Excess of β-subunit of thyrotropin (TSH) in patients with idiopathic central hypothyroidism due to the secretion of TSH with reduced biological activity

G. Faglia, P. Beck Peccoz, M. Ballabio, C. Nava

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Abstract

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.

Original languageEnglish
Pages (from-to)908-914
Number of pages7
JournalJournal of Clinical Endocrinology and Metabolism
Volume56
Issue number5
Publication statusPublished - 1983

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Thyrotropin
Hypothyroidism
Bioactivity
Serum
Thyroid Gland
Thyroid Hormones
Bone

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Excess of β-subunit of thyrotropin (TSH) in patients with idiopathic central hypothyroidism due to the secretion of TSH with reduced biological activity. / Faglia, G.; Beck Peccoz, P.; Ballabio, M.; Nava, C.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 56, No. 5, 1983, p. 908-914.

Research output: Contribution to journalArticle

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abstract = "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.",
author = "G. Faglia and {Beck Peccoz}, P. and M. Ballabio and C. Nava",
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T1 - Excess of β-subunit of thyrotropin (TSH) in patients with idiopathic central hypothyroidism due to the secretion of TSH with reduced biological activity

AU - Faglia, G.

AU - Beck Peccoz, P.

AU - Ballabio, M.

AU - Nava, C.

PY - 1983

Y1 - 1983

N2 - 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.

AB - 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.

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