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Biomedical subjects

M Ojima

Publications and source records attributed to M Ojima.

At least 91 records · Page 5Linked to original sources
PubMed1984

[A case of adrenocortical carcinoma with Cushing's syndrome presenting unusual urinary 17-ketosteroid fractionation].

A patient with adrenocortical carcinoma with Cushing's syndrome is presented. This case seems to be most characterized by its very unusual urinary 17-ketosteroid (KS) fractionation, since markedly increased etiocholanolone was not accompanied by increments of either DHEA or androsterone. Determination of the plasma adrenocorticosteroids of the patient revealed normal DHEA and DHEA-S levels, moderately increased 17-OH-pregnenolone, and markedly increased 11-deoxycortisol. Therefore, it seems plausible that the unique 17-KS fractionation of this patient would have ensued as a result of remarkably decreased C17-20 lyase activity sufficient to nullify the increased 17-OH-pregnenolone and that markedly increased etiocholanolone might have been converted from 11-deoxycortisol.

17-Hydroxycorticosteroids↗
PubMed1983

Human chorionic gonadotropin and alpha-fetoprotein in testicular germ cell tumors. An immunohistochemical study in comparison with tissue concentrations.

The relation between immunohistochemical demonstration and tissue concentration of humanchorionic gonadotropin (hCG) and alpha-fetoprotein (AFP) was examined in 17 testicular germ cell tumors. There was a good correlation between their results; e.g., a tumor with high hCG concentration contained numerous hCG positive cells, and vice versa. The immunoperoxidase localization of hCG and AFP was investigated in 57 tumors including above 17. HCG was revealed in syncytiotrophoblastic giant cells of seminoma or embryonal carcinoma as well as syncytial cells of choriocarcinoma, and on rare occasion in mononuclear cells. AFP was localized in tumor cells of yolk sac tumor or embryonal carcinoma and occasionally hyaline globules. No cell was stained concomitantly with hCG and AFP. Pathogenetical significance of cells positively stained was discussed.

Adolescent↗
PubMed1983

An immunohistochemical study of hepatoblastoma producing human chorionic gonadotropin.

High tissue concentrations of human chorionic gonadotropin (hCG) and alpha-fetoprotein (AFP) were revealed by radioimmunoassay in a hepatic tumor which was surgically removed from a two-year, eight-month-old boy manifesting sexual precocity. Histologically the tumor showed an embryonal type hepatoblastoma admixed with multinucleated tumor giant cells. The localization of native hCG and hCG-beta subunit was immunohistochemically demonstrated in some of the above giant cells, while that of alpha-fetoprotein was diffusely in the tumor cells of hepatoblastoma of embryonal type. Ultrastructural features of the giant cells were also presented.

Carcinoma, Hepatocellular↗
PubMed1983

[Diagnosis and treatment of adrenocortical tumors].

Adrenocortical tumors can be divided into two groups based on their histopathological characteristics, i.e., benign (adenoma) and malignant (carcinoma), and also classified as functioning (or hormonal) and non-functioning (or non-hormonal) tumors, depending on the presence or absence of recognizable clinical syndromes due to excessive steroids. The syndrome of functioning adrenocortical tumors includes Cushing's syndrome, primary aldosteronism and the adrenorge genital syndrome, of which a minority presents most of the specific clinical features: Cushing's syndrome; red face, typical moon face, truncal obesity, and purplisch red striae, primary aldosteronism; muscle weakness, noctural polyuria, hypertension and hypokalemia, adrenogenital syndrome; virilization or feminization, but many of them present complete clinical picture. The diagnosis of these syndromes needs to measure urinary 17-OHCS and 17-KS and plasma concentrations of cortisol, aldosterone, dehydroepiandrosterone (DHEA) and the other steroids. Dexamenthasone suppression test, various stimulation tests and the measurement of plasma ACTH are also useful for diagnosis. Usually, adrenocortical tumors can be detected preoperatively by physical examination or radiographic studies. Some are massive enough to be palpable through the abdominal wall. Some are large enough to cause displacement of the kidney, as seen intravenous urography. Most are visible by adrenal scintigraphy using 131I-iodocholesterol, computerized tomography, or adrenal arteriography. The standard treatment for adrenocortical tumors are surgical resection. Unresectable adrenocortical carcinomas may be treated with an adrenocorticolytic drug, o'p'-DDD. Metyrapone and aminoglutethimide can be also employed to inhibit the production of steroids.

