No abstract

The thyrotropin (TSH) response to thyrotropin-releasing hormone(TRH) (200 mug iv) was determined in 80 surgical patients with nontoxic multinodular goiter. The TSH reserve was normal in multinodular goiter. The TSH reserve was normal in 55 and elavated in 8 patients. No TSH response to TRH (deltaTSH less than or equal to 1 muU/ml) was detectable in 17 patients (21%). Individual and mean serum T4, FT4I and serum T3 values did not differ from normal in 13 of the TRH unresponsive patients; in 4 patients FT4I or serum T3 was marginally elevated. No statistical differences were noted for I131-uptake, PBI131 and conversion rate between controls and TRH unresponsive patients. All patients who failed to respond to TRH were euthyroid on clinical evaluation. Goiters were large multinodular and long-standing in most instances. In 12 tested subjects TRH responsiveness recovered following partial thyroidectomy. In 3 of 7 TRH unresponsive euthyroid patients tested 9-12 days post surgery a transient lack of TSH to respond to TRH was observed. Recovery of TRH responsiveness was accompanied by a significant (P IS LESS THAN 0, 02) decrease in serum T4and FT4I in the euthyroid range, whereas no change in serum T3 occurred. It is suggested that TRH unresponsiveness represents a state of preclinical hyperthyroidism maintained by autonomously functioning goiter compartments.

The effect of glucose on the release of insulin from the pancreas of 18\m=.\5 to 21\m=.\5-day-old rat foetuses has been studied in utero. Foetal hyperglycaemia was induced by a 1 h glucose infusion into pregnant rats.In foetuses from mother rats infused with saline, the blood glucose and the plasma insulin concentrations increased up to day 21\m=.\5of gestation. The blood glucose level of the foetuses never exceeded that of the mothers which remained stable from day 18\m=.\5to day 21\m=.\5of gestation.The infusion of glucose raised the foetal blood glucose concentration to that of the mothers and induced a significant increase of plasma insulin levels both in the mothers and their foetuses. The enhanced plasma insulin concentration observed in the 18\m=.\5-day-old foetuses of glucose-infused pregnant rats became greater each day up to 21\m=.\5 days.

No abstract

Serum thyroid hormone and TSH concentrations were measured before and after oral TRH (40 mg) administration in 46 women with preclinical hypothyroidism. Preclinical hypothyroidism was defined as serum T4 in the normal range, a normal or elevated basal serum TSH, and an exaggerated serum TSH response to TRH, in the absence of clinical manifestations of hypothyroidism. The results were compared to those in 22 normal women of the same age and body mass index. Overall, the patients had significantly lower mean values for basal T4 [total T4, free T4 index (FT4 index), and free T4] but not for T3; all indices of T4 were lower in those with an elevated basal TSH, but only the FT4 was lower in patients who had normal basal TSH levels and exaggerated TSH responses to TRH. Thyroid reserve, or the increase in serum thyroid hormones after TRH (delta T4, delta FT4, and delta T3) showed an inverse correlation with basal TSH (for delta T4, r = -0.518 and P less than 0.001; for delta FT4, r = -0.442 and P less than 0.05; for delta T3, r = -0.645 and P less than 0.001). Thyroid reserve was lower than normal in those with elevated basal TSH levels, but was normal in those with exaggerated TSH responses to TRH who had normal basal TSH levels. Thus, an elevated basal TSH level, even with basal serum T4 and T3 levels in the normal range, indicates deficient thyroid reserve.