02101nas a2200361 4500000000100000008004100001260001300042653001000055653002800065653001900093653002100112653003500133653001100168653002000179653002100199653002100220653002100241653002000262653002300282653001200305653001600317653002200333653001800355100001500373700001100388700001500399245009400414856004100508300001100549490000700560520115800567022001401725 1982 d c1982 Jun10aAdult10aAntibodies, Antinuclear10aAutoantibodies10aErythema Nodosum10aFluorescent Antibody Technique10aHumans10aImmunodiffusion10aImmunoglobulin A10aImmunoglobulin G10aImmunoglobulin M10aImmunoglobulins10aLeprostatic Agents10aleprosy10aMiddle Aged10aRheumatoid Factor10aThyroglobulin1 aSharma V K1 aSaha K1 aSehgal V N00aSerum immunoglobulins an autoantibodies during and after erythema nodosum leprosum (ENL). uhttp://ila.ilsl.br/pdfs/v50n2a05.pdf a159-630 v503 a
Sera from 20 patients with lepromatous leprosy complicated by erythema nodosum leprosum (ENL) were collected at the time of acute reaction and then after clinical cure four weeks later. Anti-ENL drugs used were: prednisolone (11 patients), chloroquin (6 patients), and clofazimine (3 patients). Immunoglobulins M, G, and A and autoantibodies, namely, antithyroglobulin antibody (ATA), antinuclear antibody (ANA), and rheumatoid factor (RF), were measured in these 20 paired serum samples. The mean serum concentration of IgG showed a significant elevation after clinical subsidence of the reaction, mainly in the prednisolone treated group; while those of IgM and IgA varied only marginally. Autoantibodies were detected in nine patients. Of these, three patients developed these antibodies only after remission of the reaction. Treatment with prednisolone and chloroquin, although causing subsidence of ENL, resulted in an increased incidence of ATA and/or ANA. Furthermore, it was observed that longer duration of illness, higher age group, and history of repeated attacks of ENL predisposed these patients to enhanced autoantibody formation.
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