title: Failure to detect thyroid growth-promoting activity in immunoglobulin G of patients with endemic goiter.
abstract: The [3H]thymidine incorporation assay in FRTL-5 cells was used to measure thyroid growth-stimulating antibody in the purified immunoglobulin G (IgG) fraction of patients with endemic nontoxic goiter (grade I-III) living in Italy (n = 34) or Peru (n = 37). IgG of euthyroid nongoitrous subjects living in the same endemic area (n = 25) and from an area of sufficient iodine intake were used as controls. Bovine TSH (10 mU/L) and thyroid-stimulating antibody of Graves' disease produced a significant increase in [3H]thymidine incorporation and DNA content in FRTL-5 cells. IgG from Italian or Peruvian patients with endemic goiter produced a small increase in [3H]thymidine incorporation in FRTL-5 cells (131 +/- 54% and 165 +/- 57%, respectively), which was indistinguishable from that obtained with IgG from normal nongoitrous subjects residing in endemic or nonendemic areas (167 +/- 80% and 161 +/- 36%, respectively). For comparison 18 of 25 (72%) IgG of hyperthyroid patients with Graves' disease produced clear-cut increases in [3H]thymidine incorporation (1142 +/- 1065%) and DNA content (219%) in FRTL-5 cells. IgG from patients with endemic goiter, at variance with Graves' IgG, did not cause an increase in DNA in FRTL-5 cells. All Graves' IgG that stimulated [3H]thymidine incorporation in FRTL-5 cells also stimulated cAMP production in this culture system, whereas no adenylate cyclase stimulation was produced by IgG from patients with endemic goiter. The prevalence of thyroglobulin antibody and thyroperoxidase antibody in endemic goiter patients did not differ from that in control subjects residing in the same iodine-deficient area. Our data show that sera of endemic goiter patients are devoid of thyroid growth-stimulating antibody and thyroid-stimulating antibody activities. These observations argue against a direct role of thyroid autoimmunity in the development of goiter in iodine-deficient areas.
authors.affiliation: Istituto di Endocrinologia Università di Pisa, Italy.
authors.forename: P
authors.initials: P
authors.lastname: Vitti
authors.forename: L
authors.initials: L
authors.lastname: Chiovato
authors.forename: M
authors.initials: M
authors.lastname: Tonacchera
authors.forename: G
authors.initials: G
authors.lastname: Bendinelli
authors.forename: C
authors.initials: C
authors.lastname: Mammoli
authors.forename: A
authors.initials: A
authors.lastname: Capaccioli
authors.forename: E
authors.initials: E
authors.lastname: Fiore
authors.forename: E
authors.initials: E
authors.lastname: Pretell
authors.forename: A
authors.initials: A
authors.lastname: Pinchera
mesh_terms: D000328:Adult; D000368:Aged; D001323:Autoantibodies / Q000032:analysis*; D004247:DNA / Q000096:biosynthesis; D005260:Female; D006043:Goiter, Endemic / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis*; D018828:Immunoglobulins, Thyroid-Stimulating; D008297:Male; D008875:Middle Aged; D013961:Thyroid Gland / Q000276:immunology*
chemical_list: D001323:Autoantibodies; D007074:Immunoglobulin G; D018828:Immunoglobulins, Thyroid-Stimulating; D004247:DNA