Clinical Picture
Widespread borderline tuberculoid leprosy with HIV co-infection
Lancet Infect Dis 2017; 17: 348
Dermatology and Venereology,
Hôtel Dieu de France,
Achrafieh, Beirut, Lebanon
(E Kechichian MD, R Tomb PhD)
Correspondence to:
Dr Elio Kechichian,
Dermatology and Venerology,
Hôtel Dieu de France, Achrafieh,
Beirut 00961, Lebanon
elio.kechichian@net.usj.edu.lb
348
Elio Kechichian, Roland Tomb
A 35-year-old Lebanese man who had previously lived in
Oman for 4 years presented to the outpatient clinic of the
Hôtel Dieu de France hospital, Lebanon, with a
generalised eruption of annular plaques. 4 years
previously he had consulted our clinic for ill-defined
ulcerated plaques associated with low-grade fever and
general status alteration. At that time, ecthyma, secondary
syphilis, and vasculitis were all considered during
differential diagnosis. A skin biopsy, serological testing
for syphilis (Treponema pallidum haemagglutination
assay and Venereal Disease Research Laboratory test),
HIV 1/2 enzyme immunoassay, and a recombinant
purified protein derivative (PPD) test for tuberculosis
were ordered along with a complete blood count and liver
and renal function tests. Tests came back positive for
HIV-1 and negative for syphilis and tuberculosis. The
Figure: Annular atrophic plaques with central clearing in a 35-year-old
Lebanese man
patient refused the biopsy at that time and was lost to
follow-up.
When he returned to the clinic 4 years later, he had
generalised eruption of annular hypopigmented non-
palpable atrophic plaques with central clearing (figure).
They were devoid of hair and had a pigmented rim at the
periphery. 85 lesions were counted, with the largest
located on the lower right leg and measuring 10 × 5·5 cm.
Sensory testing revealed hypoesthesia. Biopsy samples
taken 6 months previously showed non-caseating
epithelioid granulomata, focal epidermal exocytosis, and
negative acid-fast bacilli stain. PPD testing for
tuberculosis was negative. His overall health status was
good. Chest radiograph, CD4 count, and a general blood
test were within normal limits. He did not have any other
opportunistic infections and was doing well. According
to guidelines from WHO, and with his characteristic
skin lesions, histopathological findings, definite sensory
loss, and a history of residence in Oman (a country
endemic for leprosy), a diagnosis of borderline
tuberculoid leprosy was made. Clofazimine (50 mg per
day), dapsone (100 mg per day), and rifampicin (600 mg
per day) were started, and the patient was scheduled for
monthly follow-up visits. As a result of drug procurement
complications, the patient only completed 1 month of
treatment, which he tolerated well. It was too soon at the
end of his treatment for us to judge the outcome.
Leprosy prevalence in Lebanon is very low—less than
0·1 per 100 000 people—and the patient probably
contracted the disease in Oman. Multiple reports suggest
that cell-mediated immune responses to Mycobacterium
leprae are preserved at the site of disease in patients
infected with HIV. HIV prevalence in patients with
leprosy is not increased compared with the general
population, and the clinical spectrum of leprosy is not
affected by HIV co-infection. Because of the extremely
high lesion count in our patient, we speculate that HIV
might have had a role in disseminating the disease over
the body by altering peripheral M leprae-specific CD4
lymphocytes without affecting the local immunological
reaction and the granuloma formation per se.
Contributors
EK made the decision to submit the Clinical Picture for publication, and
did the literature search. RT was responsible for the figures and the final
corrections. Both authors wrote the report.
Declaration of interests
We declare no competing interests.
www.thelancet.com/infection Vol 17 March 2017