4 Indeed,

in the present extended EN-Vie study, surviving patients were followed up more than 3 additional years, and during this additional period, 8 patients received TIPS, 2 OLT, and 7 died. Thus, the present study was able to evaluate long-term outcome of BCS patients (median follow-up of almost 5 years, with a minimum of 43 months). Our updated data confirm that, in Western countries, a step-wise therapeutic strategy confers good long-term survival in patients with BCSurvival score. Most of our patients (88.5%) received long-term anticoagulation. Interestingly enough, the rate of bleeding complications in patients receiving anticoagulation was lower than that previously reported.15 This is most likely the result of more adequate prevention of PH complications as well as careful management of anticoagulation during selleck chemicals invasive procedures.15 Only 22 patients (14%) underwent angioplasty/thrombolysis as primary invasive therapy, and only 8 of them did not require further intervention, such as TIPS, surgical shunt, and/or OLT. It seems that angioplasty/stenting, although an attractive, minimally invasive technique with the potential of

restoring physiological sinusoidal flow, has low applicability in the treatment of our BCS patients. These results contrast with a recent retrospective study from China showing a great applicability and efficacy of angioplasty/stenting in a large cohort of patients with BCS.16 In our opinion, these differences could be most likely explained by different pathogenic mechanisms of hepatic venous outflow obstruction,8 because hepatic vein stenoses are less frequent in the Western world than in Eastern countries. Therefore, angioplasty/stenting remains a potentially valuable treatment of the BCS subtype with short-length stenosis and investigation of the patients’ suitability for this approach is mandatory, because the benefits are Thalidomide potentially significant. Strikingly, no additional patient

received a surgical shunt during the extended follow-up period, and thus only 3 patients (2%) received this therapeutic modality. TIPS has emerged as the preferred derivative treatment in Europe. The fact that two recent small retrospective studies from North America have shown excellent outcomes of BCS patients after surgical shunts does, in our opinion, not change the trend in current practice to prefer less-invasive over more-invasive procedures.17, 18 Moreover, we would like to emphasize that previous multicenter retrospective studies were unable to demonstrate a solid survival advantage in BCS patients treated with surgical shunts.7, 19-22 The low number of patients treated with surgical shunting in our data set precludes shedding more light on this issue. Sixty-two patients required TIPS as rescue therapy after failures of medical or minimally invasive treatments (angioplasty/stenting/thrombolysis).

If ANC decreased below 500, PEG IFN was held for 2 weeks and resumed at 90 μg if ANC PLX4032 in vitro increased to greater than 1,000. Patients would be discontinued from the study if ANC remained below 500. We assumed an SVR of approximately 40% for the 24-week and 80% for the 48-week treatment group based on results of our previous retrospective study and other studies with HCV genotype 6.16 With such expected SVR rates and a 2-sided alpha of 0.05, the power is 80% for a total sample size of 60 patients and approximately 30 patients in each arm. Continuous variables

were compared using Student’s t test if tests normality is observed, whereas nonparametric methods such as the rank sum test was used for all others. Chi-square statistics were used to compare categorical variables. Univariate and multivariate logistic regression was used to estimate adjusted odd ratios relating potential treatment predictors to SVR. Primary analysis of SVR was done by intention-to-treat. Statistical significance was defined as a two-sided P value of 0.05 or less. All statistical analysis was performed using Stata v. 9.0 (Stata Corp., College Station, TX). The study flow diagram is shown in Fig. 1. Of the 75 patients screened, 60 patients were included selleck chemicals in the trial from five clinical sites.

Twenty-seven patients were randomly assigned to 24 weeks of treatment and 33 patients were assigned to 48 weeks of treatment. All selleckchem except one patient were of Asian descent and 93% of patients were Vietnamese or Chinese Vietnamese immigrants. The one non-Asian patient was a Hispanic woman in the 24-week group. As shown in Table 1, baseline characteristics were similar in both groups. As included in the randomization process, the

