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Dysbalanced sex hormone status is an independent predictor of decompensation and mortality in patients with liver cirrhosis
AuthorFerlitsch, Arnulf ; Paternostro, Rafael ; Heinisch, Birgit B. ; Reiberger, Thomas ; Mandorfer, Mattias ; Bardach, Constanze ; Lampichler, Katharina ; Seeland, Berit ; Schwarzer, Remy ; Trauner, Michael ; Peck-Radosavljevic, Markus
Published in
Hepatology Research, 2019, Vol. 49, Issue 2, page 201-211
PublishedWiley-Blackwell, 2019
Document typeJournal Article
Keywords (EN)cirrhosis / mortality / sexual hormone / testosterone
URNurn:nbn:at:at-ubmuw:3-792 Persistent Identifier (URN)
 The work is publicly available
Dysbalanced sex hormone status is an independent predictor of decompensation and mortality in patients with liver cirrhosis [0.52 mb]
Abstract (English)


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.


Males with cirrhosis were prospectively included in this study since 2010. Sexual hormones including bioavailable testosterone, total testosterone, luteinizing hormone, folliclestimulating hormone, prolactin, and sex hormonebinding globulin as well as ChildPugh score, Model for Endstage Liver Disease (MELD) score, and hepatic venous pressure gradient were recorded. Sarcopenia was also assessed in patients with available computed tomography scans. Clinical followup for hepatic decompensation, liver transplantation, and death was recorded until May 2017.


One hundred fourteen male cirrhotic patients were included: age 55 9.4 years, MELD 13.5 (range, 720.7). Etiologies were alcoholic liver disease in 61(53.5%) patients, viral in 30 (26.3%) patients, and other in 23 (20.2%). ChildPugh scores were A in 32 (28.1%) patients, B in 48 (42.1%), and C in 34 (29.8%). Levels of bioavailable testosterone and total testosterone decreased with advanced ChildPugh score (P < 0.001 and P < 0.001) whereas prolactin increased (P = 0.002). Median bioavailable testosterone (0.8 ng/mL [0.12] vs. 1.68 ng/mL [0.072.65]; P = 0.004) and total testosterone (2.7 ng/mL [0.2312.34] vs. 7 ng/mL [0.2510]; P = 0.041) levels were lower in patients with severe portal hypertension (hepatic venous pressure gradient >12 mmHg). Median bioavailable testosterone (0.25 ng/mL [0.071.7] vs. 0.97 ng/mL [0.152.74)]; P = 0.017) and total testosterone levels (1.28 ng/mL [0.257.32] vs. 4.32 ng/mL [0.4313.47]; P = 0.031) were significantly lower in sarcopenic patients. Median followup was 13 months (0.275 months) and liverrelated events were recorded in 46 patients (40.4%; death, 31 [27.2%]). Low total testosterone was associated with an increased risk for hepatic decompensation and/or death, even after adjusting for ChildPugh score, MELD, and other relevant factors (ChildPugh score model: hazard ratio 2.503, 95% confidence interval, 1.2145.157, P = 0.013; MELD model: hazard ratio 3.065, 95% confidence interval, 1.5236.169, P = 0.002).


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

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