There were 931 females and 99 males included in this analysis. Among the first 770 cases, in whom this was available, the diagnosis of PBC (and hence its date) was made retrospectively by the investigators in 34.3% (264) of patients. Twelve cases were uniquely detected by death certificate, and these were not included in the 1,030 cases that were analyzed. The overall chi-squared heterogeneity test showed marginally statistically significant evidence for departure from the

uniform distribution (P = 0.062). More detailed analyses of individual months showed that there was a marked, highly statistically significant peak for diagnoses in the month of June (O = 115, E = 84.7, O/E = 1.36; P = 0.001). Furthermore, Poisson Bortezomib mouse modeling showed that there was evidence of sinusoidal patterning with a June peak

(P = 0.012), with goodness of fit (P = 0.302) and estimated amplitude of 0.111 (standard error = 0.044) (Table 1; Fig. 1). The numbers of patients attending liver clinics and inpatient admissions by month during 2001-2003 are given this website in Table 2. Although there were lower attendances during August and December because of staff vacations, there was no evidence of any seasonal patterning (P = 0.712). The numbers of patients by month surviving less than 5 years (i.e., late diagnoses) and numbers of patients surviving more than 10 years (i.e., early diagnoses) are given in Table 3. There was evidence of seasonality among the early diagnoses (chi-square test for heterogeneity: P = 0.035; test for sinusoidal variation: P = 0.011). However, there was no evidence

of seasonality among the late diagnoses (chi-square test for heterogeneity: P = 0.781; test for sinusoidal variation: P = 0.780). The numbers of symptomatic and asymptomatic patients by month of diagnosis are given in Table 4. There was evidence of significant sinusoidal variation among the symptomatic group (P = 0.013). There was evidence of significant heterogeneity among the asymptomatic group (P = 0.004) (Fig. medchemexpress 2). This study has found highly novel evidence of seasonal variation among cases of PBC. Rigorous statistical methods have been used to analyze high-quality, population-based data from a well-defined geographical region. The study area has very low inward or outward migration rates.12, 16, 17 Thus, the findings cannot be explained by seasonal migration. We have also reviewed our case-finding methodology very carefully and can find no reason within this for a seasonal variation in notification of new cases over this 17-year period. Case finding was carried out in consistent fashion and did not depend upon factors other than patients’ established clinical case records.

Available information on preclinical toxicology studies with PEGylated drugs did not show any PEG-related toxicities for PEGASYS® and Mircera®. In toxicity studies with Cimzia® in cynomolgus monkeys and rats conducted

with high doses of the PEGylated protein, the only PEG-related finding was vacuolation mainly in macrophages and after chronic dosing. This vacuolation did not result in functional SCH727965 nmr changes in the animals. No PEG-related effects have been reported in clinical studies with Cimzia®. Vacuolation of macrophages and some other cell types at high PEG doses was also reported for some PEGylated proteins including PEGylated haemoglobin [13, 17, 18, 22, 23]. No changes in other tissues have been reported. The larger PEG molecules do not penetrate into tissue to the extent as PEG molecules smaller than 20 kDa [37, 38]. Therefore, it can be assumed that large PEG molecules linked to a large protein, such as FVIII, will remain in circulation until FVIII is removed through the protein-related

removal mechanisms thought to be mainly in the liver. Thus, the penetration of large PEG or PEGylated rFVIII into tissues, such as brain, can be assumed to be negligible. This is supported by the toxicology studies with the PEGylated proteins and/or with PEG alone where no indication of vacuolation of neuronal cells or microglia (derived from the same lineage as macrophages) has been observed in any of the studies. ABT-263 clinical trial The 60 kDa PEG moiety in BAY 94–9027 did not show any toxicity when assessed in acute and repeat administration toxicity studies, up to the highest dose tested of 210 mg kg−1 in the acute and 11 mg kg−1 in the 4 weeks toxicity study. The large safety margins medchemexpress of the clinical dose of PEG for Cimzia®, PEGASYS® and the expected clinical dose of BAY 94–9027 to the observed vacuolation

in cells of the RES system in rats and monkeys seen only with Cimzia® (Fig. 3) suggests that long-term administration of 60 kDa PEGylated rFVIII could be a safe option. Several key points can be extracted from the experiments with 60 kDa PEG and the review of the literature on safety of high molecular weight PEG. The toxicity of a PEGylated protein is usually the same or lower than the un-PEGylated protein and the toxicity seen is related to the action of the protein moiety, not the PEG [12, 13]. The removal of the PEGylated protein from circulation is driven by mechanisms specific to the protein [12, 13], and PEGylated proteins can have reduced immunogenicity when compared to their un-PEGylated protein [4, 5, 13]. Polyethylene glycol molecules, given at low doses as in most therapeutic proteins, can be removed by the kidney and liver with low organ accumulation [33, 38].

