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Gynaecomastia is uni- or bilateral breast enlargement in males associated with benign hyperplasia of the glandular, fibrous and adipose tissue resulting from oestrogen-androgen imbalance. Asymptomatic gynaecomastia is a common finding in healthy male adults and does not have to be treated, while symptomatic gynaecomastia might be the symptoma of many pathological conditions and requires meticulous diagnosis and therapeutic management. The commonest causes of gynaecomastia in the Polish population include liver cirrhosis and drugs used to treat its complications. The current study presents the case of severe painless gynaecomastia in a patient with decompensated alcoholic liver cirrhosis, treated with spironolactone because of ascites. Breast enlargement assessed a IIb according to the Simon’s Scale or III according to the Cordova-Moschella classification, developed slowly over the two-year period of low-dose spironolactone therapy The course and dynamics of disease are described and the main mechanisms leading to its development discussed. The importance of effective treatment of patients with severe gynecomastia is emphasized as the disease may result in significant psychosocial problems.
Hypoxia is regarded as an important physiological factor that controls nephrogenesis. We investigated whether the renin-angiotensin-aldosterone system (RAAS) affects hypoxia-related target genes in developing kidneys. Newborn rat pups were treated with enalapril (30 mg/kg/d) or spironolactone (200 mg/kg/d) for 7 days. Tissue hypoxia was assessed by the uptake of a hypoxyprobe-1, pimonidazole (200 mg/kg), and the expression of hypoxia-responsive genes. In the enalapril group, hypoxia-inducible factor (HIF)-1, HIF-2, and Ets-1 protein expression were not changed, compared to the control group. In the spironolactone group, HIF-1 and Ets-1 protein expression were significantly increased by immunoblots and immunohistochemistry, whereas HIF-2 protein expression was not changed, compared to the control group. In the enalapril group, the immunoactivity of pimonidazole was not significantly different from that of the controls. However, in the spironolactone group, pimonidazole staining demonstrated that the cortex and medulla underwent severe hypoxia. In summary, our data showed that aldosterone inhibition in the developing kidney augmented the hypoxic responses, and up-regulated the expression of key mediators of hypoxia including HIF-1 and Ets-1. Angiotensin II inhibition did not affect hypoxia-related alterations in the developing kidney. The components of RAAS may differentially modulate renal hypoxia and its related target genes in the developing rat kidney.
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