37, p = 0.020), and baseline ALT > 45 for males and > 30 for females (HR 2.26, p < 0.0001) were significant predictors of treatment initiation, but not practice setting. Similarly,

only older age (HR 1.02, p < 0.0001), male gender (HR 1.42, p = 0.019) and baseline ALT > 45 for males and > 30 for females (HR 2.81, p < 0.0001) were significant independent predictors of starting treatment within the first year of treatment eligibility and not practice setting. Conclusion: The majority of patients who started treatment started within one year of becoming treatment eligible; however, approximately 40% of patients still have not started treatment on longer follow-up. Further studies are needed to determine the barriers for treatment initiation in diverse practice settings. Disclosures: Huy N. Trinh - Advisory Committees or Review Panels: BMS, Gilead; Grant/ Research Support: selleck chemicals llc BMS, Gilead; Speaking and Teaching: BMS, Gilead, vertex; Stock Shareholder: Gilead Huy A. Nguyen – Advisory Committees or Review Panels: Gilead, BMS; Speaking and Teaching: Gilead Mindie H. Nguyen – Advisory Committees or Review Panels: Bristol-Myers Squibb, Bayer AG, Gilead, Novartis, Onyx; Consulting: Gilead Sciences, Inc.; Grant/Research Support: Gilead Sciences, Inc., Bristol-Myers Squibb, Novartis AZD1208 order Pharmaceuticals, Roche Pharma AG, Idenix, Hologic, ISIS The following people have nothing to disclose: Vinh

D. Vu, Ailinh Do, Nghia H. Nguyen, Lily H. Kim, Khanh Nguyen Background. Fibrosis-regression(FR) rate in treated CHB-patients patients was similary estimated using Fibrotest and LSM (Fibros-can),

although with possible overestimation of FR by LSM related to necroinflammatory activity(NIA).(AntivirTher2009,2010) Aims. To prospectively evaluate : 1)The histological impact of strong inhibitor of HBV-replication, entecavir-motherapy [0.5mg/day], using Fibrotest-Actitest and LSM.2) The impact of presumed steatosis(Steatotest) on the treatment response. Methods. NUC-naïve CHB preincluded [19-centers,France] fol-lowed-up (FU) 上海皓元 from baseline to M6,M12 and M24-months. Viral-response(VR) defined as undetectable-HBVDNA. Results. N=177 pre-included, 15-retracted, 3-died, 5 non-applicable Fibrotest (4 flare-up ALT>600IU/L), 24 lost-of-follow-up (FU); N=137 with M6-FU included [age 45(20-83)yrs; 71%males; 84% anti-HBe(+); 43%caucasian/29%asian/28%african]. Applicable-LSM vs Fibrotest 95%vs97.2%(p<0.0001). Fibro- test presumed advanced fibrosis(AF,F2F3F4-METAVIR) in 36%(60/167) and cirrhosis 12%(N=20/167); presumed NIA (Actitest) in 74%(123/166) and baseline steatosis>1% (Steatotest) 37%(57/156). N=43 had liver biospy [size 24(5-40)] AF 56%(24/43). VR prevalences were 67% M6(N=120), 83% M12(N=105) and 86%M24(N=50). Presumed NIA [Actitest] regressed from M0 0.38(0.02) to M6 0.21(0.01), M12 0.19(0.01) and M24 0.14(0.02), all p<0.0001vsM0. 76% patients with baseline-NIA regressed at M6. Presumed AF [Fibrotest] regressed from M0 0.69(0.02) vs M6 0.59(0.03) vs M12 0.57(0.03), M24 0.

