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.

Changes in the hypothalamic-pituitary-thyroid axis during acute starvation in non-obese patients.

We investigated changes in the hypothalamic-pituitary-thyroid axis before, during, and after fasting in twenty-one non-obese euthyroid patients with psychosomatic diseases. Blood samples for free T3 (FT3), T3, free T4 (FT4), T4, reverse T3 (rT3), and TSH were obtained from all patients before and on the 5th day of fasting, and in 11 of the same individuals on the 5th day of refeeding. Serum TSH and T3 responses to TRH were also evaluated in 10 patients before and on the 5th day of fasting. During the fast, FT3, T3 and TSH levels decreased significantly and rT3 levels increased significantly whereas FT4 and T4 levels remained within the normal range. Maximal delta TSH, peak TSH levels, max delta T3, peak T3 levels, and net secretory responses to TRH decreased significantly. Peak TSH levels and max delta TSH to TRH correlated well with basal levels of TSH. A statistically significant negative correlation between basal levels of FT4 and TSH was observed. After refeeding, there was a significant increase only in TSH which returned to prefasting values. These results demonstrated that in a state of "low T3" during acute starvation a reduction in serum T3 might depend partly on TSH-mediated thyroidal secretion.

Coping behaviors of severe diabetics.

In order to study the relationship between personality and the development of diabetic retinopathy in patients with diabetes mellitus, diabetics with retinopathy (severe group) and sex-, age-, and duration-matched diabetics without complications were tested by psychological tests, and interviewed. The result of the Yatabe-Guilford personality test (Y-G) and Spielberger's State and Trait Anxiety Inventory revealed that subjects were emotionally and socially stable and well-adjusted types and less anxious in the severe group than in the mild group. The interview findings reveal that the severe group had neglected the medical treatment and the diet therapy for significantly longer periods of time and the incidence of a childhood parental separation was significantly higher in the severe group than in the mild group. Discussion focuses on the severe diabetics' coping behavior which is characterized by the neglect of medical treatment and diet therapy for extended periods of time, which in turn resulted in diabetic retinopathy and other complications. Such coping behavior is shown to be equivalent to that found in the alexithymic behavioral syndrome.

[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)

A study of thyroid function after subtotal thyroidectomy for Graves' disease: particularly on TRH tests, T3 suppression tests and antithyroid antibodies in euthyroid patients.

Of 305 patients who underwent subtotal thyroidectomy for Graves' disease between 1969 and 1975, recurrent hyperthyroidism was found in 31 (10.2%) and hypothyroidism in 18 (5.9%). The remaining 256 patients were clinically euthyroid, but an elevated serum TSH level was found in 104 (34.1%) and an elevated serum T3 level in 19 (6.28%). In 57 of 133 clinically and biochemically euthyroid patients, a TRH test, T3 suppression test and measurement of antithyroid antibodies were performed. Twenty-nine of the 57 patients (50.9%) showed an abnormal response to TRH. Eight of these (14.0%) showed an impaired or absent response. The T3 suppression test showed that 15 of the 57 patients (26.3%) were non-suppressible. Positive antithyroid antibodies, especially antimicrosomal antibodies, were more frequent in non-suppressible and TRH-non-responsive patients than in suppressible and TRH-responsive patients. It is suggested that after operation for Graves' disease: 1) only half of the clinically euthyroid patients were biochemically euthyroid, 2) of the clinically and biochemically euthyroid patients, there were many with abnormalities in TRH responsiveness and T3 suppressibility, and 3) thyroid functional status is unstable and long careful follow-up is important after operation for Graves' disease.

Responses to TRH, T3 suppression tests and histological findings by needle biopsy in patients with simple goitre in Japan.

Studies were performed in 120 patients with simple goitre, defined as relatively soft diffuse goitre. All were clinically and biochemically euthyroid and their antithyroid antibodies were negative. The TRH test was performed in 99 after the TRH test, while satisfactory biopsies of the thyroid were obtained in 37. The results showed that 28 of the 115 cases (24%) had an abnormal response to TRH; 8 (7%) were hyporesponders and 20 (17%) were hyperresponders. The T3 suppression test showed that 3 of 99 cases (3%) were non-suppressible. As determined by histological examination of the needle biopsy specimen, 17 of the 37 cases (46%) had normal follicles without lymphocytic infiltration, 10 (27%) had diffuse chronic thyroiditis, 5 (14%) had focal thyroiditis and 4 (11%) had diffuse epithelial hyperplastic change, and 1 (3%) had an adenomatous goitre. It is suggested that simple goitre defined as above includes various thyroid diseases and that the results of TRH tests, antithyroid antibody estimations and histological findings do not correlate in many patients.

Changes in thyroid function in euthyroid subjects with a family history of Graves' disease: a follow-up study of 69 patients.

TRH tests were performed in 206 clinically and biochemically euthyroid relatives of patients with Graves' disease. In 117 of the 206, T3 suppression tests were performed. Results revealed that 56 of the 206 (27.1%) showed abnormal responses to TRH. Twenty-nine of these (14.1%) revealed absent or decreased responses, and 27 (13.1%) revealed augmented responses to TRH. Eight of the 117 (6.8%) were T3 nonsuppressible. These eight subjects consisted of 4 subjects out of 17 hyperesponders and 4 subjects out of 90 normal responders. The majority of suppressible subjects (86 among 109) demonstrated normal responses to TRH. Sixty-nine of the 206 subjects were followed for 6 months to 5 yr to observe changes in their thyroid functions. Among all 69 subjects 3 became clinically thyrotoxic 12, 12, and 18 months after their initial visit, respectively, and 2 became clinically hypothyroid 2 yr after their initial visit. Since 69 subjects were clinically and biochemically euthyroid and had no goiter or exophthalmos at their initial visit, the incidence of thyrotoxicosis or hypothyroidism in these subjects could be considered to be remarkably high. It is of interest that the 3 thyrotoxic patients were TRH hyporesponders at their first visit. One patient was T3 suppressible; T3 suppression tests were not performed in the other 2 patients at their initial visit. There was no abnormality in the first TRH test in 2 relatives who became hypothyroid. It is suggested that 1) among euthyroid relatives with a family history of Graves' disease, there are many with abnormalities in TRH responsiveness and T3 suppressibility, 2) nonsuppressible subjects are more likely to be TRH hyporesponders and vice versa, 3) hyperthyroidism or hypothyroidism occurs frequently in euthyroid relatives with a family history of Graves' disease, and 4) thyrotoxicosis occurs frequently in TRH-hyporesponders, and hypothyroidism occurs in the others.

Thionamide therapy in Graves' disease: relation of relapse rate to duration of therapy.

The present study was undertaken to investigate whether there is a rational basis for the usual long periods of thionamide therapy in patients with hyperthyroid Graves' disease. Eighty untreated patients were given the minimum dose of thionamide drug needed to maintain serum thyroxine, triiodothyronine, and thyrotropin (TSH) concentrations within their normal ranges. Thyrotropin-releasing hormone (TRH) tests were done at 6 monthly intervals for 2 years. Among patients who had positive responses of TSH to TRH, approximately 10 patients every 6 months were asked to stop thionamide therapy and were followed up for at least 1 year after discontinuation of drugs. In the groups treated for 6, 12, 18, and 24 months, relapses occurred in nine of 13, five of nine, three of 12, and two of 11 patients, respectively. Values for thyroid function tests before and at the end of treatment were not different among these four groups of patients. The overall remission rates were not ascertained. However, a minimum of 1 year's treatment is recommended, at least in Japan.