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Biomedical subjects

F Witassek

Publications and source records attributed to F Witassek.

26 records · Page 2Linked to original sources
PubMed1977

[Aldosterone and renin in liver cirrhosis with ascites].

Supine plasma aldosterone and plasma renin activity were determined in patients with cirrhosis of the liver and ascites (n = 10). Most of the patients initially showed an increase in plasma aldosterone and plasma renin activity. However, values within the normal range were observed (plasma aldosterone, n = 3; plasma renin activity, n = 4). In the ascitic fluid renin activity could not be detected, whereas aldosterone concentrations correlated significantly with the respective plasma levels (r = 0.8, p less than 0.01). During therapy with spironolactone alone (n =2) or in combination with furosemide (n = 4), diuresis and natriuresis showed no correlation with changes in plasma aldosterone and/or plasma renin activity. Our results suggest that other factors than renin and aldosterone secretion may be important in the formation of ascites in patients with cirrhosis of the liver. In addition, the inverse correlation between mean arterial blood pressure and plasma renin activity (r = -0.65, p less than 0.05) found in our patients supports the assumption that the increase in renin secretion is probably induced by changes in (renal) hemodynamics.

Aldosterone↗
PubMed1977

Effect of a spirolactone on plasma and urinary aldosterone in primary aldosteronism.

In primary aldosteronism due to an adrenal adenoma (n=2), treatment with a spirolactone (160 mg Canrenone/day for 7 days) decreased plasma aldosterone and urinary aldosterone-18-glucuronide. However, in the presence of a normalization in urinary aldosterone 18-glucuronide plasma aldosterone remained elevated above normal. Continued therapy with higher doses (320 mg/day for 7 days and 480 mg/day for 28 days) did not significantly alter plasma aldosterone, while urinary aldosterone-18-glucuronide returned to values comparable to those obtained before therapy. Cessation of the drug resulted in a marked increase in plasma aldosterone and urinary aldosterone-18-glucuronide. The results indicate that in primary aldosteronism due to an adrenal adenoma, the spirolactone (Canrenone) inhibits aldosterone biosynthesis and seems to influence aldosterone degradation.

Adenoma↗
PubMed1976

[Plasma renin activity and plasma aldosterone in essential hypertension: effect of age and diastolic blood pressure].

In patients with essential hypertension a gradual decrease in basal and stimulated renin secretion was found with increasing age. Stimulated plasma aldosterone decreased similarly; however, the observed changes were less pronounced. Young patients (less than 35 years) with high renin hypertension had lower diastolic blood pressure than patients with low renin hypertension in the same age group. Contrary to these findings, a markedly higher diastolic blood pressure was observed in patients over 35 years of age with high renin hypertension than in the group of patients with low renin hypertension. These results indicate that neither high nor low renin essential hypertension patients represent homogeneous groups. Furthermore, the dissociation between changes in renin activity and plasma aldosterone points to a disturbed relationship between the renin angiotensin system and aldosterone secretion in essential hypertension.

Adolescent↗
PubMed1976

[Primary aldosteronism].

The syndrome of primary aldosteronism is caused either by an aldosterone-producing adenoma or by idiopathic bilateral adrenal hyperplasia. Hypokalemic hypertension is the leading symptome of the disease. Diagnosis is by the combination of abnormally high and non-suppressible aldosterone values with undetectable or low renin values unresponsive to postural changes or salt restriction. Patients with aldosterone-producing adenoma normally show a fall in plasma aldosterone in response to posture and ACTH-dependent circadian rhythm of aldosterone, whereas bilateral hyperplasia is characterized by postural increases in plasma aldosterone and an ACTH-independent diurnal aldosterone rhythm. These creteria serve to differentiate between adenoma and hyperplasia. An aldosterone-producing adenoma can be localized by veinography, determination of aldosterone concentration in both adrenal veins and by 131I-cholesterol scintigraphy. In our hands the determination of aldosterone in blood from both adrenal veins is the most efficient procedure. In interpreting the results, however, rhythmic and sudden changes in adrenal hormone secretion should be considered. In cases where no adrenal venous blood is obtained, 131I-cholesterol scintigraphy may be used to localize adenoma. In patients with aldosterone-producing adenomas unilateral adrenalectomy should be performed, whereas patients with idiopathic bilateral hyperplasia should receive antihypertensive therapy. As rare instances of primary aldosteronism, a case of aldosterone-producing carcinoma of the adrenal cortex and a case of presumably unilateral adrenal hyperplasia are reported.

Adenoma↗
PubMed1975

[Primary aldosteronism: diagnosis, laterality and regulation of hormone secretion].

In 16 patients with hypokalemic hypertension the combination of abnormally high and unsuppressible plasma aldosterone with low or undetectable renin activity led to the diagnosis of primary aldosteronism. To differentiate between aldosterone producing adenoma and idiopathic bilateral hyperplasia, determination of aldosterone concentration in both adrenal veins was performed in 12 patients. In 4 of these patients the two forms of primary aldosteronism could not be differentiated as in these cases only one of the two adrenal veins simultaneously showing an abnormally high aldosterone concentration could be canulated. Plasma aldosterone and plasma cortisol were determined overnight (20.00-8.00 h) at short time intervals in 8 patients with adenoma, 1 patient with carcinoma of the adrenal cortex and 3 patients with bilateral hyperplasis. In all patients with adenoma a significant correlation between aldosterone and cortisol was observed (p less than 0.05-0.001) whereas no correlation was seen in the patients with hyperplasia and carcinoma. The clinical importance of these findings is that in the presence of ACTH-dependent secretion of aldosterone the site of the adenoma can be predicted even when blood from only one adrenal vein is obtained.

Adenoma↗
PubMedDate not supplied

Abnormal glucuronidation of zomepirac in patients with cirrhosis of the liver.

The disposition of zomepirac was investigated in 18 patients with various liver diseases and in 10 healthy normal subjects in order to further test the hypothesis that glucuronidation of drugs may be spared in liver disease. Severity of the liver disease was assessed by the galactose elimination capacity. Following oral administration of zomepirac (200 mg), plasma and urinary drug concentrations were measured by high-pressure liquid chromatography. Urine was assayed before and after alkaline hydrolysis. The apparent oral clearance of zomepirac was 3.7 +/- S.D. 1.2, 3.0 +/- 0.8, and 1.8 +/- 0.6 ml . min-1 . kg-1 in normal subjects, patients with mild liver disease, and cases with cirrhosis, respectively. In patients with liver disease, the reduction in zomepirac clearance was significantly correlated with the abnormalities in galactose elimination capacity (r = 0.83, n = 18), suggesting that the functioning liver cell mass was the major determinant of the rate of zomepirac disposition. These results are not consistent with the original hypothesis but suggest that--in contrast to ether-glucuronidation--ester-glucuronidation may be abnormal in liver disease. Dosage adjustments may, therefore, be necessary in patients with cirrhosis of the liver.

Adult↗