Conclusions:  Silmitasertib There was no significant difference in delta polyp size between the examinees with gallbladder polyps and cholelithiasis and those with gallbladder polyps only. Hence, a small proportion of subjects with gallbladder polyps and cholelithiasis, such as those with thickened gallbladder walls and an interval increase in the size of the gallbladder polyps are candidates for prophylactic cholecytectomy. “
“Transient elastography (TE) is increasingly employed in clinical practice for the noninvasive detection of tissue fibrosis in patients with chronic liver disease (CLD), and particularly chronic hepatitis C virus (HCV)-related hepatitis. The present study was designed to provide

a definitive characterization of the “confounding” increase in liver stiffness (LS) following a standardized meal in a consecutive population of 125 patients with chronic HCV infection at different stages of fibrotic evolution. LS values were obtained after overnight fasting and 15, 30, 45, 60, and 120 minutes following the onset of a standardized liquid meal (400 mL, 600 Kcal, 16.7% protein, 53.8% carbohydrates, 29.5% fat). An evident increase in LS values was observed 15 to 45 minutes after the onset of the meal with return to baseline premeal

levels within 120 minutes in all patients. The peak postmeal delta increase in LS was progressively more marked with increasing stages of fibrosis (P < 0.001), becoming maximal in patients with cirrhosis. However, the probability of identifying the Metavir stage CHIR-99021 chemical structure of fibrosis, the Child-Pugh class, or the presence/absence of esophageal 上海皓元医药股份有限公司 varices with the postmeal delta increase in LS was inferior to that obtained with baseline LS values. Conclusion: The results of the present study provide definitive evidence of the confounding effect of a meal on the accuracy of LS measurements for the prediction of fibrosis stage in patients with chronic HCV hepatitis and suggest that a fasting period of 120 minutes should be observed before the performance of TE. (HEPATOLOGY 2013;) Transient elastography

(TE) is increasingly employed in clinical practice for the noninvasive detection of tissue fibrosis in patients with chronic liver disease (CLD), and particularly chronic hepatitis C virus (HCV)-related hepatitis.1 In this clinical setting, TE has been shown to be able to discriminate between at least three stages of fibrotic evolution: the absence of significant fibrosis, the presence of advanced fibrosis/cirrhosis, and an intermediate stage, often defined as a “gray area.” This distinction is useful in everyday practice for directing the need of liver biopsy,2 and overall, the use of TE, alone or in association with other noninvasive means, considerably reduces the number of liver biopsies necessary for correct patient management.

Our

results broadly confirm the results of Alvi et al. obtained with cultured macrophages and PBMCs, by showing an upregulation of IL-8 secretion by cultured AGS cells upon stimulation with recombinant HP0986 protein. Our results also support the conclusion of Alvi et al. that the HP0986 protein is presented to the human immune system as demonstrated by serologic profiling of patient samples in both the studies using sera from patients with varied geographic descent. Our results revealed presence of hp0986 locus in a significant number (31%) of clinical isolates (Fig. 1) and its prevalence was highest in strains obtained from the Indian ethnic group (88%) in Malaysia. Further, our study

appears to be in agreement with the previous observation on the prevalence of dupA, in different ethnic groups in Malaysian and Singaporean populations [40]. Similarly, the prevalence rates of FDA-approved Drug Library molecular weight other plasticity region genes were also reported by others to be in a similar range, for example, jhp0940, jhp0945, jhp0947, and jhp0949 had a prevalence rate of 23.9, 39.1, 37.7, and 45.7%, respectively, in Colombia, United States, South Korea, and Japan [41]. As all these studies have been carried out on the basis of PCR-based genotyping, it will be necessary to stress that the absence of a PCR amplicon in H. pylori could be due to different allelic structures or sequences in different clinical isolates given that it is a highly recombining and geographically compartmentalized pathogen. However, our approach included consensus sequence-based primers nested within click here the hp0986 gene which appears to be highly conserved when tested in a single strain colonizing a single patient for about 10 years [42]. Although it is possible that the

gene length in some strains could be larger than the gene annotated in strain 26695, but it may not affect the outcome of a PCR-based survey. We observed variation in transcript levels of HP0986 in some H. pylori clinical isolates which may be due to multiple factors such as difference in environmental conditions of the stomach (pH, stress, level 上海皓元 of mucin secretion etc.) or it may be an intrinsic property of an individual clinical isolate [25]. However, in vivo expression of HP0986 was limited when compared with in vitro expression (Fig. 2); decreased in vivo expression may likely be due to several reasons such as less bacterial load as the bacterium maintains low profile during infection, or it may also be due to loss of RNA during sample processing etc. [43, 44]. It was also shown that in vivo expression of CagA in gastric biopsies was lower than its in vitro expression [45] which was further consistent with a DNA microarray study wherein the in vivo CagA expression was downregulated by low pH levels [46]. The antibody response in the sera of H.

