AI Article Synopsis
- Host genetic variations, specifically human platelet antigens (HPAs), may impact the progression of fibrosis in patients with chronic hepatitis C (CHC).
- The study focused on four specific HPA polymorphisms (HPA -2, -3, -5, and -15) in 211 CHC patients while assessing serum markers related to fibrosis.
- Results indicated that patients with the HPA-15aa genotype had significantly lower levels of serum laminin compared to other genotypes, suggesting a potential role of HPA-15 in the fibrosis progression of CHC.
Article Abstract
Background: Host genetic polymorphisms influence the fibrosis progression of chronic hepatitis C (CHC) patients. Previous studies have shown the association of human platelet antigens (HPAs) polymorphisms with CHC. However, little is known regarding the association of HPAs polymorphisms with the fibrosis progression of CHC. The aim of this study was to determine the association of HPA -2, -3, -5 and -15 polymorphisms with the levels of serum fibrosis marks in CHC patients.
Methods: The HPA -2, -3, -5 and -15 were genotyped by 5'-nuclease assay in 211 CHC patients, while the serum concentration of hyaluronic acid (HA), collagen IV (CIV), amino-terminal pro-peptide of type III procollagen (PIIINP), and laminin (LN) from the same samples were measured by time resolved fluorescence immunoassay.
Results: The level of serum LN was significantly lower in CHC patients with HPA-15aa genotype compared to those with HPA-15ab/bb (P = 0.032) but did not differ among HPA-2, -3 and -5 genotypes. There were no difference in HA, CIV and PIIINP levels among HPA-2, -3,-5 and -15 genotypes.
Conclusions: This study demonstrates that HPA-15 aa polymorphism is associated lower serum LN in CHC, which suggests that HPA -15 aa may be involved in the fibrosis progression of CHC.
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| http://dx.doi.org/10.1016/j.transci.2020.102967 | DOI Listing |
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