Circulating thyrotropin bioactivity in sporadic central hypothyroidism.

摘要: The etiopathogenesis of sporadic central hypothyroidism (CH) involves pituitary and hypothalamic lesions. Pituitary CH (pCH) implies a diminished number functioning thyrotropes, accounting for the quantitative impairment TSH secretion. Hypothalamic (hCH) is characterized by normal or even increased concentrations qualitative abnormalities secretion, including decreased bioactivity circulating TSH. However, controversy still exists about actual occurrence bioinactive among patients, no data are available in pCH. Therefore, we studied 41 patients with different hypothalamic-pituitary disorders. Immunoreactive (TSH-I) ranged from 0.08-11.1 mU/L (normal, 0.24-4.0), free T4 (FT4) 0.6-8.8 pmol/L 9-18), FT3 1.2-5.4 4-8). A blunted response to TRH ( =4 mU/L, indicating prevalent hCH, was found remaining 44%. Net TSH-I increments showed significant correlation basal FT4 (P < 0.02), relevance reserve pathogenesis CH. Circulating immunoconcentrated tested bioassay ricin affinity chromatography. ratio between biological (B) immunological (I) activities reduced (n = 25; B/I, 0.38+/-0.19) compared values recorded subjects 26; 1.53+/-0.54; P 0.001) primary hypothyroid 24; 0.74+/-0.31; 0.001), but difference pCH 9; 0.36+/-0.16) hCH 16; 0.39+/-0.20) seen. B/I limited overlap (20%) highly endogenous TRH-stimulated 0.005). elevated sialylation degree molecules may explain part these findings. In conclusion, secretion common alteration lesions, contributing along