Our

results broadly confirm the results of Alvi et al. obtained with cultured macrophages and PBMCs, by showing an upregulation of IL-8 secretion by cultured AGS cells upon stimulation with recombinant HP0986 protein. Our results also support the conclusion of Alvi et al. that the HP0986 protein is presented to the human immune system as demonstrated by serologic profiling of patient samples in both the studies using sera from patients with varied geographic descent. Our results revealed presence of hp0986 locus in a significant number (31%) of clinical isolates (Fig. 1) and its prevalence was highest in strains obtained from the Indian ethnic group (88%) in Malaysia. Further, our study

appears to be in agreement with the previous observation on the prevalence of dupA, in different ethnic groups in Malaysian and Singaporean populations [40]. Similarly, the prevalence rates of see more other plasticity region genes were also reported by others to be in a similar range, for example, jhp0940, jhp0945, jhp0947, and jhp0949 had a prevalence rate of 23.9, 39.1, 37.7, and 45.7%, respectively, in Colombia, United States, South Korea, and Japan [41]. As all these studies have been carried out on the basis of PCR-based genotyping, it will be necessary to stress that the absence of a PCR amplicon in H. pylori could be due to different allelic structures or sequences in different clinical isolates given that it is a highly recombining and geographically compartmentalized pathogen. However, our approach included consensus sequence-based primers nested within Androgen Receptor antagonist the hp0986 gene which appears to be highly conserved when tested in a single strain colonizing a single patient for about 10 years [42]. Although it is possible that the

gene length in some strains could be larger than the gene annotated in strain 26695, but it may not affect the outcome of a PCR-based survey. We observed variation in transcript levels of HP0986 in some H. pylori clinical isolates which may be due to multiple factors such as difference in environmental conditions of the stomach (pH, stress, level 上海皓元 of mucin secretion etc.) or it may be an intrinsic property of an individual clinical isolate [25]. However, in vivo expression of HP0986 was limited when compared with in vitro expression (Fig. 2); decreased in vivo expression may likely be due to several reasons such as less bacterial load as the bacterium maintains low profile during infection, or it may also be due to loss of RNA during sample processing etc. [43, 44]. It was also shown that in vivo expression of CagA in gastric biopsies was lower than its in vitro expression [45] which was further consistent with a DNA microarray study wherein the in vivo CagA expression was downregulated by low pH levels [46]. The antibody response in the sera of H.

Decompensated liver disease at presentation was found in 125 patients, and 70 had undergone transplantation for AIH, 57 had not undergone a liver biopsy, click here 39 did not have available data on autoantibodies or gamma globulins, three had only family history of AIH, and 256 did not have AIH as their final diagnosis.

Other cases excluded were for suspicion of overlap syndromes with primary biliary cirrhosis and primary sclerosing cholangitis (n = 97) and pediatric cases (n = 68). Drugs were suspected to have induced the AIH in 24 of 261 (9.2%) cases: minocycline (n = 11), nitrofurantoin (n = 11), and cephalexin and Prometrium, in one case each. These were suspected on clinical grounds because of current use of these drugs at the time of diagnosis. None of the patients continued with the drugs past the date of presentation, and none were rechallenged. The demographic and biochemical data in the study cohort of the 24 DIAIH patients and the 237 other AIH patients is demonstrated in Table 1. The median follow-up of the DIAIH patients was 36 months (13-77); and in the other AIH patients, 36 months (15-79) (P = NS). The DIAIH patients were referral patients from states other than Minnesota in 19 of 24 (79%) and selleck chemical in 160 of 237 (68%) in the other AIH patients (P = NS). A similar proportion of patients had antinuclear antibodies and smooth muscle antibody seropositivity