1C). Immunoblot analysis confirmed that hepatocyte populations from regenerating livers were enriched with cells that expressed keratin (K)7, a marker of immature hepatocytes (Fig. 4B). Hepatocytic cells from regenerating livers also expressed Ihh and Shh ligands (Fig. 4B), and immunostaining of 48-hour cytospins from regenerating (but not

sham-operated) livers co-localized expression buy Hydroxychloroquine of Shh and albumin (Supporting Fig. 1D). Thus, the aggregate data provide conclusive evidence that hepatocytic cells expressing progenitor markers and Hh ligands or target genes increase as the liver regenerates after PH. Hh ligands are known to promote the proliferation of various progenitors. Therefore, it was important to determine whether the proliferative activity of hepatocytic or ductular cells increased as these populations became enriched with Hh-responsive cells. Mice received a single injection of BrdU 2 hours before sacrifice to label cells that were engaged in DNA synthesis. The numbers of hepatocytes and ductular cells with BrdU nuclear staining increased significantly after PH (Fig. MLN2238 4C, D). As with Gli2-staining (Fig. 4A), BrdU nuclear staining peaked first in hepatocytes, and then in ductular cells. PH also increased nuclear accumulation

of Ki67, another S-phase marker, in both cell populations (Supporting Fig. 2A, B). Thus, increased proliferative activity in hepatocyte and ductular cell populations closely paralleled their enrichment with Hh-responsive cells. To determine how Hh-pathway activation impacts regenerative responses, post-PH, mice were treated with cyclopamine, a specific Smo antagonist that abrogates Hh signal transduction32

or vehicle (olive oil) before PH and at regular intervals (every 24 hours) after PH. As expected, cyclopamine did not prevent induction of Hh ligands (data not shown). However, it attenuated induction of Gli1 and Gli2 mRNAs (Fig. 5A) and proteins (Fig. 5B), and inhibited mRNA/protein expression of sFRP1 (Fig. 5A) and Ptc (Fig. 5B), two other Gli-regulated genes. Inhibiting Hh MCE公司 signaling also reduced mRNA or protein expression of various progenitor markers, such as AFP, Fn14, and keratin (K)19 after PH (Fig. 5C), and prevented cells that expressed AE1/AE3 or muscle pyruvate kinase (Mpk) (other progenitor markers) from accumulating in the liver (Fig. 5D). In addition, it attenuated fibrogenic repair, as evidenced by decreased expression of α-SMA and collagen mRNAs, α-SMA protein, and picrosirius red staining (Fig. 5E). Cyclopamine inhibition of Hh-regulated responses was associated with significantly reduced survival after PH.

The archaeal genus, Methanobrevibacter, was enriched in enterotype 3, indicating

that the availability of hydrogen disposal pathways may be important in determining the composition of the enterotype. Evaluation of 98 individuals in North America indicated that long-term dietary practices were the most likely determinant of enterotype in each individual, with protein and animal fat correlating with Deforolimus nmr predominance of Bacteroides and Prevotella correlating with carbohydrate intake.[13] The infant gut is presumed to be sterile in utero and acquires microbes during the process of birth or immediately thereafter.[14-17] Transition from facultative anaerobes to strict anaerobes in neonates was originally thought to occur after the first week of life, but molecular studies suggest that the transition occurs very rapidly.[16, 17] In developing buy KPT-330 countries, microbial colonization of the gut appears to reach maximal levels almost immediately.[17] The relative abundance of the various constituents of the gut microbiota changes presumably in response to changing dietary patterns. Significant numbers of carbohydrate-fermenting bacteria, including Bacteroides-Prevotella and Clostridium coccoides-Eubacterium rectale (Clostridium cluster XIV) appear at the time of weaning.[17]

