Serum carboxypeptidase A activity (CPase) was measured using carbonaphthoxy-1-phenylalanine as the substrate in various types of diabetes mellitus and the clinical implications of CPase in relation to pancreatic disorders were also discussed. Remarkably low level of CPase was observed in diabetics complicated with pancreatic cancer or chronic pancreatitis (pancreatic diabetics). In growth-onset type and maturity-onset type diabetics (primary diabetics), no remarkable decrease was found in CPase activity, if they were under good control. Very low CPase activity, however, was frequently found in primary diabetics with duration longer than 15 years. Abnormality of pancreatic uptake of ⁷⁵Se-selenomethionine and/or some degrees of dysfunction in pancreozymin-serection test were found in diabetics with low CPase level, especially in pancreatic diabetics. These results suggest that the determination of CPase is a useful screening method for detecting pancreatic disorders in patients with diabetes mellitus.

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Changes of blood pressure (BP), creatinine clearance (Ccreat), plasma renin activity (PRA), plasma aldosterone concentration (PAC) and urinary excretion of adrenaline and noradrenaline (uAD, uNAD) were studied in 5 normal subjects following i. v. infusion of 1-sarcosine, 8-isoleucine angiotensin II (sar¹, ile⁸-A II) and angiotensin II (A II). The effects of variable sodium balance on these changes were studied as well. Sar¹, ile⁸-A II demonstrated variable agonistic activities at 4 sites of A II action, i.e., C_creat, PRA and PAC. There seemed to be a reciprocal relation between agonistic and antagonistic activities (latter being evaluated by antagonism against A II-induced changes of BP, Ccreat, PRA and PAC) of sar¹, ile⁸-A II at each of sites, which would rather suggest similarity than heterogeneity of A II receptors at these sites. It was disclosed that agonistis activities on BP, PRA and PAC were dependent on sodium balance, i.e., most agonistic during sodium repletion and least active during sodium depletion. The implications of these findings were discussed.

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1-sareosine, 8-isoleucine angiotensin II (sar¹, ile⁸-A II), was infused intravenously in 68 subjects with hypertensive, body fluid and electrolyte disorders and changes of blood pressure (BP), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were studied. Most low-renin subjects showed elevation of BP and PAC and reduction of PRA. Four of 10 high-renin, hypertensive subjects showed reduction of BP and PRA. Many high-renin, normotensive subjects showed elevation of PRA and more or less reduction of PAC. Reduction of BP was less predictable. Changes of BP, PRA and PAC of normoreninemic subjects were variable. Subjects with Bartter's syndrome and renal tubular acidosis showed a significant reduction of BP indicating subclinical volume deficit. Marked elevation of BP was observed in subjects with Cushing's syndrome and hypertensive subjects with pheochromocytoma. Failure of inducing BP reduction in many subjects with renovascular hypertension presents a problem as a means of screening for such patients. From data of BP, PRA and PAC of subjects with both extremes of PRA, it was inferred that sar¹, ile⁸-A II is both agonistic and antagonistic at 3 sites of A II, i.e., BP, PRA and PAC in man. Factors other than renin and angiotensin appeared to be involved in hypertension seen in Cushing syndrome and pheochromocytoma.

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A Patient, 44-year-old woman, with idiopathic Addison's disease with goiter and ovarian dysfunction was studied endocrinologically and immunologically. She had a 26-year history of goiter, a 14-year history of severe oligomenorrhea and a 5-year history of Addison's disease. In recent three years, she had been treated with 20mg of hydrocortisone per day.Plasma cortisol levels before hydrocortisone administration were very low and urinary 17KGS levels did not respond to ACTH-Z. Plasma ACTH levels before hydrocortisone administration were high. Peripheral thyroid hormone levels were normal but response of plasma TSH to TRH injection was high and prolonged. ¹³¹I-uptake in thyroid gland was very high. Thyroid gland aspiration biopsy revealed infiltrations of many lymphocytes in the gland. Plasma gonadotrophins levels were very high and response to synthetic LH-RH were excessive. Thyroglobulin antibody and thyroid microsomal antibody were found in her sera. Specific adrenal antibody against zona fasciculata cells of dog adrenal cortex was also found by immunofluorescence method. Ovarian antibody, parietal cell antibody and antinuclear factor were not detected. Leukocyte mygration inhibition test using rabbit adrenal tissue was normal. These findings indicate that her goiter was caused by chronic thyroiditis and oligomenorrhea was caused by ovarian failure.

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A case of Plummer-Vinson syndrome is reported. The patient was a 43-year-old woman, with the chief complaint of dysphagia, manifesting glossitis and other oral symptoms, and had hypochromic anemia. Administration of chalybeate was followed by early disappearance of dysphagia and glossitis, as well as the improvement of anemia. It was emphasized that this syndrome develops frequently in women in middle age, that is, the age in which the incidence of upper esophageal cancer is high. In view of this, it is important in the diagnosis of this syndrome to eliminate the possibility of malignancy, which makes mandatory the scrupulous examination of the subpharyngo-esophageal region by means of fluorosccpy and endoscopy. The routine roentgen and endoscopic examinations having been performed in this country are not reliable in detecting the pathology. The effectiveness of chalybeate suggested an intimate relation between iron deficiency and the development of dysphagia, angular stomatitis and glossitis.

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