Dermatology: Practical and Conceptual


222 Letter  |  Dermatol Pract Concept 2019;9(3):13

Dermatology Practical & Conceptual

A Case of Lepromatous Leprosy Clinically 
Masquerading as Vasculitis

Ali Sadeghinia1, Shadi Azizzadeh-Roodpishi1, Maryam Daneshpazhooh1,  
Kambiz Kamyab2, Amin Kiani1, Hamidreza Mahmoudi1

1 Department of Dermatology, Autoimmune Bullous Diseases Research Center, Tehran University of Medical Sciences, Tehran, Iran

2 Department of Dermatopathology, Razi Hospital, Tehran University of Medical Sciences, Tehran, Iran

Key words: leprosy, vasculitis, skin lesions, misdiagnosis

Citation: Sadeghinia A, Azizzadeh-Roodpishi S, Daneshpazhooh M, Kamyab K, Kiani A, Mahmoudi H. A case of lepromatous leprosy 
clinically masquerading as vasculitis. Dermatol Pract Concept. 2019;9(3):222-224. DOI: https://doi.org/10.5826/dpc.0903a13

Accepted: February 14, 2019; Published: July 31, 2019

Copyright: ©2019 Sadeghinia et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, 
which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: None.

Competing interests: The authors have no conflicts of interest to disclose.

Authorship: All authors have contributed significantly to this publication.

Corresponding author: Hamidreza Mahmoudi, MD, Autoimmune Bullous Diseases Research Center, Razi Hospital, Vahdate-Eslami 
Square, 11996, Tehran, Iran. Email: hr_mahmoody@yahoo.com

Introduction

Leprosy is a chronic infectious disease caused by Mycobacte-

rium leprae affecting mostly skin and nervous system. It can 

have different clinical manifestations and can even mimic 

diseases of autoimmune origin and of vasculitis [1, 2]. Here, 

we discuss a patient with an 8-year misdiagnosis of vasculitis 

that turned out to be leprosy.

Clinical Presentation

A 32-year-old man was referred to the dermatology clinic 

at Razi Hospital, Tehran, Iran, complaining of erythema-

tous lesions for 8 months and a history of distal peripheral 

neuropathy for 8 years. He suffered from recurrent chronic 

punched-out ulcers on extremities with scar formation. 

He was diagnosed with vasculitis, most likely polyarteritis 

nodosa, because of the presence of lower limb ulcers, periph-

eral neuropathy, and livedoid-like skin changes. No skin 

biopsy was done at the time to help confirm the diagnosis. He 

was under treatment by rheumatologists before referral to our 

clinic and had been treated for 1 year with azathioprine (100 

mg/day) and prednisolone (10 mg/day) to control neuropathy.

Physical examination revealed diffuse erythematous 

urticarial plaques on the patient’s trunk. Poikilodermic 

changes were evident on his face and neck. He had bilateral 

hand and foot muscle atrophy and paresthesia. A few heal-

ing ulcers were evident on his ankles (Figure 1). The lesions 

were not painful and he had no associated joint pain. Neural 

examination revealed profound sensory impairment. Labo-

ratory examination only showed an elevated erythrocyte 

sedimentation rate of 56 mm/hour. No previous biopsy had 

been done.

In the context of these findings, vasculitis, autoimmune 

connective tissue disease (ACTD), mycosis fungoides, and 

leprosy were the most likely differential diagnoses.

A punch biopsy was taken from urticarial trunk lesions. 

Microscopic view revealed perivascular, perifollicular, and 

perineural infiltration of mononuclear inflammatory cells 

and histiocytes. In addition, hypertrophied nerve bundles 

were seen. No signs of vasculitis were evident. Acid-fast 

organisms were detected in Ziehl-Neelsen stain, especially 



Letter  |  Dermatol Pract Concept 2019;9(3):13 223

Conclusions

Leprosy is a neglected tropical disease. 

It still infects a considerable population 

in developing countries. It has cutaneous 

and neurological manifestations and can 

also present with clinical manifestations 

resembling vasculitis [1].