among the two groups (Table 1). Trial of discontinuation of immunosuppression was only tried in 14 of 24 (58%) of the DIAIH patients. A significantly 上海皓元医药股份有限公司 higher proportion of patients with DIAIH were able to discontinue their immunosuppressive therapy compared with

other AIH patients (100% versus 35%) (P < 0.0001) (Table 1) and showed no relapse at 36 (12-58) months in the DIAIH patients. In general, liver tests at presentation were higher and jaundice more common in the DIAIH group, but the differences were not significantly different (Table 1). Patients with nitrofurantoin-induced and minocycline-induced AIH are shown in Table 2. A very similar proportion of the DIAIH and the rest of the AIH group had typical and compatible histology according to the histological characterization presented by Hennes et al.17 (Table 3). None of the DIAIH patients had atypical histology, and only one patient from the rest of the AIH group had atypical histology. This patient fulfilled diagnostic criteria for AIH, although histology was similar to histology observed in primary biliary cirrhosis. The severity of inflammation and fibrosis was not significantly different between the two groups (Table 3). There was a tendency toward a higher stage score in the AIH than in the DIAIH group, but the difference was not significant (Table 3). However, cirrhosis was not present in any of the DIAH patients, whereas cirrhosis was found among 5 of 24 (20.

Decompensated liver disease at presentation was found in 125 patients, and 70 had undergone transplantation for AIH, 57 had not undergone a liver biopsy, this website 39 did not have available data on autoantibodies or gamma globulins, three had only family history of AIH, and 256 did not have AIH as their final diagnosis.

Other cases excluded were for suspicion of overlap syndromes with primary biliary cirrhosis and primary sclerosing cholangitis (n = 97) and pediatric cases (n = 68). Drugs were suspected to have induced the AIH in 24 of 261 (9.2%) cases: minocycline (n = 11), nitrofurantoin (n = 11), and cephalexin and Prometrium, in one case each. These were suspected on clinical grounds because of current use of these drugs at the time of diagnosis. None of the patients continued with the drugs past the date of presentation, and none were rechallenged. The demographic and biochemical data in the study cohort of the 24 DIAIH patients and the 237 other AIH patients is demonstrated in Table 1. The median follow-up of the DIAIH patients was 36 months (13-77); and in the other AIH patients, 36 months (15-79) (P = NS). The DIAIH patients were referral patients from states other than Minnesota in 19 of 24 (79%) and IWR-1 nmr in 160 of 237 (68%) in the other AIH patients (P = NS). A similar proportion of patients had antinuclear antibodies and smooth muscle antibody seropositivity

among the two groups (Table 1). Trial of discontinuation of immunosuppression was only tried in 14 of 24 (58%) of the DIAIH patients. A significantly 上海皓元 higher proportion of patients with DIAIH were able to discontinue their immunosuppressive therapy compared with

other AIH patients (100% versus 35%) (P < 0.0001) (Table 1) and showed no relapse at 36 (12-58) months in the DIAIH patients. In general, liver tests at presentation were higher and jaundice more common in the DIAIH group, but the differences were not significantly different (Table 1). Patients with nitrofurantoin-induced and minocycline-induced AIH are shown in Table 2. A very similar proportion of the DIAIH and the rest of the AIH group had typical and compatible histology according to the histological characterization presented by Hennes et al.17 (Table 3). None of the DIAIH patients had atypical histology, and only one patient from the rest of the AIH group had atypical histology. This patient fulfilled diagnostic criteria for AIH, although histology was similar to histology observed in primary biliary cirrhosis. The severity of inflammation and fibrosis was not significantly different between the two groups (Table 3). There was a tendency toward a higher stage score in the AIH than in the DIAIH group, but the difference was not significant (Table 3). However, cirrhosis was not present in any of the DIAH patients, whereas cirrhosis was found among 5 of 24 (20.

Decompensated liver disease at presentation was found in 125 patients, and 70 had undergone transplantation for AIH, 57 had not undergone a liver biopsy, selleck kinase inhibitor 39 did not have available data on autoantibodies or gamma globulins, three had only family history of AIH, and 256 did not have AIH as their final diagnosis.

