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. Author manuscript; available in PMC: 2017 May 1.
Published in final edited form as: Gastroenterology. 2016 Feb 2;150(5):1219–1230.e6. doi: 10.1053/j.gastro.2016.01.032

Table 2.

Independent predictors of liver damage (presence of steatosis, NASH, and fibrosis stage F2-F4) in 1149 patients of the Liver Biopsy cross-sectional Cohort.

Steatosis NASH Fibrosis F2-F4
OR 95% CI P-value OR 95% CI P-value OR 95% CI P-value
Age, years 1.01 0.99-1.02 0.32 1.01 1.00-1.02 0.17 1.02 1.01-1.04 <0.001
Gender, F 0.44 0.28-0.69 <0.001 0.66 0.51-0.86 0.002 0.66 0.47-0.91 0.011
BMI, Kg/m2 0.96 0.94-0.98 0.001 1.01 0.99-1.03 0.13 0.98 0.95-0.99 0.014
IFG/T2DM, yes 1.43 0.86-2.45 0.17 1.93 1.41-2.64 <0.001 2.95 2.07-4.23 <0.001
PNPLA3, number of I148M alleles 1.90 1.37-2.68 <0.001 1.70 1.41-2.04 <0.001 1.63 1.32-2.02 <0.001
TM6SF2, E167K 1.64 0.85-3.50 0.14 1.62 1.12-2.39 0.010 1.41 0.92-2.12 0.11

rs641738, number of T alleles 1.42 1.07-1.91 0.015 1.18 1.00-1.40 0.050 1.30 1.06-1.70 0.012

OR: odds ratio; CI: confidence interval; BMI: body mass index, IFG: impaired fasting glucose; T2DM: type 2 diabetes mellitus.

Logistic regression models were used to test the association of demographic, clinical, and genetic factors with liver damage. In addition to predictors shown above, models were adjusted for statin use and indication for liver biopsy (severe obesity vs. increased liver enzymes in NAFLD. Genetic analyses were calculated by using an additive model, except for TM6SF2 where a dominant model was used due to few homozygotes for the 167K mutant allele.

The reference group was defined by the absence of steatosis, NASH and fibrosis (F0-F1). NASH diagnosis was based on the criteria reported in the Methods section.