proportion of patients with advanced fibrosis stage 3-4 and HCV RNA levels ≥800,000 IU/mL were similar in the 24- and 48-week groups: 26% and 27% for advanced fibrosis and 74% and 64% for high HCV RNA levels, respectively. Steatosis was noted in 33% versus 52% (P = 0.36) and excess iron was found in 28% versus 24% (P = 0.35) in the 24-week and 48-week groups, respectively. Average baseline viral loads in both groups was over 6.2 ± 1.0 log IU/mL. Seventy-eight percent of patients in the 24-week group and 82% of patients in the 48-week group adhered to the assigned duration of therapy (P = 0.70). RVR, complete EVR, and SVR results are shown in Fig. 2. Of the subgroup of 39 patients who had HCV RNA PCR testing at week 4 of therapy, 17 of 20 (85%) in the 24-week treatment group and 12 of 19 (63%) achieved RVR but this difference (22%, 95% confidence interval [CI]: −05% to 49%) was not statistically significant (P = 0.12). RVR was a significant predictor of SVR in the 48-week group and trending towards significance in the 24-week group: 14 of 17 (82%) and 10 of 12 (83%) of those with RVR achieved SVR compared to 1 of 3 (33%) and 2 of 7 (29%) for the 24-week and 48-week groups, respectively (P = 0.

19, 22 All patients participating in the eight clinical trials signed appropriate consent forms and all studies were approved by the institutions’ Human Subjects Committees. In this analysis, patients with HCV genotypes 1-6 who were assigned 48 weeks of interferon alfa-2a monotherapy, peginterferon alfa-2a monotherapy, or peginterferon alfa-2a/ribavirin combination therapy, and had baseline and posttreatment Selleck GDC 0068 (i.e., week 72) biopsies, were included. The impact on histologic response was evaluated by three categories of virologic response: (1) degree of virologic response: SVR, relapsers,

patients with breakthrough, and nonresponders; (2) time to HCV RNA undetectability: rapid viral response (RVR; weeks 0-4), complete early virologic response (cEVR; weeks 5-12), 24-week undetectable (weeks 13-24), and never undetectable; and (3) duration of viral suppression: none, <24 weeks, 24 to 48 weeks, and 48 weeks. Because HCV RNA was assessed only at certain time points (i.e., baseline, weeks 4, 12, 24, 48, 60, and 72), a precise measure of the duration of viral suppression could not be obtained. For this reason, patients were grouped to the

duration of viral suppression categories based on the midpoints of the minimum and maximum duration of suppression according to the assessment schedule. The Wnt tumor virologic response categories were defined as follows: SVR (undetectable HCV RNA at 24-weeks after end of treatment); relapsers (undetectable HCV RNA at end of treatment but detectable at 24 weeks after end of treatment); breakthroughs (initially undetectable HCV RNA but later detectable while on treatment);

and nonresponders (HCV RNA detectable learn more throughout treatment; never became undetectable). Missing HCV RNA test results at the end of treatment or 24 weeks after the end of treatment were counted as HCV RNA detectable. Because the analysis included only patients with both baseline and posttreatment biopsies, very few patients had missing HCV RNA test results. Histologic outcome was determined on the basis of changes in the METAVIR NIF activity and fibrosis scores from baseline to 24 weeks after the end of treatment. Patients were classified with respect to the activity grade and fibrosis stage as either: improved (decrease of ≥1 categories from baseline to follow-up); stable (no change in category from baseline to follow-up); or worsened (increase of ≥1 categories from baseline to follow-up). Biopsies from all patients in the eight clinical trials were evaluated in a blinded fashion by a single pathologist. All liver biopsies were required to be a minimum of 1 cm in size. All biopsy samples had a minimum of four portal tracts. Biopsies that were <1 cm in size or had less than four portal tracts were considered inadequate and were excluded.

Many RO4929097 mouse of these were analyzed here for the first time. Overall findings show that four nonsynonymous SNPs are related to the rate of metabolism of alcohol. These are ADH1B Thr60Ser, ADH1C Gly78X, ADH1C Arg272Gln, and ADH1C Ile350Phe, which explain 2.5%, 9.0%, 8.4%, and 12.3% of the variability in the metabolic rate, respectively. Our findings

do not support the theoretical models predicting alterations in the AUC, with lowest values in carriers of the ADH1B 48His allele, but are consistent with the model predicting lower AUC in carriers of nonmutated ADH1C enzymes compared with carriers of mutated enzymes.6 The current study confirms the lack of effect of the ADH1B Arg48His in the metabolic rate of alcohol in white subjects, in agreement with independent studies,11–13 and, with the single exception of the polymorphism ADH1B Thr60Ser, it rules out a major effect in vivo for the rest of the ADH1B polymorphisms analyzed. Although consistent evidence has indicated

