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  • Title: [Electrolyte balance in arterial hypertension (continuation)].
    Author: Siegenthaler W, Lüscher T.
    Journal: Z Gesamte Inn Med; 1980 Oct 01; 35(19):suppl 97. PubMed ID: 7210751.
    Abstract:
    In patients with arterial hypertension as most frequent disturbance of the electrolyte balance a hypopotassaemia is observed. Examinations of our working team on 517 patients with hypertension exhibited a prevalence of the hypopotassaemia of 3%, in which case in the greater part of these patients (1.6%) a decrease of the serum potassium levels induced by diuretics was present. In the other patients in 1.2% of the cases a secondary and only in 0.2% of the patients a primary aldosteronism was diagnosed as underlying cause. The leading clinical symptom of the primary aldosteronism is a hypopotassaemic hypertension. The diagnosis of the disease is ascertained by the proof of a pathologically increased plasma aldosterone concentration and of a decreased and non-measurable renin activity, respectively. Since these peripheral hormone values do not allow a differential diagnosis between an adenoma producing aldosterone and an idiopathic hyperplasis of the adrenal cortex, further investigations for the differentiation of these two main forms of the primary aldosteronism must be performed. These investigations are: Phlebography of the suprarenal bodies, determination of the aldosterone concentration in the blood of the adrenal veins and iodine-131-cholesterol scintigraphy. Patients with an adenoma producing aldosterone are unilaterally adrenalectomized, while an operative intervention has no essential influence of the behaviour of the blood pressure in cases with idiopathic hyperplasia of the adrenal cortex. Therefore, these cases must be treated antihypertensively. A pseudo-primary aldosteronism, also shows a hypopotassaemic hypertension as leading symptom. In contrast to the genuine primary aldosteronism this disease, differs by the proof of low plasma aldosterone levels. A pseudo-primary aldosteronism is caused by the exogenic supply of mineralocorticoid-effective substances. A hypopotassaemia in patients with Cushing's syndrome should, above all when it is very expressed, attract the suspicion to a cortisol-producing carcinoma of the adrenal cortex. The hypopotassaemia in these patients is caused by additional abnormally high tumour production of mineralocorticoid-effective steroids.
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