Izmir protocol is safe, cheap and easy to carry out. “
“The greatest challenges of managing people with hemophilia (PWH) are in the developing countries. Not only do almost 80% of PWH reside in these find more countries but there is also significant lack of knowledge of this condition as well as diagnostic infrastructure and therapeutic options. Under these conditions, judicious utilization of resources becomes a matter of paramount importance with emphasis on early

diagnosis and physical therapy combined with best practises of factor replacement that is possible. However, the situation is rapidly evolving with greater allocation of resources for clotting factor concentrates (CFC) in large parts of the developing world. This has raised the possibility of initiating early prophylaxis with modest doses of CFC. These innovations do need to be combined with the classic concepts of comprehensive care to cover the management of chronic musculoskeletal complications and surgical interventions as needed. The introduction of molecular genetics click here for carrier detection and counseling is also very important. This chapter describes the comprehensive care model

for PWH in developing countries. “
“Summary.  Haemophilia A and B are rare X-linked conditions. Elevated rates of HIV and hepatitis C related malignancies in these patients are well reported, however rates of other types of cancers are not. Therefore,

a retrospective literature review of cancer in patients with haemophilia was conducted. A Medline search of articles from January 1966 to July 2009 utilizing the keywords haemophilia, leukaemia, malignancy, mortality, neoplasm and cancer was performed. The articles were reviewed and additional relevant publications were located from the references. Data on age, type and severity of haemophilia, HIV status, type of malignancy and outcomes were recorded as available. Thirty-two cases of leukaemia were identified as well as 159 malignant solid tumours. Specific incidence and prevalence rates could not be calculated due to the limited nature of the information available in the reports. Many types of malignancy have been reported in persons with haemophilia MCE irrespective of infection with HIV and hepatitis C yet prevalence and incidence rates compared to the general population remain unknown. Patients with haemophilia can manifest non infectious related malignancies and symptomatic patients should be evaluated accordingly. “
“Summary. Continuous infusion (CI) of factor VIII (FVIII) is an effective method for replacement therapy in haemophilia. Recently, concerns have been raised regarding association of CI with the development of inhibitors. The aim of this study was to gain information on the current practices in Europe regarding CI and the true inhibitor incidence after this mode of therapy.

Chart reviews and prospective data collection were supplemented by additional ascertainment of deaths and transplants through the end of 2008 for patients included in the retrospective study only (n = 112) and through February 2010 for the remaining patients check details (n = 756) under a data use agreement with the Scientific Registry of Transplant Recipients (SRTR). The study cohort utilized for this report included 868 adult liver transplant candidates for whom the first living liver donor was evaluated between February 28, 2002 and August 31, 2009.

For these candidates, median follow-up was 4.6 years (range: 4 days to 7.9 years). Data from DDLT recipients not enrolled in A2ALL but transplanted at A2ALL centers were obtained from SRTR for comparison with A2ALL patients who received DDLT during the same period. The cumulative incidence function was calculated using SAS macro “comprisk.”7 The

MELD scores reported were calculated on laboratory data only8 and ignored MELD exception scores used in organ allocation. Survival analyses, starting at the time of evaluation of each subject’s first potential donor, were employed to compare mortality after LDLT to the conventional transplant strategy of waiting for and potentially receiving DDLT. The non-LDLT group thus included those who received DDLT, those who remained on the waitlist without receiving a liver transplant at study end, and those who died prior to receiving a DDLT. LDLT (n = 4) or DDLT (n = 2) procedures that were aborted intraoperatively due

to recipient conditions were considered transplants. Domino transplants mTOR inhibitor were classified as DDLTs (n = 1). A Cox regression method employing sequential stratification to compare the effect of receipt of LDLT with not receiving LDLT over the entire period of observation was utilized for the primary analysis.1 The sequentially stratified Cox model was adjusted for baseline covariates of age, HCC, hepatitis C virus (HCV), cholestatic liver disease, and MELD score, all determined at the time of first donor evaluation. Multiplicative interactions (effect MCE modification) between LDLT, HCC, and MELD score were evaluated. An additional Cox regression analysis of posttransplant mortality was performed starting on the day of transplant and compared LDLT versus DDLT adjusted for age, HCC, HCV, cholestatic liver disease, and MELD score at transplant. Survival probabilities in the tables and figures were calculated in the following manner. Survival in the absence of receipt of LDLT was estimated from a Cox regression censored at LDLT. This model was adjusted for age, HCC, HCV, cholestatic disease, and MELD score as above. Depiction of probabilities of survival that encompass both the waiting period for liver transplantation and posttransplant period were estimated by multiplying the waitlist survival probability at the respective LDLT median transplant time by the posttransplant survival probability for LDLT recipients.

