Interestingly, MBL is able to interact with TLR2 in the phagosome to initiate proinflammatory signaling,42 which thereby might also play a role in infection after OLT. Gene association studies have several potential limitations which should be taken into consideration when interpreting the results. One is that selection bias may arise from the fact that not all patients were included (patients were excluded because DNA was absent or because of perioperative morbidity or mortality
within the first 7 days after transplantation). However, frequencies for the studied SNPs in recipients were comparable in both cohorts. Another limitation is that the study may suffer from bias due to population stratification. In our study, however, a similar association was observed in a second independent cohort, despite differences in treatment regimes and donor genotype frequencies. An additional theoretical limitation is the possibility that the evaluated polymorphisms may not be directly GSK 3 inhibitor associated with CSI, but instead may be associated with other factors
BYL719 molecular weight that influence that clinical endpoint. However, the multivariate analyses identify each of the separate SNPs, the number of risk-conferring SNPs, sex, and antimicrobial prophylaxis as independent risk factors for infection. In conclusion, the genetic profile of the lectin complement activation pathway has a major impact on bacterial infection after liver transplantation. These observations also confirm the importance of the liver as primary source of the lectin complement pathway
constituents: MBL, FCN2, and MASP2. Further studies on these genetic risk factors in liver transplantation 上海皓元 could contribute to novel infection prevention strategies and improvement of postoperative outcome. This should be evaluated in prospective intervention studies. Such an approach based on lectin complement pathway genes might in time lead to more personalized treatment protocols and improved survival after OLT. We thank Rolf Vossen and Willem Verduyn for technical assistance, and Dr. James Hardwick for his advice regarding the final text. Additional Supporting Information may be found in the online version of this article. “
“Treatment for chronic hepatitis B (CHB) over the last two decades has drawn on immune-based interferon-α (IFN-α) or direct-acting antiviral agents in the category of nucleos(t)ide analogues (NAs). Over this time, various combinations of these two treatment approaches have been submitted to trials, but with disappointing gains over the respective monotherapies. This has been offset in part by the positive impact that these therapies have had on the lives of patients with CHB in significantly reducing the risk of development of progressive liver disease and hepatocellular carcinoma.1 Equally dramatic has been the observed reversal of hepatitis B virus (HBV)-associated fibrosis and cirrhosis, with a commensurate decrease in the need for liver transplantation.