Other cases excluded were for suspicion of overlap syndromes with primary biliary cirrhosis and primary sclerosing cholangitis (n = 97) and pediatric cases (n = 68). Drugs were suspected to have induced the AIH in 24 of 261 (9.2%) cases: minocycline (n = 11), nitrofurantoin (n = 11), and cephalexin and Prometrium, in one case each. These were suspected on clinical grounds because of current use of these drugs at the time of diagnosis. None of the patients continued with the drugs past the date of presentation, and none were rechallenged. The demographic and biochemical data in the study cohort of the 24 DIAIH patients and the 237 other AIH patients is demonstrated in Table 1. The median follow-up of the DIAIH patients was 36 months (13-77); and in the other AIH patients, 36 months (15-79) (P = NS). The DIAIH patients were referral patients from states other than Minnesota in 19 of 24 (79%) and see more in 160 of 237 (68%) in the other AIH patients (P = NS). A similar proportion of patients had antinuclear antibodies and smooth muscle antibody seropositivity

among the two groups (Table 1). Trial of discontinuation of immunosuppression was only tried in 14 of 24 (58%) of the DIAIH patients. A significantly medchemexpress higher proportion of patients with DIAIH were able to discontinue their immunosuppressive therapy compared with

other AIH patients (100% versus 35%) (P < 0.0001) (Table 1) and showed no relapse at 36 (12-58) months in the DIAIH patients. In general, liver tests at presentation were higher and jaundice more common in the DIAIH group, but the differences were not significantly different (Table 1). Patients with nitrofurantoin-induced and minocycline-induced AIH are shown in Table 2. A very similar proportion of the DIAIH and the rest of the AIH group had typical and compatible histology according to the histological characterization presented by Hennes et al.17 (Table 3). None of the DIAIH patients had atypical histology, and only one patient from the rest of the AIH group had atypical histology. This patient fulfilled diagnostic criteria for AIH, although histology was similar to histology observed in primary biliary cirrhosis. The severity of inflammation and fibrosis was not significantly different between the two groups (Table 3). There was a tendency toward a higher stage score in the AIH than in the DIAIH group, but the difference was not significant (Table 3). However, cirrhosis was not present in any of the DIAH patients, whereas cirrhosis was found among 5 of 24 (20.

Additional Supporting Information may be found in the online version of this article. “
“Mutations in hemochromatosis protein (HFE) or transferrin receptor 2 (TFR2) cause hereditary hemochromatosis (HH) by impeding production of the liver iron-regulatory hormone, hepcidin (HAMP). This Ibrutinib order study examined the effects of disruption of Hfe or Tfr2, either alone or together, on liver iron loading and injury in mouse models of HH. Iron

status was determined in Hfe knockout (Hfe−/−), Tfr2 Y245X mutant (Tfr2mut), and double-mutant (Hfe−/−×Tfr2mut) mice by measuring plasma and liver iron levels. Plasma alanine transaminase (ALT) activity, liver histology, and collagen deposition were evaluated to assess liver injury. Hepatic oxidative stress was assessed by measuring superoxide dismutase (SOD) activity and F2-isoprostane levels. Gene expression was measured by real-time polymerase chain reaction. Hfe−/−×Tfr2mut mice had elevated hepatic iron with a periportal distribution and increased plasma iron, transferrin saturation, and non-transferrin-bound iron, compared with Hfe−/−, Tfr2mut, and wild-type (WT) mice. Hamp1 expression was reduced to 40% (Hfe−/− and Tfr2mut) and 1% (Hfe−/−×Tfr2mut) of WT values. Hfe−/− ×Tfr2mut mice had elevated plasma ALT activity and mild hepatic inflammation with scattered FK506 chemical structure aggregates of

infiltrating inflammatory cluster of differentiation 45 (CD45)–positive cells. Increased hepatic hydoxyproline levels as well as Sirius red and Masson’s Trichrome staining demonstrated advanced portal collagen deposition. Hfe−/− and Tfr2mut

