Six months after the treatment, a follow-up ultrasound examination showed nearly complete resolution of the cyst. This case illustrates the effectiveness of the PAIR procedure as a nonsurgical alternative for the management of hydatid cysts and emphasizes the importance of considering the extent and type of the hydatid lesion when the choice is being made between surgical and nonsurgical approaches. The authors thank Jon E. Rosenblatt, M.D. (Division of Clinical Microbiology, Mayo Clinic, Rochester, MN), for providing the microbiology HM781-36B molecular weight images and James C. Andrews, M.D. (Division of Vascular and Interventional

Radiology, Mayo Clinic, Rochester, MN), for reviewing the manuscript. “
“We report a case of gastric anisakiasis presenting as a submucosal tumour that was completely resected by endoscopic submucosal dissection. A 55-year-old woman without an obvious history of raw-fish consumption or severe abdominal pain was referred to our hospital for a comprehensive examination of a gastric submucosal tumour detected by barium gastrography. Dabrafenib clinical trial Gastroscopy revealed a 2 cm diameter

submucosal tumour at the greater curvature of the gastric mid-body (Figure 1A). Endoscopic ultrasound (EUS) revealed a heterogeneous hypoechoic mass with a hyperechoic core (Figure 1B). The lesion occupied the submucosa and muscularis propria. The possibility of a malignant tumour could not be excluded, because the

tumour was newly identified and showed a heterogeneous pattern on the EUS images. ESD was performed after obtaining the patient’s informed consent 3 months after the initial gastroscopy. Submucosal dissection during ESD was difficult because of severe fibrosis. The submucosal tumour was completely resected but complicated by a tiny perforation, which was managed by application of endoclips. Pathological examination of the lesion revealed a granulomatous lesion with prominent eosinophilic infiltration and a lumen-like click here structure consistent with the characteristics of gastric anisakiasis (Figure 2A,2B). Contributed by “
“We have read with great interest the study by Solà et al.1 Two years ago, our group showed that terlipressin has an affinity to V2 receptors.2 Resultant hyponatremia has been suggested,2-4 and it is now supported by this large, retrospective clinical study with a relevant control group. The observed hyponatremia is likely a result of both V1a and V2 receptor activation. Terlipressin induces natriuresis via V1a receptor stimulation.5 The combination with V2 receptor–induced antidiuresis due to an increased abundance of aquaporin 2 in the renal collecting duct is likely responsible for the observed hyponatremia.

Results: We achieved SBDC under the conventional method in 200 out of 281 patients (71.2%). Among patients who underwent the conventional and guide-wire method, we achieved http://www.selleckchem.com/products/Neratinib(HKI-272).html SBDC in 264 out of 281 patients

(94.0%). Eleven out of 65 patients (16.9%), who moved on to the guide-wire method, developed PPP, though, moving on to the guide-wire method was the risk factor for PPP in multivariate analysis [Odd's ratio;4.14, p = 0.005]. Among patients who underwent the guide-wire method, PPP occurred only in the PGC group (PGC vs WGC; 11/49 (22.4%) vs 0/12 (0%), p = 0.101). It was supposed that PGC would contribute to PPP. The final cumulative rate of SBDC and PPP were 98.2% (276/281) AZD6244 concentration and 7.5% (21/281), respectively. Conclusion: In patients with naïve choledocholithiasis and difficult cannulation under conventional method, using the guide-wire method was effective for SBDC. However, moving on to the guide-wire method itself, especially PGC, was the risk factor for PPP. Key

Word(s): 1. bile duct cannulation; 2. choledocholithiasis; 3. post-ERCP pancreatitis Presenting Author: CHOL KYOON CHO Additional Authors: CHOONG YOUNG KIM, HEE JOON KIM, HYUN JONG KIM, JIN SHICK SEOUNG Corresponding Author: CHOL KYOON CHO Affiliations: Chonnam National University Medical School, Chonnam National University Medical School, Chonnam National University Medical School, Chonnam National University Medical School Objective: Gallbladder tuberculosis is an extremely rare disease. It can mimic other gallbladder disease, because accurate preoperative diagnosis is difficult and diagnosis is made by histopathologic examination after cholecystectomy Methods: A 54 year old man was visited our hospital

