Since inhibitors usually occur Aloxistatin chemical structure within the first 50 EDs, many physicians prefer not to switch FVIII products during this time. On the other hand, it should be acknowledged that switching between different FVIII products was not associated with an enhanced risk of inhibitor development in the large cohorts of patients with <50 EDs evaluated in the CANAL and RODIN studies [13, 14]. Similarly, intensive treatment and/or surgery are well known determinants of inhibitor development [36, 37]. Therefore, it sounds reasonable to avoid switching FVIII product in the

peri-operative period, although, no robust evidence is available to support a specific role of product switch in the inhibitor formation after surgery and intensive treatment [36, 37]. Patients with a family history of inhibitors or a severe F8 gene

defect are also known to be at high inhibitor risk, however, no observation has been reported in the literature indicating an increased inhibitor risk when switching FVIII U0126 in vivo products in these conditions. Patients with a previous history of inhibitors, including those who achieved success after immune tolerance induction (ITI), are usually considered at risk of inhibitor recurrence. It may be reasonable to surmise that, in this situation, the introduction of a new FVIII product could break the tolerance to FVIII. On the other hand, successful ITI outcome was reported with FVIII products different from that eliciting the inhibitor formation [57]. In patients with MHA inhibitor

prevalences between 3% and find more 13% are reported, but these cross-sectional studies did not take exposure to FVIII concentrate into account [3-6]. As patients with MHA receive factor VIII replacement therapy infrequently for bleeds or surgery, it is especially important to express the inhibitor risk as a function of EDs. This was done in the INSIGHT study that included 2711 persons with MHA (FVIII 0.02–0.40 IU mL−1) from Europe and Australia [7]. The inhibitor risk at 50 EDs was 6.7% (95% CI, 4.5–8.9) and at 100 EDs the risk further increased to 13.3% (95% CI, 9.6–17.0). Furthermore, this study demonstrated that the risk of inhibitor development in patients with MHA remains present after 50 EDs and even after 100 EDs. Thus, in contrast to severe haemophilia A the risk of inhibitor development does not level off after 50EDs and patients with MHA are at lifelong risk of inhibitors, requiring continuous vigilance. This necessitates frequent testing for inhibitors, especially after intensive FVIII replacement for major bleedings or surgery. Inhibitors in patients with MHA develop at a median age of 37 years after a median of 29 EDs [7, 8] In about half the patients (57%), the baseline FVIII drops below 0.01 IU mL−1 as the inhibitor cross-reacts with the endogenous FVIII, changing the phenotype into severe haemophilia A [7].

Since inhibitors usually occur GSK126 in vitro within the first 50 EDs, many physicians prefer not to switch FVIII products during this time. On the other hand, it should be acknowledged that switching between different FVIII products was not associated with an enhanced risk of inhibitor development in the large cohorts of patients with <50 EDs evaluated in the CANAL and RODIN studies [13, 14]. Similarly, intensive treatment and/or surgery are well known determinants of inhibitor development [36, 37]. Therefore, it sounds reasonable to avoid switching FVIII product in the

peri-operative period, although, no robust evidence is available to support a specific role of product switch in the inhibitor formation after surgery and intensive treatment [36, 37]. Patients with a family history of inhibitors or a severe F8 gene

defect are also known to be at high inhibitor risk, however, no observation has been reported in the literature indicating an increased inhibitor risk when switching FVIII selleck products in these conditions. Patients with a previous history of inhibitors, including those who achieved success after immune tolerance induction (ITI), are usually considered at risk of inhibitor recurrence. It may be reasonable to surmise that, in this situation, the introduction of a new FVIII product could break the tolerance to FVIII. On the other hand, successful ITI outcome was reported with FVIII products different from that eliciting the inhibitor formation [57]. In patients with MHA inhibitor