that the ADH1B*3 allele (48 Arg+370 Cys) is associated with variability in alcohol metabolism,35, 36 this allele is specific to African subjects12 and is not relevant to white subjects (Table 4). In contrast to ADH1B, genetic variation in ADH1C seems to be relevant to alcohol metabolism in whites (Table 5), even after the use of correction for the huge multiple comparison problem presented by the set of data presented in this study. There is little CB-839 ic50 information on the effect in vivo of the gene variants associated with decreased ethanol metabolic rate. For example, the ADH1B Thr60Ser seems to be rather conservative, but in contrast the ADH1C Gly78X likely results in largely dysfunctional enzyme. These gene variants have been described

very recently, and no functional in vitro studies have been performed so far. The identification of polymorphisms related to decreased alcohol metabolism in whites carried out in this study is likely to have relevant implications, and not only because of the clear relationship between the polymorphisms and the ethanol elimination rate shown in Table 5: Although no major association of these SNPs was observed with the Cmax and the association with the AUC value is weak, the functional significance of the observed decrease in the metabolic rate associated with variant alleles is of crucial click here importance, because in this study the alcohol challenge was based on a single dose, whereas alcohol consumption follows a pattern of multiple dosing, and therefore alcohol accumulation and eventually higher concentrations in blood are expected to occur in carriers of the variant allozymes as compared with noncarriers. No effect of CYP2E1 polymorphisms on alcohol pharmacokinetics or effects was observed in this study. We analyzed the most common CYP2E1 variant allele in the 5′ flanking region, CYP2E1*5, which showed a minor allele frequency equal to 3.4%.

Importantly, the risk score remained MI-503 chemical structure the significant prognostic risk factor (hazard ratio [HR] 1.36, 95% CI 1.13-1.64, P = 0.001 for OS) (Table 3). We next carried out ROC analysis to assess predictive performance of 3-year OS of 65-gene risk scores in a pooled test cohort and

compared it with other clinical variables that showed significance in univariate analysis (tumor size, vasculature invasion, grade, and AFP). The AUC of risk score (0.699; 95% CI, 0.636-0.764) is very close to that of tumor size (0.691; 95% CI, 0.628-0.755), the most significant clinical variable in univariate analysis (Fig. 3). Taken together, these findings suggest that the risk score retains its prognostic relevance even after the classical clinicopathological prognostic features have been taken into account. We further tested the independence of the risk score over current staging systems. Pexidartinib When the risk score was applied to patients with early stage (BCLC stage A) and intermediate and advanced stage (BCLC stage B and C) HCC, it successfully identified high-risk patients in different BCLC stages (Fig. 4). The risk score was also independent of American Joint Committee on Cancer (AJCC) stages (Supporting Fig. 3). We next tested whether a new risk score can improve the discrimination of prognosis over BCLC stages. Performance of the combined model (BCLC and risk score)

is substantially improved over the baseline models with only BCLC and risk score as evidenced by an increase of AUC from ROC analysis (Supporting Fig. 4A). Moreover, subset selleck products ROC analysis within each BCLC stage clearly demonstrated an incremental value of risk score over current staging system (Supporting Fig. 4B). Because vasculature invasion is the clinical variable best known to be significantly associated with

OS of HCC after surgical resection,27–31 we next tested how independent the new risk score is of vasculature invasion. As expected, the prognosis of patients without vasculature invasion was significantly better than that of patients with invasion (Supporting Fig. 5A). When the risk score-based stratification was applied separately to invasion-positive and -negative patients, it successfully identified high-risk patients in both subgroups (Supporting Fig. 5B,C). Importantly, when all stratifications were combined together the risk score even identified patients without vasculature invasion whose risk was worse than or similar to that of patients with invasion (Supporting Fig. 5D). We next examined the potential association of risk score with underlying liver disease by including Child-Pugh class and cirrhosis information into the analysis. As expected, Edmondson grade reflecting pathological characteristics of tumors showed an incremental association with risk score. The number of patients with a high risk score is slightly increased in higher grades.