presenting abdominal discomfort. He had medical history of hypertension and diabetes mellitus. He was treated with endoscopic retrograde cholangiopancreatogram for common bile duct stone removal by 6 months ago. learn more He was afebrile, there were tenderness in right upper quadrant area and no Murphy’s sign on physical examination. In laboratory findings, complete blood count showed only leukocytosis and other blood chemistries and viral serologic markers were normal. Serum CA 19-9 was elevated.(115.2 U/ml) Abdominal computed tomography(CT) revealed diffuse wall thickening of gallbladder and several gallstones. Based on these findings, preoperative diagnosis was thought be xanthogranulomatous cholecystitis or gallbladder cancer. Results: In operative findings, sever adhesion between gallbladder, omentum, common bile duct, and transverse colon was observed and gallbladder was thickened, distended and inflamed. We performed cholecystectomy and transverse colon segmental resection, because there were cholecysto-colonic fistula.

This review discusses these emerging new paradigms of INH-induced DILI and highlights recent insights into the mechanisms, as well as points to the existing large gaps in our understanding of the pathogenesis. Isoniazid (INH) remains a widely used and effective first-line agent for the treatment of tuberculosis, although newer drugs are being developed to face the challenge of emerging multidrug-resistant strains of Mycobacterium

tuberculosis.[1] Mitomycin C research buy Acute tuberculosis is mostly treated with a multidrug therapy approach (including rifampicin or pyrazinamide), but INH monotherapy is typically used in the treatment of latent tuberculosis. Shortly after its introduction to the market in 1952, INH was recognized to be associated with Talazoparib in vitro rare cases of liver injury, and the drug received a black box warning as early as 1969. The exact incidence of INH-induced liver injury is difficult to estimate retrospectively, mainly due to notorious underreporting and the contribution of comedications to these adverse effects.

However, recent comprehensive prospective studies that included patients from different countries have revealed that the incidence of serious INH-induced liver injury is well in the previously published range of 1–3% of treated (exposed) patients.[2-4] Thus, these numbers place INH among the top-ranking drugs regarding their potential to cause drug-induced liver injury (DILI), although the absolute numbers of INH-related DILI cases are smaller

than those of other drugs that are given to much larger patient populations. Despite extensive research over several decades, the underlying mechanisms of INH-induced DILI have remained poorly understood. One of the reasons is the complexity of these mechanisms and the difficulty to distinguish between drug-related mechanisms (that determine the hazard) and patient-related see more mechanisms (that determine the actual risk) (Fig. 1a). Traditionally, the drug-specific mechanisms (determined by the chemotype) have included the generation of reactive metabolites leading to hepatocellular injury, while the patient-specific determinants of susceptibility have long been considered to be genetic polymorphisms and other mutations in genes coding for some of the drug-metabolizing enzymes involved in the bioactivation and detoxication pathways of INH. However, recent analyses on mechanisms and risk factors associated with INH hepatotoxicity have revealed that there are still important gaps in our understanding of its pathogenesis;[5-7] therefore, these classical paradigms need to be revisited. For example, novel experimental data suggest that there may be previously unrecognized mechanisms, including INH-induced activation of the adaptive and innate immune system, disruption of endogenous metabolism, and mitochondrial dysfunction that may be implicated in INH hepatotoxicity.

Las is transmitted by the Asian citrus psyllid (ACP) Diaphorina citri (Hemiptera: Psyllidae) in a persistent manner, but its interactions with the psyllid vector, particularly at the organ and cellular levels, are poorly understood. We have tested several fluorescence in situ hybridization

(FISH) protocols and three nucleic acid probes for the localization of Las in haemolymph smears and dissected organs of ACP adults that fed on Las-infected plants in the field or laboratory and in sections from Las-infected citrus leaves. Las was detected by FISH and confocal laser scanning microscopy in the filter chamber, midgut, Malpighian tubules, haemolymph, salivary glands, Opaganib clinical trial ovaries and in muscle and fat tissues of ACP that acquired Las from infected plants, as well as in the phloem of infected citrus leaves. Las appeared

as pleiomorphic bodies or short thin rods that were much more dispersed and individually distinct in citrus leaf phloem and in ACP haemolymph, but more densely aggregated in cells of the salivary glands and other ACP organs and tissues. Our results provide the first in situ demonstration of Las infection in various psyllid organs and tissues and show the near-systemic infection of ACP by Las. “
“A total of 241 isolates of Phytophthora infestans were collected in 1997, 2006 and 2007 in eight European countries and characterized with molecular markers (simple sequence repeats, SSR genotypes) and phenotypic traits selleck inhibitor such as sensitivity to fungicides, mating type and aggressiveness. The mating type distribution changed from mainly A1 in 1997 to a majority of A2 in 2007. No resistant isolates were detected for