prevalences between 3% and selleck kinase inhibitor 13% are reported, but these cross-sectional studies did not take exposure to FVIII concentrate into account [3-6]. As patients with MHA receive factor VIII replacement therapy infrequently for bleeds or surgery, it is especially important to express the inhibitor risk as a function of EDs. This was done in the INSIGHT study that included 2711 persons with MHA (FVIII 0.02–0.40 IU mL−1) from Europe and Australia [7]. The inhibitor risk at 50 EDs was 6.7% (95% CI, 4.5–8.9) and at 100 EDs the risk further increased to 13.3% (95% CI, 9.6–17.0). Furthermore, this study demonstrated that the risk of inhibitor development in patients with MHA remains present after 50 EDs and even after 100 EDs. Thus, in contrast to severe haemophilia A the risk of inhibitor development does not level off after 50EDs and patients with MHA are at lifelong risk of inhibitors, requiring continuous vigilance. This necessitates frequent testing for inhibitors, especially after intensive FVIII replacement for major bleedings or surgery. Inhibitors in patients with MHA develop at a median age of 37 years after a median of 29 EDs [7, 8] In about half the patients (57%), the baseline FVIII drops below 0.01 IU mL−1 as the inhibitor cross-reacts with the endogenous FVIII, changing the phenotype into severe haemophilia A [7].

On the other hand, animals in Lt/HF group decreased energy expenditure with lost BAT compensations and developed more severe lipid and glucose intolerance, hepatic steatosis, inflammation and hepatocyte ballooning. Contrary to our expectations, cBATX caused a further recruitment of iBAT both in St/C and St/HF groups, which could compensate energy expenditure loss by excised tissue, but not in Lt/HF group. Ad-MSCs population in St/HF group was higher (Sca-1: >95%, CD29: >99%, CD44: >60%, CD105: >40%) with abundant differentiation capacity to WAT and iBAT than that in Lt/HF group. Interestingly,

Ad-MSCs Tx significantly improved body weight gain, energy expenditure loss and findings of NAFLD with the appearance of donor cell derived iBAT in Lt/HF group. Conclusion: Impaired metabolic compensation in adipose tissues resulted in progression of NAFLD, which Selumetinib chemical structure was based on deteriorated Ad-MSCs capacity. New approach targeted this pathway as cell transplantation could be a potent strategy for preventing NAFLD. Disclosures: Kohichiroh Yasui – Grant/Research Support: AstraZeneca K.K., CHUGAI Pharmaceutical Co., Ltd., Dainippon Sumitomo Pharma Co., Ltd., Eisai Co., Ltd., FUJIFILM Medical Co., Ltd., Merck Serono, MSD K.K., Otsuka Pharmaceutical Co., Ltd. Yoshito Itoh – Grant/Research Support: MSD KK, Bristol-Meyers

Squibb, Dain-ippon Sumitomo Pharm. Co., Ltd., Otsuka Pharmaceutical Co., Chugai Pharm Co., Ltd, Mitsubish iTanabe Pharm. Co.,Ltd., HCS assay Daiichi Sankyo Pharm. Co.,Ltd., Takeda Pharm. Co.,Ltd., AstraZeneca K.K.:, Eisai

Co.,Pharm.Ltd, FUJIFILM Medical Co.,Ltd. The following people have nothing to disclose: Taichiro Nishikawa, Hisakazu Nakajima, Satoru Sugimoto, Ikuyo Itoh, Kazuki Koudou, Tomoki Nakajima, Kanji Yamaguchi, Michihisa Moriguchi, Yoshio Sumida, Hironori Mitsuyoshi, Masahito Minami The pathogenesis of liver injury and inflammation this website in nonalcoholic steatohepatitis (NASH) is obscure. We have previously reported that toxic free fatty acids induce hepatocyte lipoapoptosis in vitro by activating the TRAIL receptor (TR). The AIMS of this study were to examine the role of TR-mediated signaling in a murine model of NASH. METHODS: TR knockout (TR−/−) mice, mice with conditional deletion of caspase-8 in hepatocytes (Casp8Δhepa) and wild-type (WT) littermates were fed a diet high in saturated fat, cholesterol and fructose (FFC) or chow for 6 or 3 months, respectively. RESULTS: FFC-fed WT and TR−/− mice had comparable caloric intake and activity. However, the FFC-fed TR−/− mice had reduced liver triglyceride content, lower serum ALT values, and hepatocyte apoptosis by TUNEL assay as compared to WT mice. Moreover, TR−/− mice displayed attenuation of liver fibrosis by mRNA levels of collagen-1a and Sirius red staining.

