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Biomedical subjects

K Haruyama

Publications and source records attributed to K Haruyama.

At least 37 records · Page 2Linked to original sources
PubMed1982

[The localization of aldosterone-producing adenoma on computed tomography--a comparative study with adrenal scintigraphy and plasma aldosterone concentration in the adrenal or renal vein].

The evaluation of computed tomography (CT) for detecting aldosterone-producing adenoma in primary aldosteronism was performed by comparison with adrenal scintiscan; determination of aldosterone in adrenal or renal veins, retroperitoneal pneumography and adrenal venography was reliable for diagnosis of adrenal tumors in pheochromocytoma or Cushing's syndrome, but not so effective for small adenoma of primary aldosteronism. An abdominal CT scan was performed on six patients with primary aldosteronism, one with idiopathic hyperaldosteronism and one with glucocorticoid responsive hyperaldosteronism; in an attempt to evaluate the utility of this noninvasive procedure. Diagnosis of hyperaldosteronism was made by demonstrating the elevated plasma aldosterone concentration and aldosterone secretion rate, normal excretion rate of urinary 17-OHCS and 17-KS, and low plasma renin activity. The CT scan correctly predicted unilateral adrenal adenoma in all the patients with primary aldosteronism of which the findings were identical to those demonstrated by surgery. The diameter of these tumors ranged from 10 X 7 X 6 to 19 X 17 X 14 mm. Also the CT scan in idiopathic hyperaldosteronism and glucocorticoid responsive hyperaldosteronism showed bilateral adrenal hyperplasia and bilateral normal adrenal glands, respectively. The pathological findings in these two cases disclosed the adrenal hyperplasia of zona glomerulosa and adrenal hyperplasia of zona subglomerulosa accompanied by a normal thickness of the adrenal gland, respectively. The precision of the CT scan, adrenal scintigraphy and determination of plasma aldosterone in the adrenal or renal veins were almost equal to the diagnosis of the localization of adrenal adenoma. It is concluded that the CT scan is a noninvasive and most useful method for the localization of aldosterone-producing adenoma and helpful in distinguishing adrenal adenoma from adrenal hyperplasia.

Adenoma↗
PubMed1982

[The effect of trilostane, a new inhibitor of adrenal steroid biosynthesis, on blood pressure, plasma aldosterone and other steroid hormones, serum potassium and plasma renin activity in primary aldosteronism (author's transl)].

Six patients with primary aldosteronism (PA), one with idiopathic hyperaldosteronism (IHA), one with glucocorticoid responsible hyperaldosteronism (GRHA) and eight with essential hypertension (EH) were treated with trilostane (MWD-1822) (4 alpha, 5-epoxy-17 beta-hydroxy-3-oxo-5 alpha-androstane-2 alpha-carbonitrile), an inhibitor of adrenal steroid biosynthesis, for 9-47 days with a daily dose of 30-960 mg. Blood pressure decreased slightly and gradually from 30 min. to 360 min, plasma aldosterone (PAC) and cortisol concentration (F) decreased, and plasma dehydroepiandrosterone concentration (DHEA) increased 120 min. after the administration of a single dose of 120 mg of trilostane. In the patients with PA, IHA and GRHA on long term therapy with trilostane, blood pressure decreased, PAC and F were depleted, serum improved within normal limits and DHEA increased, but plasma progesterone concentration (Prog.) changed variously and plasma renin activity (PRA) remained suppressed. In the patients with EH, systolic pressure decreased in 5 out of 8 (under - 20 mmHg), and diastolic pressure decreased in 3 out of 8 (under - 10 mmHg), DHEA increased in all, but the changes in serum potassium, PAC, F, Prog. and PRA were various. There was no remarkable reaction after the administration of trilostane. It is concluded that trilostane is an effective inhibitor of 3-hydroxysteroid dehydrogenase in vivo and that it is useful in the treatment of primary aldosteronism and other hypertension due to hyperproduction of aldosterone.

Adult↗
PubMed1982

Two cases of low-renin hypertension thought to be due to excessive secretion of unknown mineralocorticoid.

