Abstract

Traditional Chinese medicine (TCM) syndrome is an important basis for TCM diagnosis and treatment. As Child-Pugh classification as well as compensation and decompensation phase in liver cirrhosis, it is also an underlying clinical classification. In this paper, we investigated the correlation between single nucleotide polymorphisms (SNPs) of Interleukin-10 (IL-10) and TCM syndromes in patients with hepatitis B cirrhosis (HBC). Samples were obtained from 343 HBC patients in China. Three SNPs of IL-10 (−592A/C, −819C/T, and −1082A/G) were detected with polymerase chain-reaction-ligase detection reaction (PCR-LDR). The result showed the SNP-819C/T was significantly correlated with Deficiency syndrome (P = 0.031), but none of the 3 loci showed correlation either with Child-Pugh classification and phase in HBC patients. The logistic regression analysis showed that the Excess syndrome was associated with dizzy and spider nevus, and the Deficiency syndrome was associated with dry eyes, aversion to cold, IL-10-819C/T loci, and IL-10-1082A/G loci. The odds ratio (OR) value at IL-10-819C/T was 4.022. The research results suggested that IL-10-819C/T locus (TC plus CC genotype) is probably a risk factor in the occurrence of Deficiency syndrome in HBC patients.

Highlights

  • Hepatitis B virus (HBV) infection is a major health problem in China

  • We investigated the correlation between single nucleotide polymorphisms (SNPs) of Interleukin-10 (IL-10) and Traditional Chinese medicine (TCM) syndromes in patients with hepatitis B cirrhosis (HBC)

  • The results showed that IL-10-819C/T locus was significantly correlated to Deficiency syndrome (P = 0.031), and IL10 gene loci (−592A/C, −819C/T, and −1082A/G) were not correlated to either Child-Pugh classification or compensation and decompensation phase in HBC patients

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Summary

Introduction

Hepatitis B virus (HBV) infection is a major health problem in China. It is one of the major causes of virus-related liver diseases such as liver cirrhosis (LC) and hepatocellular carcinoma (HCC) [1, 2]. During the course of HBV infection, liver is gradually damaged by this hepatotropic DNA virus, presenting a wide variety of clinical manifestations ranging from an asymptomatic carrier state to chronic hepatitis B (CHB), and to HBC, even to HCC [2, 4]. Whether chronic HBV infection would be developed to CHB or even LC, the process is affected by many factors such as hereditary susceptibility of patients

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