The presence of esophageal and gastric varices was noted and classified according to the Japanese Research Society of Portal Hypertension

(7). During the procedure, 2 gastric biopsy specimens were taken from each patient. One biopsy specimen was taken from the antrum and one from the fundus for histopathological examination. Biopsy specimens were analyzed by the same histopathologist Abiraterone manufacturer during the study period. The gastritis was classified as either chronic active or nonactive. Nonactive gastritis was defined by the presence of mononuclear cell infiltration and active gastritis by the presence of neutrophils and/or erosions. H Pylori infection was reported on the histology. Children with Portal hypertension were subsequently

studied. The underlying liver disease, the duration of evolution of the disease, the medical treatment, the presence of systemic or gastrointestinal symptoms, and the indications for upper STI571 cost gastrointestinal endoscopy were recorded for those patients. The patients were divided into 2 groups. Group 1 included 190 patients with Portal hypertension without liver cirrhosis (i.e. Portal Cavernoma,Peri Portal fibrosis due to Schistomaisis and congenital hepatic fibrosis). Group 2 included 60 patients with liver disease progressing toward cirrhosis (infectious hepatitis, Idiopathic cirrhosis, Progressive Familiar Intra hepatic Cholestasis (PFIC), Wilson disease, or other metabolic liver diseases.) The x2 test was used to compare qualitative variables, and the Fisher exact test for comparison between small groups. P < 0.05 was considered significant. The study was approved by Al Nileen University Ethical committee. Results: Among 2000 patients enrolled during the study period, 250 (12.5%) received a diagnosis of Portal hypertension and were therefore included in the study. The median age of the patients at the time of endoscopy was 5 years 9 months (range, 5 months–15 years). The median time between the diagnosis of liver disease and endoscopy was 2 years 3 months (range, 2 months–8 years). Table

1 summarizes the clinical selleck chemicals characteristics of the patients. Portal Hypertensive Gastropathy was found in 150 of 250 patients (60%). Moderate PHG was found in 104 of 250 patients and severe PHG in 41 patients (31 of whom had liver cirrhosis). Esophageal varices were found in 135 of 250 patients (54%) (Grade I, n = 52; grade II, n = 62; and grade III, n = 21). The hemorrhagic aspect of the esophageal mucosa was observed in 21 patients. No patient had gastric varices (8). Gastritis was found in 145 of 250 (58%) patients (antrum, n = 70; fundus, n = 75). No glandular atrophy or intestinal metaplasia was seen in the patients in the study. In the group 2 patients (n = 60), PHG was found in 35 patients with Liver Cirrhosis associated with chronic gastritis (active, n = 25; nonactive, n = 20). Esophageal varices were found in 15 patients.

The presence of esophageal and gastric varices was noted and classified according to the Japanese Research Society of Portal Hypertension

(7). During the procedure, 2 gastric biopsy specimens were taken from each patient. One biopsy specimen was taken from the antrum and one from the fundus for histopathological examination. Biopsy specimens were analyzed by the same histopathologist find more during the study period. The gastritis was classified as either chronic active or nonactive. Nonactive gastritis was defined by the presence of mononuclear cell infiltration and active gastritis by the presence of neutrophils and/or erosions. H Pylori infection was reported on the histology. Children with Portal hypertension were subsequently

studied. The underlying liver disease, the duration of evolution of the disease, the medical treatment, the presence of systemic or gastrointestinal symptoms, and the indications for upper Selleckchem Ku-0059436 gastrointestinal endoscopy were recorded for those patients. The patients were divided into 2 groups. Group 1 included 190 patients with Portal hypertension without liver cirrhosis (i.e. Portal Cavernoma,Peri Portal fibrosis due to Schistomaisis and congenital hepatic fibrosis). Group 2 included 60 patients with liver disease progressing toward cirrhosis (infectious hepatitis, Idiopathic cirrhosis, Progressive Familiar Intra hepatic Cholestasis (PFIC), Wilson disease, or other metabolic liver diseases.) The x2 test was used to compare qualitative variables, and the Fisher exact test for comparison between small groups. P < 0.05 was considered significant. The study was approved by Al Nileen University Ethical committee. Results: Among 2000 patients enrolled during the study period, 250 (12.5%) received a diagnosis of Portal hypertension and were therefore included in the study. The median age of the patients at the time of endoscopy was 5 years 9 months (range, 5 months–15 years). The median time between the diagnosis of liver disease and endoscopy was 2 years 3 months (range, 2 months–8 years). Table

