Risk factors for type-1 reactions in borderline leprosy patients.
Type-1 or reversal reactions are the major cause of nerve damage and disability in leprosy. We wished to determine whether there were any clinical or laboratory markers that identified patients with an increased risk of type-1 reaction. 42 (31%) of 136 Nepalese borderline leprosy patients (97 male, 39 female; age range 7-73 years) had a type-1 reaction during the first 2 years of multi-drug therapy. Before therapy, 41 (98%) of the 42 patients were seropositive for antibodies to one of three mycobacterial antigens. Seropositivity for IgM antiphenolic-glycolipid-1 (PGL-1) antibodies, but not IgG anti-lipoarabinomannan or anti-Mycobacterium leprae 35 kDa protein antibodies, was significantly associated with subsequent manifestation of a type-1 reaction (p less than 0.001). The concentration of IgM anti-PGL-1 antibodies in serum was significantly higher in patients in whom a type-1 reaction developed. The risk attributable to anti-PGL-1 seropositivity was independent of leprosy class, skin smear positivity, and the presence of other anti-M leprae antibodies (adjusted odds ratio = 8.7, p less than 0.001). In the 87 patients who had a lepromin test, anti-PGL-1 seropositivity and lepromin reactivity were significant independent risk factors for subsequent reaction. 78% of patients with positive lepromin reactivity and IgM anti-PGL-1 antibodies had type-1 reactions. Patients with these risk factors should be carefully monitored during antimicrobial therapy to permit early initiation of anti-inflammatory treatment thus minimising permanent nerve damage and resultant disability.
Mycobacterial Research Laboratory, Anandaban Leprosy Hospital, Kathmandu, Nepal.
P W
PW
Roche
W J
WJ
Theuvenet
W J
WJ
Britton
D000293:Adolescent; D000328:Adult; D000368:Aged; D000907:Antibodies, Bacterial / Q000032:analysis; D000911:Antibodies, Monoclonal / Q000032:analysis; D000942:Antigens, Bacterial; D015415:Biomarkers / Q000097:blood; D002648:Child; D004342:Drug Hypersensitivity / Q000209:etiology / Q000276:immunology*; D005260:Female; D006017:Glycolipids / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular; D007428:Intradermal Tests; D015439:Leprosy, Borderline / Q000188:drug therapy / Q000276:immunology*; D015441:Leprosy, Tuberculoid / Q000188:drug therapy; D008070:Lipopolysaccharides / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009166:Mycobacterium leprae / Q000276:immunology; D009443:Neuritis / Q000139:chemically induced / Q000276:immunology*; D010523:Peripheral Nervous System Diseases / Q000139:chemically induced / Q000276:immunology*; D012307:Risk Factors
D000907:Antibodies, Bacterial; D000911:Antibodies, Monoclonal; D000942:Antigens, Bacterial; D015415:Biomarkers; D006017:Glycolipids; D008070:Lipopolysaccharides; C050016:lipoarabinomannan; C045169:phenolic glycolipid I, Mycobacterium leprae