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[What role does secondary hyperaldosteronism play in decompensated liver cirrhosis?].

In 29 untreated resting patients with cirrhosis of the liver and ascites plasma aldosterone levels were determined. The determinations were performed with a radioimmunoassay using highly specific antibodies without chromatography. Seven aldosterone values were decreased, 18 were normal and only four were increased. The median of the values was 107 pg/ml and differed not from that of healthy persons. In 20 other patients, in which application of diuretics had already been started, 14 plasma aldosterone levels were increased. The median was 332 pg/ml und thus far above the normal range. Secondary aldosteronism in connection with decompensated cirrhosis of the liver arises mainly under therapy with diuretics.

Aldosterone↗

Hyperaldosteronism associated with liver metastases.

Plasma aldosterone levels were measured in 50 patients with confirmed liver metastases from various histologically proved primary tumors. None of these patients had electrolyte abnormalities or history of benign liver disease, congestive heart failure, hypertension, or renal disease. Patients with edema, ascites, or both had significantly greater elevation of plasma aldosterone levels compared to nonedematous patients; these patients also demonstrated a substantial degree of hepatic dysfunction as evidenced by lower serum albumin levels and higher bilirubin and alkaline phosphatase levels. This study provides a rational basis for the use of the specific aldosterone inhibitor spironolactone in the treatment of patients with advanced metastatic liver disease and edematous states.

Aldosterone↗

[Conceptual basis and diagnosis of primary hyperaldosteronism].

Primary aldosteronism comprises two different conditions, the tumoral form usually caused by an adenoma and the idiopathic form due to nodular hyperplasia of the two adenals. More rarely, an adenoma of the adrenal cortex, glucocorticosteroid-sensitive hyperplasia, and angiotensin-sensitive adenoma or an autonomous nodule transformed to primary tumoral hyperplasia, may be observed. Primary alderosteronism may be conceived as a spectrum of genetic abnormalities which express themselves either by hyperplasia or by a tumour. A defect in steroid genesis and prolonged stimulation of the cortex would lead to the formation of nodules which may become autonomous and generate a tumour. Hypertension may be isolated. Detection requires three sampling of serum potassium in all hypertensive patients, a study of the aldosterone-renin axis when the value is less than 3.6 mEq, or whenever the hypertension is severe or resistant to treatment. The diagnosis is made by the association of an increased plasma aldosterone level before getting up in the morning and a plasma renin unaffected by orthostatism. The choice of medical or surgical treatment depends on the uni- or bilateral anatomic substrate. Computerised tomography, very sensitive but not specific, like hormonal studies, often provides incomplete answers. Adrenalectomy is indicated in the presence of a mass of centimetric proportions with concordant results of the dynamic test. In other situations, investigations are continued with the search for an aldosterone gradient by selective venous sampling. This is very valuable to determine the lateralisation but fails in 25% of cases, and its results have to be compared with those of imaging techniques: CT scan, venography and, when necessary, scintigraphy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗

[Primary hyperaldosteronism caused by monolateral adrenal hyperplasia].

We have reported two patients with unilateral adrenal hyperplasia as a rare cause of primary aldosteronism, and discussed the literature on this subject. When diagnosed by NMR-CT imaging and selective sampling from adrenal veins, the treatment of this disorder appears to be surgical. Whether its pathogenesis is related to the more common varieties of primary aldosteronism is open to speculation according to metabolic findings.

Adrenal Glands↗