We studied the frequency, pattern and outcome of renal dysfunction in patients with cirrhosis using ADQI-IAC definitions. Methods: Consecutive patients attending outpatient clinics in Colombo BMS-907351 molecular weight North Teaching Hospital, Ragama, were prospectively recruited and followed up. Results: Of 277 patients with cirrhosis and stable serum creatinine, 27 (9.7%) had serum creatinine >1.5 mg/dl (current cut-off), and 23/27 (85%) fulfilled criteria for HRS2. 65/277 (23.5%) had eGFR <60 ml/min [ADQI-IAC cut-off for chronic kidney disease (CKD)], but 42/65 (64.6%) did not fulfil criteria for HRS2. Compared to cirrhotics without

CKD, the CKD group were older (61.4 vs 53.7 years; p < 0.0001), more likely to be female (50.8% vs 19.3%; p < 0.0001), more likely to have cryptogenic cirrhosis (67.7% vs 41%; p < 0.0001), and Child-Pugh class B or C (95.4% vs 74%; p < 0.001). As expected, they had higher MELD scores (16.6 vs 13.5; p < 0.0001). 58/277 (20.9%) died during follow-up [mean 9.8 months (SD 4.5)]. After adjusting for

other variables, CKD independently increased risk of death 3.3-fold (Nagelkerke R Square test). Conclusion: Compared to HRS criteria, the ADQI-IAC definition detects more than twice the number of cirrhotic patients with CKD. As the presence of CKD is associated with increased mortality, further studies are needed to determine whether prognosis can be improved in such patients by treating acute deterioration PLX4032 in vivo of CKD with available treatments for HRS1. Key Word(s): 1. renal dysfunction; 2. cirrhosis; 3. CKD; 4. HRS; Presenting Author: QINGCHUN FU Additional Authors: XIAOJIN WANG, ZHAOXIA LUO, LIUDA NI, LI LI, JINJIN CHEN, FENG ZHOU, LIQIN SHI, YINPENG JIN, GUANGXIU LV, XIANG HU, CHENGWEI CHEN Corresponding Author: XIANG HU, CHENGWEI CHEN Affiliations: shanghai liver diseases research center; Shenzhen Beike Cell Engineering Research Institute Objective: The study is aimed to evaluate the safety and feasibility of infusions of human umbilical cord mesenchymal

stem cells (hUCMSCs) in patients with decompensated liver cirrhosis (DLC). Methods: It is in an open, dose escalation study. Three doses of hUCMSCs are 5.0 E+7 cells, 1.0 E+8 cells and 2.0 E+8 cells, respectively. The cells were administrated selleckchem with IV infusion. Each patient received 3 times infusion every the fourth day, with a follow-up for 52 weeks. The criteria for Adverse Event (AE) was mainly in accordance to the NCI-CTCAE 4.0 version. The study got an approval from IRB, and all subjects have signed ICF before study enrollment (ClinicalTrials.gov identifier: NCT01342250). Results: 20 patients were recruited (14 male and six female, mean age 54.2 ± 5.9 years) from Nov 2010 to May 2011. 17 of them were diagnosed as HBV, while one was HCV. All patients were tolerant with the infusion. Two patients died for complications after 6 months of the first infusion.

Therefore, we analyzed the outcomes of endoscopic resection VX-770 clinical trial for gastric neoplasm in patients with LC. Methods: From January 1995 to December 2012, 120 patients with LC (case group) underwent endoscopic resection for gastric neoplasm at Asan Medical Center. To compare the clinical outcomes, age, sex, and tumor size-matched control group (n = 360) were selected from patients without LC. In addition, we analyzed the changes in the outcomes of the

Child-Pugh classification after the procedure. Methods: From January 1995 to December 2012, 120 patients with LC (case group) underwent endoscopic resection for gastric neoplasm at Asan Medical Center. To compare the clinical BMS-777607 outcomes, age, sex, and tumor size-matched control group (n = 360) were selected from patients without LC. In addition, we analyzed the changes in the outcomes

of the Child-Pugh classification after the procedure. Results: Among total 120 patients of the liver cirrhosis group (median age 68.5 years, men 103 patients), 106 patients(88.3%) were in Child-Pugh A classification and 14 patients (1.2%) were in Child-Pugh B. The complete/curative resection rates were 100%/97.5% in the

