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Dysbalanced sex hormone status is an independent predictor of decompensation and mortality in patients with liver cirrhosis
Author(s) -
Paternostro Rafael,
Heinisch Birgit B.,
Reiberger Thomas,
Mandorfer Mattias,
Bardach Constanze,
Lampichler Katharina,
Seeland Berit,
Schwarzer Remy,
Trauner Michael,
PeckRadosavljevic Markus,
Ferlitsch Arnulf
Publication year - 2019
Publication title -
hepatology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.123
H-Index - 75
eISSN - 1872-034X
pISSN - 1386-6346
DOI - 10.1111/hepr.13253
Subject(s) - decompensation , medicine , testosterone (patch) , cirrhosis , gastroenterology , sex hormone binding globulin , ascites , luteinizing hormone , endocrinology , liver disease , portal venous pressure , liver transplantation , alcoholic liver disease , hormone , prolactin , androgen , transplantation , portal hypertension
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 in this study since 2010. Sexual hormones including bioavailable testosterone, total testosterone, luteinizing hormone, follicle‐stimulating hormone, prolactin, and sex hormone‐binding globulin as well as Child–Pugh score, Model for End‐stage Liver Disease (MELD) score, and hepatic venous pressure gradient were recorded. Sarcopenia was also assessed in patients with available computed tomography scans. Clinical follow‐up for hepatic decompensation, liver transplantation, and death was recorded until May 2017. Results One hundred fourteen male cirrhotic patients were included: age 55 ± 9.4 years, MELD 13.5 (range, 7–20.7). Etiologies were alcoholic liver disease in 61(53.5%) patients, viral in 30 (26.3%) patients, and other in 23 (20.2%). Child–Pugh 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 Child–Pugh score ( P < 0.001 and P < 0.001) whereas 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 bioavailable testosterone (0.25 ng/mL [0.07–1.7] vs. 0.97 ng/mL [0.15–2.74)]; P = 0.017) and total testosterone levels (1.28 ng/mL [0.25–7.32] vs. 4.32 ng/mL [0.43–13.47]; P = 0.031) were significantly lower in sarcopenic patients. Median follow‐up was 13 months (0.2–75 months) and liver‐related 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 Child–Pugh score, MELD, and other relevant factors (Child–Pugh score model: hazard ratio 2.503, 95% confidence interval, 1.214–5.157, P = 0.013; MELD model: hazard ratio 3.065, 95% confidence interval, 1.523–6.169, P = 0.002). Conclusion 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.