1 summarizes the clinical selleck chemicals characteristics of the patients. Portal Hypertensive Gastropathy was found in 150 of 250 patients (60%). Moderate PHG was found in 104 of 250 patients and severe PHG in 41 patients (31 of whom had liver cirrhosis). Esophageal varices were found in 135 of 250 patients (54%) (Grade I, n = 52; grade II, n = 62; and grade III, n = 21). The hemorrhagic aspect of the esophageal mucosa was observed in 21 patients. No patient had gastric varices (8). Gastritis was found in 145 of 250 (58%) patients (antrum, n = 70; fundus, n = 75). No glandular atrophy or intestinal metaplasia was seen in the patients in the study. In the group 2 patients (n = 60), PHG was found in 35 patients with Liver Cirrhosis associated with chronic gastritis (active, n = 25; nonactive, n = 20). Esophageal varices were found in 15 patients.

84,86 Hui et al.86 indicated that differences in FD symptoms correlated with psychological factors such as negative perception of major life events rather than with the number of stressful life events experienced. Chen et al.87 demonstrated that severity of stressful life events was positively correlated with disturbance of gastric myoelectric activity

in FD patients. Coping pattern is a psychological factor associated with FD symptoms.84,86,88 Several psychological studies have found that effective coping strategies play a role in mitigating anxiety, depression, and somatic problems.88,89 Cheng et al.89 designed flexible coping psychotherapy for enhancing coping flexibility of FD patients and check details demonstrated that the psychotherapy significantly changed FD symptom severity. Finally, familial factors may include psychological, environmental or genetic factors, which may contribute to abdominal symptoms of FD patients. Ahn et al.90 found that family function score was lower in an FD group than in a normal control group, and Ochi

et al.91 suggested that parental criticism experienced in early life may underlie Small molecule library in vitro the psychological background of FD patients and correlated with their abdominal symptoms. All of these results add support to the theory of psychosocial disturbances in the pathogenesis of FD. Statement 17. Gastric acid may be responsible for the symptoms in a subset of patients with functional dyspepsia. Grade of evidence: moderate. Level of agreement: a: 89.5%; b: 10.5%; c: 0%; d: 0%; e: 0%; f: 0%. Because anti-secretory

therapy is effective in some patients with FD,92,93 it is thought that gastric acid may play a role in the pathogenesis of FD. However, selleck inhibitor it has not been clearly demonstrated that excessive gastric acid is a pathogenetic factor in FD, and data on the amount of gastric acid secretion in patients with FD are lacking. Results of studies from Asian countries are controversial.94–96 Proton pump inhibitors (PPIs) are believed to be beneficial in a subset of patients with FD. This positive response is mainly confined to patients with ulcer-like and reflux-like dyspepsia.92 Patients with postprandial pain are reported to have a high prevalence of pathological acid exposure, which suggests that patients who respond to acid-suppressive therapy might have non-erosive reflux disease.97 Several studies have suggested a role for increased duodenal acid exposure or duodenal or gastric hypersensitivity to acid in the pathogenesis of symptoms in some patients with FD.76,98–100 These factors might explain the beneficial effects of acid-suppressive treatment for FD. However, the prevalence and pathogenetic role of these abnormalities in Asian patients with FD remains to be further explored. Statement 18. Helicobacter pylori may play a role in pathogenesis of functional dyspepsia. Grade of evidence: moderate. Level of agreement: a: 52.6%; b: 31.6%; c: 5.3%; d: 10.

16, 18, 23, 26-28 There are no satisfactory therapies for severe SOS; the best current results (46% complete response rate, defined as total serum bilirubin <2 mg/dL and resolution of multiorgan failure) are with intravenous defibrotide.35 Defibrotide, a mixture of porcine oligodeoxyribonucleotides, has

