Z Gastroenterol 2018; 56(05): e49
DOI: 10.1055/s-0038-1654664
POSTER
Hepatologie
Georg Thieme Verlag KG Stuttgart · New York

Dysbalanced sex hormone status is an independent predictor of decompensation and mortality in patients with liver cirrhosis

R Paternostro
1   Internal Medicine III, Division of Gastroenterology and Hepatology, Vienna, Austria
,
B Heinisch
1   Internal Medicine III, Division of Gastroenterology and Hepatology, Vienna, Austria
,
T Reiberger
1   Internal Medicine III, Division of Gastroenterology and Hepatology, Vienna, Austria
,
M Mandorfer
1   Internal Medicine III, Division of Gastroenterology and Hepatology, Vienna, Austria
,
B Seeland
1   Internal Medicine III, Division of Gastroenterology and Hepatology, Vienna, Austria
,
R Schwarzer
1   Internal Medicine III, Division of Gastroenterology and Hepatology, Vienna, Austria
,
M Trauner
1   Internal Medicine III, Division of Gastroenterology and Hepatology, Vienna, Austria
,
M Peck-Radosavljevic
1   Internal Medicine III, Division of Gastroenterology and Hepatology, Vienna, Austria
,
A Ferlitsch
1   Internal Medicine III, Division of Gastroenterology and Hepatology, Vienna, Austria
› Author Affiliations
Further Information

Publication History

Publication Date:
09 May 2018 (online)

 

Background & Aims:

Endocrinological abnormalities including low testosterone levels are prevalent in cirrhosis. We assessed sexual hormone status in regard to hemodynamic abnormalities and its impact on hepatic decompensation and survival.

Methods:

Males with cirrhosis were prospectively included since 2010. Sexual hormones including bioavailable testosterone, total testosterone, luteinizing- and follicle-stimulating-hormone, prolactin, sex-hormone-binding-globulin as well as Child-Pugh score, MELD and hepatic-venous-pressure-gradient were recorded. Clinical follow-up for hepatic decompensation, liver transplantation and death was recorded until May/2017.

Results:

114 male cirrhotic patients were included: Age 55 ± 9.4, MELD 13.5 (7 – 20.7), ALD 61 (53.5%), viral 30 (26.3%), other 23 (20.2%), Child-Pugh-Score: A: 32 (28.1%) B: 48 (42.1%), C: 34 (29.8%). Levels of bioavailable-testosterone and total-testosterone decreased with advanced Child-Pugh-Score (p < 0.001; p < 0.001) while prolactin increased (p = 0.002). Median bioavailable-testosterone [0.8 ng/ml (0.1 – 2) vs. 1.68 ng/ml (0.07 – 2.65); p = 0.004] and total-testosterone [2.7 ng/ml (0.23 – 12.34) vs. 7 ng/ml (0.25 – 10); p = 0.041] levels were lower in patients with severe portal hypertension (hepatic-venous-pressure-gradient > 12 mmHg). Median follow-up was 13 months (0.2 m-75 m) and in 46 patients (40.4%; death: 31 (27.2%)] liver-related events were recorded. Low total-testosterone was associated with an increased risk for hepatic decompensation and/or death, even after adjusting for Child-Pugh-Score, MELD and other relevant factors (Child-Pugh-Score-Model: HR: 2.503 95%CI: 1.214 – 5.157, p = 0.013; MELD-Model: HR: 3.065 95%CI: 1.523 – 6.169, p = 0.002).

Conclusion:

In parallel to increasing severity of cirrhosis, levels of testosterone decline while prolactin levels increase. However, low testosterone levels are independently associated with a higher risk for hepatic decompensation and mortality.