α-Subunit and β-subunit of TSH were measured in the sera of five patients with idiopathic central hypothyroidism due to the secretion of biologically inactive TSH, in seven normal controls matched for bone age and sex, and in five subjects with mild primary thyroid failure before and after TRH (200 μg, iv) stimulation. Basal serum α-subunit concentration in patients did not differ from that in normal controls (mean ± SD, 0.40 ± 0.20 vs. 0.38 ± 0.28 ng/ml; P, NS) whereas TSH and TSH-β were significantly higher in patients (TSH, 1.51 ± 0.74 vs. 0.59 ± 0.53 ng/ml, P <0.025; TSH-β, 0.56 ± 0.18 vs. 0.10 ± 0.02 ng/ml, P <0.001). The concentration of TSH-β was also significantly higher in patients with central hypothyroidism than in subjects with mild primary thyroid failure (0.56 ± 0.18 vs. 0.24 ± 0.08 ng/ml; P <0.01), although serum TSH levels did not differ in the two groups (1.51 ± 0.74 vs. 2.16 ± 0.52 ng/ml; P, NS). α-Subunit was significantly higher in primary hypothyroid subjects (1.50 ± 0.87, P <0.05 compared with patients with central hypothyroidism). After TRH, α-subunit, TSH, and TSH-β net increases (peak) were significantly higher in patients with central hypothyroidism than in normal controls (α-subunit: 0.95 ± 0.5 vs. 0.47 ± 0.19 ng/ml, P <0.05; TSH: 7.1 ± 3.1 vs. 2.9 ± 1.8 ng/ml, P <0.005: TSH-β: 0.89 ± 0.35 vs. 0.22 ± 0.18 ng/ml, P <0.005), whereas they did not significantly differ from those recorded in hypothyroid controls. The β/α ratio, which was 1.67 ± 0.86 in patients and 0.35 ± 0.18 in normal controls (P <0.005), slightly decreased after TRH to 1.24 ± 0.78 in patients, but remained unchanged in normal controls (0.39 ± 0.1). After TRH the α-subunit peak occurred at 20 min both in patients and in controls, whereas TSH and TSH-β peaked at 60 min in patients and at 20 min in controls. One patient was given oral TRH (40 mg/day for 4 weeks). The β/α ratio fell from 1.85 to 0.13. Interestingly, serum thyroid hormones, which did not increase after iv TRH and after the first doses of oral TRH, showed a definite increase. Sera from two patients were filtered on Sephadex G-100: in one of them TSH-β eluted in the same position as labeled reference standard, whereas in the other one radioimmunoassayable TSH-β eluted near the void volume. The above data indicate that in patients with idiopathic central hypothyroidism due to biologically inactive TSH there is an excess of circulating TSH-β and suggest that TRH is implicated in the secretion of TSH of full biological potency.
|Number of pages||7|
|Journal||Journal of Clinical Endocrinology and Metabolism|
|Publication status||Published - 1983|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism