Amyloid goiter: Report of the clinical, histological and biochemical features of five cases

Rivka Gal, Shmuel Shtrasburg, Miriam Luria, Beatrice Lifschitz Mercer, Sami Viskin, Shoshana Yakar, Mordechai Pras

Research output: Contribution to journalArticlepeer-review


The clinical course and pathological findings of five cases of amyloid goiter in patients with AA amyloidosis are presented. The underlying diseases which caused the amyloidosis were: chronic recurrent multifocal sterile osteomyelitis, acne conglobata, tuberculosis, and two cases of familial Mediterranean fever. All presented with a hard, moderately rapidly growing thyroid mass, mimicking a malignant thyroid tumor. Four patients underwent excisiorial biopsy or partial thyroidectomy, after which they developed hypothyroidism. The fifth case was discovered at an autopsy. Histologically, in all cases, the thyroid follicles were scarce, many had an atrophic appearance, surrounded by amyloid deposits and associated with adipose metaplasia of the stroma. The amyloid was potassium permanganate Congo red sensitive, and reacted with anti-AA antibodies by the avidin biotin immunoperoxidase method in all cases. The amyloid fibrils, extracted from the thyroid tissue of each of the five cases, revealed two protein bands in 17% SDS polyacrylamide gel electrophoresis: One band (of about 5 kD) ran faster than the usual 8.5 kD amyloid A protein, and the other (of about 9.5 kD) ran slower. Both proteins reacted with rabbit anti-human AA polyclonal antiserum in Western immunoelectroblot. It is concluded that in our cases amyloid goiter was associated with two SAA related protein chains, that were codeposited in the thyroid in the form of fibrils, accompanied by large amounts of mature adipose tissue.

Original languageEnglish (US)
Pages (from-to)119-125
Number of pages7
Issue number2
StatePublished - 1995


  • Aa amyloidosis
  • Amyloid goiter

ASJC Scopus subject areas

  • Internal Medicine


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