INDIRECT EVIDENCE TO SUGGEST THAT PROLACTIN INDUCES SALT RETENTION INCIRRHOSIS

Prolactin is known to have renal sodium retention properties in animal s. In man, only two studies have suggested a similar effect in healthy volunteers or in patients with microprolactinoma. Since hyperprolacti nemia is frequently observed in liver disease, this prospective study of 19 patients evaluated the influence of prolactin on urinary electro lytes excretion in cirrhosis. Basal hyperprolactinemia was found in 14 out of 19 cases. The effect of serum prolactin elevation on renal sod ium and potassium excretion was studied in all patients after thyrotro pin-releasing hormone stimulation (200 mu g), with seven consecutive h ourly urinary samples. Patients were separated into two groups accordi ng to amount of prolactin discharge after thyrotropin-releasing hormon e injection. Group I included patients with ''low prolactin release'', defined as the difference between basal and peak prolactin values (De lta prolactin)<1000 mu u/ml (n=8), and no change in natriuresis could be observed. In contrast, in group II with a ''high PRL release'' (Del ta prolactin>1000 mu u/ml, n=11), significant reductions in urinary so dium (p<0.01) and potassium (p<0.02) excretion were observed, which la sted until the third hour after thyrotropin-releasing hormone injectio n. A significant correlation was found between peak prolactin values a nd the decrements of natriuresis (r=0.70, p<0.02). The pattern of urin ary electrolyte changes and the stability of the ratio U-K/U-K+Na sugg est a possible sodium-retaining effect of prolactin localized proximal ly to the distal tubule. (C) Journal of Hepatology.