ABSTRACT Background 70.8% male), median GDF‐15 was 2880 (1850–4770) pg/mL. GDF‐15 correlated with hepatic dysfunction (MELD Spearman's ρ : 0.50; albumin ρ : −0.57), HVPG ( ρ : 0.47), systemic inflammation (C‐reactive protein ρ : 0.45; interleukin 6 IL‐6 ρ : 0.55; procalcitonin ρ : 0.58), liver stiffness ( ρ : 0.67) and enhanced liver fibrosis test ( ρ : 0.64) (all p < 0.001). GDF‐15 was higher in patients with detectable bacterial DNA in blood (3520 vs. 2250 pg/mL; p < 0.001) and correlated with lipopolysaccharide ( ρ : 0.34; p = 0.010) and lipoteichoic acid ( ρ : 0.37; p = 0.004). Platelet activation was not linked to GDF‐15 after adjusting for liver disease severity, yet patients with undetectable GPIIb/IIIa activation after stimulation showed significantly higher GDF‐15. Over a median follow‐up of 51.5 (26.0–58.2) months, 38 patients decompensated and 21 died (61.9% liver‐related). GDF‐15 (aHR per 100 pg/mL: 1.015; 95% CI: 1.004–1.026; p = 0.007) predicted decompensation risk independently of HVPG, MELD, albumin and IL‐6. Similarly, GDF‐15 was associated with higher risk of all‐cause (HR: 1.019; 95% CI: 1.009–1.029; p < 0.001) and liver‐related mortality (HR: 1.019; 95% CI: 1.007–1.032; p = 0.002). Conclusions GDF‐15 is a promising biomarker in cirrhosis that reflects disease‐driving pathomechanisms and independently predicts decompensation and mortality.
Hofer et al. (Mon,) studied this question.