Risk factors associated with type 2 diabetes mellitus in patients with chronic hepatitis B: a cross-sectional study with pair-matched controls

cally, 54.7% were mixed ancestry, 31.4% Black African, 10.4% White and 3.5% Asian. Median duration of follow up was 5.3 (IQR 2.4–8.5) years and 7.1% were HIV coinfected, median CD4 at baseline 249 cells/mm (IQR 127–422). HBV genotypes (n = 94) were predominantly genotype A (50%) and D 42.6%) with B (1%), C (3.2%) and E (3.2%). At diagnosis, median HBV viral load was 468 (IQR 51–3357) IU/ml, 68.1% being <2000 IU/mL with a median ALT 28 U/L (IQR 19–48). In those biopsied (n = 85), median Ishak necro-inflammatory stage and fibrosis grade scores were 5 (IQR 3–7) and 3 (IQR 1–3) respectively and 17% had a fibrosis score of ≥5. An ALT >40 U/L predicted for a fibrosis score ≥3 [OR 3.9 (1.4– 11.0], p < 0.009 whilst median ALT was significantly higher in those with a viral load of >2000 IU/mL, p < 0.0001. Age, greater or <30 years, did not predict for differences in ALT, viral load or histological findings, p = NS. During follow up, 15.3% (n = 110) met criteria for HBeAg-negative immune escape chronic HBV infection, the majority male (82%). Treatment was given to 25.3% (n = 182) of the cohort. In those with CHB mono-infection, 62.3% used Lamivudine, 37% Tenofovir and 3.8% aInterferon. In the treated group, pre-treatment median ALT [49 U/L (IQR 27–88)] was significantly higher than ALT at last follow up [28 U/L (IQR 18–44)], p < 0.0001. During follow-up 3.5% (n = 25) HBsAg seroconverted at a median 61 months (IQR 43–82) while 4.2% developed hepatocellular carcinoma with median survival of 4 months (IQR 2–9). CONCLUSIONS: Most HBeAg-negative CHB patients remain in the immune control phase during follow-up with 15%, mostly men, progressing to the immune escape phase. Elevated ALT predicted for higher viral load and greater fibrosis which supports its use as a surrogate marker for therapy requirement in resource constrained settings.