Abstracts Asociación Mexicana del Hígado (AMH) 2023
More infoThe clinical course of hepatitis C virus infection (HCV) is modulated by environmental factors and genetic polymorphisms that interact with the virus, such as the low-density lipoprotein receptor (LDLR) and ligand Apolipoprotein E (ApoE); both are associated with lipid metabolism. However, the relationship of these genes with liver damage has not been jointly evaluated in Mexicans. The study aimed to identify a relationship between the LDLR polymorphism (C*52T, rs14158) and ApoE haplotype in anti-HCV positive patients with liver damage in a subpopulation of West Mexico.
Materials and PatientsThis cross-sectional study included 152 naïve anti-HCV positive patients; 110 were viral load (VL) positive (+ve), and 42 were VL negative(-ve). A medical-nutritional evaluation was registered. LDLR and ApoE genotypes were assessed by allelic discrimination. Comparative statistical analysis was performed between VL+ve and VL-ve adjusted by genotype distribution and liver damage. Written informed consent was obtained from the participants. The Institutional Review Board approved this study.
ResultsThe patients (85F/67M) were 49.8±12 years of age with a BMI of 27.7±5.4. VL +ve patients showed glucose homeostasis abnormalities (glucose >100 mg/dL, HOMA-IR >2.5); low levels of cholesterol, triglycerides, VLDL, and LDL, compared to VL-ve patients (p<0.001), as well as high-above-normal ALT, AST, GGT (p<0.001) and low platelets (p<0.001). A 61.1% (58/95) of the VL+ve patients had a high risk for fibrosis (FIB-4), and 35.7% (35/98) had severe fibrosis (APRI). A 10% (11/110) of the VL+ve patients were carriers of the TT LDLR/ApoE3 genotype in which 90% (10/11) had moderate/severe liver damage compared to the C allele carriers (CC, CT), whereas the VL-ve patients had 0% of the TT LDLR genotype (p=0.035) with a lower proportion of liver damage.
ConclusionsThe presence of the TT LDLR/ApoE3 genotypes in VL+ve patients with hepatic function abnormalities suggests that it may be a valuable marker for risk of liver damage to avoid disease progression and to implement preventive strategies among the Mexican population.
Ethical statement
The protocol was registered and approved by the Ethics Committee. The identity of the patients is protected. Consentment was obtained.
Declaration of interests
None
Funding
None