Biomedical subjects

C E Kater

Publications and source records attributed to C E Kater.

51 records · Page 3Linked to original sources

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↗

PubMed1981

The zonal origins of the mineralocorticoid hormones in the 21-hydroxylation deficiency of congenital adrenal hyperplasia.

The 0800 h plasma concentrations of the mineralocorticoid hormones, 18-hydroxydeoxycorticosterone (18-OHDOC), deoxycorticosterone (DOC), corticosterone, 18-hydroxycorticosterone (18-OHB), and aldosterone, in six patients with nonsalt-losing congenital adrenal hyperplasia revealed two groupings of these steroids: in one group, DOC, 18-OHB, and aldosterone were significantly elevated (P less than 0.001) at 51.7 +/- 18.0, 70.8 +/- 14.2, and 22.7 +/- 3.0 ng/dl, respectively; in the other group, corticosterone and 18-OHDOC were normal at 363.6 +/- 76.0 and 7.8 +/- 1.1 ng/dl, respectively. No significant increases in response to upright posture were observed in DOC, 18-OHB, or aldosterone. After a 1-h Cortrosyn stimulation test, the already elevated levels of DOC, 18-OHB, and aldosterone showed slight additional increases, but the normal levels of corticosterone and 18-OHDOC changed little within the normal unstimulated range. In these patients certain mineralocorticoid hormone patterns permit the identification of the zonal origins of steroids. The normal and fixed levels of 18-OHDOC and corticosterone, zona fasciculata steroids, are similar to those of cortisol and imply deficiency of formation and of their precursor, zona fasciculata DOC, a 21-hydroxylated steroid. Both the mineralocorticoid and glucocorticoid pathways distal to 21-hydroxylation are impaired in the zona fasciculata. However, the elevated and partially responsive levels of DOC, 18-OHB, and aldosterone imply that there is greater activation of 21-hydroxylation in the zona glomerulosa than in the zona fasciculata, with its normal fixed steroid levels, and that the elevated level of DOC is primarily from this zone.

18-Hydroxycorticosterone↗

PubMed1979

[Effect of saralasin infusion on glomerular filtration rate and sodium excretion in hypertensive patients (author's transl)].

Saralasin (S) infusion, at a dose of 10 micrograms/kg/min IV, decreased Glomerular Filtration Rate (GFR) in 18 hypertensive patients. This effect was more pronounced in those patients with angiotensinogenic hypertension due to the somation of the effects of S upon renal vasculature and systemic arterial pressure. A decrease in urinary sodium excretion was also observed being more intense in those patients whose systemic pressure also decreased during S infusion. In group II (10 hypertensive patients) infusion of S in increasing doses (0.1, 0.5, 1.0, 5.0 and 10.0 micrograms/kg/min) a progressive decrease in GFR was observed only when the arterial pressure also decreased. However urinary sodium excretion decreased progressively as S doses increased. This effect was not related to S effect upon arterial pressure. This observation indicates that S, like angiotensin II, has a direct effect upon the renal tubules evoking an increase of sodium reabsorption.

Angiotensin II↗

PubMedDate not supplied

Hypertension and economic activities in São Paulo, Brazil.

A study of the prevalence of hypertension was undertaken among workers in 10 subsectors of the economy in São Paulo, a major urban-industrial area of Brazil. Included in the study were 5500 subjects 15-65 years of age, employed in 57 randomly selected firms. Hypertension rates (DBP greater than or equal to 90 mm Hg) were higher among males up to 44 years of age. There was a decreasing gradient from mild to moderate and severe forms in all groups. Severity tended to increase with age in all groups. Black males showed higher rates than whites (29.2% vs 16.7%, p less than 0.05), the excess being partially accounted for by moderate and severe forms (40% vs 20%). Subjects who overworked showed a trend toward higher hypertension rates. Higher rates in four subsectors (metallurgy, finance, transport, and journalism), aside from the distribution of known risk factors and job selection, may reflect a variety of work-related stressors.

Adolescent↗

PubMedDate not supplied

Studies of impaired aldosterone response to spironolactone-induced renin and potassium elevations in adenomatous but not hyperplastic primary aldosteronism.

Spironolactone (SPL) corrects hypertension, hypokalemia, and hyporeninemia in patients with primary hyperaldosteronism (PHA) by blocking mineralocorticoid (MCH) receptors. We evaluated the effect of continuous SPL treatment (100 to 300 mg/day for 7 days to 9 years) on plasma renin (PRC), potassium, aldosterone (PA), 18-hydroxycorticosterone (18-OHB), deoxycorticosterone (DOC), and corticosterone (B) concentrations and 24-hour urinary excretion of aldosterone (UA) in 24 patients with PHA (15 with an aldosterone-producing adenoma [APA] and nine with idiopathic PHA [IHA]). Despite the normalization of PRC and K in both APA and IHA patients by SPL, UA and PA failed to increase in APA (55.8 +/- 8.8 to 51.4 +/- 7.3 micrograms/24 hr and 54.0 +/- 9.4 to 44.6 +/- 6.2 ng/dl, respectively) in contrast to rises in IHA patients (22.3 +/- 2.5 to 69.3 +/- 10.3 micrograms/24 hr and 16.0 +/- 1.0 to 49.9 +/- 9.9 ng/dl). Similar corrections with amiloride (20-40 mg/day for 2 months) in one patient with APA produced a three- to fourfold increase in UA and PA. In addition, while on SPL the characteristic fall or no change in PA and 18-OHB during upright posture persisted in all APA patients despite further increases in PRC (4.48 +/- 1.15 to 7.86 +/- 1.89) and K (4.0 +/- 0.1 to 4.3 +/- 0.1). The patterns of the aldosterone precursors, DOC, B, and 18-OHB, and their ratios to acute stimulation with cosyntropin were not altered by SPL. Thus, SPL treatment causes a sustained impairment of the aldosterone secretory response to normalized PRC and K, but not to ACTH stimulation, only in patients with APA.