Chart reviews and prospective data collection were supplemented by additional ascertainment of deaths and transplants through the end of 2008 for patients included in the retrospective study only (n = 112) and through February 2010 for the remaining patients selleck kinase inhibitor (n = 756) under a data use agreement with the Scientific Registry of Transplant Recipients (SRTR). The study cohort utilized for this report included 868 adult liver transplant candidates for whom the first living liver donor was evaluated between February 28, 2002 and August 31, 2009.

For these candidates, median follow-up was 4.6 years (range: 4 days to 7.9 years). Data from DDLT recipients not enrolled in A2ALL but transplanted at A2ALL centers were obtained from SRTR for comparison with A2ALL patients who received DDLT during the same period. The cumulative incidence function was calculated using SAS macro “comprisk.”7 The

MELD scores reported were calculated on laboratory data only8 and ignored MELD exception scores used in organ allocation. Survival analyses, starting at the time of evaluation of each subject’s first potential donor, were employed to compare mortality after LDLT to the conventional transplant strategy of waiting for and potentially receiving DDLT. The non-LDLT group thus included those who received DDLT, those who remained on the waitlist without receiving a liver transplant at study end, and those who died prior to receiving a DDLT. LDLT (n = 4) or DDLT (n = 2) procedures that were aborted intraoperatively due

to recipient conditions were considered transplants. Domino transplants Deforolimus research buy were classified as DDLTs (n = 1). A Cox regression method employing sequential stratification to compare the effect of receipt of LDLT with not receiving LDLT over the entire period of observation was utilized for the primary analysis.1 The sequentially stratified Cox model was adjusted for baseline covariates of age, HCC, hepatitis C virus (HCV), cholestatic liver disease, and MELD score, all determined at the time of first donor evaluation. Multiplicative interactions (effect 上海皓元 modification) between LDLT, HCC, and MELD score were evaluated. An additional Cox regression analysis of posttransplant mortality was performed starting on the day of transplant and compared LDLT versus DDLT adjusted for age, HCC, HCV, cholestatic liver disease, and MELD score at transplant. Survival probabilities in the tables and figures were calculated in the following manner. Survival in the absence of receipt of LDLT was estimated from a Cox regression censored at LDLT. This model was adjusted for age, HCC, HCV, cholestatic disease, and MELD score as above. Depiction of probabilities of survival that encompass both the waiting period for liver transplantation and posttransplant period were estimated by multiplying the waitlist survival probability at the respective LDLT median transplant time by the posttransplant survival probability for LDLT recipients.

HA had the best correlation with a correlation coefficient value of 0.62. These variables were included

in multivariate analysis and achieved an R square value of 0.511 to predict CPA. Using the backwards selection method, selleck chemicals three serum markers (HA, α2-macroglobulin and platelet count) which remained significant were included in the final model and achieved an R square value of 0.46 to predict CPA. Using this model the predicted CPA was calculated for each patient. The mean predicted CPA was 7.70 (range: 0.98-28.2) and the mean variance between the predicted and measured CPA was 2.78. The final model had an AUROC of 0.86 (95% CI, 0.78-0.95) to predict those patients with a CPA≥10% and a cut point of 8.7 had a sensitivity of 80.8% and specificity of 85.2%. The AUROC of the model to predict patients with a CPA ≥ 20% was 0.96 (95% CI, 0.91-1.00) and a cut point of 10.7 had a sensitivity of 100% and specificity of 89%. A similar predictive ability of the final

model was found in the validation set. Conclusion: This study has for the first time GSI-IX developed a serum biochemical model using CPA as the reference standard. The model has the potential to improve the prediction of liver related clinical outcomes and non-invasively measure changes liver collagen with the use of anti-fibrotic agents. Disclosures: Enrico Rossi – Patent Held/Filed, UNIVERSITY OF WA Gary P. Jeffrey – Advisory Committees or Review Panels: MSD, Novartis The following people have nothing to disclose: Yi Huang, Bastiaan de Boer, Leon Adams, Gerry C. MacQuillan, Max K. Bulsara Background and aims: Vitamin D deficiency was found to have impacts on both negative outcome of IFN-α2b/ribavirin treatment and severe liver fibrosis in chronic hepatitis C patients (CHC).

