Markers of erythrocyte turnover are linked to liver cirrhosis stage

Background: Rheological stasis in the splanchnic system could induce erythrocyte sequestration and lysis during liver cirrhosis. Markers of erythrocyte turnover might therefore respond to the severity of portal hypertension. Hence, we investigated the relation between cirrhosis stage and glycated hemoglobin (HbA1c), as HbA1c derives from a chemical reaction which dependents on the lifespan of erythrocytes.

Methods: Patients followed at Mainz University were prospectively enrolled between 2012 and 2013. Clinical scores (Child Pugh) and laboratory markers of erythrocyte turnover (HbA1c, reticulocytes, haptoglobin) were assessed. Multiparameter comparisons were performed by ANOVA tests and univariat analysis was based on Chi² tests.

Results: Patients (N = 153) with liver cirrhosis, age 57 ± 12 years (mean ± SD) and predominantly male gender (n = 100, 65.4%) were analyzed. Liver cirrhosis was due to ethanol consumption (n = 80, 52.3%), hepatitis C (n = 38, 24.8%), hepatitis B (n = 19, 12.4%), NASH (n = 8, 5.2%) and other causes (n = 8, 5.2%). HbA1c decreased significantly from 5.8 ± 1%, 5.6 ± 1.5% and 4.9 ± 0.7% (mean ± SD), by comparing Child Pugh stages (A, B and C), respectively (P = 0.01). Moreso, patients grouped by HbA1c ≤5.0% showed a significantly higher rate of Child Pugh C cirrhosis (P = 0.007). In coherence with compensatory erythrocyte production, reticulocytes increased throughout progressive Child Pugh stages, from 1.86 ± 0.7, 2.4 ± 1.2 to 2.8 ± 1.8 (mean ± SD), respectively (P = 0.004). However serum haptoglobin decline did not follow progressive cirrhosis stages (P = 0.412).

Conclusion: Progressive liver cirrhosis increases erythrocyte turnover, which eventually reduces HbA1c concentration in the systemic circulation. HbA1c might therefore guide assessment of portal hypertension in patients with liver cirrhosis.