Adenoma↗

PubMedDate not supplied

[Importance of percutaneous venous catheterization in the identification of the origin of hyperandrogenism].

Selective percutaneous venous catheterization (SPVC) was performed to ascertain the source of androgen excess (AE) in 3 virilized women (12, 50 and 58y) in whom hormonal and radiologic investigation (ultrasonography and computerized tomography) was inconclusive. In all cases, elevated testosterone levels remained unsuppressed with dexamethasone, but were adequately suppressed by normal basal DHEA-S and cortisol. SPVC for T and F determinations (and the T/F ratio) were performed before surgery in all cases and during surgery in case 3. A T/F ratio of 152.4 and 71.8 (with an ovary-peripheral vein gradient [OPG] of 637 and 1173 ng/dl) identified the right and left ovary as the source of androgen excess respectively in cases 1 and 2, whereas the T/F ratio (87.4 and 97.2) and OPG (749 and 1162 ng/dl) were increased in both ovaries in patient 3. Thus, lateralization was evident in cases 1 (R ovary Leydig cell tumor) and 2 (L ovary hemangioma and stromal luteinization) whereas bilateral production in case 3 was confirmed by biopsy (PCO). Pre-operative identification of the origin of AE by SPVC is essential in defining proper treatment for patients suspected of harboring a neoplasia. Because it is not widely available nor devoid of complications, SPVC should only be indicated in hirsute/virilized women whose basal plasma testosterone and DHEA-S levels are in the tumoral range, i.e. higher than 150 ng/dl and 700 micrograms/dl, respectively.

Androgens↗

PubMedDate not supplied

[Standardization and clinical applications of the rapid and prolonged ACTH stimulation tests in patients with primary and secondary adrenal insufficiency].

Some methodological aspects of the rapid ACTH stimulation test (RST) and the prolonged ACTH stimulation test (PST) remain heterogeneous, e.g. administration routes, time of the day, duration, interpretation criteria and clinical indications. To standardize both tests we studied the serum cortisol responses to ACTH in 16 normal subjects, 16 patients with Addison's disease (AD), 14 with hypopituitarism (HP) of different etiologies and 13 patients on chronic glucocorticoid (CG) treatment (doses equivalent to 5-20 mg/d of prednisone for at least 6 months). For the RST, 250mcg of Cortrosina Organon were injected as an IV bolus and blood collected before and 60 minutes later, whereas for the PST, 250mcg of Cortrosina-Depot Organon were injected IM, every 8 hours for 3 days, and blood drawn daily between 8 and 9 o'clock AM. The post-ACTH cortisol value was the single parameter chosen to interpret both tests (the absolute or percent increase was of no further value). The 95% lower confidence limits (mean minus 1.64 SD) for the RST and the 3rd day of PST were 19.1 and 49.0mcg/dL, respectively. AD patients did not increase cortisol in response to both the RST (1.1 +/- 1.2 to 1.2 +/- 1.1mcg/dL) or the PST (1.2 +/- 1.3 to 2.0 +/- 1.7mcg/dL). However, whereas 22 out of 27 patients with HP and CG showed a modest cortisol increase to the RST (1.6 +/- 2.3 to 5.6 +/- 4.7 mcg/dL), all had a gradual and nearly normal response on the 3rd day of the PST (1.6 +/- 2.1 to 29.6 +/- 16.6mcg/dL).(ABSTRACT TRUNCATED AT 250 WORDS)

Addison Disease↗

PubMedDate not supplied

[Congenital adrenal hyperplasia and pregnancy].

About 90% of CAH cases are due to 21-hydroxylase (21-OH) deficiency. There are decreased cortisol and increased ACTH secretions; and elevated cortisol precursors and androgens. CAH is an important factor of menstrual disorders and infertility. Pregnancy is very much uncommon in the classic form, and 90% of reported cases belong to the postnatal form. The authors present two patients with classic form of CAH (21-OH deficiency) who became pregnant. They had been treated in early childhood (2-4 years old) with glucocorticoids and had surgical correction of the ambiguous external genitalia. During pregnancy, daily prednisone dose was raised to 5 mg twice, serum levels of 17-hydroxyprogesterone (17-OHP) and androgens were monthly measured. The 17-OHP levels remained high (about 1.6 ng/dl), and androgens (testosterone, androstenedione, SDHEA) levels remained normal. Cesarean section was performed in both cases; newborns were normal and 17-OHP was within normal limits. Adequate early replacement therapy has improved fertility and pregnancy.

17-alpha-Hydroxyprogesterone↗

PubMedDate not supplied