Research Article

Evaluation of a histocompatibility antigen related to hepatitis B virus in patients with hepatocellular carcinoma in the western Brazilian Amazon

Published: April 25, 2013
Genet. Mol. Res. 12 (2) : 1336-1346 DOI: https://doi.org/10.4238/2013.April.25.5
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Abstract

Hepatocellular carcinoma is an infection of variable incidence that can be caused by hepatitis B virus (HBV), which is endemic in the Amazon region. The diagnosis of HBV can be performed through the use of serum markers such as the hepatitis B surface antigen. The chronic HBV can cause mutagenesis and carcinogenesis, being the susceptibility of infection due to allele human leukocyte antigen (HLA). Thus, we evaluated the clinical, molecular and laboratory profile (histocompatibility complex) of HBV in 22 patients with hepatocellular carcinoma in Amazonia, including 18 males and 4 females, using a blood sample for generic HLA class II. The results showed increased frequency of disease evolution in adults between 25 and 64 years old, who comprised 19 of the 22 patients studied. Most patients (16/22) presented high levels of alpha-fetoprotein and transaminases (14/22). The most common HLA alleles were DRB1*04 (8/44), DRB1*08 (9/44), DRB*03 (16/44), and DQB1*04 (9/44). When we compared specific phenotype frequencies of HLA-DRB1* between patients and controls, we found that patients had a significantly higher frequency of allele DRB1*08 and a significantly lower frequency of DRB1*07 and DRB1*12 compared to previous studies on Asian and Amazonian populations suggesting ethnic differences. We suggest that alleles HLA-DRB*08, HLA-DRB*03 and HLA-DQB1*04 may be risk factors for hepatocellular carcinoma in Amazon.

Hepatocellular carcinoma is an infection of variable incidence that can be caused by hepatitis B virus (HBV), which is endemic in the Amazon region. The diagnosis of HBV can be performed through the use of serum markers such as the hepatitis B surface antigen. The chronic HBV can cause mutagenesis and carcinogenesis, being the susceptibility of infection due to allele human leukocyte antigen (HLA). Thus, we evaluated the clinical, molecular and laboratory profile (histocompatibility complex) of HBV in 22 patients with hepatocellular carcinoma in Amazonia, including 18 males and 4 females, using a blood sample for generic HLA class II. The results showed increased frequency of disease evolution in adults between 25 and 64 years old, who comprised 19 of the 22 patients studied. Most patients (16/22) presented high levels of alpha-fetoprotein and transaminases (14/22). The most common HLA alleles were DRB1*04 (8/44), DRB1*08 (9/44), DRB*03 (16/44), and DQB1*04 (9/44). When we compared specific phenotype frequencies of HLA-DRB1* between patients and controls, we found that patients had a significantly higher frequency of allele DRB1*08 and a significantly lower frequency of DRB1*07 and DRB1*12 compared to previous studies on Asian and Amazonian populations suggesting ethnic differences. We suggest that alleles HLA-DRB*08, HLA-DRB*03 and HLA-DQB1*04 may be risk factors for hepatocellular carcinoma in Amazon.