IWR-1 in vitro antithrombotic and profibrinolytic effects in vitro and in vivo. However, its mechanism of action in the treatment of SOS is not known. The complete recovery of some patients with severe SOS and multiorgan failure suggests that the drug has biologic effects in humans.35 Numerous other approaches to treatment of severe SOS have been reported (tissue plasminogen activator, intravenous N-acetylcysteine, human antithrombin III concentrate, activated protein C, prostaglandin E1, prednisone, topical nitrate, vitamin E plus glutamine, and use of a liver assist device), but none can be currently recommended. Transhepatic shunts have been placed in patients with SOS to reduce portal pressure and mobilize ascites, but neither serum bilirubin levels nor patient outcomes were improved. Patients with persistent ascites and normal serum bilirubin have undergone successful portosystemic shunts. Peritoneovenous

shunts for intractable ascites have been unsuccessful. Successful liver transplants for severe SOS have been reported but in most centers, patients at risk for recurrent malignancy are low-priority candidates for liver transplant. Prevention of sinusoidal BTK inhibitor injury is likely to be a more effective strategy for improving transplant outcomes selleck inhibitor than treatment. Prophylactic ursodeoxycholic acid reduces the frequency of cholestasis in general and GVHD-related cholestasis specifically and improves

outcomes, compared to placebo.2 Hyperbilirubinemia is common when patients are neutropenic and febrile and have gut mucosal injury from the conditioning regimen. Hepatocyte retention of conjugated bilirubin is mediated by endotoxins, interleukin-6, and tumor necrosis factor-α. Although this disorder is often referred to as “cholestasis of sepsis”, it occurs in patients with fever alone and in the presence of localized infection in the lungs and soft tissues. Acute GVHD (Fig. 2) develops in up to 70% of allograft patients, depending on the degree of HLA-match between donor and patient, the intensity of GVHD prophylaxis, and whether T cells are depleted from the donor inoculum. Prophylaxis with ursodiol has greatly decreased the frequency of jaundice after transplant and has altered the clinical phenotype of GVHD.2 In retrospect, what had been called hepatic GVHD is a mélange of three processes. The first process is jaundice developing in a patient with cutaneous and intestinal GVHD.

Specimens obtained using ESD were fixed with buffered formalin and stained with hematoxylin and eosin. Gastritis scores in non-neoplastic mucosa obtained from the same region of gastric neoplasm and being far enough from it were independently evaluated by two specialists (MI and TB) using the updated Sydney system [16]. Endoscopic evaluation of atrophic gastritis was determined according to the criteria of Kimura and Takemoto [17]. Pathologic

NVP-AUY922 cost diagnosis of each neoplasm was judged according to the criteria of the Japanese Classification of Gastric Carcinoma [18]. Fasting sera were collected and stored at −80 °C until use. Serum anti-H. pylori antibody titers (E-plate; Eiken, Japan), serum PG levels (LZ test; Eiken, Tokyo, Japan), and serum gastrin levels (Gastrin RIA Kit II; Dainabot, Tokyo, Japan) were evaluated [19]. If the antibody titer FK506 in vivo was >10 IU/L, the patients were considered H. pylori-positive. PG I ≤ 70 ng/mL and PG I/II≤3 were regarded as PG-positive, indicative of gastric mucosal atrophy [10]. We classified the patients into four groups, group A (Hp(−), PG(−)),group B (Hp(+), PG(−)), group C (Hp(+), PG(+)),

and group D (Hp(−), PG(+)), according to the ABC method, and investigated the patients in group A. We determined the presence of H. pylori infection using immunohistochemical staining with a polyclonal rabbit anti-H. pylori antibody (Dako, Tokyo, Japan) as previously described [20]. Sections of fixed tissues (4 μm) were deparaffinized and rehydrated. After heat-induced this website epitope retrieval (95 °C, 20 minutes) in citrate buffer (pH 6.0), endogenous peroxidase was quenched with 0.3% H2O2 in methanol for 10 minutes, followed by rinsing with phosphate-buffered

saline (PBS, pH 7.2). Non-specific binding was blocked with PBS containing 5% skim milk for 20 minutes. The sections were rinsed with PBS and incubated with primary antibodies overnight at 4 °C. We used the labeled streptavidin-biotin method (Dako, LSAB2 System-HRP, Japan), and diaminobenzidine-hydrogen peroxidase was used for color development. The tissues were finally counterstained lightly with hematoxylin. Statistical analyses for comparing categorical data were performed using the χ2-test and Fisher’s exact test, and the Wilcoxon rank sum test was used for numerical data, as appropriate. The cumulative incidence rate of metachronous gastric tumors was evaluated using Kaplan–Meier analysis. We used multivariate logistic regression for discriminant function. A p value of <.05 was considered significant. The JMP statistical software (SAS Institute Inc., Cary, NC, USA) was used for all calculations. We evaluated the serum markers (anti-H. pylori antibody and PGs) and classified patients into four groups (A, B, C, and D) as previously described [21]. Of 271 patients, 30 (11.1%) were classified into group A, and 71, 153, and 17 were classified into group B, group C, and group D, respectively (Table 1).