mice had less hepatic inflammation and collagen deposition. Liver F2-isoprostane levels 上海皓元医药股份有限公司 were elevated, and copper/zinc and manganese SOD activities decreased in Hfe−/−×Tfr2mut, Tfr2mut, and Hfe−/− mice, compared with WT mice. Conclusion: Disruption of both Hfe and Tfr2 caused more severe hepatic iron overload with more advanced lipid peroxidation, inflammation, and portal fibrosis than was observed with the disruption of either gene alone. The Hfe−/−×Tfr2mut mouse model of iron-induced liver injury reflects the liver injury phenotype observed in human HH. (HEPATOLOGY 2012) Primary and secondary iron overload disorders are important causes of liver disease and associated morbidity worldwide.1 The most common primary iron overload disorder is hereditary hemochromatosis (HH), which affects approximately 1 in 200 individuals of Northern European descent.2 There are four types of HH; the most common, HH type 1, is caused primarily by homozygosity for the C282Y mutation in the hemochromatosis protein (HFE).3 Iron overload disease develops in up to 30% of these individuals and can result in significant hepatic, pancreatic, cardiac, or musculoskeletal tissue damage.4 Juvenile, or HH type 2, is rare and is caused by mutations in hemojuvelin (HJV) or hepcidin (HAMP).

However, this does not mean that metabolic factors are not selleck screening library important in patients with CHB. In fact, one Chinese study of patients with CHB showed co-existence of MetS was associated with a greater risk of cirrhosis (OR 1.7), and this has recently been confirmed in North America.42 Further, the strength of association with cirrhosis increased progressively with the number of MetS components present (OR of 1.4, 2.6, 4.1, 4 and 5.5 for patients with one, two, three, four and five components of MetS, respectively).43

The key pathogenic processes documented in studies elsewhere include insulin resistance, hypoadiponectinemia and oxidative stress.1 Their importance in contributing to NAFLD has been reiterated in Asian studies. It is beyond the scope of this article to review the pathogenesis of NAFLD44 but data on recent studies implicating genetic factors will be briefly discussed. Until recently, the genetic contribution to NAFLD has been largely ignored because alterations in lifestyle have been blamed for click here the fatty liver epidemic. This perception is likely to change with the publication of studies such as the one by Schwimmer

et al. in the USA, who observed a high frequency of fatty liver among siblings (59%) and parents (79%) of children with NAFLD.45 This has fuelled interest in genetic studies. However, most of these studies in Asia (and elsewhere) have mainly involved evaluation of candidate genes. The latter were chosen for their known associations with insulin resistance, medchemexpress MetS, inflammatory and adipocytokine responses and hepatic fibrogenesis. Most of the reported studies are small and underpowered to detect significant differences. As expected, single nucleotide polymorphisms (SNPs) related to genes coding for tumor necrosis factor-alpha (TNF-α), TNF-α

related apoptosis-inducing ligand (TRAIL), leptin, adiponectin, peroxisome proliferator-activated receptors (PPAR) and angiotensin receptors have showed significant association.46–48 but the findings have not been consistent.49 To date, there has been only one adequately powered candidate gene study in Asian subjects with fatty liver. Lean Indian men with NAFLD were found to carry two gain-of-function single-nucleotide polymorphisms (SNPs) within the gene encoding apolipoprotein 3 (APOC3).50 The variant allele carriers had a 30% increase in plasma apolipoprotein C3 and a 60% increase in plasma triglycerides and marked insulin resistance. The prevalence of NAFLD among carriers of the two variant SNPs (C-482T and T-455C) was 38% (absent in wild type homozygotes). Through its effects on inhibiting hepatic lipase activity and delaying catabolism of triglyceride-rich particles, the physiological actions of APOC3 are pro-steatotic; inheritance of variants, known to be associated with increased APOC3 levels, would exacerbate this tendency.

However, this does not mean that metabolic factors are not MK-2206 important in patients with CHB. In fact, one Chinese study of patients with CHB showed co-existence of MetS was associated with a greater risk of cirrhosis (OR 1.7), and this has recently been confirmed in North America.42 Further, the strength of association with cirrhosis increased progressively with the number of MetS components present (OR of 1.4, 2.6, 4.1, 4 and 5.5 for patients with one, two, three, four and five components of MetS, respectively).43

The key pathogenic processes documented in studies elsewhere include insulin resistance, hypoadiponectinemia and oxidative stress.1 Their importance in contributing to NAFLD has been reiterated in Asian studies. It is beyond the scope of this article to review the pathogenesis of NAFLD44 but data on recent studies implicating genetic factors will be briefly discussed. Until recently, the genetic contribution to NAFLD has been largely ignored because alterations in lifestyle have been blamed for Daporinad manufacturer the fatty liver epidemic. This perception is likely to change with the publication of studies such as the one by Schwimmer

