Diabetes impacts liver stiffness in chronic hepatitis C patients with and without virological cure: a longitudinal study

Abstract

Background: Transient elastography is controversial as a follow-up tool in chronic hepatitis C (CHC) patients. The aim was to assess the variation of liver stiffness measures and its associated factors on a cohort of CHC individuals composed of naïve, sustained virological response (SVR) and non-responder patients (NR).Methods: This was a longitudinal study in CHC patients who were followed with clinical, laboratorial and serial elastography (Fibroscan®). The rate of progression of liver stiffness was calculated and the associated factors for progression were assessed by multiple linear regression analysis. Results: Four hundred and six patients were included: 29% naïve, 24% NR and 47% SVR who were followed for 44 (35-53) months. There was a significant decrease in liver stiffness among SVR patients [11.8 (9.2) kPa vs 8.8 (8.4) kPa (p<0.001)], a trend for liver stiffness increasing in NR group [6.6 (5.2) kPa vs 7.1 (4.5) kPa; p=0.069)] and no change of liver stiffness in naïve group [6.3 (3.0) vs 6.0 (3.8); p=0.22]. The related factors for liver stiffness progression were lack of SVR (p=0.002) and diabetes (p=0.05). In non-diabetic SVR group, a negative rate of progression (- 0.047 kPa/month) was found compared to the highest rate in diabetic non-responder patients (+ 0.044 kPa/month). Diabetics with SVR showed a rate of (+) 0.037 kPa/month while in non-diabetic non-responder patients the ratio was (+) 0.028 kPA/month.Conclusion: Despite SVR, liver stiffness in diabetic patients progresses, suggesting that a close follow-up of diabetic patients should remain even after SVR.

Effect of MTTP -493G/T, I128T, Q95H and Q244E polymorphisms on hepatic steatosis in patients with chronic hepatitis

“… 5 , 6 , 7 Interestingly, diabetes mellitus was reported to be a factor that independently affected liver stiffness after DAA treatment despite SVR. 8 The underlying mechanisms involving the presence of steatosis, especially before treatment, can be alcohol consumption, being overweight, obesity, diabetes type 2 mellitus, HCV genotype, Human Immunodeficiency Virus (HIV) coinfection, and genetic polymorphisms in genes, such as Transmembrane six Superfamily member 2 ( TM6SF2 ), Patatin-Like Phospholipase Domain Containing 3 ( PNPLA3 ) and Microsomal Triglyceride Transfer Protein ( MTTP ). 9 , 10 , 11 , 12 , 13 In this context, the role of host and viral characteristics associated with genetic polymorphisms in liver fat accumulation in chronic hepatitis C was investigated in the present study.…”