Furthermore, GpIb and VWF are also necessary for platelet-to-platelet cohesion [2]. Aggregation of platelets within the growing haemostatic plug is promoted by the interaction with a second receptor on platelets, the GpIIb/IIIa (or integrin αIIbβ3) which after activation binds to VWF and fibrinogen, recruiting more platelets into a stable plug. Both these binding activities of VWF are the highest in the largest VWF multimers. Second, VWF is a specific carrier of factor VIII (FVIII) in plasma. VWF protects FVIII from proteolytic degradation, prolonging its half-life in circulation and efficiently

selleck chemicals localizing it at the site of vascular injury. Each monomer of VWF has one binding domain, located in the first 272 amino acids of the mature subunit (D’–D3 domain) able to bind one FVIII molecule. These functions are explored by an array of laboratory ICG-001 assays, but no one reflects the whole spectrum of VWF activities. The deficiency or abnormal function of VWF causes von Willebrand’s disease (VWD), the most frequent inherited bleeding disorder [3]. VWD is heterogeneous because molecular defects can occur in more than one of the functional domains of the multimeric glycoprotein. As a consequence VWD is classified in three different types: partial quantitative deficiency (type 1), qualitative deficiency (type 2) and complete quantitative deficiency (type 3). Tests for the

correct diagnosis of VWD ideally have to explore the most important VWF properties: the antigenic level of VWF (VWF:Ag); the VWF–platelet GpIb interaction (VWF:RCo); the VWF–subendothelium–collagen interaction (VWF:CB); the VWF–FVIII interaction (VWF:FVIIIB) and the capacity of VWF to be organized into multimers.

Factor VIII procoagulant activity (FVIII:C) is also included in the diagnostic work-up, because it reflects the ability of VWF to protect it from degradation and is a useful complement in suspecting type 2N variants (see below). Table 1 summarizes the functional test for VWD diagnosis. With find more these tests, a useful classification in VWD types can be reached. The VWF:RCo explores the interaction of VWF with the platelet GpIb/IX/V complex and is still the standard method for measuring VWF activity. Abnormal VWF:RCo/VWF:Ag ratio (<0.6) usually indicates the presence of qualitative variants (type 2 VWD). Both aggregometric and turbidimetric methods appear useful. The aggregometric test however may be difficult to standardize and presents a low sensitivity at very low VWF concentrations (usually <10 U dL−1). Furthermore, careful calibration and standardization are essential [4]. In the recent years, the sensitivity of VWF:RCo has been significantly improved by using ELISA assays with recombinant GpIb [5,6]. The improved sensitivity of the ELISA VWF:RCo assay should enhance the reliability of the ratio determination, which however is difficult to obtain at very low VWF:Ag concentration.

Furthermore, GpIb and VWF are also necessary for platelet-to-platelet cohesion [2]. Aggregation of platelets within the growing haemostatic plug is promoted by the interaction with a second receptor on platelets, the GpIIb/IIIa (or integrin αIIbβ3) which after activation binds to VWF and fibrinogen, recruiting more platelets into a stable plug. Both these binding activities of VWF are the highest in the largest VWF multimers. Second, VWF is a specific carrier of factor VIII (FVIII) in plasma. VWF protects FVIII from proteolytic degradation, prolonging its half-life in circulation and efficiently

STA-9090 nmr localizing it at the site of vascular injury. Each monomer of VWF has one binding domain, located in the first 272 amino acids of the mature subunit (D’–D3 domain) able to bind one FVIII molecule. These functions are explored by an array of laboratory Selleck Temsirolimus assays, but no one reflects the whole spectrum of VWF activities. The deficiency or abnormal function of VWF causes von Willebrand’s disease (VWD), the most frequent inherited bleeding disorder [3]. VWD is heterogeneous because molecular defects can occur in more than one of the functional domains of the multimeric glycoprotein. As a consequence VWD is classified in three different types: partial quantitative deficiency (type 1), qualitative deficiency (type 2) and complete quantitative deficiency (type 3). Tests for the

correct diagnosis of VWD ideally have to explore the most important VWF properties: the antigenic level of VWF (VWF:Ag); the VWF–platelet GpIb interaction (VWF:RCo); the VWF–subendothelium–collagen interaction (VWF:CB); the VWF–FVIII interaction (VWF:FVIIIB) and the capacity of VWF to be organized into multimers.