et al. in the USA, who observed a high frequency of fatty liver among siblings (59%) and parents (79%) of children with NAFLD.45 This has fuelled interest in genetic studies. However, most of these studies in Asia (and elsewhere) have mainly involved evaluation of candidate genes. The latter were chosen for their known associations with insulin resistance, medchemexpress MetS, inflammatory and adipocytokine responses and hepatic fibrogenesis. Most of the reported studies are small and underpowered to detect significant differences. As expected, single nucleotide polymorphisms (SNPs) related to genes coding for tumor necrosis factor-alpha (TNF-α), TNF-α

related apoptosis-inducing ligand (TRAIL), leptin, adiponectin, peroxisome proliferator-activated receptors (PPAR) and angiotensin receptors have showed significant association.46–48 but the findings have not been consistent.49 To date, there has been only one adequately powered candidate gene study in Asian subjects with fatty liver. Lean Indian men with NAFLD were found to carry two gain-of-function single-nucleotide polymorphisms (SNPs) within the gene encoding apolipoprotein 3 (APOC3).50 The variant allele carriers had a 30% increase in plasma apolipoprotein C3 and a 60% increase in plasma triglycerides and marked insulin resistance. The prevalence of NAFLD among carriers of the two variant SNPs (C-482T and T-455C) was 38% (absent in wild type homozygotes). Through its effects on inhibiting hepatic lipase activity and delaying catabolism of triglyceride-rich particles, the physiological actions of APOC3 are pro-steatotic; inheritance of variants, known to be associated with increased APOC3 levels, would exacerbate this tendency.

preparation; 4. randomised prospective trial; 5. sodium phosphate tablet Presenting Author: SATOSHI ASAI Additional Authors: NAOKI FUJIMOTO, KOUJIROU TANOUE, EISUKE AKAMINE, MIKIO NAMBARA, NORIFUMI HIROOKA, NORIFUMI HIROOKA, HIDEO YANAGI, MINORU OGAWA, ATSUHIRO OGAWA Corresponding

Author: SATOSHI ASAI Affiliations: Tane General Hospital, Tane General Hospital, Tane General Hospital, Tane General Hospital, Tane General Hospital, Tane General Hospital, Tane General Hospital, Tane General Hospital, Tane General Hospital Objective: One of major causes of pain during colonoscopy is looping of the instrument during insertion through the sigmoid colon, which causes discomfort PD0325901 cell line by stretching of the mesentery. There are a lot of studies in colonoscope techniques, but they are not assessed objectively with respect to colonoscope passage through the sigmoid colon without loop formation. The aim of this study is to determine whether cap-fitted colonoscopy and water immersion increase the success rate of insertion through the sigmoid without loop formation. Methods: A total of 1005 patients were randomized to standard colonoscopy, cap-fitted colonoscopy Tipifarnib or water immersion technique. All examinations were performed under a magnetic endoscope imaging device.

The main outcome was the success rate of insertion without loop formation. Results: The success rate of insertion without loop formation was 37.5%, 40.0%, and 53.8% in the standard, cap, and water groups, respectively (standard-water p = 0.00014, cap-water p = 0.00186). There were no significant differences among the groups about the cecal intubation rate, the cecal intubation time and the number of polyps >5 mm per patient. Conclusion: Water immersion increased the success rate of insertion through the sigmoid colon without loop formation. This practical technique, just to prepare a cap and water, is useful without compromising cecal intubation rate, cecal intubation time, or polyp detection rate. Key Word(s): 1. Water immersion; 2. water navigation colonoscopy; 3. water assisted colonoscopy; 4. cap fitted colonosocpy MCE Presenting Author: JACOBUS ALBERTUS AUWYANG Additional Authors: SETYOKO SETYOKO Corresponding Author: JACOBUS ALBERTUS AUWYANG

Affiliations: Tugurejo Hospital Objective: Poor bowel preparation accounts for 20% of failed colonoscopies and can also lead to failure to detect pathology during the procedure. We aimed to identify independent factors affecting bowel preparation in colonoscopy. Methods: 249 consecutive colonoscopies performed in 2011–2013 were identified. Data were retrospectively collected on age, gender, patients’ medical co-morbidities, history of previous surgery and malignancy, type and effectiveness of bowel preparation, medication used during the procedure, and endoscopic findings such as presence of diverticular disease. Logistic regression analysis was used to identify independent factors affecting bowel preparation in colonoscopy. Results: Male gender (OR 0.