This study presents a cross-sectional analysis of the hormonal alterations of patients with visceral leishmaniasis. The diagnosis was established by the bone marrow aspiration and polymerase chain reaction test. Primary adrenal insufficiency was observed in 45.8% of patients; low aldosterone/renin plasma ratio in 69.4%; low daily urinary aldosterone excretion in 61.1%; and low transtubular potassium gradient in 68.0%. All patients had normal plasma antidiuretic hormone (ADH) concentrations, hyponatremia, and high urinary osmolality. Plasma parathyroid hormone was low in 63%; hypomagnesemia was present in 46.4%, and increased Mg++EF in 100%. Primary thyroid insufficiency was observed in 24.6%, and secondary thyroid insufficiency in 14.1%. Normal follicle-stimulating hormone plasma levels were present in 81.4%; high luteinizing hormone and low testosterone plasma levels in 58.2% of men. There are evidences of hypothalamus-pituitary-adrenal axis abnormalities, inappropriate aldosterone and ADH secretions, and presence of hypoparathyroidism, magnesium depletion, thyroid and testicular insufficiencies.

SUMMARYThere are few reports linking hyponatremia and visceral leishmaniasis (kala-azar). This is a study of 55 consecutive kala-azar patients and 20 normal individuals as a control group. Hyponatremia and serum hypo-osmolality were detected in 100% of kalaazar patients. High first morning urine osmolality (750.0 ± 52.0 vs. 894.5 ± 30.0mOsm/kg H 2 O, p < 0.05), and high 24-hour urine osmolality (426.0 ± 167.0 vs. 514.6 ± 132.0 mOsm/kg H 2 O, p < 0.05) demonstrated persistent antidiuretic hormone secretion. Urinary sodium was high (82.3 ± 44.2 vs.110.3 ± 34.7 mEq/L, p < 0.05). Low seric uric acid occurred in 61.8% of patients and increased fractional urinary uric acid excretion was detected in 74.5% of them. Increased glomerular filtration rate was present in 25.4% of patients. There was no evidence of extracellular volume depletion. Normal plasma ADH levels were observed in kala-azar patients. No endocrine or renal dysfunction was detected. It is possible that most hyponatremic kala-azar patients present the syndrome of inappropriate antidiuretic hormone secretion.

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In this Century Cardiovascular Disease (CVD) is the most common isolated cause of death in developed countries. Many studies have suggested that men with low testosterone levels present higher incidence of components of metabolic syndrome and are at a greater risk of developing CVD. Testosterone can affect the development of atherosclerosis in the coronary arteries. While this androgen seems to have a cardioprotective effect by benefiting endothelial function, inducing vasodilation, and reducing fat mass, insulin resistance and chronic inflammation, it also appears to increase endothelin, thromboxane A2 and reactive oxygen species and renal smooth muscle cells. The relation between testosterone and coronary disease in men has been the focus of study of many authors. Most studies point to a neutral and/or protective effect of endogenous testosterone in male cardiovascular health. Unfortunately, many intervention studies have not been able to confirm this effect with testosterone therapy. More studies are needed to elucidate the pathogenic mechanisms of testosterone in cardiovascular health and to evaluate androgen receptor polymorphisms and their physiological responses to testosterone.