Prolactin responses to hypoglycemia and thyrotropin-releasing hormone in anorexia nervosa.

Although prolactin (PRL) responses to thyrotropin-releasing hormone (TRH) have been described by many investigators, PRL secretion after insulin stimulation has rarely been documented in patients with anorexia nervosa (AN). We investigated PRL responses to TRH (500 micrograms) and insulin (0.1 U/kg) in 19 women with AN and 10 normal women. Levels of PRL stimulation at 60 min and later following insulin administration were significantly lower in AN than in normal women. PRL increased by at least 10 micrograms/ml after insulin in 42% of women with AN and in 70% of normal women. The maximum PRL increase (max delta PRL) did not differ after the two stimulations in the normal women. However, in AN, the max delta PRL after insulin stimulation (17.2 +/- 4.0 micrograms/l, mean +/- SEM) was significantly lower than that after TRH (49.1 +/- 6.4 micrograms/l). These findings suggest that anorectic women may have a disturbance in hypothalamic functions. Insulin-induced hypoglycemia is useful to determine the integrity of the hypothalamic-pituitary axis for PRL secretion, in combination with TRH stimulation.

Serum thyrotropin (TSH) responses to thyrotropin-releasing hormone (TRH) in patients with anorexia nervosa and bulimia: influence of changes in body weight and eating disorders.

Serum thyrotropin (TSH) responses to thyrotropin-releasing hormone (TRH) were studied in 47 women with anorexia nervosa (AN) (group I) and in 11 bulimic patients of normal weight (group II). In group I, TSH responses were low in nine patients, delayed in 32 and normal in six. Patients with a normal TSH response had a lesser degree of anorexia than those with a delayed TSH response. Bulimia and vomiting were more frequently observed in the low response group. The maximum increase in TSH concentrations following TRH administration in the group I patients with vomiting (4.0 +/- 0.90 microU/ml, mean +/- S.E.) was significantly lower than that in the group I patients without vomiting or in normal controls (11.2 +/- 0.82 microU/ml and 11.1 +/- 2.34 microU/ml, respectively). Twenty-five patients with abnormal TSH responses in group I were retested after weight gain. Initially, TSH responses were low in six and delayed in 19. Following weight recovery, responses continued to be abnormal in five of the six and in eight of the 19, respectively. The symptoms of eating disorders continued in all patients with abnormal TSH responses even after weight recovery, whereas patients with normal responses after weight gain recovered from all symptoms. Of 11 patients in group II, six had abnormal TSH responses to TRH; the responses were delayed in four and low in two. Patients with normal responses had a lesser degree of eating disorder, compared with abnormal responders. These observations suggest that abnormal TSH responses in patients with AN were not necessarily due to weight loss alone; rather, they may be related to the eating disorder itself.

Abnormal serum prolactin responses to luteinizing hormone-releasing hormone (LHRH) in patients with anorexia nervosa and bulimia.

Abnormal responses of serum prolactin (PRL) to luteinizing hormone-releasing hormone (LHRH) stimulation have been observed in anovulatory women and in hypogonadal patients. Various endocrinological abnormalities have been demonstrated in patients with anorexia nervosa (AN). The present study was undertaken to further investigate responses of serum PRL, growth hormone (GH), luteinizing hormone (LH) and follicle stimulating hormone (FSH) to LHRH stimulation in 65 patients with AN and in 12 patients with bulimia before therapy and in the AN patients after several months of treatment, and in comparison to 12 normal women of the same age. Serum PRL responses to LHRH were positive (peak PRL levels greater than 25 ng/ml and delta increase in PRL greater than 10 ng/ml) in 16.9% of AN and 16.6% of bulimic patients; they were negative (absent) in all controls. Following restoration of the AN patients to normal body weight, the PRL responses to LHRH became normalized in those patients whose eating disorder behavior also returned to normal. However, in those patients whose eating disorder patterns continued to be abnormal, abnormal PRL responses persisted. The bulimic patients were of normal body weight, and yet had abnormal PRL responses. Thus, the responses of PRL correlated more closely with the behavior of the underlying eating disorder rather than with body weight gain or normal body weight.

[A long-term follow-up study of patients with chronic lymphocytic thyroiditis--with special reference to histological findings].

It is generally believed that in the long-term observation of chronic thyroiditis, the goiter decreases in size with thyroid hormone therapy and the thyroid function drops gradually. On the other hand, the histological changes in so-called Hashimoto's thyroiditis have been recognized to show progressive loss of epithelium and increased fibrosis. In this study, goiter size, thyroid function, thyroid microsomal and thyroglobulin antibodies and histology in needle biopsy were investigated in 75 patients with chronic thyroiditis during an interval of more than ten years. Among 75 cases, 8 (11%) were hypothyroid at the first medical examination. Among 21 cases who received no treatment, 7 (33%) became hypothyroid during the period of more than ten years. Among 54 cases with thyroid hormone therapy, 16 (30%) showed a remarkable reduction in size of goiter, but among 21 cases without thyroid hormone therapy only 3 (14%) showed a remarkable reduction. This paper discusses changes in titers of thyroidal antibodies in 47 cases. Among these 47 cases, 21 increased titer of thyroglobulin antibody during the period of more than ten years. 10 (48%) out of these 21 cases showed a remarkable reduction in size of goiter. But among 11 cases with a decrease of titer of thyroglobulin antibody, only one (9%) showed a remarkable reduction in size of goiter. On the other hand, titer of thyroid microsomal antibody increased in 33 cases. 9 (27%) out of these 33 cases showed a remarkable reduction in size of goiter. Only one (13%) of 8 cases, which decreased titer of thyroid microsomal antibody, showed a remarkable reduction in size of goiter.(ABSTRACT TRUNCATED AT 250 WORDS)