fluazinam and mandipropamid, whereas the proportion selleck compound of isolates resistant to mefenoxam (MFX) was high and increased over the years. There was no genetic link between mating type and MFX resistance. Aggressiveness (product between lesion expansion and sporulation capacity) was slightly higher for MFX-resistant compared to sensitive isolates and for isolates collected later compared to earlier in the same season. It was about equally high for A1 and A2 types, and for French isolates in 1997 and British isolates in 2007, but lower for French isolates in 2007. Six different SSR genotype families were distinguished. In 1997, populations were dominated by genotype families I and III/IV, which significantly declined in 2007 being largely displaced by genotype families II (‘blue 13’ type) and V, which are by coincidence mainly A2 MFX resistant and A1 MFX sensitive, respectively. However, mating type and MFX resistance were genetically not linked to SSR genotypes. “
“The application of silicon (Si) reduces the intensity of diseases in several economically important crops.

However, one patient of a family was classified into the cluster different from her family, suggesting that E-PAS detected the sample distinct from that of her family on the transmission

route. Conclusions:  The E-PAS to output phylogenetic tree was developed since requisite material was sequence data only. E-PAS could expand to determine HBV genotypes as well as transmission routes. “
“Background and Aim:  There are insufficient data on renal safety during long-term adefovir dipivoxil (ADV) treatment. We aimed to elucidate the incidence and risk factors of renal impairment in chronic hepatitis B (CHB) patients treated Vemurafenib molecular weight with ADV. Methods:  We retrospectively enrolled 687 CHB patients (51.4% with compensated cirrhosis) treated with ADV alone (18.2%) or in combination with lamivudine (81.8%) for more than 12 months. Renal

function was measured using the estimated glomerular filtration rate (eGFR), and renal dysfunction was defined as mild (20–30% decrease), moderate (30–50%), or severe (more than 50%). Results:  During the median treatment duration CP-868596 chemical structure of 27 months, 72 patients (10.5%) developed renal impairment, which was mild in 77.8% of cases, moderate in 20.8% of cases, and severe in one patient. The cumulative incidence of renal impairment at 1, 3, and 5 years was 2.6%, 14.8%, and 34.7%, respectively. Modification of the dosing interval or discontinuation of ADV was required in seven and three patients, respectively, and none of them showed a further decline in the eGFR. Although a univariate analysis revealed age, the number of exposure to radio-contrast dye, liver cirrhosis, and hepatocellular carcinoma as risk factors selleckchem of renal impairment, age was the only significant risk factor identified in the multivariate analysis (odds ratio = 1.048, 95% confidence interval = 1.019–1.076, P = 0.001). Conclusions:  Renal impairment in long-term ADV users was relatively frequent, but serious renal toxicity was rare, and

all cases were safely managed. Careful monitoring of renal function is required, especially in older patients. “
“Early detection and differentiation of malignant from benign pancreatic tumors is very essential as mass-forming pancreatitis is a frequently encountered problem. Positron emission tomography (PET) has a role in establishing the diagnosis of pancreatic carcinoma when the conventional imaging modalities or biopsies are nondiagnostic. In this prospective study, the utility of fluorodeoxyglucose (FDG)-PET/computed tomography (CT) in the characterization of mass-forming lesions of the pancreas was reported. 18F-FDG-PET/CT was prospectively performed in 87 patients diagnosed to have periampullary or pancreatic mass. Lesions with focally increased FDG uptake in PET/CT were considered malignant, whereas those with diffuse or no FDG uptake were considered benign. Semiquantitative analysis with maximum standardized uptake value (SUVmax) was also calculated.

showing bile acid–dependent liver growth and regeneration.18 Serum ALT and AST levels were higher in both cholic acid–fed groups, but not different between WT and KO mice (data not shown).