medchemexpress Researches proved that vitamin D binding protein (GC), rs7041 G>T, rs4588 C>A contribute to negative treatment response, while DHCR7 GG homozygosis involves in severe liver fibrosis. The study aimed to asses whether the GC, CYP2R1, DHCR7 can affect the outcome of combined therapy (IFN-α2b/ribavirin) and explore the relationship between those SNPs and liver fibrosis in CHC patients. Methods: 526 northern Chinese CHC patients were genotyped for the GC, CYP2R1_rs10741657, DHCR7_rs12785878 polymorphisms, 271 of them received a recombinant IFN-α2b/ribavirin combination for 48 weeks. 321 CHC patients who underwent liver stiffness measurement (fibroscan) were analyzed. Results: The genotype distributions of those SNPs in CHC patients did not deviate from H-W equilibrium. Analysis results between SNPs and treatment response are presented in table. After multiple analysis (adjusted factors: gender, HCV RNA baseline, IL28B C/C), CYP2R1 AA genotype can predict successful treatment response (OR=2.89, 95% CI=1.32-6.28, P = 0.008 for RVR; OR=3.67, 95% CI=1.17-11.50, P = 0.

We hypothesized that bile duct biopsies might be more useful for diagnosing AIP and more closely reflect the histopathology of the pancreas than ampullary biopsies because the bile duct is commonly involved in AIP. Therefore, we carried out a clinicopathological study to examine the usefulness of endoscopic biopsies from Vater’s ampulla and the bile duct for discriminating

between AIP and PSC or pancreatobiliary cancers. The present PLX4032 concentration study consisted of 26 AIP patients (all associated with cholangitis), 3 patients with IgG4-related sclerosing cholangitis (without AIP), 6 PSC patients and 27 pancreatobiliary carcinoma patients. Patients with AIP or IgG4-related sclerosing cholangitis were examined in a single disease group named IgG4-related sclerosing cholangitis (IgG4-SC). All patients were diagnosed and treated at Hokkaido University Hospital from April 2006 to February 2009. After excluding four AIP patients without cholangitis, all patients diagnosed with AIP, IgG4-SC, and PSC at our institute RXDX-106 chemical structure were included in the present study. During the same period, we examined a total of 128 consecutive patients with pancreatic cancer and a total of 248 consecutive patients with bile duct cancer. Of the 128 patients with pancreatic cancer, 119 patients were excluded because of no biliary drainage (n = 5), no surgical treatment

(n = 94) or biliary drainage only (n = 20).

Of the 248 patients with pancreatic cancer, 230 patients were excluded because of no biliary drainage (n = 16), no surgical treatment (n = 67), biliary drainage only (n = 66) or transpapillary bile duct biopsy only (n = 81). All pancreatobiliary carcinoma patients 上海皓元医药股份有限公司 who underwent endoscopic retrograde cholangiopancreatography (ERCP) and ampullary and bile duct biopsies during this period were also included in the present study. The mean ages and male/female ratios were as follows: IgG4-SC, 68 years, 23/6; PSC, 44 years, 1/5; and pancreatobiliary carcinoma, 66 years, 22/5. The clinical presentations of patients with IgG4-SC included obstructive jaundice (13/29, 45%), mild abdominal pain (2/29, 7%) and bodyweight loss (1/29, 3%). Two patients (7%) were found to have elevated biliary enzymes based on a blood test. The remaining 11 patients (38%) did not have any subjective symptoms and were found to have abnormalities on a radiological examination for routine medical screening or follow-up for extra-pancreatobiliary diseases. PSC patients presented with serological liver dysfunction (4/6, 67%) and jaundice (2/6, 33%). Pancreatobiliary carcinoma patients had obstructive jaundice (21/27, 78%), elevated biliary enzymes (4/27, 15%), mild abdominal pain (1/21, 4%) and mild back pain (1/21, 4%).