1 second, INR 1,080; Antinuclear Antibody titer 1/100. BNO and USG of the abdomen were normal. The patient was treated

with prednisone 1 mg/kg a day for 2 weeks, then tappered over 2 weeks, omeprazole 20 mg twice a day, and sucralfate syrup 30 ml three times a day before meal. After a year, patient came again with epigastric abdominal pain, palpable purpuric rash in both of lower legs but without melena and joint pain. Oesophagogastroduodenoscopy showed oesophagitis LA grade A and pangastritis. Biopsy result was chronic gastritis without H. pylori. Normal 0 false false false. Management still consists of the therapy on complication and definitive therapy. Conclusion: HSP patient with gastrointestinal involvement may experience recurrent symptoms after a year relieved symptoms. Key Word(s): 1. Henoch-Schönlein Cabozantinib supplier purpura; 2. pangastritis; 3. hematuria; 4. osteoarthritis pedis bilateral Presenting Author: JI HYUN SONG Additional Authors: SANG GYUN KIM, SU JIN CHUNG, HAE YEON KANG Corresponding Author: JI HYUN SONG Affiliations: Seoul National University College of Medicine, Seoul National University Hospital Gangnam Center, Seoul National University Hospital Gangnam Center Objective: Subepithelial Akt inhibitor mass is a relatively common finding in upper gastrointestinal endoscopy.

The aim of this study was to evaluate the natural course of asymptomatic subepithelial masses in upper gastrointestinal tract and analyze the risk factors of the subepithelial masses increasing in size. Methods: From 2004

to 2011, 2126 subepithelial masses in upper gastrointestinal tract were detected, and 935 were followed up using endoscopy. Results: The find more lesion size at initial endoscopy was 8.7 mm (range 1–100 mm). During a mean follow-up of 35.2 ± 21.2 month (range 6–96 month), 903 subepithelial masses (96.6%) were showed no interval change, 32 lesions (3.4%) were increased at least 25% in diameter with mean increment 5.0 ± 4.0 mm (range 1–15 mm). The risk of increasing subepithelial mass was significant in overlying mucosal changes (hyperemia, erosion, or ulcer) (OR = 8.22, 95% CI 1.48–45.70) and hard consistency (OR = 10.348, 95% CI 1.10–97.35). We evaluated the increasing velocity as size increment divided by follow-up years. The increasing velocity was faster (0.44 ± 2.12 mm/year, range 0.00–15.00 mm/year) for large lesions (≥2 cm) than small lesions (0.07 ± 0.38 mm/year, range 0.00–5.14 mm/year for <2 cm) (p < 0.001). Conclusion: Most of the small subepithelial masses were showed no interval change during 8 year follow-up period. Regular follow-up with endoscopy may be considered in small (<2 cm) subepithelial masses with intact overlying mucosa. Key Word(s): 1. Subepithelial mass; 2. upper gastrointestinal tract; 3.

11, 13 Sinusoidal Ibrutinib nmr dilation is associated with higher right atrial pressures, similar to that observed in patients with cardiac cirrhosis.11, 13 In contrast to cardiac failure, the extent of dilation as well as fibrosis is more severe in patients with Fontan circulation.11, 13 After a failed Fontan procedure (at least in patients with cavopulmonary anastomosis), the back pressure on the liver is usually continuous

(i.e., nonpulsatile), as opposed to the back pressure secondary to problems such as tricuspid regurgitation (i.e., pulsatile). This continuous high venous pressure may explain why liver dysfunction is frequent after a Fontan procedure. The exact mechanism for the development of fibrosis with cardiac dysfunction is unknown. Fibrosis in cardiac cirrhosis or after Fontan palliation may develop independent

of inflammation and, potentially, driven by repetitive mechanical stretch and compression of sinusoid and other resident cells as a result of passive congestion.14 This, along with hypoxia driven by a low cardiac output, may lead to significant structural and function alteration of the liver parenchyma. Hepatic complications of a failed Fontan are, in part, related to selleck screening library the duration of follow-up.11, 15, 16 As compared to a duration of less than 5 years, the odds of hepatic complications for a post-Fontan duration of 11-15 years is 4.4 (confidence interval [CI]: 1.1-17.2) and 9.0 (CI: 2.2-36.2), for a duration of 16-20 years.15 Furthermore, the extent of hepatic fibrosis on pathological specimens is strongly correlated

