Rumi Masunaga

Cushing's syndrome induced by hypersecretion of cortisol from only one of bilateral adrenocortical tumors

A case of Cushings syndrome induced by the unilateral (right side) dominance of cortisol secretion in the face of bilateral adrenal tumors is reported. The adrenal tumor resected on the right side was a so-called black adenoma and histologically without any findings of nodular hyperplasia. After resection of the adrenal adenoma, no findings of cortisol hypersecretion from the remaining adrenal tumor on the left side were observed until the present, suggesting that the tumor of the left adrenal gland is a nonfunctioning adenoma. These data imply that the adrenal adenomas have primarily developed from the adrenal gland itself, rather than from micronodular hyperplasia by corticotropin stimulation, and that one of these tumors produces excess hormones initially by corticotropin stimulation, but the other remains in cell proliferation.

Cushing's syndrome with cortisol hypersecretion from one of bilateral adrenocortical adenomas: Report of a case

We report herein the case of a 40-year-old man with Cushings syndrome, diagnosed by clinical manifestations and endocrinological studies, who was found to have bilateral adrenocortical adenomas, one of which hypersecreted cortisol. The Cushings syndrome was therefore attributed to primary adrenocortical disease, and the right adrenal tumor was resected and histologically diagnosed as a so-called black adenoma. After resection of the right tumor, the left adrenal tumor showed no signs of cortisol hypersecretion for the 23 months of follow-up until the patient died of peritonitis subsequent to the rupture of a duodenal ulcer. The left adrenal tumor was examined at autopsy and found to be a cortical adenoma. These data imply that the adrenal adenomas developed primarily from the adrenal gland itself, and that one of the tumors was well differentiated and secreted excess hormones, while the other remained in cell proliferation without hypersecretion.

Effect of Somatostatin and Dopaminergic Agents on Bovine Pituitary Phosphodiesterase Activity

The effects of somatostatin and dopaminergic agents on pituitary cyclic nucleotide phosphodiesterases that had been partially purified through DEAE cellulose column chromatography were studied. Somatostatin, L-dopa, dopamine and CB-154(2-bromo-alpha-ergocriptine) competitively inhibited the pituitary cyclic AMP phosphodiesterase activity, especially that of the low Km enzyme. This inhibition was most potent in the case of somatostatin and CB-154.

Immunoreactive Creatine Kinase-MB and Creatine Kinase Isozyme Concentrations During Treatment of Hypothyroid Patients

Using a highly sensitive enzyme immunoassay (EIA) system, we determined creatine kinase isozymes, namely creatine kinase-MB and creatine kinase-MM, in sera of patients suffering from primary hypothyroidism with concomitant signs of myocardial affections before and during treatment. After oral administration of L-thyroxine, the augmented mass concentrations of serum creatine kinase-MB and creatine kinase-MM, and the increased catalytic activity concentrations of serum total creatine kinase and creatine kinase-MB gradually decreased in inverse proportion to the increased concentrations of serum triiodothyronine (T3) and thyroxine (T4). By the 6th to 8th week after treatment, the elevated levels of serum total creatine kinase and creatine kinase-MB catalytic activity concentrations (assayed by a routine method) and serum creatine kinase-MM mass concentrations (assayed by EIA) declined to normal values, while serum T3, T4, and thyroid stimulating hormone attained normal values. Serum creatine kinase-MB mass concentrations (assayed by EIA), however, still remained at the higher level, without complete recovery from myocardial damage, as shown by electrocardiogram (ECG). These data indicate that metabolic distortion still exists in the myocardium, as revealed by the high creatine kinase-MB mass concentration, especially as assayed by EIA, even though the plasma levels of thyroid hormones had returned to normal.