01798nas a2200325 4500000000100000008004100001260001300042653001000055653001600065653002300081653001900104653001800123653001100141653001600152653001600168653001100184653001200195653000900207653002700216653002600243100001500269700001500284700001600299245009100315856004100406300001000447490000700457520099400464022001401458 1982 d c1982 Mar10aAdult10aAmyloidosis10aAntibody Formation10aAutoantibodies10aCryoglobulins10aFemale10aHepatitis A10aHepatitis B10aHumans10aleprosy10aMale10aOceanic Ancestry Group10aTreponemal Infections1 aWangel A G1 aWegelius O1 aDyrting A E00aA family study of leprosy: subcutaneous amyloid deposits and humoral immune responses. uhttp://ila.ilsl.br/pdfs/v50n1a07.pdf a47-550 v503 a

One group of 11 aboriginal families, consisting of 27 persons with leprosy and 43 unaffected family members, and a second group of 26 patients with leprosy were studied in the Northern Territory of Australia. Amyloid deposits were sought in fine needle aspirates of subcutaneous fat and serological investigations relevant to amyloidosis and to the humoral immune response were done. The study showed unexpectedly high frequencies of amyloid deposits, evidence of persisting hepatitis B virus (HBV) infection, and antibodies to smooth muscle, to skin basement membrane, and to extractable nuclear antigens (ENA). Compared with unaffected family members, patients with leprosy had increased serum alpha-lipoprotein (alpha-LP) and were more often hepatitis B surface antigen (HBsAg) carriers but, contrary to expectations, the presence of amyloid, the alpha-LP level, serum amyloid associated (SAA) protein, and the HBsAg carrier state all appeared unrelated to the type of leprosy.

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