with elevated hepatic venous pressures (r = 0.83; P = 0.003), low cardiac index, and ventricular function.11 Hepatic dysfunction correlates best with a low cardiac index and ventricular function. After selleck chemicals llc cardiac transplantation, 1-year actuarial survival is 89% in patients with preserved ventricular function, as compared to 56% in those with failing ventricular function (P = 0.04).17 Progression to cirrhosis may even be observed within 10 years of the initial Fontan surgery.18 The majority of hepatic complications are incidentally discovered. In patients with Fontan circulation followed for a median of 12 years, elevated liver function tests (30% abnormal transaminases and 32% abnormal bilirubin), coagulopathy (58%), hepatomegaly (53%), cirrhosis (26%), and hepatic masses (3%) are recognized.19 PH with gastroesophageal varices may develop, resulting in increased risk of gastrointestinal hemorrhage; hepatocellular carcinoma (HCC) may also develop. Liver function test and coagulation abnormalities (especially protein C deficiency), particularly in patients with Fontan circulation, are common.20, 21 The approach to abnormal liver function tests is similar to other patients with liver disease. However, there are salient features that may be unique to patients with CHD.

This study identifies sheep as H. canis reservoirs potentially important in zoonotic or foodborne transmission. Helicobacter canis was originally isolated from a child with gastroenteritis [1]. Its identification in dogs suggested that pets were reservoirs facilitating zoonotic transmission [2]. Subsequently, H. canis was isolated from a dog with hepatitis [3], a colony of Bengal cats with endemic diarrhea [4], and healthy cats [5]. In these cases, H. canis’ role in hepatic and intestinal disease was given further plausibility by extensive prior experimental enterohepatic

Helicobacter use in mouse inflammation Ceritinib cost and neoplasia models [6-8]. Since H. canis has been cultured from bacteremic humans [9-12]. It has also been identified in a duodenal biopsy from a Crohn’s disease patient [13] and in a liver biopsy from an autoimmune hepatitis patient [14]. Most of these reports state that the patient had dog or cat ownership history, and all of these authors hypothesized zoonotic transmission. As H. canis was previously identified in dogs, cats, and humans, it has not been known to naturally infect other species. Here we report H. canis isolation from sheep feces, expanding its host range and raising important questions regarding potential avenues for zoonotic or foodborne transmission. Fecal samples were collected from 22 sheep in sterile Brucella broth containing MK-8669 purchase 20% glycerol.

These sheep were from a single open flock of Dorsets, Hampshires, and Dorset-Hampshire crosses used in teaching and research. The cohort’s average age was 4 (range of 1–10) and consisted of 21 predominantly multiparous ewes and 1 ram. Collection was approved by the Committee on Animal Care of the Massachusetts Institute of Technology. Samples were plated on 5% sheep blood agar (Thermo Fisher Scientific, this website Lenexa, KS, USA) and CVA (Cefoperazone-Vancomycin-Amphotericin B) agar (BD, Franklin Lakes, NJ, USA), and cultured at 37 °C under microaerobic conditions in vented jars containing N2, H2, and CO2 (80 : 10 : 10). Helicobacter-positive samples were identified by colony morphology,

phase contrast microscopy, Gram-negative staining, and Helicobacter genus-specific 16S rRNA PCR [15]. Isolate species identity and clonality were confirmed by RFLP and REP-PCR [15, 16]. Biochemical testing was performed using the Remel RapID NH kit (Thermo Fisher Scientific). DNA was extracted from pure cultures for 16S rRNA sequencing and a neighbor joining phylogenetic tree was constructed based on sequence similarity [17]. All isolates were evaluated for HeLa cell cytotoxicity as previously described, with H. hepaticus strain 3B1 as a positive control [18]. Fecal culture yielded mixed bacterial populations that made separation of Helicobacter-associated colony morphologies technically difficult. Despite this, four isolates, namely, MIT 12-7708, MIT 12-7709, MIT 12-7728, and MIT 12-7730 were recovered. RFLP showed H.

This study identifies sheep as H. canis reservoirs potentially important in zoonotic or foodborne transmission. Helicobacter canis was originally isolated from a child with gastroenteritis [1]. Its identification in dogs suggested that pets were reservoirs facilitating zoonotic transmission [2]. Subsequently, H. canis was isolated from a dog with hepatitis [3], a colony of Bengal cats with endemic diarrhea [4], and healthy cats [5]. In these cases, H. canis’ role in hepatic and intestinal disease was given further plausibility by extensive prior experimental enterohepatic

Helicobacter use in mouse inflammation Rapamycin and neoplasia models [6-8]. Since H. canis has been cultured from bacteremic humans [9-12]. It has also been identified in a duodenal biopsy from a Crohn’s disease patient [13] and in a liver biopsy from an autoimmune hepatitis patient [14]. Most of these reports state that the patient had dog or cat ownership history, and all of these authors hypothesized zoonotic transmission. As H. canis was previously identified in dogs, cats, and humans, it has not been known to naturally infect other species. Here we report H. canis isolation from sheep feces, expanding its host range and raising important questions regarding potential avenues for zoonotic or foodborne transmission. Fecal samples were collected from 22 sheep in sterile Brucella broth containing Selleck Opaganib 20% glycerol.