We hypothesized that bile duct biopsies might be more useful for diagnosing AIP and more closely reflect the histopathology of the pancreas than ampullary biopsies because the bile duct is commonly involved in AIP. Therefore, we carried out a clinicopathological study to examine the usefulness of endoscopic biopsies from Vater’s ampulla and the bile duct for discriminating

between AIP and PSC or pancreatobiliary cancers. The present find more study consisted of 26 AIP patients (all associated with cholangitis), 3 patients with IgG4-related sclerosing cholangitis (without AIP), 6 PSC patients and 27 pancreatobiliary carcinoma patients. Patients with AIP or IgG4-related sclerosing cholangitis were examined in a single disease group named IgG4-related sclerosing cholangitis (IgG4-SC). All patients were diagnosed and treated at Hokkaido University Hospital from April 2006 to February 2009. After excluding four AIP patients without cholangitis, all patients diagnosed with AIP, IgG4-SC, and PSC at our institute RG7420 were included in the present study. During the same period, we examined a total of 128 consecutive patients with pancreatic cancer and a total of 248 consecutive patients with bile duct cancer. Of the 128 patients with pancreatic cancer, 119 patients were excluded because of no biliary drainage (n = 5), no surgical treatment

(n = 94) or biliary drainage only (n = 20).

Of the 248 patients with pancreatic cancer, 230 patients were excluded because of no biliary drainage (n = 16), no surgical treatment (n = 67), biliary drainage only (n = 66) or transpapillary bile duct biopsy only (n = 81). All pancreatobiliary carcinoma patients MCE who underwent endoscopic retrograde cholangiopancreatography (ERCP) and ampullary and bile duct biopsies during this period were also included in the present study. The mean ages and male/female ratios were as follows: IgG4-SC, 68 years, 23/6; PSC, 44 years, 1/5; and pancreatobiliary carcinoma, 66 years, 22/5. The clinical presentations of patients with IgG4-SC included obstructive jaundice (13/29, 45%), mild abdominal pain (2/29, 7%) and bodyweight loss (1/29, 3%). Two patients (7%) were found to have elevated biliary enzymes based on a blood test. The remaining 11 patients (38%) did not have any subjective symptoms and were found to have abnormalities on a radiological examination for routine medical screening or follow-up for extra-pancreatobiliary diseases. PSC patients presented with serological liver dysfunction (4/6, 67%) and jaundice (2/6, 33%). Pancreatobiliary carcinoma patients had obstructive jaundice (21/27, 78%), elevated biliary enzymes (4/27, 15%), mild abdominal pain (1/21, 4%) and mild back pain (1/21, 4%).

L-Fabp expression decreased 10-fold following HSC activation, concomitant with depletion of LDs. Primary HSCs isolated from L-FABP−/− mice contain fewer LDs than wild-type (WT) HSCs, and exhibit up-regulated expression of genes involved in HSC activation. Adenoviral L-Fabp transduction inhibited activation of passaged WT HSCs and increased both the expression

of prolipogenic genes and also augmented intracellular lipid accumulation, including triglyceride and FA, predominantly palmitate. Freshly isolated HSCs from L-FABP−/− mice correspondingly exhibited decreased palmitate in the free FA pool. To investigate whether L-FABP deletion promotes GDC 0068 HSC activation in vivo, we fed L-FABP−/− and WT mice a high-fat diet supplemented with trans-fatty acids and fructose (TFF). TFF-fed L-FABP−/− mice exhibited reduced hepatic steatosis along with decreased LD abundance and size compared to WT mice. In addition, TFF-fed L-FABP−/− mice exhibited decreased hepatic fibrosis, with reduced expression of fibrogenic genes, compared to WT mice. Conclusion: L-FABP deletion