17-Hydroxycorticosteroids↗
PubMed1980

Plasma concentrations of 18-hydroxy-11-deoxycorticosterone and 18-hydroxycorticosterone simultaneously measured in normal subjects and adrenocortical disorders.

A method for the simultaneous measurement of 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) and 18-hydroxycorticosterone (18-OH-B) in human peripheral plasma has been developed. The present method consists of extracting plasma with dichloromethane, separating the 18-OH-DOC and 18-OH-B from other steroids on a Sephadex LH-20 column and quantitating each steroid by radioimmunoassay. The mean plasma level of 18-OH-DOC at 8:00 a.m. was 8.2 +/- 3.9 ng/100 ml (mean +/- S.D.) in normal males. It was 7.8 +/- 2.6 ng/100 ml in the follicular phase of normal females and 11.5 +/- 2.8 ng/100 ml in the luteal phase. The corresponding level of 18-OH-B in normal males was 10.3 +/- 4.2 ng/100 ml and in the follicular and luteal phases of normal females was 12.4 +/- 4.5 ng/100 ml and 13.8 +/- 4.1 ng/100 ml, respectively. No sex differences nor difference between the phases of the menstrual cycle was confirmed. Plasma levels of the two steroids were not rarely high in patients with Cushing syndrome due to adrenocortical hyperplasia and carcinoma, primary aldosteronism, idiopathic hyperaldosteronism and congenital 17 alpha-hydroxylase deficiency, while they were usually within the normal range in cases of Cushing syndrome due to adrenocortical adenoma. These steroid levels were significantly low in patients with Addison's disease.

18-Hydroxycorticosterone↗
PubMed1979

[In vivo and in vitro studies on 18-hydroxy-11-deoxycorticosterone and 18-hydroxycorticosterone in normal subjects and in those with various adrenocortical disorders (author's transl)].

Simultaneous measurement of 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) and 18-hydroxycorticosterone (18-OH-B) in the peripheral plasma was carried out on normal subjects and in patients with adrenocortical disorders. The mean plasma levels of 18-OH-DOC at 0800h in normal males and in the follicular and luteal phases of normal females were 8.2 +/- 3.9 ng/100 ml (Mean +/- SD), 7.8 +/- 2.6 ng/100ml and 11.5 +/- 2.8 ng/100ml, respectively. The corresponding levels of 18-OH-B in normal males and in the follicular and luteal phases of normal females were 10.3 +/- 4.2 ng/100ml, 12.4 +/- 4.5 ng/100ml and 13.8 +/- 4.1 ng/100ml, respectively. No differences between the sexes nor the phases of the menstrual cycle were confirmed. ACTH stimulation increased plasma concentrations of 18-OH-DOC and 18-OH-B by 5.1 and 4.4 times respectively, while dexamethasone markedly decreased these 2 steroids. An upright posture increased these steroids significantly. In patients with Cushing syndrome, plasma levels of these 2 steroids were rarely high in cases with adrenocortical hyperplasia and adrenocortical carcinoma, while they were usually within the normal range in adrenocortical adenoma. These 2 steroid levels were increased in primary aldosteronism, idiopathic hyperaldosteronism and congenital 17 alpha-hydroxylase deficiency. They were decreased in Addison's disease and the salt-loosing type of congenital 21 alpha-hydroxylase deficiency. Patients with congenital 21 alpha-hydroxylase deficiency (simple form) showed elevated levels of 18-OH-DOC and normal levels of 18-OH-B. In vitro production of 18-OH-DOC and 18-OH-B was studied by tissue slices of the normal adrenal cortex, adrenocortical carcinoma causing Cushing syndrome, aldosteronoma and nodular hyperplasia with hyperaldosteronism. In the normal adrenal cortex, the mean production rates of 18-OH-DOC and 18-OH-B were 31 and 26 ng/g tissue/hr, respectively. ACTH and angiotensin II significantly increased the production of both 18-OH-DOC and 18-OH-B. In adrenocortical carcinoma, the production of these steroids was markedly diminished and not stimulated with either ACTH or angiotensin II. Aldosteronoma tissue produced these 2 steroids 20 to 40 times that of the normal adrenal tissue and was significantly increased with the addition of ACTH and angiotensin II. Nodular hyperplasia with hyperaldosteronism produced much 18-OH-DOC and 18-OH-B, but did not respond to ACTH and angiotensin II.

18-Hydroxycorticosterone↗