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Biomedical subjects

J Hirai

Publications and source records attributed to J Hirai.

At least 55 records · Page 3Linked to original sources
PubMed1986

[Clinical study of non-Hodgkin's lymphoma--results of the Kanazawa University-Kurume University Cooperative Study on Malignant Lymphomas].

Ninety-two patients with previously untreated non-Hodgkin's lymphoma (NHL) were studied multidisciplinarily. The high incidence of NHL in elderly men (older than 60 years) was confirmed. With regard to the initial site, 51 patients (55.5%) were affected in the nodal region while other patients were affected in the extranodal or Waldeyer's ring region. Eighty-two patients (89.1%) were diagnosed as having diffuse lymphoma, and 47 of these patients were further classified into large cell type (LSG classification). Surface marker analysis revealed that the incidence of B cell-type NHL was twice as high as that of T cell-type NHL. All patients were entered into a randomized trial of radiotherapy and/or combination chemotherapies (ACOP, ACOP-E and AclBEP regimens) according to clinical stage. More than 90% of the patients with early-stage NHL achieved complete remission (CR), and the CR rate for patients with advanced-stage disease was about 50%. All patients with CS I NHL are still alive at 27 months after diagnosis, and the survival rate of patients with CS II NHL at 35 months after diagnosis is 80%. However, the median survival time of patients with advanced-stage disease was estimated to be 16 months.

Adult↗
PubMed1985

The constant plasma 18-hydroxycorticosterone to aldosterone ratio: an expression of the efficacy of corticosterone methyloxidase type II activity in disorders with variable aldosterone production.

Aldosterone and 18-hydroxycorticosterone (18-OHB) are produced by the adrenocortical zona glomerulosa. Under normal conditions, plasma 18-OHB levels parallel and are influenced by the same trophic factors that regulate aldosterone production. To evaluate corticosterone-methyl-oxidase II activity, the final step of aldosterone biosynthesis, in conditions associated with chronic derangements of the pituitary-adrenal and/or renal-adrenal axis, we measured the plasma 18-OHB to aldosterone ratio, cortisol, PRA or plasma renin concentration, and potassium (K) in 104 such patients and 15 normal subjects. The 18-OHB to aldosterone ratios in the pituitary-adrenal group were not significantly different from normal regardless of elevated or reduced ACTH and/or cortisol levels [patients with Cushing's syndrome, 3.55 +/- 0.68 (+/-SE); ACTH deficiency, 2.03 +/- 0.34; 21-hydroxylase deficiency, 3.09 +/- 0.23; normal subjects, 2.50 +/- 0.15]. The renal-adrenal group also had normal ratios regardless of plasma renin concentration and K levels [patients with aldosterone-producing adenomas, 2.85 +/- 0.15; idiopathic hyperaldosteronism, 2.14 +/- 0.19; salt-losing nephropathy, 3.06 +/- 0.54; Bartter's syndrome, 2.89 +/- 0.20; isolated (hyporeninemic) hypoaldosteronism, 3.20 +/- 0.39]. Only in patients with 17 alpha-hydroxylase deficiency (230.1 +/- 118.6) was the ratio abnormally high. Chronic perturbations of aldosterone production by ACTH, the renin-angiotensin system, and/or K did not alter this last step of aldosterone biosynthesis (corticosterone-methyloxidase II), as defined by their plasma concentrations. Any influence of these trophic factors must be proximal to the site of 18-OHB production.

18-Hydroxycorticosterone↗
PubMed1982

The mineralocorticoid hormone pathways in hypertension with hyperaldosteronism.

Simultaneous measurement of the 0800-hr plasma concentrations of deoxycorticosterone (DOC), corticosterone (B), 18-hydroxycorticosterone (18-OHB), aldosterone, 18-hydroxydeoxycorticosterone (18-OHDOC) and cortisol (F) in four types of primary aldosteronism provides evidence for primary adrenal disease. Elevated DOC with normal F concentrations in the presence of elevated 18-OHB and aldosterone, and suppressed renin concentration suggests a primary adrenal abnormality of the zona glomerulosa (ZG). Steroid production by the zona fasciculata (ZF), F, 18-OHDOC, and most often B, is normal. These patterns exist only for primary adrenal hyperplasia, aldosterone-producing adenoma (APA), and aldosterone-producing adrenocortical carcinoma (AP-Ca). Elevated DOC levels are rarely found in patients with idiopathic hyperaldosteronism (IHA or adrenal hyperplasia) and suggest that IHA is not a primary adrenal disorder and should be excluded from the syndrome of primary aldosteronism as they have been heretofore.