Factor VIII procoagulant activity (FVIII:C) is also included in the diagnostic work-up, because it reflects the ability of VWF to protect it from degradation and is a useful complement in suspecting type 2N variants (see below). Table 1 summarizes the functional test for VWD diagnosis. With see more these tests, a useful classification in VWD types can be reached. The VWF:RCo explores the interaction of VWF with the platelet GpIb/IX/V complex and is still the standard method for measuring VWF activity. Abnormal VWF:RCo/VWF:Ag ratio (<0.6) usually indicates the presence of qualitative variants (type 2 VWD). Both aggregometric and turbidimetric methods appear useful. The aggregometric test however may be difficult to standardize and presents a low sensitivity at very low VWF concentrations (usually <10 U dL−1). Furthermore, careful calibration and standardization are essential [4]. In the recent years, the sensitivity of VWF:RCo has been significantly improved by using ELISA assays with recombinant GpIb [5,6]. The improved sensitivity of the ELISA VWF:RCo assay should enhance the reliability of the ratio determination, which however is difficult to obtain at very low VWF:Ag concentration.

Finally, qHBsAg and qHBeAg were measured in stored samples, so a falsely low titer might have been seen because the natural Tanespimycin decay of viral proteins led to error in the titers. In conclusion, we report a

systematic analysis of 2 years of serial qHBsAg and qHBeAg data for patients treated with ETV. The baseline level of qHBsAg and the on-treatment decline of qHBeAg in HBeAg(+) patients were proved to be highly useful in predicting VR and SR, respectively, and this lends support to the clinical utility of quantitative serological markers. In addition, these inexpensive and simple assays provide insight into the dynamic nature of

the association between qHBsAg, qHBeAg, and HBV DNA in patients receiving antiviral therapy; further studies are warranted to validate and explore their potential role. “
“Aim:  Dietary habits NU7441 solubility dmso are involved in the development of chronic inflammation; however, the impact of dietary profiles of hepatitis C virus carriers with persistently normal alanine transaminase levels (HCV-PNALT) remains unclear. The decision-tree algorithm is a data-mining statistical technique, which uncovers meaningful profiles of factors from a data collection. We aimed to investigate dietary profiles associated with HCV-PNALT using a decision-tree algorithm. Methods:  Twenty-seven HCV-PNALT and 41 patients with chronic hepatitis C were enrolled in this study. Dietary habit was assessed using a validated semiquantitative food frequency questionnaire. A decision-tree algorithm was created by dietary variables, and was selleckchem evaluated by area under the receiver operating characteristic curve analysis (AUROC). Results:  In multivariate

analysis, fish to meat ratio, dairy product and cooking oils were identified as independent variables associated with HCV-PNALT. The decision-tree algorithm was created with two variables: a fish to meat ratio and cooking oils/ideal bodyweight. When subjects showed a fish to meat ratio of 1.24 or more, 68.8% of the subjects were HCV-PNALT. On the other hand, 11.5% of the subjects were HCV-PNALT when subjects showed a fish to meat ratio of less than 1.24 and cooking oil/ideal bodyweight of less than 0.23 g/kg. The difference in the proportion of HCV-PNALT between these groups are significant (odds ratio 16.87, 95% CI 3.40–83.67, P = 0.0005). Fivefold cross-validation of the decision-tree algorithm showed an AUROC of 0.6947 (95% CI 0.5656–0.8238, P = 0.0067). Conclusion:  The decision-tree algorithm disclosed that fish to meat ratio and cooking oil/ideal bodyweight were associated with HCV-PNALT.