However, serum total bile acid levels in cholic acid–fed KO mice were approximately five-fold higher and hepatic bile acid levels three-fold higher than in WT mice, suggesting defective ability to regulate serum and liver bile acid levels (Fig. 6C,D). Expression of the sinusoidal bile acid uptake transporters Ntcp, Slco1a1, and Slco1b2 were lower in both cholic acid–fed groups (Fig. 7A). Expression of the latter two genes was also lower in chow-fed KO mice. Expression of the basolateral efflux transporters Abcc3 (Mrp3) and Abcc4 (Mrp4) was not different, PCI32765 although there was a trend toward higher buy KU-60019 Abcc4 levels in KO mice. Among the canalicular transporters, expression of Bsep (Abcb11) was lower in cholic acid–fed KO mice, whereas Abcb4 (Mdr2) was up-regulated in both cholic acid–fed

groups (Fig. 7B). Expression levels of other sinusoidal transporters were similar between the cholic acid–fed groups. Of the bile acid regulatory genes, expression of farnesoid X receptor (FXR) was lower in both cholic acid–fed groups. However, Shp-1 expression, a downstream target of FXR, was up-regulated in both WT and KO mice on a cholic acid diet (Fig. 7C). Fgf4r levels were similar in all four groups. Expression of constitutive androstane receptor (CAR) was lower in both cholic acid–fed groups and in chow-fed KO mice. However, despite lower expression levels of CAR, KO mice had higher expression of the downstream target of CAR, Cyp2b10. This result suggests that activation of CAR, possibly by a post-transcriptional mechanism, occurs in KO mice and may represent

a find more protective mechanism to down-regulate bile acid biosynthetic genes. PPARα expression was higher in both cholic acid groups whereas pregnane X receptor expression was lower in cholic acid–fed KO mice. After H&E staining, histology samples from WT mice showed mildly increased lobular inflammation on cholic acid diet (Fig. 8). On the other hand, cholic acid–fed KO mice had increased ductular reaction and greater lobular inflammation on cholic acid diet along with increased pericellular fibrosis on reticulin staining. Staining for F-actin showed that WT mice on cholic acid diet had dilated bile canaliculi, likely reflecting the choleretic effect of bile acids (Fig. 8, bottom panel). However, the interconnected lattice-like structure of canaliculi was preserved in WT livers on cholic acid diet. On the other hand, KO mice on cholic acid diet had canaliculi that were not only dilated but also tortuous and distorted (Fig. 8P). Formation and excretion of bile is one of the important functions of the liver. This task is achieved by the coordinated action of multiple proteins and cellular organelles.

The final two primary alliances that formed were very unusual since they were all speckled males (alliances 6 and 8). In both pooled periods the mixed sex mean CoA was less than the community average (and close to the

female-female mean CoA) and associations involved every age class combination. In prehurricane years all but three Selleck Roxadustat males and four females had strong mixed sex associations, whereas in posthurricane years only 15 of 23 males and 14 of 24 females had strong mixed sex associations. All other data were similar for both data sets and is presented together. The vast majority of associations were within social clusters, the few that were cross cluster involved Central males with Northern and Southern females. The highest

CoAs were between mothers and speckled offspring, and one association of an uncle and niece (known through documented multigenerational maternal-offspring relationships). The majority of first order alliances did not have equally strong CoAs with females, indicating they were not always together when with females. In some of the alliances, only CFTR activator one male had strong associations with females. The majority of the females involved in strong mixed sex associations were reproductively active (pregnant, with a calf, or both). Of those that were not involved in mixed sex strong associations, only five were of age to be reproductively active. Despite large changes in demography, the basic pattern of social structure characteristics of this community remained consistent with previous long-term analyses, including definitive social clusters (Elliser and Herzing 2012), sex preferences, and overall association patterns (Elliser and Herzing, in press). This is contrary to what has been described for other species, where demographic changes resulted in altered behavior and social structure/grouping (bottlenose dolphins: 上海皓元 Lusseau and Newman 2004; marmosets: Lazaro-Perea et al. 2000; chimpanzees: Lehmann and Boesch 2004;

killer whales: Matkin 2008; bottlenose dolphins: Elliser and Herzing 2011). However, some changes in spotted dolphin social structure were observed after the hurricanes. There was lower social differentiation, younger age of alliance formation and increased overall cohesion within clusters and across age class. This suggests that responses to demographic upheaval differ between populations and/or species, with varying degrees of change in social structure as they adapt to new conditions. One of the most striking results was that despite losing many individuals and an overall decrease in community size, the Northern, Central, and Southern clusters remained discrete (although the Central cluster appeared more closely connected with the Southern cluster prehurricane and then with the Northern cluster posthurricane) and group size remained the same, even though social differentiation within the clusters decreased.