case group and 91.9%/91.9% in the control group (p = 0.60 and p = 0.70, respectively). The median procedural time was 33.5 minutes in the case group and 33.7 selleck chemical minutes in the control group (p = 0.930). Bleeding was observed in 7 cases of the case group (5.83%) and in 16 cases of the control group (4.44%) after the procedure (p = 0.673). No perforation occurred in the control group and 4 cases of microperforation occurred in the control group (p = 0.576). The median follow up period after the procedure in the case group and the control group was 29.2 months and 44.24 months, respectively. In the case group, 4 of 106 cases of Child-Pugh A were changed to Child-Pugh B (3.3%) and none of 14 cases of Child-Pugh B were changed to Child-Pugh C after undergoing endoscopic resection. Conclusion: Endoscopic resection for gastric neoplasm can be performed in LC patients with a comparable efficacy and safety to the patients without LC. Also, endoscopic resection does not worsen the Child-Pugh classification in the majority of the patients. Key Word(s): 1. Endoscopic resection; 2. liver cirrhosis; 3.

The slightly Palbociclib price increased DILI susceptibility in CYP2E1*1A/*1A carriers may even be solely attributed to the reactive oxygen pathway without the need to postulate CYP2E1-mediated metabolism of acetylhydrazine to hepatotoxins. If this downstream mechanism played a major role, then CYP2E1*1A/*1A may even be a risk factor for DILI associated with other drugs, and this should be investigated in future studies. The genetically polymorphic NAT2 metabolizes some therapeutically important drugs such as isoniazid and sulfonamides. The *4 allele is considered

the wild-type because the resulting protein is functionally fully active. The prevalence of genetic NAT2 variants associated with intermediate and slow acetylator status is between 40% and 70% in Caucasians, and 10% and 40% in Asians.63, 64 In a rather small study, all six

patients who developed liver injury upon sulfonamide intake were phenotyped as NAT2 slow acetylators.65 For Etoposide isoniazid, a number of case series and case-control studies have identified NAT2 slow acetylator genotypes as risk factors for isoniazid-induced liver injury,66 but a recent meta-analysis confirmed such an association only for Asian populations (odds ratio 2.5) whereas an elevated risk was not confirmed when data from patients of different ethnic origins was analyzed.58 In the aforementioned prospective study with isoniazid monotherapy, no such association was observed either.59 The role of uridine diphosphate glucuronosyltransferase 2B7 (UGT2B7), along with CYP2C8 and adenosine triphosphate–binding cassette C2 (ABCC2), variants was investigated in a study comparing 24 patients with diclofenac hepatotoxicity to two

groups of controls: 48 patients on diclofenac and 112 who did not take the drug.41 The authors substantiated an elevated risk in patients harboring at least one UGT2B7*2 allele. Because UGT2B7*2 is believed to lead to an increased function of the enzyme, increased hepatotoxicity could be explained by the UGT2B7-mediated production selleck inhibitor of larger amounts of the diclofenac acyl glucuronide, which then forms covalent protein adducts leading to cell damage. Overall, the authors concluded that the UGT2B7*2 and the ABCC2 −24CT variants contributed significantly to the risk of diclofenac-induced DILI, whereas CYP2C8 plays no important role. Glutathione S-transferases (GSTs) are conjugation enzymes that may exert a double protective action against hepatotoxicity by “neutralizing” reactive phase 1 drug metabolites as well as other ROS involved in downstream hepatotoxic mechanisms. Based on such a possible nonspecific protective mechanism, a recent CGAS used a mixed DILI cohort and analyzed GST polymorphisms associated with DILI.30 Patients with a double GSTT1-GSTM1 null genotype had a significant 2.7-fold increased risk of DILI.

Similarly, when myeloid DCs were stimulated with CD40L in the presence of HCV core, p9 enhanced IL-12 production by inhibiting HCV core-induced as well as CD40L-induced IL-10. Moreover, in vitro, p13 potentiated the effect of maturation stimuli on human and murine DC, increasing their IL-12 production and stimulatory activity, which resulted in enhanced proliferation and IFN-γ production

by responding T-cells. Finally, immunization with p13-treated murine DC induced stronger anti-HCV T-cell responses not only in wildtype mice but also in HCV transgenic mice and in mice transiently expressing HCV core in the liver. Conclusion: These results suggest that IL-10 inhibiting peptides may have important applications to enhance anti-HCV XL765 concentration immune responses by restoring the immunostimulatory capabilities of DC. (HEPATOLOGY 2011.) Chronic infection caused by hepatitis C virus (HCV) is characterized by low or nil antiviral T-cell responses, whereas viral clearance is associated with strong and multispecific T-cell responses.1 Among other mechanisms, production of immunosuppressive

