A 59-year-old man diagnosed with borderline lepromatous leprosy developed reddish patches and plaques on the face, which progressively enlarged and spread to the trunk and limbs (Figure 1A–D). Other superficial nerves appeared normal. Biopsy showed plasmocytic and lymphocytic infiltration in the nerve tract, and was 4+ acid-fast bacilli (AFB)–stain positive suggesting Mycobacterium leprae (Figure 2A and B); this was confirmed by real-time polymerase chain reaction (PCR). The HLA-B*13:01 test was negative. Two weeks after rifampin, dapsone, and clofazimine (World Health Organization multidrug therapy [WHO MDT] regimen) were started, the skin lesions (hypochromic macules) became red, edematous, and enlarged (Figure 3A–D). Both ulnar nerves became tender and thickened; ultrasonography showed reduction of blood flow (Figure 4A and B). Collectively these findings indicated a type 1 conversion reaction (T1R) (Figure 2C). One year after prednisone was started (40 mg/day for 3 months with progressive tapering), the T1R was found to be completely resolved.
In leprosy, type 1 and type 2 reactions—whether spontaneous or related to treatment—are the main causes of morbidity. T1Rs result from cell-mediated immunity affecting up to 30% of susceptible individuals.1 Nonpolar forms of leprosy are the primary risk factor for the occurrence of T1Rs.2 Systemic corticosteroids remain the mainstay of treatment of T1Rs.
Nery JA, Bernardes Filho F, Quintanilha J, Machado AM, Oliveira S de S, Sales AM, 2013. Understanding the type 1 reactional state for early diagnosis and treatment: a way to avoid disability in leprosy. An Bras Dermatol 88: 787–792.