Hepatitis B virus (HBV) infection is the leading cause of severe chronic liver disease. This article provides a critical view of the importance of genomic medicine for the study of HBV infection and its clinical outcomes in Latin America. Three levels of evolutionary adaptation may correlate with the clinical outcomes of HBV infection. Infections in Latin America are predominantly of genotype H in Mexico and genotype F in Central and South America; these strains have historically circulated among the indigenous population. Both genotypes appear to be linked to a benign course of disease among the native and mestizo Mexicans and native South Americans. In contrast, genotypes F, A and D are common in acute and chronic infections among mestizos with Caucasian ancestry. Hepatocellular carcinoma is rare in Mexicans, but it has been associated with genotype F1b among Argentineans. This observation illustrates the significance of ascertaining the genetic and environmental factors involved in the development of HBV-related liver disease in Latin America, which contrast with those reported in other regions of the world.

Hepatitis B virus (HBV) infection may be underestimated among high-risk individuals in regions of low HBs antigenemia. This study aimed to assess HBV serological markers, genotypes, and risk factors in Mexican patients with risk of HBV infection and low socioeconomic status. Demographics, clinical, and risk factor data were collected in patients with HIV (n = 289), HCV (n = 243), deferred blood donors (D-BD) (n = 83), and two native populations, Mixtecos (n = 57) and Purepechas (n = 44). HBV infection was assessed by HBsAg, anti-HBc, and HBV-DNA testing. Overall, patients had low education and very-low income. Totally, HBsAg prevalence was 16.5% (113/684) ranging from 0.7% (HCV) to 37.3% (D-BD), while anti-HBc was 30.2% (207/684). Among 52 sequences, genotypes H (n = 34, 65.4%), G (n = 4, 7.7%), subgenotypes F1b (n = 7, 13.5%), A2 (n = 6, 11.5%), and D4 (n = 1, 1.9%) were detected. Surgeries, sexual promiscuity, and blood transfusions had a differential pattern of distribution. In HCV patients, single (OR = 5.84, 95%Cl 1.91-17.80, P = 0.002), MSM (OR = 4.80, 95%Cl 0.75-30.56, P = 0.097), and IDU (OR = 2.93, 95%CI 1.058-8.09, P = 0.039) were predictors for HBV infection. While IDU (OR = 2.68, 95%CI 1.08-6.61, P = 0.033) and MSM (OR = 2.64, 95%CI 1.39-5.04, P = 0.003) were predictors in HIV patients. In this group, MSM was associated with HBsAg positivity (OR = 3.45, 95%CI 1.48-8.07, P = 0.004) and IDU with anti-HBc positivity (OR = 5.12, 95%CI 2.05-12.77, P < 0.001). In conclusion, testing with a combined approach of three different HBV markers, a high prevalence of HBV infection, a differential distribution of HBV genotypes, including subgenotypes F1b, A2, and D4, as well as risk factors in low-income Mexican risk groups were detected.

This study suggests that the CD36 (rs1761667) AA genotype is associated with higher fat intake and more instances of advanced LF in CHC patients.

ObjectiveTo identify nonalcoholic steatohepatitis (NASH) and liver stiffness in Mexican subjects with different body mass index (BMI).MethodsA cross-sectional study was conducted in 505 adults. Risk for NASH was defined as the presence of one or more of the following biochemical and metabolic parameters (BMPs): fasting glucose ≥100 mg/dl, triglycerides (TG) ≥150 mg/dl, homeostatic model assessment of insulin resistance (HOMA-IR) ≥2.5, aspartate aminotransferase (AST) >54 IU/L and alanine aminotransferase (ALT) >42 IU/L. Body mass index measurement and nutritional assessment were performed by standard procedures. Liver fibrosis stage was determined by liver stiffness measurement using transitional elastography (TE) or by liver biopsy (LB).ResultsRisk for NASH was 57% (290/505). Most BMPs values incremented by BMI category. Among 171 at-risk patients, 106 subjects were evaluated by TE and 65 subjects by LB. Abnormal liver stiffness (≥6.0 kPa) was prevalent in 54% (57/106) of the cases, whereas by LB, 91% (59/65) of patients with obesity had NASH and liver fibrosis. Furthermore, liver fibrosis was prevalent in 46% (6/13) in normal weight individuals, whereas 4.6% (3/65) of patients with a BMI ≥ 35 kg/m2 showed no histopathological abnormalities. Overall, 67.8% (116/171) of the patients had abnormal liver stiffness or NASH. The normal weight patients with liver damage consumed relatively a higher fat-rich diet compared to the other groups whereas the remaining subgroups shared a similar dietary pattern.ConclusionYoung patients with overweight and obesity showed a high prevalence of altered BMPs related to abnormal liver stiffness assessed by TE and NASH by LB. Early diagnostic strategies are required to detect the risk for NASH and avoid further liver damage in populations with a rising prevalence of obesity by defining the risk factors involved in the onset and progression of NASH.