Table 1.
Baseline characteristics of patients at the time of diagnosis of liver cirrhosis.
Our cohort was predominantly male with a median age of 55 years at the time of diagnosis. The most common etiologies of cirrhosis were alcoholic liver disease (ALD) and viral hepatitis and the baseline characteristics of these subcohorts are compared on the two rightmost columns. Patients with ALD usually presented at later stages of liver disease with higher CPS and MELD. Most deaths occurred in this group (68 patients, 32.2%).
Fig 1.
Decompensation events present at the time of diagnosis of liver cirrhosis.
In total, half of the patients (50.0%) already had decompensated cirrhosis at baseline. Decompensations were most common in ALD patients (75.4%), while patients with cirrhosis due to viral hepatitis less frequently presented with decompensations at baseline (19.0%). Patients with both ALD and viral hepatitis as causes of cirrhosis showed similar decompensation rates as the overall population.
Table 2.
Chronic liver disease-related complications and decompensation events present at the time of diagnosis of cirrhosis; overall and according to etiology.
“Any complications” were defined as ascites, hepatic encephalopathy (HE) and/or variceal bleeding. Other liver-related events were spontaneous bacterial peritonitis (SBP), hepatocellular carcinoma (HCC) and portal vein thrombosis (PVT). Half of the patients (238, 50.0%) had some decompensation event at baseline, with the most common being ascites (199, 41.8%). Cirrhosis due to ALD had the highest ratio of decompensations at baseline (75.4%), especially most variceal bleeding events–absolute and relative to cohort size (39 bleeding events, 18.5%).
Table 3.
Child Pugh Score (CPS) and Model for End-stage Liver Disease (MELD) Score at the time of diagnosis of cirrhosis and according to etiology of liver disease.
At baseline, 22.1% of patients already had a Child Pugh Stage C and 33.4% had a MELD Score greater than 15. Patients with cirrhosis due to ALD usually presented with the highest CPS and MELD scores.
Fig 2.
Changes from baseline to last follow-up in Child Pugh Score (CPS), MELD score, platelet count, and liver stiffness (transient elastography in kPa) for patients with cirrhosis due to alcoholic liver disease (ALD), chronic hepatitis C (CHC) or other reasons.
Box and whiskers graph (5–95% percentile whiskers) of paired measurements (diagnosis and latest follow-up) for the main singular etiologies of cirrhosis in our cohort: ALD, CHC and “other”. Patients with ALD had higher scores at baseline, but showed improvement in CPS over time. Patients with chronic hepatitis C presented at earlier stages of liver disease. We found a significant effect of hepatitis C virus eradication (SVR12) on CPS and MELD, on platelet count as well as on liver stiffness. For the ALD cohort, not enough paired measurements of liver stiffness were obtained. Level of significance: * = p <0.05, ** = p < 0.01, *** = p < 0.001.
Fig 3.
Systemic inflammation increased with liver disease.
We found increasing levels of c-reactive protein (CRP, in mg/L) as a marker of systemic inflammation with increasing severity of liver disease, measured in Child-Pugh Score (CPS) and Model for End-stage Liver Disease (MELD) score (Box and whiskers, 5–95% percentile; p < 0.001).
Fig 4.
Spearman correlation matrix for CPS and MELD (two-tailed) at the time of diagnosis.
When comparing score and laboratory parameters at baseline, we found a strong correlation between CPS and MELD for CRP as a marker for systemic inflammation. We also found a strong inverse correlation for serum HDL levels with disease progression–expressed as increasing CPS and MELD. The association with LDL was not as strong and no significant correlation was found for triglycerides or HbA1c. Patients with advanced chronic liver disease were regularly anemic, as shown here in a strong inverse correlation with hemoglobin levels and CPS/MELD. Level of significance: * = p <0.05, ** = p < 0.01, *** = p < 0.001.
Table 4.
Dyslipidemia and liver disease (values in median (IQR)).
Shown here are serum levels of LDL, HDL, and triglycerides of the included patients, divided by etiologies, Child Pugh Score (CPS), and MELD strata. We found steep declines in HDL levels with the progression of liver disease. Consequentially, ALD patients, who in general presented at more advanced stages of liver disease, had the lowest HDL levels. We found similar patterns for LDL and triglycerides, but not as significant. LDL levels were highest in the “cholestatic and AIH” subcohort, mainly due to the highly elevated levels among patients with primary biliary cholangitis.
Fig 5.
Kaplan-Meier estimates of two-year survival in patients with liver cirrhosis due to alcoholic liver disease and viral hepatitis.
After a follow-up of twelve months, the overall survival in the viral hepatitis group was significantly better (95.1% vs. 75.8%, log rank p < 0.001). After 24 months, 90.2% of patients in the viral hepatitis cohort were still alive compared to 71.1% in the ALD cohort (log rank p < 0.001).