Chinese medicine syndrome distribution of chronic hepatitis B virus carriers in immunotolerant phase.

OBJECTIVE: To explore Chinese medicine (CM) syndrome distribution of chronic hepatitis B virus (HBV) carriers in immunotolerant phase (ITP). METHODS: One hundred and eighty-five chronic HBV carriers in ITP, seen in the Third Affiliated Hospital of Sun Yat-sen University from May 2009 to December 2010, were admitted in an observational study under the guidance of CM. Patients' CM symptoms and signs, demographics, liver biochemistries, and qualitative HBV DNA were recorded in the questionnaires. CM syndromes were then differentiated to 15 detailed types and analyzed by generalization. Lastly, the location, pathogenic factors and nature of the disease were also assessed. RESULTS: When CM syndrome patterns were differentiated to 15 types, there were 27 (15%) no syndrome cases, 94 (50%) single syndrome cases and 64 (35%) compound syndromes cases. The main detailed syndromes included Liver (Gan)-qi depression (LQD), Kidney (Shen)-qi deficiency (KQD), Spleen (Pi)-qi deficiency (SQD) and Kidney-yang deficiency (KYAD). After CM syndromes generalized to five types, their frequency was Spleen-Kidney deficiency (SKD)>LQD>inner dampness-heat retention (IDHR)>Liver-Kidney deficiency (LKD)>blood stasis blocking collateral (BSBC). SKD and LQD occupied 64%. The disease location included Liver, Gallbladder (Dan), Spleen, Stomach (Wei) and Kidney. The pathogenic factors were mainly qi stagnation, qi deficiency, yang deficiency, concurrently dampness-heat and blood stasis. The deficiency syndrome was more than excess syndrome in its nature. CONCLUSIONS: Most of chronic HBV carriers in ITP have their CM syndrome, and the most common types are SKAD, LQD. This study suggests that the natural history may be improved through breaking the state of immune tolerance or shorten the time of ITP by strengthening Spleen-Kidney and reliving Liver qi.

Therapeutic effect of traditional Chinese medicine on coagulation disorder and accompanying intractable jaundice in hepatitis B virus-related liver cirrhosis patients.

AIM: To observe the therapeutic effects of new traditional Chinese medicine (TCM) therapy on coagulation disorder and accompanying intractable jaundice in HBV-related liver cirrhosis patients. METHODS: Using stratified random sampling according to fibrinogen (Fib) levels, 145 liver cirrhosis patients due to hepatitis B complicated by coagulation disorder were treated. Of them, 70 in research group were treated with TCM by "nourishing yin, cooling blood and invigorating blood circulation" and Western medicine, 75 in control group were treated with conventional Western medicine. The indexes of liver function, coagulation function and bleeding events were observed and compared. RESULTS: The prothrombin time (PT) was shorter and the fibrinogen (Fib) level was higher in the research group than in the control group (Fib = 1.6-2.0 g/L, 1.1-1.5 g/L, and < or = 1.0 g/L). The total bilirubin (TBIL) level was significantly lower in the research group than in the control group, except for the subgroup of FIB < or = 1.0 g/L. CONCLUSION: TCM therapy can improve coagulation fuction and decrease TBIL.

[Effects of glycyrrhizin on the expression of hepatitis B virus and Toll like receptors 2,4 in HepG2.2.15 cells expressing low HBsAg].

OBJECTIVE: To investigate the effects of glycyrrhizin (GL) on the expression of hepatitis B virus e antigen (HBeAg), HBV DNA, Toll-like receptors 2,4 (TLR2,4) and proliferation of cells in HepG2.2.15 cell line. METHODS: Real-time PCR examined HBV DNA, ELISA examined HBsAg, HBeAg and MTT examined the proliferation of cells. FCM examined the positive percent of cells expressing TLR2,4 before and after stimulated with GL, in contrast to the blank group. RESULTS: The expression of HBsAg was low in the cell line, so e antigen was studied. The total HBeAg mean was significantly difference on the second day after stimulated (P<0.01), but only in the group with 400 microg/ml HBeAg decreased significantly in contrast to the blank group (P<0.05), the group with 800 microg/ml increased significantly in contrast to the other groups (P<0.01). The total HBV DNA mean on the third day after stimulated was significant, only the group with 50 microg/ml decreased in contrast to the blank group, but P>0.05, the other four groups increased. The intensity of TLR4 expression in the cells was significantly higher than that of the control group (P<0.05), both of total mean TLR2,4 increased significantly (P<0.01). The four groups except the group with 200 microg/ml increased significantly in no dose-dependent manner (P<0.05). GL in three goups under 200 microg/ml all could make cells proliferate, but only 200 microg/ml group had significant difference compared to the blank group (P<0.05). Both 400 and 800 microg/ml groups inhibited the growth of cells (P<0.01). The proliferation of cells were notably negative correlated with the expression of HBeAg, HBV DNA (P<0.05). CONCLUSION: The study suggestes GL could inhibit or promote HBV DNA replicating and e antigen secreting in mutative HepG2.2.15 cell line, the correlation between the proliferation of cells and the both are negative. GL could upregulate TLR2,4 in no dose-dependent manner. Influencing HBV maybe have no correlation to up regulating TLR2,4 by GL at least in vitro.