[A case of hyperthyroidism with pancytopenia and the etiological study of its haematological disorders (author's transl)].
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Biomedical subjects
Publications and source records attributed to M Kawato.
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The direct inhibitory action of somatostatin (cyclized SRIF) on the pancreatic endocrine function was investigated by a technique using pancreaticoduodenal arteriovenous system in vivo. Somatostatin was infused for 20 minutes at a speed of 2.5 mug/minute into the superior pancreaticoduodenal vein and femoral artery were measured before and every 5 minutes throughout the experiment for 30 minutes. The results were compared with those obtained from the control experiment which was carried out in the same time schedule under infusion of physiologic saline solution instead of somatostatin. Next, the effect of somatostatin on the glucose-induced insulin release from the pancreas was also evaluated. The following findings were obtained. (1) Somatostatin infused at a speed of 2.5 mug/minute into the superior pancreaticoduodenal artery caused a statistically significant inhibition of plasma levels of IRI and IRG and also pancreatic output of these hormones. With the sessation of somatostatin infusion an abrupt rise of the hormones were seen. This "rebound" phenomenon was more pronounced in insulin secretion than in glucagon. No significant changes in the plasma glucose levels in either the pancreaticoduodenal vein or the femoral artery throughout the experiment were found. (2)During infusion of somatostatin at a speed of 1.25 mug/minute, insulin response to glucose injected into the pancreaticoduodenal artery in a small dose, as well as having no effect on the plasma glucose level in systemic circulation, was also significantly inhibited. From these findings obtained by direct experiment using the pancreaticoduodenal arterio-venous system, it was confirmed that somatostatin exhibits a direct inhibitory action on pancreas endocrine in a very low concentration in vivo, and it was suggested that this action might be partly due to a reduction in pancreatic circulation.
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In order to evaluate the clinical usefulness of the TRH stimulation test in predicting premyxedematous state in chronic thyroiditis, serum TSH response to the i. v. injection of TRH was determined in 58 patients with chronic thyroiditis proven by needle or open biopsy. TSH radioimmunoassay was done by a double antibody technique, and the degree and pattern of TSH response were assessed based on our criteria established by the results obtained from 9 normal controls. According to Woolner's classification, 35 cases were diagnosed as diffuse type. 19 cases as focal type and 4 cases as hyperplastic. The basal levels of TSH were above the normal range in 71.4% of diffuse thyroiditis, whereas 36.8% of the patients with focal thyroiditis had an abnormally high basal TSH level. Responses of serum TSH to TRH was exaggerated in 67.1% of all patients; 80.0% in diffuse type and 47.4% in focal type. Concerning TSH response curve, 15 patients were judged as "prolonged", and 8 patients as "delayed" response. No weak responder in the TRH test was found in patients with high basal TSH level, 91% of whom had an exaggerated response. Serum levels of thyroxine and triiodothyronine inversely correlated with basal, maximal TSH levels (p less than 0.01) and increment of TSH (delta TSH) after TRH injection (p less than 0.01). Thyroidal uptake of I131 also inversely correlated with basal TSH level (p less than 0.05) but not with maximal TSH and delta TSH. From the fact that an elevation of basal TSH level and its hyperresponsiveness to TRH administration develop in a much more exaggerated fashion compared to the changes in other parameters of thyroid function, it was concluded that TRH test provides a useful rationale for the early diagnosis of premyxedema in chronic thyroiditis.
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