Consecutive patients with compensated cirrhosis and without hepatocellular carcinoma (HCC) were prospectively

enrolled. Baseline LSM was assessed at enrollment, then at a 6-12-month interval. Esophagogastroduodenoscopy and ultrasonography were performed regularly for surveillance Midostaurin molecular weight of varices and HCC. Liver disease progression (LDP) was defined as portal hypertension (PHT) progression (development of varices, varices growth, variceal bleeding, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy), HCC occurrence and liver-related death. Hepatic decompensation was defined as variceal bleeding, ascites, spontaneous bacterial peritonitis, or hepatic encephalopathy. Clinical event included hepatic decompensation and SB203580 price HCC development. Two hundred and twenty patients were enrolled. In a median follow-up period of 36.9 months, LDP were detected in 49 patients including 30 PHT progression (10 variceal development, 11 variceal growth, 9 hepatic decompensation) and 19 HCC developments. The cumulative incidence of LDP, PHT progression and HCC development at 3 years was 20.7%, 12.8% and 9.1% respectively. Multivariate analyses showed baseline

LSM is an independent predictor of PHT progression (HR: 1.05, 95% Cl: 1.02-1.09) and LDP (HR: 1.04, 95% Cl: 1.01-1.07); however, not of HCC occurrence. Assessed with area under receiver operating characteristic curve, the performance of baseline LSM in predicting PHT progression and hepatic decompensation was 0.744 and 0.929 respectively. With 17 and 21.1 kilopascal as the cut-offs, the negative predictive value was 92% and 99% respectively. Patients with baseline LSM≥17kPa and 14kPa without serial changes had higher risk of MCE PHT progression

and LDP respectively. Conclusions: For patients with compensated hepatic cirrhosis, LSM was an independent predictor of PHT and LDP, but not of HCC occurrence. Baseline LSM was useful to exclude PHT progression and hepatic decompensation. Patients with baseline LSM≥17 kilopascal without serial change had higher risk of PHT progression. Disclosures: The following people have nothing to disclose: JIng-Houng Wang, Seng-Kee Chuah, Sheng-Nan Lu, Chao-Hung Hung, Chung-Mou Kuo, Wei-Chen Tai, ShueShian Chiou Background Gastroesophageal variceal hemorrhage is an important complication of cirrhosis. We investigated the in-hospital mortality and its risk factors after variceal hemorrhage in a large sample, using a nationwide Japanese database. Methods Data on the patients with variceal hemorrhage were collected for a total of 39 months from a nationwide administrative database covering approximately 1,000 hospitals. The risk factors for fatal outcome due to variceal hemorrhage was analyzed with receiver operating characteristics (ROC) curves and univariate and multivariate logistic regression. Comorbidities were assessed by using Charlson Comorbidity index.

0001), and both 2-APB and SKF96363, store-operated calcium channels (SOCs) inhibitors, completely inhibited ATP-induced [Ca2+]i increases after restoration PD0325901 price of extracellular Ca2+. ATP promoted the proliferation and migration of HCC cells and the growth of HCC in nude mice. Suramin, P2Y2R specific siRNA, and 2-APB inhibited ATP-induced HCC cell proliferation and migration and HCC growth (P < 0.05 and P < 0.01). Conclusion: P2Y2R was up-regulated in human HCC cells and mediated ATP-induced

human HCC cell proliferation and migration and HCC growth through SOCs-mediated Ca2+ signaling, suggesting that P2Y2R may play important role in the development and progression of inflammation-associated HCC and targeting P2Y2R may be a promising therapeutic strategy against human HCC. CT99021 purchase Key Word(s): 1. P2Y2 receptor; 2. HCC; 3. ATP; Presenting Author: HYE JIN KIM Additional Authors: BEOM YONG YOON, SE YOUNG PARK, SE WOONG HWANG, SUN HYUNG KANG, HEE SEOK MOON, JAE KYU SEONG, EAUM SEOK LEE, SEOK HYUN KIM, BYUNG SEOK LEE, HEON YOUNG LEE Corresponding Author: HYE JIN KIM Affiliations: Chungnam National University Objective: Transarterial chemoembolization (TACE) have been applied for treating hepatocellular carcinoma (HCC), but procedure-related complications can be a serious problem. Methods: Liver abscess is most common infectious complication

