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Thyroid function in the elderly.

Thyroid dysfunction is common in older individuals, yet the diagnosis is often complicated by atypical clinical presentations and difficulty in interpretation of laboratory tests. An understanding of the alterations in thyroid function occurring normally as a consequence of the aging process is necessary for correct laboratory diagnosis of thyroid dysfunction in the elderly. There are subtle alterations in hypothalamic and pituitary function but normal feedback control of TSH secretion persists. In the thyroid itself, morphologic changes develop with age, but have little impact on thyroid hormone economy. Thyroidal secretion of thyroxine decreases, but parallels the decrease in thyroxine degradation rate, resulting in unaltered plasma thyroxine levels. Decreased peripheral conversion of thyroxine to triiodothyronine causes a fall in triiodothyronine concentrations. Nonthyroidal illnesses in the elderly may perturb the laboratory assessment of thyroid function by producing isolated high or low thyroxine levels in euthyroid individuals.

Adult↗
PubMed1979

Amyloid goitre in familial Mediterranean fever.

Three patients known to suffer from familial Mediterranean fever (FMF), systemic amyloidosis and chronic renal failure developed large amyloid goitres. Amyloid goitre is an extremely rare complication of systemic amyloidosis not previously described in FMF. The clinical and pathological features of these three cases were similar to those previously described in amyloid goitre. In two of the patients abnormalities in thyroid function were consistent with those documented in chronic renal failure. There was evidence of hypothyroidism in a third patient. There was no evidence of amyloid induced dysfunction of other endocrine organs.

Adult↗
PubMed1977

Thyroid dysfunction in chronic renal failure. A study of the pituitary-thyroid axis and peripheral turnover kinetics of thyroxine and triiodothyronine.

Thyroid function was evaluated in 46 patients with end-stage kidney disease and 42 normal subjects. Patients were studied before and after the institution of maintenance hemodialysis (HD) and after renal transplantation (RT). Serum total triiodothyronine concentrations (TT(3), ng/100 ml, mean+/-SD) were 63+/-17 and 83+/-22 in the non-HD and HD groups, respectively. Values from normal subjects were 128+/-25 and from RT patients 134+/-20. The TT(3) was in the hypothyroid range (<78 ng/100 ml; 2 SD below normal mean) in 80% of non-HD and 43% of HD patients. Mean serum total thyroxine concentration (TT(4)), although within the normal range, was lower than the control value. T(4)-binding globulin capacity was also slightly lower but the difference was not statistically significant. Among patients whose TT(4) was 1 SD below the normal mean, the free T(4) index was equally depressed, suggesting that factors other than decreased binding capacity might be responsible for the low TT(4). In addition, there was a 37% incidence of goiter. Mean serum thyroid-stimulating hormone (TSH) was not elevated and the TSH response to thyrotropin-releasing hormone (TRH) was distinctly blunted, suggesting the possibility of pituitary dysfunction as well. In vivo (125)I-l-T(4) and (131)I-l-T(3) kinetics during 0.2 mg/day of l-T(4) replacement showed marked reduction in T(3) turnover rate in the uremic patients, both before and during HD; the values (mug T(3)/day, mean+/-SD) for the different groups were as follows: normal, 33.8+/-6.1; non-HD, 13.5+/-2.6; HD, 12.9+/-3.1; and RT, 30.3+/-7.1. The low T(3) turnover rate was due to impaired extrathyroidal conversion of T(4) to T(3). The mean percent+/-SD of metabolized T(4) converted to T(3) was 37.2+/-5.8 in normal subjects, 15.7+/-3.1 in non-HD, 12.8+/-1.7 in HD, and 34.0+/-14.7 in RT patients. In contrast, thyroidal T(3) secretion rate was not different between the control and the three patient groups. Thus, it appears that uremia affects thyroid function at several levels: (a) subnormal pituitary TSH response to TRH; (b) possible intrathyroidal abnormalities as suggested by slightly decreased TT(4) and high incidence of goiter; and (c) abnormal peripheral generation of T(3) from T(4). Restoration of renal function with RT resulted in normalization of all parameters of thyroid function with the exception of blunted or absent TSH response to TRH. The latter may be a direct consequence of glucocorticoid administration.

Adult↗
PubMed1980

Effect of streptozotocin diabetes on the hypothalamic-pituitary-thyroid axis in the rat.

Studies of the hypothalamic-pituitary-thyroid axis have been performed in streptozotocin (STZ)-diabetic Wistar rats and their controls. Plasma PBI concentration, plasma and pituitary TSH, contents, and hypothalamic TRH content were measured by RIA in basal and stimulated conditions. Compared to controls, rats made diabetic by 6.0 or 7.5 mg STZ/100 g BW showed decreased plasma PBI and TSH and diminished pituitary TSH content, with greater alterations in rats receiving the highest STZ dose. Both diabetic groups showed an almost 50% reduction of hypothalamic TRH content in comparison with the mean control value. After thyroidectomy, pituitary TSH secretion increased in diabetic, ad libitum fed, and semistarved animals, but it was lower in the diabetic group in which the reduction in plasma PBI was similar or greater. To evaluate pituitary sensitivity to the inhibitory action of L-T4 on TSH secretion in diabetes, thyroidectomized control (Thx-C), thyroidectomized diabetic (Thx-D), and thyroidectomized semistarved (Thx-S) rats were injected twice daily for 7 days with either saline or a fractional L-T4 dose of 0.25, 0.50, or 1.00 microgram/100 microgram/100 g BW. In Thx-D rats, a daily dose of 1.00 microgram L-T4 was sufficient to normalize pituitary TSH secretion, while a dose of 2.00 microgram was required to induce a similar effect in the Thx-C and Thx-S animals. Pituitary TSH content was increased in the Thx-C group with increasing T4 doses. No modification in this parameter was seen in the Thx-D and Thx-S animals. The fact that diabetes caused a reduction in the hypothalamic TRH content indicates that the primary cause of pituitary-thyroid alterations in STZ-diabetic rats lies in the hypothalamus, although the metabolic imbalance induced by diabetes and, in less degree, by undernutrition could also be partly responsible for some of the described modifications.

Animals↗