02048nas a2200325 4500000000100000008004100001260001300042653002600055653002400081653003800105653001600143653001100159653002100170653002100191653001200212653002400224653002500248100001500273700002100288700001200309700002400321700001300345700001400358245018100372856004100553300001100594490000700605520109600612022001401708 1990 d c1990 Sep10aAntibodies, Bacterial10aAntigens, Bacterial10aEnzyme-Linked Immunosorbent Assay10aGlycolipids10aHumans10aImmunoglobulin G10aImmunoglobulin M10aleprosy10aLipopolysaccharides10aMycobacterium leprae1 aMeeker H C1 aSchuller-Levis G1 aFusco F1 aGiardina-Becket M A1 aSersen E1 aLevis W R00aSequential monitoring of leprosy patients with serum antibody levels to phenolic glycolipid-I, a synthetic analog of phenolic glycolipid-I, and mycobacterial lipoarabinomannan. uhttp://ila.ilsl.br/pdfs/v58n3a07.pdf a503-110 v583 a

Sequential serum samples from leprosy patients at various stages of antibacterial treatment were tested by an ELISA for antibodies to phenolic glycolipid I (PGL-I), a synthetic PGL-I analog (ND-BSA), and lipoarabinomannan (LAM) from Mycobacterium tuberculosis to determine if these antibodies could be useful in monitoring response to therapy. Among patients with positive initial anti-PGL-I IgM, a significant decrease in this antibody was seen over time (p less than 0.01), whether assayed by PGL-I or ND-BSA. The two antigens showed good agreement in the detection of decrease in anti-PGL-I IgM. The greatest decrease was seen in patients with a high initial anti-PGL-I IgM and a high bacterial index (BI). Patients with a declining BI were seen to have generally declining antibody levels to PGL-I and to LAM; in those patients with a fluctuating BI, antibody levels were less predictable. We conclude that antibodies to PGL-I and LAM can be useful in following response to therapy in leprosy patients and that either the native PGL-I or ND-BSA can serve as antigen for the ELISA.

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