Overview
Cirrhotic male hypogonadism syndrome, also known as endocrine deficiency-cirrhosis syndrome, West-Cordova syndrome (Silvestrini-Corda syndrome). Its main clinical features are gynecomastia, testicular atrophy and hypogonadism on the basis of cirrhosis. This syndrome is more common in patients with decompensated cirrhosis.
Etiology
Blood estrogen levels increase and urinary excretion increases in cirrhosis due to decreased inactivation of estrogen and increased conversion of androgens to estrogen. Increased estrogen levels can cause male feminization through feedback inhibition of the hypothalamic-pituitary-gonadal axis leading to decreased secretion of gonadotropins and adrenocorticotropic hormone and decreased secretion of androgens.
Symptoms
Gynecomastia gradually appears on the basis of cirrhosis, which can be unilateral or bilateral, with the right side being the most common, showing nodular elevation of the nipple or areola in mild cases, and resembling the female breast in severe cases, which may be distended and painful, but without milk secretion. In addition, there are male testicular atrophy, scanty pubic hair, loss of libido, thinning of voice, often accompanied by spider nevus and liver palms caused by skin capillary dilatation.
Examination
Serum levels of E2 and E3 are increased, and testosterone and its metabolites are decreased.
Diagnosis
In the presence of gynecomastia and other hypogonadism on the basis of cirrhosis, the diagnosis can be made by measuring the increased levels of E2 and E3 in the serum and the decreased levels of testosterone and its metabolites.
Treatment
The treatment of this disease is mainly for the treatment of primary liver disease, with the reduction of primary disease and the improvement of liver function, the male gonadal function can gradually improve. Androgen therapy has also been reported to have some efficacy.