Z Gastroenterol 2016; 54 - KV184
DOI: 10.1055/s-0036-1586960

Association of controlled attenuation parameter (CAP) and HbA1c in patients with fatty liver

A Arslanow 1, J Geisel 2, F Lammert 1
  • 1Saarland University Medical Center, Department of Medicine II, Homburg/Saar, Deutschland
  • 2Saarland University Medical Center, Institute of Clinical Chemistry and Laboratory Medicine, Homburg/Saar, Deutschland

Background and aim: Chronic liver diseases and serum glycosylated hemoglobin (HbA1c) levels are linked to one another through the metabolic syndrome. Our aim was to analyze for the first time the potential association between hepatic steatosis, using the controlled attenuation parameter (CAP), and HbA1c.

Patients and methods: At a tertiary referral center in Deutschland, we evaluated 212 outpatients. Steatosis was assessed non-invasively using CAP, which quantifies the degree of ultrasound attenuation based on transient elastography (Fibroscan). Serum HbA1c and liver function tests were measured with standardized clinical chemistry assays. The NAFLD susceptibility variant PNPLA3 p.I148 M was genotyped using Taqman assays.

Results: Overall, 93.4% presented with non-alcoholic liver disease (113 men, median age 52 years). Median CAP was 293 dB/m (100 – 400), and 171 (80.7%) presented with elevated CAp ≥238 dB/m, indicating marked steatosis. Median BMI was 30.2 kg/m2 (17.2 – 47.4), median HbA1c 5.6% (3.7 – 10.4), and serum ALT activities 45 U/l (9 – 301). The frequency of elevated CAP increased with higher serum HbA1c levels (rs= 0.230, P = 0.001). Patients with both steatosis and increased HbA1c levels (HbA1c≥6.0%) displayed significantly (P = 0.001) higher CAP values as compared to those with normal levels (312 vs. 286 dB/m). As compared to non-diabetics, CAP values and HbA1c levels were higher in diabetics (322 vs. 282 dB/m and 6.8 vs. 5.3%, both P < 0.001). In total, 49.0% carried at least one PNPLA3 p. 148 M risk allele. When stratifying for the PNPLA3 genotype, the genetic association of elevated CAP with higher serum HbA1c levels is maintained only for carriers of the p.I148 allele but not in carriers of the risk allele [M]. Overall, the risk for steatosis was independently associated with HbA1c, BMI, ALT and age as determined by multivariate linear regression analysis (all p ≤0.013).

Conclusions: Non-invasive risk stratification and follow-up of steatosis in patients with the metabolic syndrome is needed because of potential progression to steatohepatitis. Steatosis as assessed by CAP is associated with HbA1c in non-diabetic individuals, and the combination of these non-invasive markers improves individual risk assessment of patients with chronic liver diseases.