These sheep were from a single open flock of Dorsets, Hampshires, and Dorset-Hampshire crosses used in teaching and research. The cohort’s average age was 4 (range of 1–10) and consisted of 21 predominantly multiparous ewes and 1 ram. Collection was approved by the Committee on Animal Care of the Massachusetts Institute of Technology. Samples were plated on 5% sheep blood agar (Thermo Fisher Scientific, selleck chemicals llc Lenexa, KS, USA) and CVA (Cefoperazone-Vancomycin-Amphotericin B) agar (BD, Franklin Lakes, NJ, USA), and cultured at 37 °C under microaerobic conditions in vented jars containing N2, H2, and CO2 (80 : 10 : 10). Helicobacter-positive samples were identified by colony morphology,

phase contrast microscopy, Gram-negative staining, and Helicobacter genus-specific 16S rRNA PCR [15]. Isolate species identity and clonality were confirmed by RFLP and REP-PCR [15, 16]. Biochemical testing was performed using the Remel RapID NH kit (Thermo Fisher Scientific). DNA was extracted from pure cultures for 16S rRNA sequencing and a neighbor joining phylogenetic tree was constructed based on sequence similarity [17]. All isolates were evaluated for HeLa cell cytotoxicity as previously described, with H. hepaticus strain 3B1 as a positive control [18]. Fecal culture yielded mixed bacterial populations that made separation of Helicobacter-associated colony morphologies technically difficult. Despite this, four isolates, namely, MIT 12-7708, MIT 12-7709, MIT 12-7728, and MIT 12-7730 were recovered. RFLP showed H.

More studies need to be conducted to obtain more information about variations in therapy and efficacy for different

genotypes. Several different treatment regimens for treating patients with hepatitis D have been evaluated in the past.11 Nucleosides and nucleotides were ineffective for HDV infections in multiple studies. For genotypes 1 and 2, Aslan et al.12 previously postulated a primary immune-mediated disease with elevated levels of CD4+ T cells, and this makes an immunomodulatory compound such as interferon click here a reasonable therapeutic choice. In 1991, the first 12-month interferon treatment study was published by Rizzetto’s group; a biochemical response was found, although a virological response was not achieved.13 In 2006, the first data for a small group (n = 16) treated with PEG-IFNα2b were presented,6 and a sustained virological response was shown in 43% of the patients. Wedemeyer et al.5 have now put hepatitis D therapy with PEG-IFN back into the limelight. Their data demonstrate buy Doxorubicin that PEG-IFN is at present the only reasonable therapeutic option for HDV infection. HDV coinfection leads to hepatitis B e seroconversion and low HBV DNA levels, which are typical signs of delta hepatitis dominating an HBV infection.14 This constellation can

cause severe hepatitis with a high risk of decompensating end-stage liver disease or hepatocellular carcinoma development, and this makes optimal treatment necessary. In light of the current results and previous studies already showing the ineffectiveness of nucleos(t)ide therapy, we are faced with the question whether there is any role for these compounds in treating patients chronically coinfected with hepatitis B and hepatitis D. ADV has lost its role as a first-line therapy selleck chemical for chronic hepatitis B over the last years, and to date, there are no available data addressing the prognosis of treatment with entecavir or tenofovir in these cases. Anyway, although no significant suppression of HBsAg was noticed in the PEG-IFN–alone group, HDV RNA clearance was achieved to the same degree found in the PEG-IFN and ADV group. In addition, HBsAg levels could be further reduced with combination therapy.

In this cohort, HDV replication correlated with serum HBsAg levels.15 HBsAg reduction might be a prognostic factor for possible clearance in the future because HDV needs HBsAg as an envelope protein. Thus, is there a reasonable indication for combination therapy? With respect to HBsAg levels, this therapeutic scheme had the most profound effect. Because an HBsAg decline is a positive predictor of successful therapy in hepatitis B e antigen–positive patients with chronic hepatitis B monoinfections,16 combination therapy might also be favorable in HBV/HDV-coinfected patients with hepatitis B e antigen and/or a high viral load. A positive effect provided by combination therapy in these patients must be evaluated in future studies.

