Implications of estradiol and progesterone in pulmonary vasodilatation in cirrhotic patients.

Abstract

The derangement of sex hormone serum levels in cirrhotic patients is well-delineated, and increased levels of progesterone and estradiol have been associated to hyperventilation in cirrhotic patients. These hormones have a well-known role in the regulation of vascular tone. The aim of this study was to evaluate whether sex hormone levels contribute to pulmonary vasodilatation (PV) and gas exchange abnormalities in cirrhosis. Contrast transesophageal echocardiography, arterial blood gases, parameters of liver function, pulmonary function test, estradiol and progesterone levels were determined in 45 male cirrhotic patients. Nineteen of 45 patients (42.2%) presented PV. Hyperventilation (pressure arterial of CO2< or =35 mmHg) was correlated to progesterone levels (p<0.05) and pressure arterial of CO2 was high in patients with PV (p<0.005) and Child class B and C (p<0.01). Hypoxemia (pressure arterial of O2<80 mmHg) had inverse correlation with progesterone (p<0.05) and estradiol (p<0.05) levels and pressure arterial of O2 was low in patients with Child class B and C (p<0.05). PV was present in patients with high estradiol levels (p<0.05), high progesterone levels (p<0.005) and Pugh class B and C (p<0.05). Logistic regression analysis identified progesterone as the sole independent factor associated to PV (p<0.0005). Multivariate linear regression showed that PV was the sole independent factor related to both pressure arterial of CO2 (p<0.05) and pressure arterial of O2 (p<0.01) levels. PV was independently associated to gas exchange abnormalities in cirrhosis. Progesterone and estradiol were related with PV in cirrhotic patients.