attenuates both diet-induced hepatic steatosis and fibrogenesis, despite the observation that L-Fabp paradoxically promotes FA and LD accumulation and inhibits HSC activation in vitro. These findings highlight the importance of cell-specific modulation of hepatic lipid metabolism in promoting fibrogenesis in nonalcoholic fatty liver disease. (Hepatology 2013) Nonalcoholic fatty liver disease (NAFLD) encompasses a Decitabine order spectrum of pathology ranging from simple steatosis to nonalcoholic steatohepatitis (NASH) and cirrhosis.1 Neutral lipid storage in hepatocytes, principally in the form of triglyceride, predisposes individuals to the subsequent development and progression of NASH,2 although much is still poorly understood regarding the metabolic regulation and clinical significance of distinctive storage pools of intrahepatic medchemexpress lipid. Among these intracellular storage compartments, lipid droplets (LDs) have emerged as a focal point of interest.3

LDs are specialized spherical organelles composed of a core of neutral lipids surrounded by proteins known as perilipins (Plins), which play key roles in regulating aspects of intracellular trafficking, signaling, and cytoskeletal organization.4 Understanding the pathways that regulate metabolic flux in LDs is likely to provide insight into the mechanisms of lipid-mediated liver injury.5 Hepatic stellate cells (HSCs) are the major effectors of hepatic fibrogenesis, characterized in their quiescent state by abundant LDs containing predominantly retinyl esters, triglyceride, and cholesterol ester along with cholesterol, phospholipids, and fatty acids (FAs).6, 7 In the course of hepatic injury, quiescent HSCs undergo phenotypic changes including enhanced cell proliferation, loss of LDs, expression of α-smooth muscle actin (α-SMA), and excessive production of extracellular matrix (ECM).

The finding that liver iron levels were unaffected in Dmt1liv/liv mice indicates that hepatocyte DMT1 is dispensable for the overall iron economy of the liver. In addition, the observation that hepatic iron accumulation and deposition of iron in hepatocytes were unaffected in Metabolism inhibitor double-mutant Hfe−/−;Dmt1liv/liv and Trfhpx/hpx;Dmt1liv/liv mice demonstrates that hepatocyte DMT1 is not required for development of hepatic iron overload characteristic of hemochromatosis or hypotransferrinemia. Furthermore, no alterations were found in levels of plasma iron, total iron-binding capacity, transferrin saturation, or hemoglobin in single- or double-mutant

Dmt1liv/liv mice, suggesting that inactivation of hepatocyte DMT1 does not affect systemic iron metabolism. The first clue that DMT1 was dispensable for hepatic iron accumulation was provided by studies of the Dmt1−/− mouse, which found that Dmt1−/− neonates had 3 times normal liver iron levels.[9] However, this observation was confounded by the fact that the Dmt1−/− mice had severe anemia and prominent extramedullary erythropoiesis in the liver. Hepatic iron accumulation in Dmt1−/− mice was directly investigated by administering a single IP dose of 5 mg of iron dextran.[9] The iron dextran injection resulted in a large

increase in levels of liver iron, in Trametinib research buy hepatocytes as well as macrophages. Although these observations indicated that an IP injection of a pharmacologic dose of iron (in a nonphysiological form) could load iron into the liver in the absence of DMT1, it is unclear how relevant these data are to usual pathways of hepatic iron uptake and accumulation. Therefore, in the present study, we assessed the role of DMT1 in hepatic iron uptake by IV administering physiologic forms of iron—transferrin or ferric citrate as NTBI18—and by using animal models of human disorders of iron overload. Similar to HFE-related hemochromatosis patients, Hfe−/− mice hyperabsorb MCE公司 dietary iron