18-Hydroxydesoxycorticosterone↗
PubMed1982

Regulation of the mineralocorticoid hormones in adrenocortical disorders with adrenocorticotropin excess.

Chronic stimulation by adrenocorticotropin (ACTH) of the adrenal cortex produces different plasma mineralocorticoid hormone (MCH) patterns, depending on the amount of glucocorticoid hormones (cortisol) concurrently generated and the degree of activation of the renin angiotensin system (RAS). Patients with Cushing's disease or the ectopic ACTH-excess syndrome have normal or low production of the MCHs, aldosterone and 18-hydroxycorticosterone (18-OHB), by the zona glomerulosa (ZG), elevated cortisol and deoxycorticosterone (DOC) levels, and high-normal to elevated production of the MCHs corticosterone (B) and 18-hydroxydeoxycorticosterone (18-OHDOC) by the zona fasciculata (ZF). Prolonged administration of superphysiologic doses of ACTH to normal subjects yields similar patterns. Patients with simple virilizing 21-hydroxylase deficiency (21-OHD) have impaired ZF production of B and 18-OHDOC and elevated DOC, 18-OHB, and aldosterone secretion secondary to the superimposed RAS stimulation of the ZG. Patients with 17 alpha-hydroxylase deficiency (17 alpha-OHD) have elevated levels of the ZF MCHs DOC, B, 18-OHDOC, and 18-OHB and a functionally suppressed ZG. Patients with 11 beta-hydroxylase deficiency (11 beta-OHD) have only elevated production of DOC by the ZF and suppressed RAS and aldosterone. A significant negative correlation between cortisol and aldosterone concentrations suggests that cortisol is involved in the ACTH-mediated inhibition of aldosterone formation.

18-Hydroxydesoxycorticosterone↗
PubMed1980

Clinical evaluation of biventriculo-cineangiographic findings in hypertensive left ventricular hypertrophy.

In the present study, we demonstrated that hypertensive left ventricular hypertrophy can be divided angiographically into symmetrical (SH) and asymmetrical septal hypertrophy (ASH) groups. In the SH group, the dynamics of the septal wall and the free wall were almost the same as those of the control group. On the other hand, the ASH group rather resembled the HCM group in the thickness and dynamics of the septal wall and the free wall as well as in the septal configuration. The most characteristic difference of the ASH and HCM groups from the SH group was in the significantly greater thickness of the septal wall at end diastole. However, in view of the developmental mechanism of hypertensive heart, it is interesting to note that the more the septal-free wall ratio increases, the more the thickness of the septal wall increases in the SH group.

Adult↗
PubMed1980

Clinical manifestation of adrenocorticotropin-determined plasma concentrations of mineralocorticoid hormones.

Chronic oversecretion of adrenocorticotropin (ACTH) in Cushing's disease and partial adrenal insufficiency results in a plasma pattern of mineralocorticoid hormones (MCHs) in which deoxycorticosterone, 18-hydroxycorticosterone and aldosterone remain within normal limits. In patients with deficiencies of 17 alpha- and 21-hydroxylation, the entire MCH pathway may be initially stimulated by ACTH alone in the presence of reduced cortisol production. An ACTH-induced intra-adrenal factor reflected by levels of cortisol production, or cortisol itself, may determine MCH levels by its inhibition (high) or lack of inhibition (low) of 11 beta- and 18-hydroxylation.

Adenoma↗
PubMed1979

Adrenocorticotropin inhibition of mineralocorticoid hormone production.

1. Adrenocorticotropin (ACTH)-induced steroidogenesis, obtained by continuous administration of ACTH for 3 days, produces in man (a) sustained elevations of plasma deoxycorticosterone and cortisol concentrations, (b) transient elevations of plasma aldosterone and 18-hydroxycorticosterone concentrations that return to near-control values, and (c) brisk initial increases in plasma 18-hydroxydeoxycorticosterone and corticosterone concentrations that fall to 20-68% of peak values 30 h thereafter. 2. Dexamethasone (8 mg/day, orally) treatment for 2 days in man permits a greater postural increase in plasma aldosterone and 18-hydroxycortisone concentrations. A dampening effect of ACTH is suggested. 3. An ACTH-initiated inhibition of 11 beta- and 18-hydroxylation is proposed to be operative in regulation of mineralocorticoid hormones.

18-Hydroxycorticosterone↗