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Employment: Gilead Sciences; Patent Held/Filed: Gilead Sciences; Stock Shareholder: Gilead Sciences, Pfizer Hongmei Mo – Employment: Gilead Science Inc The following people have nothing to disclose: Viktoria Gontcharova Background: A recently discovered novel surface receptor involved in click here HCV entry, the Niemann-Pick C1-like 1 cholesterol (NPC1L1), is an HCV entry factor amendable to therapeutic intervention. Previously, DNA sequencing studies revealed that nonsynonymous variants in NPC1L1 are collectively common in general population. The aim of the present study was to elucidate whether genetic variants of the NPC1L1 are linked to the antiviral response in a group of patients with JNK activity inhibition chronic hepatitis C (CHC). Methods: We included 38 patients with CHC genotype 1 treated with pegylated interferon alpha2 and ribavirin (20 patients with SVR and 18 null responders). The whole coding sequence of NPC1L1 gene was amplified by 30 different

PCR reactions. PCR products were barcoded and sequenced in a Junior-454 deep-sequencing platform (Roche). The resulting reads were aligned against the human genome (GRCh37) using BLAT algorithm and the variants were identified using GATK Unified genotyper. The functional consequence of the

sequence variants were determined using SNPEff algorithm and association studies with patient phenotypes were performed using Plink suite. Results: 24 different sequence variants in NPC1L1 gene were identified in total in the 38 patients sequenced. 15 were small insertions and deletions (indels), whereas 9 of them constitute single nucleotide variants (SNV), from which 6 had been already learn more reported in dbSNP database. According to a negative selection of deleterious sequence variants in the normal population, most of the identified variants were predicted to play synonymous or regulatory roles in the gene. Nevertheless, even with this limited sample size, association studies shown significative association between two of the sequence variants (a single nucleotide substitution and a single base deletion) with therapy response (rs186726309 and a novel SNV, Chr7: 44575955Del(G)). Additionally, a new SNV has been found which is not present in dbSNP database (Crh7: 44561370) and is present in a low frequency in our cohort; and produces a significant aminoacid change (S919C) in the coding region of the gene. Conclusions.

Failure to observe a relationship between alcohol consumption GSK-3 inhibitor and advanced fibrosis may reflect the fact that these factors are likely to have influenced entry into HCV treatment. Patients with advanced fibrosis would have been encouraged

to seek treatment, whereas heavy drinkers may have been unwilling or too ill to commit to treatment. Integrated care and aggressive follow-up by phone and in the clinic may have contributed to the high treatment completion rates and SVR achieved in this cohort, but adherence may also have been, in part, the result of the patients’ stable life circumstances and support of the family. In addition to stable insurance coverage, over 60% were married and 80% were either employed or retired. We did not assess the prevalence or severity of alcohol dependence BMN 673 chemical structure in this study, but it seems likely that both are lower in privately insured cohorts with high marriage and employment rates than among the inner-city clinic patients and veterans studied by Chang et al.17 and Anand et al.,9 respectively. Socioeconomic stability and less-severe alcohol dependence may have contributed, in part, to the rapid drop in regular drinking

observed in response to HCV diagnosis and the further decrease once HCV treatment was initiated. We do not believe that these findings were obtained because our cohort was unique. An increasing percentage of the U.S. population is enrolled in integrated health care plans. Except for extremes of income, membership of the Kaiser Sacramento Health Care Plan is representative of the total area’s population,19 and demographics of the Sacramento area are similar to those for the United States as a whole. This is

important, because, although HCV+ rates are relatively low among individuals who are privately insured or on Medicare, this is such a large population that it accounts for 46% of the HCV+ patients in the U.S. household population (Third National Health and Nutrition Survey, National Center for Health Statistics, 1994, unpublished data). Our finding that failure to abstain for find more 6 months before HCV treatment was related to significantly higher risk of treatment failure in moderate, but not heavy, drinkers was also unexpected. This finding is counterintuitive and is based on a relatively small sample. Therefore, it needs to be replicated in a larger sample to determine whether or not it may have occurred by chance. Meanwhile, the fact that pretreatment abstinence was not associated with treatment outcome in the cohort as a whole suggests that requiring 6 months of abstinence before treatment is less critical to outcome than ensuring that patients are committed to treatment and providing close monitoring and ancillary care.