Finally, qHBsAg and qHBeAg were measured in stored samples, so a falsely low titer might have been seen because the natural Talazoparib decay of viral proteins led to error in the titers. In conclusion, we report a

systematic analysis of 2 years of serial qHBsAg and qHBeAg data for patients treated with ETV. The baseline level of qHBsAg and the on-treatment decline of qHBeAg in HBeAg(+) patients were proved to be highly useful in predicting VR and SR, respectively, and this lends support to the clinical utility of quantitative serological markers. In addition, these inexpensive and simple assays provide insight into the dynamic nature of

the association between qHBsAg, qHBeAg, and HBV DNA in patients receiving antiviral therapy; further studies are warranted to validate and explore their potential role. “
“Aim:  Dietary habits RAD001 purchase are involved in the development of chronic inflammation; however, the impact of dietary profiles of hepatitis C virus carriers with persistently normal alanine transaminase levels (HCV-PNALT) remains unclear. The decision-tree algorithm is a data-mining statistical technique, which uncovers meaningful profiles of factors from a data collection. We aimed to investigate dietary profiles associated with HCV-PNALT using a decision-tree algorithm. Methods:  Twenty-seven HCV-PNALT and 41 patients with chronic hepatitis C were enrolled in this study. Dietary habit was assessed using a validated semiquantitative food frequency questionnaire. A decision-tree algorithm was created by dietary variables, and was check details evaluated by area under the receiver operating characteristic curve analysis (AUROC). Results:  In multivariate

analysis, fish to meat ratio, dairy product and cooking oils were identified as independent variables associated with HCV-PNALT. The decision-tree algorithm was created with two variables: a fish to meat ratio and cooking oils/ideal bodyweight. When subjects showed a fish to meat ratio of 1.24 or more, 68.8% of the subjects were HCV-PNALT. On the other hand, 11.5% of the subjects were HCV-PNALT when subjects showed a fish to meat ratio of less than 1.24 and cooking oil/ideal bodyweight of less than 0.23 g/kg. The difference in the proportion of HCV-PNALT between these groups are significant (odds ratio 16.87, 95% CI 3.40–83.67, P = 0.0005). Fivefold cross-validation of the decision-tree algorithm showed an AUROC of 0.6947 (95% CI 0.5656–0.8238, P = 0.0067). Conclusion:  The decision-tree algorithm disclosed that fish to meat ratio and cooking oil/ideal bodyweight were associated with HCV-PNALT.

Finally, qHBsAg and qHBeAg were measured in stored samples, so a falsely low titer might have been seen because the natural Atezolizumab order decay of viral proteins led to error in the titers. In conclusion, we report a

systematic analysis of 2 years of serial qHBsAg and qHBeAg data for patients treated with ETV. The baseline level of qHBsAg and the on-treatment decline of qHBeAg in HBeAg(+) patients were proved to be highly useful in predicting VR and SR, respectively, and this lends support to the clinical utility of quantitative serological markers. In addition, these inexpensive and simple assays provide insight into the dynamic nature of

the association between qHBsAg, qHBeAg, and HBV DNA in patients receiving antiviral therapy; further studies are warranted to validate and explore their potential role. “
“Aim:  Dietary habits MAPK Inhibitor Library cell line are involved in the development of chronic inflammation; however, the impact of dietary profiles of hepatitis C virus carriers with persistently normal alanine transaminase levels (HCV-PNALT) remains unclear. The decision-tree algorithm is a data-mining statistical technique, which uncovers meaningful profiles of factors from a data collection. We aimed to investigate dietary profiles associated with HCV-PNALT using a decision-tree algorithm. Methods:  Twenty-seven HCV-PNALT and 41 patients with chronic hepatitis C were enrolled in this study. Dietary habit was assessed using a validated semiquantitative food frequency questionnaire. A decision-tree algorithm was created by dietary variables, and was selleck screening library evaluated by area under the receiver operating characteristic curve analysis (AUROC). Results:  In multivariate

analysis, fish to meat ratio, dairy product and cooking oils were identified as independent variables associated with HCV-PNALT. The decision-tree algorithm was created with two variables: a fish to meat ratio and cooking oils/ideal bodyweight. When subjects showed a fish to meat ratio of 1.24 or more, 68.8% of the subjects were HCV-PNALT. On the other hand, 11.5% of the subjects were HCV-PNALT when subjects showed a fish to meat ratio of less than 1.24 and cooking oil/ideal bodyweight of less than 0.23 g/kg. The difference in the proportion of HCV-PNALT between these groups are significant (odds ratio 16.87, 95% CI 3.40–83.67, P = 0.0005). Fivefold cross-validation of the decision-tree algorithm showed an AUROC of 0.6947 (95% CI 0.5656–0.8238, P = 0.0067). Conclusion:  The decision-tree algorithm disclosed that fish to meat ratio and cooking oil/ideal bodyweight were associated with HCV-PNALT.