and deposit the excess in hepatocytes, starting with periportal hepatocytes.[3] Here, we observed a similar pattern of iron deposition in the liver of Hfe−/− mice lacking hepatocyte DMT1 (Hfe−/−;Dmt1liv/liv), indicating that DMT1 is dispensable for hepatocyte iron accumulation in this animal model. Also, similar to hemochromatosis patients, Hfe−/− mice have elevated levels of plasma NTBI, even when transferrin is not fully saturated.[12] Most plasma NTBI is rapidly cleared by hepatocytes and is therefore believed to be a significant contributor to hepatic iron deposition.[11, 12] If so, our studies suggest that hepatocyte DMT1 is not required for NTBI uptake because hepatic iron levels were similar in Hfe−/− mice with or without hepatocyte DMT1. The likelihood that hepatocyte DMT1 is dispensable for the hepatic uptake of NTBI is strongly supported by our observation that hepatic iron accumulation and iron deposition in hepatocytes were unaffected in Trfhpx/hpx mice lacking hepatocyte DMT1 (Trfhpx/hpx;Dmt1liv/liv mice).

3). The

5-HT4 agonist mosapride decreased the length and frequency of LDCs but markedly promoted distal colon propulsive activity through increasing RPMCs.4). 5-HT at low concentrations (∼5 uM) strongly inhibited all activities, likely due to direct action on muscle. 5). When segmentation occurs, it replaces RPMCs, it is slow at 3.6 short-lasting contractions/min and occurs in the mid and distal colon. Conclusion: LDCs are dependent on 5-HT3 receptor activation. 5-HT3 antagonists mostly reduce RPMCs and segmentations but RMPCs and segmentation do not require 5-HT3 receptor activation and the motor patterns can increase in the presence of 5-HT3 antagonists. 5-HT4 receptor activation, promotes propulsion by creating short-lasting proximal LDCs and vigorous distal RPMCs. Key Word(s): 1. colonic motility; 2. 5-HT4 receptor; 3. 5-HT3 receptor; Presenting Author: MOHAMMADREZA ABDOLLAHI Additional Authors: MOHAMMADHOSSEIN SOMI Corresponding Author: MOHAMMADREZA ABDOLLAHI BTK inhibitor in vivo Affiliations: Young Researchers and Elite Club, Tabriz Branch, Islamic Azad University,; Liver and Gastrointestinal Selleck Erlotinib Diseases Research Center, Tabriz University of Medical Sciences Objective: An enlarging body of evidence supports the importance of the colonic polyp as a precursor to the development of colorectal cancer. Although there are exceptions, most authors agree that the majority of polyps are found in the distal 25 cm. of the colon. In this study we aimed to analyze the relationship

of age and gender with location of large intestine polyps in Tabriz University of medical science clinic clients through colonoscopy. Methods: All 上海皓元 records (n = 3650) patients undergoing colonoscopy from 2008 to 2012 at Tabriz University of Medical science were analyzed.

We also evaluated the age, gender, having polyp, location of polyps and relationship between them. We used t-test for descriptive variables and Chi-square tests to compare categorical variables. Results: Out of 3650 patients, 1984 males (54.3%) and 1666 females (45.7%), polyps were detected in 545 patients (15%). Mean age of our patients was 48.7 ± 18.6 [5–100]. The mean age in males were 48.7 ± 19.3 and in females were 48.6 ± 17.8. From those who had polyp 326 patients were male (59.8%) and 219 patients were female (40.2%). The most common age range in patients who had polyp was 60–70 year (22.4%). Most common locations of polyp were in rectum (26.5%), sigmoid (25.5%), ascending colon (14.9%), descending colon (14.4%), transverse colon (13.1%), anal canal (3.6%), all colon (1%) and cecum (1%) in those who had polyps, respectively. Polyp location in males were in rectum (28.4%), sigmoid (25.8%), ascending colon (16.3%), transverse colon (13.2%), descending colon (11%), anal canal (3.1%), cecum (1.4%) and all colon (0.8%), respectively. Polyps location in females were in sigmoid (25%), rectum (23.8%), descending colon (19.4%), ascending colon (12.9%), transverse colon (12.9%), anal canal (4.4%), all colon (1.2%) and cecum (0.