during post-TACE period. Results: We describe three cases of necrotizing liver abscess after TACE in hepatocellular carcinoma. First case, a 79-year-old man, with 2.6 cm sized HCC in S4, was treated by TACE for two times during 2 months. About 1 month after the last TACE, abdominal CT scan revealed a gas containing liver abscess. Antibiotics and percutaneous transhepatic drainage was performed. MCE Cholangiography via drainage catheter showed

findings of bile duct necrosis. The patient improved condition and removed the catheter. Second case, a 68-year-old man, with four HCC in S4, 5, 7, 8, was treated by TACE for three times during 2 years. Two new lesions was found in S6/7, was performed by TACE. About 2 days later the patient had a fever and abdominal pain. Abdominal CT scan reveal a necrotizing liver abscess and percutaneous transhepatic drainage was performed. Two month later, the abscess improved and catheter removed. Third case, a 75-year-old man was performed embolization due to HCC rupture. After 1 month, abdominal CT scan revealed necrotizing liver abscess. Antibiotics and percutaneous transhepatic drainage was performed. However, the abscess persisted despite of treatment for 5 months. Conclusion: Physicians should be alerted to necrotizing liver abscess after TACE in patient with variable clinical manifestations. Key Word(s): 1. TACE; 2. HCC; 3.

84; CI, 1.30-6.76; for BMI ≥27.5 kg/m2), presence of diabetes or IFG (OR, 4.45; CI, 1.10-30.00), and the PNPLA3 148M allele (OR, 1.62; CI, 1.00-7.00; per each 148M allele). The only independent predictors of advanced steatosis were higher

BMI (OR, 3.60; CI, 1.39-9.22;for BMI ≥27.5 kg/m2) and the 148M PNPLA3 allele (OR, 6.03; CI, 1.23-5.00; per each 148M MK-8669 in vivo allele). Similarly, higher BMI (OR, 2.38; CI, 1.22-4.82; for BMI ≥27.5 kg/m2) and the 148M PNPLA3 allele (OR, 1.70; CI, 1.07-2.74; per each 148M allele) were independently associated with NAS >2. Because the phenotypic expression of the I148M PNPLA3 polymorphism has been reported to be dependent on the presence of acquired cofactors triggering steatosis, including click here obesity and alcohol, we next evaluated whether the association of the 148M allele and severe steatosis was dependent on the presence of severe overweight (BMI, ≥27.5 kg/m2) and a positive history of alcohol intake. Either one of these acquired risk factors was present in 82 (35%) of patients, and this condition was associated with a higher prevalence of steatosis (60 of 82 [73%] versus 86 of 153 [56%]; P = 0.01) and severe steatosis (13 of 82 [16%] versus 11 of 153 [7%]; P = 0.04). The PNPLA3 148M allele was associated with a progressive increase in the prevalence of severe steatosis in patients with, but not in those without, acquired

上海皓元医药股份有限公司 cofactors, that is, severe overweight and regular consumption of any amount of alcohol (Fig. 1; P = 0.001 in patients with cofactors). Independent

predictors of advanced fibrosis at multivariate logistic regression analysis are presented in Table 4. Advanced fibrosis was associated with older age (OR, 4.17; CI, 2.21-8.13; for age >50 years), HBeAg positivity (OR, 2.53; CI, 1.16-5.72), but not with gender and viral load. Interestingly, advanced fibrosis was also independently associated with a positive history of any degree of alcohol consumption (OR, 2.09; CI, 1.02-4.32) and higher BMI (OR, 1.11; CI, 1.02-1.22; per g/m2), that is, two known risk factors for steatosis, whereas the association of advanced fibrosis with severe steatosis was not independent of these variables, although a nonsignificant trend was observed (OR, 2.56; CI, 0.98-7.60). Similarly, there was a trend for an independent association of NAS with advanced fibrosis, when this variable was introduced in the model in substitution of severe steatosis (OR, 1.15; CI, 0.98-1.35; P = 0.08). This is the first study demonstrating an association between the 148M PNPLA3 allele and an increased risk of both steatosis of any degree and severe steatosis in CHB patients. The association with severe steatosis was particularly evident in patients with comorbidities, such as increased body mass and abnormal alcohol intake.