The microbiota continues to change during childhood and adolescence. Bifidobacterium genus is abundant in children and declines in abundance with age, Bacteroides genus increased through childhood and adolescence and became very abundant in adults, while E. rectale was most abundant in adolescents and declined in adults.[18] Although it is likely that diet is the primary driver of these changes in microbial community abundance, the secondary

influence of these changes on human metabolism is not understood, and their significance cannot be discounted. The gut microbiota derives its nutrition from several sources (Table 1). These include ingested dietary components (carbohydrates, proteins, and lipid) and host-derived MCE公司 components including shed epithelial cells and mucus. The gut microbiota uses these substrates to generate energy for cellular processes and for growth. During the process of utilizing these substrates, the microbiota produces several metabolites that influence human health and metabolism. Carbohydrate fermentation leads to the production of short-chain fatty acids (SCFA) that are utilized by the host.[19] Protein fermentation gives rise to phenolic metabolites that may exert deleterious effects in the host.[20] Both the intestine and the liver have the capacity to detoxify these metabolites.[21] The gut microbiota also synthesizes several molecules such as vitamin K and constituents of the vitamin B.[11, 22] Some of these may directly contribute to human nutrition through their absorption from the bowel. Vitamin B12 produced by the gut microbiota is unlikely to be available directly to the host.

To find more resources, please visit the American Migraine Foundation(http://kaywa.me/ir2eb) Acalabrutinib in vivo “
“Many patients with chronic headache report that their pain typically arises from the neck or, more specifically, the base of the skull. Often that pain arises on one side or the other and extends forward to involve the top of the head, the temple, the forehead, the eye or some combination thereof.

These are termed cervicogenic (ie, “born of the neck”) headaches. Residing in those areas of the skull base are the occipital nerves. Irritation/inflammation of those nerves may cause a specific type of “neuralgiform” pain: occipital neuralgia. More commonly, however, those nerves serve as major “on-ramps” to the “superhighway” upon which travel the pain Erlotinib chemical structure signals that produce migraine and other types of headache. If one can block traffic on these busy on-ramps, then it may be possible to halt the flow of pain signal on the superhighway and thus—at least temporarily—halt head pain. Such is the

logic of occipital nerve blocks (ONBs) for suppression of chronic headache. The blocks themselves are relatively simple to perform. Your physician will use a small needle to inject a solution into the area around the nerves; the composition of that solution differs according to physician experience and preference but most often contains a long-acting local anesthetic and a steroid anti-inflammatory drug. Insertion of the needle is not especially painful,

but infusion of the solution may cause temporary discomfort. Pain relief can occur with startling rapidity, frequently within 15 minutes of the block(s). For those who experience relief, the duration of the therapeutic response varies widely: a day or so up to weeks . . . even months. When the procedure is performed by an experienced healthcare provider, complications of ONBs are quite rare. Because these are sensory nerves, you may experience some temporary numbness over the regions supplied MCE by the nerves. Because the local anesthetic may diffuse into areas close to the lower brain stem and upper spinal cord, transient (hours at most) difficulty speaking or swallowing have been reported. And, as with all steroid therapy, caution should be taken to minimize the amount of steroid injected over any given period of time. Occipital nerve blocks are not for everyone, but for selected patients they can prove a more effective means of suppressing chronic headache than any oral medication. Frequently asked questions: 1 How long will it take? Typically no more than a minute or two; the procedure usually is performed in a regular examination room and does not require any preparation on the patient’s part. “
“The review articles by Chai NC et al[1, 2] comprehensively address obesity and headache, conditions associated with a substantial personal and societal impact.

In this article, we present data on a critical role of OATP1B transporters to liver physiology. Although we had recently shown the importance of OATP1B transporters to hepatic drug disposition using Slco1b2−/− mice,7 the role of this transporter R788 solubility dmso to liver-specific glucose and cholesterol metabolism through modulation of TR signaling pathways, particularly with its remarkable effect on hepatic GLUT2 expression, was completely unexpected. Indeed, we would have predicted that because several OATP transporters have been shown to be capable of mediating cellular uptake of THs,1 absence of a single

isoform would not affect hepatic physiology in such a way. However, the role of transport in TH activity is supported by findings in the central nervous system, where mutations in MCT-8 (SLC16A2) have been shown to result in mental retardation due to reduced neuronal TH entry.19, 20 It is remarkable that despite the multiplicity of transporters expressed in liver capable of TH transport, OATP1B transporters appear to have a dominant role in controlling hepatic hormone status both in mice and in humans. It should be noted that a recent buy Atezolizumab study by van der Deure et al.21 suggested that OATP1B1 can also transport TH metabolites such as iodothyronine

