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Lepromatous leprosy with drug reaction

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Lepromatous leprosy with drug reaction
Rebecca D. Baxt, M.D., M.B.A.
Dermatology Online Journal 6(1): 9

Department of Dermatology, New York University

PATIENT: 61-year-old man

DURATION: Twenty years

DISTRIBUTION: Face, arms, and trunk

HISTORY: Cutaneous changes have been present for years. A new pruritic eruption has been present for the last two months. Enalapril was started two and one-half months ago. Medications include digoxin, coumadin, simvastatin, amlodipine, and hydrochlorothiazide. Medical history includes atrial fibrillation, hypercholesterolemia, gastritis, and a history of dapsone resistance. He did not tolerate clofazimine due to gastrointestinal side effects. He has most recently been maintained on rifampin 300 mg twice daily and ethionamide 25 mg daily.

Figure 1Figure 2

PHYSICAL EXAMINATION: There was leonine facies with loss of eyebrow hair. Violaceous plaques and erythematous patches were found on the chest, back, abdomen and arms. There was also hypoesthesia of the fingertips.


HISTOPATHOLOGY: There is a superficial and deep perivascular and periadnexal inflammatory infiltrate that is composed of lymphocytes, foamy histiocytes, and numerous eosinophils. There is focal spongiosis. A Fite stain failed to show acid-fast bacilli.

DIAGNOSIS: Lepromatous leprosy with a drug reaction

COMMENT: Leprosy is a chronic, cutaneous infectious disease caused by Mycobacterium leprae. The route of infection is unknown; however, prolonged close contact is thought to be required for transmission. Cases have been reported to be transmitted from armadillos.[1]

Patients are classified into multibacillary or paucibacillary groups based on the presence or absence of bacilli in skin biopsy specimens.[2] Patients are also classified according to Ridleyís system: polar tuberculoid, borderline tuberculoid, borderline, borderline lepromatous, subpolar lepromatous, and polar lepromatous. Polar tuberculoid and polar lepromatous leprosy are stable diseases, but patients classified as any of the other types can upgrade to a tuberculoid pattern of more resistance or downgrade to a lepromatous pattern of less resistance.

Lepromatous leprosy patients have widely disseminated disease. Ill-defined, symmetric, flesh-colored nodules are the classic lesions. With progressive disease, the bacilli infiltrate the dermis and cause thickening with the classic leonine facies as seen in our patient. Hair loss, especially of the eyebrows, is common as seen in our patient. Hair loss may extend over the body but not the scalp. Some lesions may be hypoesthetic. Loss of eccrine sweating from sympathetic nerve involvement is common.[3] Subpolar lepromatous and polar lepromatous patients frequently develop erythema nodosum leprosum, and subpolar lepromatous patients may develop reversal reactions. Multibacillary patients with drug resistance or noncompliance can have relapse.

The World Health Organizationís recommendations for treatment are as follows: paucibacillary disease - dapsone 100 mg daily and rifampin 600 mg each month for six months; multibacillary disease - dapsone 100 mg daily, rifampin 600 mg each month, clofazimine 50 mg daily, and 300 mg each month with or without rifampin 600 mg each month for two years.[2] In the United States, patients are usually treated for a longer period of time, and often for life, especially if they have multibacillary disease.


1. Taylor JP; Vitek I; Enriquez V; Smedley JW. A continuing focus of Hansenís disease in Texas. American Journal of Tropical Medicine and Hygiene, 1999 Mar, 60(3):449-52 PubMed.

2. Chemotherapy of leprosy. Report of a WHO Study Group. World Health Organization Technical Report Series, 1994, 847:1-24 PubMed.

3. Nations SP; Katz JS; Lyde CB; Barohn RJ. Leprous neuropathy: an American perspective. Seminars in Neurology, 1998, 18(1):113-24 PubMed.

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