There are some previous reports of 

leprosy mimicking vasculitis and ACTD 

clinically. Hsieh and Wu [2] reported a 

man with arthritis, joint deformities, 

paresthesia, malar rash, photosensitiv-

ity, and laboratory test results indicative 

of systemic lupus erythematous, treated 

for 3 years with no disease control. He 

had generalized, ill-defined skin lesions 

with peripheral sensorimotor neuropa-

been documented. Screening implemen-

tations were performed for his family 

members.

invading cutaneous nerves and arrec-

tor pili muscles (Figures 2 and 3). 

The density of bacilli in the patient’s 

smears (bacterial index) was 4+ (10-

100 bacilli in average field) and mor-

phological stain was solid-stained (liv-

ing). With the presence of erythematous 

skin lesions, neuropathy, and muscle 

atrophy; histopathological features, 

especially perineural involvement; and 

detection of acid-fast bacilli, our final 

diagnosis was leprosy and most likely 

borderline lepromatous form.

Following diagnosis, multidrug ther-

apy against Mycobacterium leprae (ML) 

was started. Rifampin (600 mg/month), 

clofazimine (300 mg/month and 50 mg/

day), and dapsone 100 mg/day were 

prescribed for a 12-month treatment 

course. After 1 year, the patient’s skin 

is clear and no disease progression has 

Figure  3. Multiple acid-fast organisms, 

Ziehl-Neelsen stain (red staining) (original 

magnification ×100). [Copyright: ©2019 Sa-

deghinia et al.]

Figure 2. Perivascular, perifollicular, and perineural infiltration of mononuclear inflamma-

tory cells and histiocytes (loose granuloma); hematoxylin and eosin staining (original magni-

fication ×4 and 40) (A-D); acid-fast organisms in Ziehl-Neelsen stain (red staining) (original 

magnification ×40) (E, F). [Copyright: ©2019 Sadeghinia et al.]

A

C

E

D

F

B

Figure 1. Poikilodermic change (A); urticarial patches/plaques on trunk (B); atrophy of foot 

muscles and chronic ulcer, ankle (C). [Copyright: ©2019 Sadeghinia et al.]

A

C

B



224 Letter  |  Dermatol Pract Concept 2019;9(3):13

Early detection of leprosy is criti-

cal in order to prevent its sequels. Phy-

sicians should have a higher clinical 

awareness about ML clinical features. 

It is important to consider it as a dif-

ferential diagnosis of atypical cases of 

neuropathy or suspicious cases of vas-

culitis and ACTD.

References

1. Sampaio L, Silva L, Terroso G, et al. Han-

sen’s disease mimicking a systemic vasculi-

tis. Acta Reumatol Port. 2011;36(1):61-64.

2. Hsieh TT, Wu YH. Leprosy mimicking lu-

pus erythematosus. Dermatologica Sinica. 

2014;32(1):47-50.

case of leprosy with mostly neural fea-

tures. A probable cause of skin lesions 

could be the immunosuppression caused 

by azathioprine and prednisolone con-

sumption. The recurrent leg ulcers may 

have been due to neuropathy directly 

caused by ML infection and trauma 

and the Lucio leprosy phenomenon, 

which is a rare reaction in untreated 

lepromatous leprosy and is character-

ized by recurrent crops of leg ulcers due 

to direct invasion of ML to the vessels’ 

wall [1]. If a recent onset ulcer had been 

available for biopsy, the histopathologi-

cal features of this phenomenon could 

have been noted.

thy. After skin biopsy the diagnosis of 

leprosy was made.

Sampaio et al [1] reported a woman 

with symmetric polyarthritis, subcuta-

neous nodules, leg ulcers, and paresthe-

sia of the distal extremities. First impres-

sion was primary vasculitis or ACTD, 

but biopsy showed ML infection.

Our patient had a history of chronic 

sensorimotor neuropathy with new urti-

carial trunk lesions. His condition was 

mistreated as neuropathy due to vascu-

litis for a long time before skin mani-

festations, possibly caused by the use 

of immunosuppressive drugs, became 

apparent. This patient had a neglected