sulphates (T4S) and that T4S plasma levels are different in individuals harboring the SLCO1B1 c.521C>T polymorphism, but the SNP was not associated with statistically significant changes to parent TH levels. However, their data show that the level

of fT4 at least in healthy volunteers appeared slightly higher in individuals harboring the polymorphism (521CC versus 521CT/TT, 14.8 ± 0.2 versus 15.6 ± 0.3; P = 0.06). In accordance with those medchemexpress findings, we show that absence of Oatp1b2 manifests as altered hepatocellular response to THs, whereas plasma levels of fT3 and TSH are unchanged and the levels of fT4 are slightly but significantly higher in knockout mice. Biological activity of THs is partly controlled by conversion of circulating T4 to the more active T3 catalyzed by intracellular iodothyronine 5′-deiodinases. In nonhepatic tissues 5′-deiodinase type 2 (DIO2), catalyzes the conversion of T4 to T3 and therefore controls the cellular activity, whereas DIO1 catalyzes the conversion of T4 to equimolar amounts of T3 and the biologically inactive reverse T3 and thereby modulates the plasma levels of T3.22-24 Linking Oatp1b2 to hepatic TH function was clearly supported by our observation that expression of the widely studied and well-defined TR target gene, Dio1, a sensitive marker of hepatic TH status,25, 26 was markedly reduced in livers of Slco1b2−/− mice. Biological activity of THs arises from activation of intracellular nuclear hormone receptors.27 TRβ is the predominant TR in the liver and is thought to mediate the cholesterol-lowering effects of TH therapy.

3 and >4.3 log IU/ml found in 26%, 48% and 26%, respectively. Prevalence of HBV variants was significantly

related to: sex (p=0.02), male were more likely to have BCP and BCP+PC; age (p=0.01), WT associated with younger patients; ethnicity (p<.001) WT and BCP found in Caucasians (51% and 49%), PC and BCP+PC found more frequently in black African (55% and 43%); HBV genotypes (p<.0001) WT and BCP found in genotype A (43% and 52%) while PC and BCP+PC found in D (32% and 36%) and E (50% and 41%) ; fibrosis stage (p<.0001) BCP, BCP+PC were associated with F>1 (52% and 50%) and WT and PC associated with F<1 (81% and 76%), HBsAg titers (p<.0001) WT associated with >4.3 log IU/ml (63%) while BCP, PC and BCP+PC associated with a titer <4.3logIU/ml (82%, 77%, 83%), HBV DNA levels (p<.0001) WT associated with a level >4.3 log IU/ml (73%) while PC associated with a level <3 .3log IU/ml (37%), In multivariate

analysis HBV variants were significantly click here and independently associated: WT with e(+) (p<.002) and high HBsAg titer (p<.01); BCP with more severe fibrosis (F >1) (p<.001); BCP+PC with more severe fibrosis (F >1)(p<.002), e(-) (p<.0001), genotypes D (p<.01) and E (p<.0001). Conclusions: PC and BCP+PC variants found more frequently in e(-) status. Patients with BCP and BCP+PC variants were more likely to have more severe fibrosis (F >1). We confirm a strong correlation between HBV variants and HBV genotypes independently from ethnicity and IL28B genotypes. Disclosures: Nathalie Boyer – Board Membership: MSD, find protocol JANSSEN; Speaking and Teaching: BMS Tarik Asselah – Consulting: BMS, Boehringer-Ingelheim, Roche, Merck-Schering Plough, Gilead, Janssen Patrick Marcellin