Two patients with low renin hypertension showing an increased urinary excretion with 17-KS, with normal level of plasma deoxycorticosterone and no signs of virilization were reported. Dexamethasone induced reduction in blood pressure and elevation of serum K, in spite of acceleration of the renin-angiotensin-aldosterone system. Thus, it has been inferred that the hypertension was not associated with adrenogenital syndrome but was due to excessive production of an unknown mineralocorticoid.

17-Hydroxycorticosteroids↗
PubMed1981

[The effects of dexamethasone and captopril on plasma aldosterone response to exogenous angiotensin II in normal men (author's transl)].

The response of plasma aldosterone to exogenous angiotensin II was evaluated in five normal volunteers on three occasions, once without endogenous ACTH or angiotensin II suppression (control), once with ACTH suppression (dexamethasone) and once with ACTH and angiotensin II suppression (dexamethasone and captopril). Plasma aldosterone concentration (PAC) fell from a control of 6.8 +/- 1.6 (mean +/- SEM) to 4.4 +/- 0.4 ng/dl with dexamethasone (p less than 0.05) and to 1.8 +/- 0.2 ng/dl with dexamethasone and captopril (p less than 0.001). PAC increased dose-dependently upon infusion rates of angiotensin II (0.2, 0.4, 0.8, 1.0, 1.2, 2.5 and 5.0 ng/kg/min) on each occasion, but aldosterone responsiveness to infused angiotensin II (change and percentage from base line levels) was not altered by the suppression of endogenous ACTH secretion with dexamethasone with each incremental infusion of the octapeptide. However, change in PAC caused by angiotensin II in the suppression of ACTH and angiotensin II was greater than that in the control at an infusion rate of 0.2 ng/kg/min (p less than 0.05), 1.2 ng/kg/min (p less than 0.05) and 2.5 ng/kg/min (p less than 0.01), and it was also greater than that in the suppression of ACTH at an infusion rate of 0.2 ng/kg/min (p less than 0.05) and 2.5 ng/kg/min (p less than 0.01). These results demonstrate that in normal men, base line aldosterone levels are controlled not only by the renin-angiotensin system, but also, in part, by ACTH. The aldosterone response to angiotensin II, however, does not depend upon endogenous ACTH secretion, an action of angiotensin II on the pituitary to release ACTH. Simultaneous administration of dexamethasone and captopril may be a useful tool to assess the sensitivity of aldosterone production in the adrenal glomerulosa with exogenous angiotensin II since endogenous ACTH and angiotensin II can be suppressed by these medications.

Adult↗
PubMed1980

[A simple method for measuring aldosterone secretion rate using 125I-aldosterone (authors' transl)].

A simplified radioimmunoassay system for aldosterone secretion rate was developed by using radioiodine-labelled aldosterone and highly specific antiserum to aldosterone. An antibody was produced in rabbits by injecting aldosterone-oxime coupled with bovine gamma-globulin once a month. Aldosterone-oxime was labelled with 125I by using the chloramine T method described by Hunter and Greenwood. 3 ml of a twenty-four-hour urine specimen was used for the radioimmunoassay. Following CH2Cl2 extraction, pH 1 hydrolysis was carried out for twenty-four hours. Separation of the aldosterone extract was achieved by paper chromatography (hexane:benzene:methanol:water = 1:9:5:2.5). The minimum measurable concentration was under 1pg, and adequate intraassay and interassay precision were obtained. Aldosterone secretion rate was 89.6 +/- 25.8 (mean +/- SD)mug/day in normal subjects and was similar in low- and normal-renin essential hypertension. Significant high values (806.4 +/- 65.8mug/day) were obtained in primary aldosteronism and were slightly high in secondary aldosteronism and high-renin essential hypertension. The aldosterone secretion rate correlated positively with plasma aldosterone level (r = 0.731, p < 0.01). Aldosterone secretion rates were obviously higher than plasma levels in primary and idiopathic aldosteronism. From these results, it is concluded that this method is a very useful and reliable one for measuring aldosterone secretion rate and for discriminating primary aldosteronism from low-renin essential hypertension. it is superior in its simplicity, and there is no need to use a liquid scintillation counter.

Aldosterone↗