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PubMed1975

Clinical uses of thyrotropin-releasing hormone.

Knowledge about the physiology of the endocrine glands has been expanded in the past several years. It now appears that the secretion of the various pituitary hormones is conditioned by specific releasing hormones secreted in the hypothalamus. Thyrotropin-releasing hormone conditions the pituitary to release thyroid-stimulating hormone when the serum thyroid hormone concentration falls below a certain level. A radioimmunoassay for TSH helps the physician to distinguish the different etiologies of hypothyroidism, to confirm the diagnosis of "euthyroid" Graves' disease and to evaluate pituitary function.

Humans↗
PubMedDate not supplied

[Indices of the pituitary-thyroid system in residents of cities with various fluorine concentrations in drinking water].

The thyroid 131I consumption, the hypophyseal thyrotropic hormone content and the blood serum total thyroxin and triiodothyronine concentrations were studied in equal groups of healthy humans and donors, living in two cities with an enhanced or decreased fluorine content in drinking water. Iodine deficiency and adaptive amplification of the hypophyseal-thyroid system, not ensuring an absolute compensation, were found in the citizens, using drinking water with an increased fluorine content, accompanied by an augmented incidence of functional disturbance, which structure remained relatively unchanged.

Drinking↗
PubMed1982

Comparison of pituitary-thyroid function in patients with endstage renal disease and in age- and sex-matched controls.

The response to i.v. bolus thyrotropin-releasing hormone (TRH) of 14 dialysis patients with end-stage renal disease (ESRD) was compared to the response of 14 age- and sex-matched renal clinic patients (controls) with normal renal function (serum creatinine concentrations less than 1.2 mg/dl). The mean basal serum levels of thyrotropin (TSH) were similar in the two groups. There was no difference between the two groups in the mean maximal increase in TSH after TRH (6.3 microU/ml and 7.2 microU/ml in ESRD and control groups, respectively); The rate of fall in TSH from 60 to 90 min after TRH was slower in the ESRD group than in the controls. The mean increase in serum triiodothyronine (T3) concentration after TRH was similar in both groups (25.4 ng/dl, ESRD; 18.4 ng/dl, controls). As previously reported, basal serum T3 content was subnormal in the ESRD patients. Serum thyroxine (T4) concentrations were comparable in control and ESRD groups and did not change significantly during the 90-min TRH test in either group. We conclude that ESRD patients, clinically stable on dialysis, have normal pituitary TRH responsiveness and normal thyroidal response to endogenous TSH secretion, as compared with an age- and sex-matched group of patients with normal renal function. The results of this study support the contention that ESRD patients are eumetabolic.

Adult↗