– Consulting: Roche, Gilead, BMS, Vertex, Novartis, Janssen-Tibotec, MSD, Boehringer, Pfizer, Abbott, Alios BioPharma; Grant/Research Support: Roche, Gilead, BMS, Novartis, Janssen-Tibotec, MSD, Alios BioPharma; Speaking and Teaching: MCE Roche, Gilead, BMS, Vertex, Novartis, Janssen-Tibotec, MSD, Abbott The following people have nothing to disclose: Michelle Martinot-Peignoux, Mar-tine Lapalus, Cédric Laouénan, Ana Carolina Cardoso, Roberto J. Carvalho-Filho, Ahmed El Ray, Simon Gosset Background and Aim: Replication of the hepatitis B virus (HBV) DNA genome proceeds via an RNA pregenome (HBV RNA), transcribed from cccDNA present in the nuclei of infected hepatocytes. Treatment of HBV infection with nucleos(t)ide analogues (NUC) suppresses HBV DNA synthesis by blocking reverse transcription, but does not affect HBV RNA synthesis. We hypothesized that during NUC therapy HBV pregenomes continue to be incorporated in viral particles and subsequently are secreted into the bloodstream. For this, we developed a sensitive assay to measure HBV RNA in plasma. Patients and Methods: HBV RNA (see below), HBV DNA (COBAS TaqMan – Roche), and HBsAg (Architect – Abbott) were measured in plasma of 10 chronic hepatitis B patients (5 HBeAg-positive and 5 negative) who received NUC therapy (7 entecavir and 3 tenofovir).

Thus, current evidence goes against a linear association of ALT with CVD events. Why GGT may be more strongly linked than ALT to vascular outcomes is not entirely clear. GGT levels may capture processes relevant to atherogenesis, but such observations are currently speculative and further studies are needed. Liver imaging is inevitably a more reliable method for diagnosing NAFLD than elevated liver enzymes; for example, the use of routine ultrasound has been reported to have a sensitivity of 89% and specificity of 93% for the identification of fatty liver.26 However, linkages of liver enzymes with incident events have been more carefully considered in recent meta-analyses as

discussed above. Data from five studies with imaging-diagnosed NAFLD are summarized in Table 2. The individual study end points are not uniform, and have been specified in the table. Two reports related to subjects with T2DM,27, 28 and both are based on the same cohort (the selleck products Valpolicella Heart Diabetes Study). The first

report was a nested case-control selleckchem study for incident CVD events over 5 years and reported an increased risk of events (odds ratio [OR] 1.53, 95% CI 1.1-1.7) after controlling for several risk factors, including the metabolic syndrome.27 The second report used the full cohort data, and the results were broadly similar.28 Of the three remaining imaging studies,29-31 only one had outcomes based on incident CVD events, including both fatal and nonfatal events for a population with NAFLD graded as simple steatosis.30 Among 1,221 participants, 231 had simple steatosis; the incidence of CVD was higher in these 231 subjects (11 CVD events) than in subjects without NAFLD (10 events). Multivariate analyses indicated that NAFLD was a predictor of CVD independent of conventional risk factors (OR 4.12, 95% CI 1.58-10.75, P = 0.004); however, with such small numbers, the CI was inevitably very broad. The last study prospectively followed up 7,372 patients discharged with a diagnosis of fatty liver, using the Danish Death Registry to obtain information on mortality data.29 Comparative general

population data were based on national CVD mortality rates for each sex in 5-year age groups and calendar periods under observation. The standardized mortality ratio (SMR) for CVD in those with fatty liver was 2.1 (95% CI 1.8-2.5). The latter study was limited in its ability MCE to consider the extent to which such excess risk was accounted for by established risk factors. Another study investigated the association of GGT with mortality, assessing whether accompanying ultrasound-determined liver steatosis strengthened the observed associations.31 The study followed subjects (including those with baseline CVD) for a mean of 7.2 years. The association of GGT levels alone with CVD mortality only became significant when comparing subjects with GGT levels in the highest quintile with those in the lowest quintile (HR 1.86, 95% CI 1.10-3.

Methods: To evaluate possibilities of modern ultrasound examination in patients with tumors of the esophagus using scanning polypositioning

from different approaches for exact diagnostics of local spread and effectiveness of the treatment. Results: Capabilities of ultrasound imaging of the esophagus throughout it were studied using the ultrasound machine of expert class Aplio MX Toshiba. The study was carried out from suprasternal and parasternal approaches in B-mode gray scale and color mapping to include the “cine-loop”. For optimal ultrasound imaging of the esophagus throughout its duration during the study there was developed an algorithm for consistency of application specific sensors and ultrasonic “windows.” In the cases specified in the diagnosis of tumors during PI3K inhibitor the study their size, structure and condition of the surrounding organs and tissues were estimated, as well as a calculated diameter of the esophageal wall thickness and the width of the lumen outside the affected area. On the proposed program ultrasonically 54 patients with verified diagnosis of esophageal cancer were examined. 42 (77.8%) men and 12 (22.2) women aged 53 to 76 years. Of these, 7 (13%) had ingurieswas of the esophagus, 41 (76%) patient-of the middle thoracic part and