cytokines such as interleukin 10 (IL-10)2, 3 has been postulated as responsible for this lack of efficient immunity. IL-10 is a pleiotropic cytokine traditionally considered as immunosuppressive and antiinflammatory, produced by many cell types (reviewed4), which exerts its effects by inhibiting www.selleckchem.com/products/Sunitinib-Malate-(Sutent).html macrophage and dendritic cell this website (DC) functions. In chronic HCV infection, patients have high serum levels of IL-10,5, 6 associated with incomplete responses to interferon IFN therapy.7 Interestingly,

these levels decline after successful treatment.6 IL-10 is produced in these patients by antigen-stimulated CD4 and CD8 T-cells, regulatory T-cells,3, 8, 9 and DC10-12 which in turn activate IL-10-producing T-cells.13In vitro experiments have demonstrated that some HCV proteins interacting with monocytes induce the production of IL-10.14, 15 Due to its antiinflammatory properties, IL-10 has been used therapeutically in HCV patients with liver fibrosis.16 Although administration of IL-10 decreased hepatic inflammation and fibrosis, HCV RNA levels increased, and antiviral CD4 and CD8 T-cells shifted from a Th1 to a Th2 cytokine profile. All these data suggest that overexpression of IL-10 in chronic HCV infection may contribute to the lack of efficient antiviral T-cell responses. Indeed, IL-10 is a key factor in determining viral clearance versus chronic infection in the LCMV murine model, and its inhibition converted a chronic into an acute infection, which could be controlled by the immune response.17, 18 Thus, for chronic HCV infection, inhibition of IL-10 would potentially enhance the efficacy of antiviral responses and, ultimately, lead to viral clearance.

4,5 Accordingly, HBV genotyping is still not CHIR-99021 research buy recommended as part of the management of chronic hepatitis B in regional guidelines.6–8 In this article, we describe recent advances in the impact of HBV genotype on the clinical outcomes and responses to antiviral treatments in chronic hepatitis B patients. In addition, the interactions between HBV genotype and other viral factors, such as viral load and viral mutants, will be reviewed. According to the homogeneity

of virus sequences, at least 10 HBV genotypes (A to J) and several subtypes have been defined by divergence in the entire HBV genomic sequences, respectively, >8% for genotypes and 4–8% for subtypes.9–11 Except for the newly identified genotypes I and J, the geographic and ethnic distributions of HBV genotypes and subtypes are well characterized (Table 1). Genotype A is highly prevalent in sub-Saharan Africa (subtype A1), Northern Europe (subtype A2), and Western Africa (subtype A3). Genotypes B and C are common in Asia. At present, genotype B is divided into B1–B6 subtypes. Among them, B1 is isolated in Japan, B2–5 are found in East Asia, and B6 is found in indigenous populations living in the Arctic, such as Obeticholic Acid nmr Alaska, Northern Canada and Greenland. Genotype C, including subtypes C1–C5, mainly

exist in East and Southeast Asia. Genotype D with subtypes D1–D5 is prevalent in Africa, Europe, the Mediterranean region and India. Genotype E is restricted to West Africa. Genotype F with 4 subtypes (F1–F4) is found in Central and South America. Genotype G has been reported in France, Germany and the United States. The eighth genotype, H, is found in Central America.4,9–13 Recently, genotype I, a novel inter-genotypic recombination among genotypes A, C, and G was isolated in Vietnam and Laos.14–16 The newest HBV genotype,

J, was identified in the Ryukyu islands in Japan, and this genotype has a close relationship with gibbon/orangutan genotypes and human genotype C.17 The correlation of HBV genotype distribution with modes of transmission was selleck products commented upon in our original landmark review in the Journal of Gastroenterology and Hepatology.4 For example, genotypes B and C are prevalent in highly endemic areas, such as Asian countries, where perinatal or vertical transmission plays an important role in spreading HBV, whereas the remaining genotypes are frequently found in areas where horizontal transmission (close personal conduct between young children, blood or sexual contamination between adults) is the main mode of transmission. Accordingly, genotyping HBV can serve as an epidemiologic tool for the investigation of maternal transmission, familial clustering and geographic distribution of HBV strains.18 The results of several studies indicate that HBV genotype can influence the short- and long-term outcomes of HBV infection (Table 2). Recent studies suggested that acute infection with HBV genotype A may increase the risk of progression to chronic infection.