastir, Tunisia autosomal recessive, diffuse, non-epidermolytic, palmo-
4
Department of plantar keratosis caused by mutations in SERPINB7 [1].
Anatomopathology, Farhat NPPK is characterized by well-demarcated, reddish,
Hached hospital, Sousse, Tunisia diffuse, and mild palmoplantar hyperkeratosis extending
5
Department of Hematology, to the dorsal surfaces of the hands and feet, inner wrists,
Farhat Hached hospital, Sousse, ankles, and Achilles tendon area [1]. A high frequency
Tunisia of hyperhidrosis on the palms and soles has been noted
<elounibouraoui@yahoo.fr> [1]. A previous report showed possible involvement of
inflammatory aspects associated with the pathogenesis
of NPPK [2]. Here, we report a case of NPPK in a
patient with rheumatoid arthritis (RA) and discuss the
References possibility of the involvement of inflammatory aspects
in the pathogenesis of NPPK.
A 52-year-old woman presented with scaly erythema on
1. Yoshida M, Kudoh J, Homma Y, Kawabe K. Safety and efficacy of both palms and soles since infancy. She had not received
silodosin for the treatment of benign prostatic hyperplasia. Clin Interv any treatment for her cutaneous lesions. Two years earlier,
Aging 2011 ; 6 : 161-72. she developed arthritis of her fingers and was seen by a
EJD, vol. 34, n° 1, January-February 2024 93