6 (11%) patients had cancer of the lower third. By histological type, in most patients- 42 (77.8%)- a squamous cell carcinoma, was diagnosed,12 (22.2%) patients had adenocarcinoma. Patients http://www.selleckchem.com/products/bmn-673.html with tumors of the esophagus were divided into three groups. The first group consisted of 7 (13.0%) patients who were ambulatory monitoring with newly diagnosed disease. The second group consisted of 38 (70.4%) patients with

a diagnosis of esophageal cancer stage III-IV, who had severe comorbidities, contraindications to radical surgery and palliative therapy. The third group consisted MCE公司 of 9 (16%) patients who received chemo radiation therapy after previously accomplished a variety of surgical procedures. Distant metastases mainly in the liver and lungs were diagnosed in 22.2% of patients 1 and 2 groups. Satisfactory and good ultrasound imaging of tumors of the esophagus with the middle third was obtained 36 out of 41 (88%) patients, which provided important additional information on the nature of the tumor lesion. Conclusion: Ultrasound examination for cancer of the esophagus to evaluate the spread of tumors local of its wall and can be used at any stage of the examination of patients. Integrated ultrasound diagnosis in patients with cancer of the esophagus allows for a single study to visualize tumor size, the character of the structure, identify enlarged lymph nodes, and evaluate the state of the or pharynx and the abdominal cavity, which helps to clarify the stage of disease.

89-42.23, P < 0.001), whereas the rs8099917 genotypes played no role in achieving SVR with or without RVR. Conclusion: The rs8099917 TT genotype is significantly independently predictive of RVR, which is the single

best predictor of SVR, in Asian HCV-2 patients. (Hepatology 2011) Peginterferon/ribavirin combination therapy is recommended for patients with hepatitis C virus (HCV) infection. Among the pretreatment virological variables, the presence of a hepatitis C virus genotype 2 (HCV-2) or HCV-3 infection is the most powerful predictor of a sustained virological response (SVR).1 Patients infected with HCV-2/HCV-3 have significantly better virological responses after antiviral SAHA HDAC therapy in comparison with patients

infected with HCV-1/HCV-4. Although a rapid virological response (RVR) rate of 62% to 87% and an SVR rate of 80% to 93% can be achieved after 24 weeks of peginterferon/ribavirin combination therapy in patients with HCV-2/HCV-3 infection,2-7 up to 30% and 20% of patients still fail to attain RVR and SVR, respectively, with the current standard-of-care regimen.8-10 There clearly exists a genotype-specific difference in the viral kinetics.11 Beyond the virological elements, the diversity of host genetic factors among different races partially accounts for variations in treatment responses. Studies based on genome-wide association studies have shown that single nucleotide polymorphisms (SNPs) at and/or near the Akt inhibitor interleukin-28B (IL-28B) gene, which encodes interferon-λ, play a critical role in the treatment of HCV-1 infection.12-15 The linkage of the genetic variants to the on-treatment and posttreatment responses of HCV-2 patients has not been well investigated; there have been discordant results

regarding its role in treatment outcomes in recent studies using Caucasian populations.14, 16 In the current study, therefore, we aimed to elucidate the role of IL-28B polymorphisms in the treatment response with respect to viral kinetics in a large Chinese cohort residing in Taiwan with HCV-2 infection. medchemexpress ALT, alanine aminotransferase; AST, aspartate aminotransferase; CI, confidence interval; EOTVR, end-of-treatment virological response; EVR,early virological response; HCV, hepatitis C virus; HCV-#, hepatitis C virus genotype #; IL-28B, interleukin-28B; OR, odds ratio; PCR, polymerase chain reaction; RVR, rapid virological response; SD, standard deviation; SNP, single nucleotide polymorphism; SVR, sustained virological response. We retrospectively recruited 497 consecutive therapy-naive patients from Taiwan with chronic hepatitis C and HCV-2 infection who underwent the current standard-of-care regimens.8-10 Patients received peginterferon alfa-2a (180 μg/week) or peginterferon alfa-2b (1.5 μg/kg/week) subcutaneously and oral ribavirin according to body weight (<60 kg, 800 mg/day; 60-75 kg, 1000 mg/day; and >75 kg, 1200 mg/day).