Just as email effectively killed the Acalabrutinib hand-stamped letter, the mobile device has changed the way we do everything from reading books to watching sports. What will this new era hold? Some analysts see longer acting products that will alter and confront accepted methods of treatment; a potential redistribution

of the existing products because of lower prices of recombinants, driven by companies having to look for new markets, with a related potential for surplus; and new players who will challenge the incumbents as they bring gene-transfer therapies and treatments to trial and begin to market them [2]. Innovation in the pharmaceutical industry will forever change the landscape in which it operates. And Erlotinib cost our community

will feel the impact of that change in all its aspects. At the WFH, we are here to serve all who have bleeding disorders and we welcome all treatment products as long as they are safe and prove useful to those individuals and countries in need. And this movement in the industry seems rather positive as it indicates we may have greater quantities and variety of products with which to treat those in need. Against this backdrop of changing faces and products, we will also see a shift from an economic perspective. Developing markets – the BRICS countries (Brazil, Russia, India, China and South Africa) as well as Mexico, Turkey and Ukraine – will account for one-third of the world’s GDP by 2020 – just 6 years away [3]. Twenty years beyond that, if infrastructure, regulatory environments and distribution systems evolve and improve, developing markets will have caught up with more mature markets. While disruption will be cause for much reflection on – and re-definition of – business models, for people affected by a bleeding disorder,

it heralds a time of celebration for a number of reasons [2]: Factor replacement therapy usage per patient will increase in developing markets; The improved convenience of longer acting therapies in the pipeline could begin to encourage more 上海皓元医药股份有限公司 people, particularly adults, to consider ongoing prophylaxis therapy; We expect to see acceptance of the real possibility of lower priced recombinant and possibly plasma-derived therapies in emerging markets; We will come closer to achieving treatment for all. These are opportunities we cannot afford to miss. Collectively, we must connect more effectively to technology and not allow ourselves to be complacent. We cannot stop advocating for better treatment, and better access to treatment, regardless of geography, the level of medical knowledge, or the wealth of a nation. The bleeding disorders community has the power, the means, and the potential knowledge to bridge, and eradicate, the divide between the developed and developing worlds we serve.

Neutrophil-gelatinase associated lipocalin (NGAL) is an iron-transporting this website protein with increased renal excretion in nephrotoxic

or ischemic kidney injury. We aimed to test the hypothesis that urinary NGAL measurement is useful to monitor acute kidney injury in cholemic nephropathy. Methods: Chow-fed (controls) or norUDCA (0.125% w/w)-treated CL57/BL6 mice were subjected to CBDL for 8 weeks. Urinary NGAL levels were determined at time of harvesting using a commercially available ELISA kit (Lipocalin-2/NGAL DuoSet Mouse, R&D Systems, DY1857). In brief, samples were incubated with detection antibody, labeled with streptavidin-HRP and subsequently measured at 450 nm. Results: Chow-fed CBDL mice exhibited significantly elevated

urinary NGAL levels (29.6 ± 4.2 ng/ ml) compared to norUDCA-treated CBDL mice (9.4 ± 1.8 ng/ ml, p<0.05). NorUDCA treatment significantly ameliorated the degree of selleck compound nephritis and kidney fibrosis and consequently to a significantly reduced renal hydroxyproline content (466 ± 107 μg/g vs. 797 ± 160 μg/g in controls, p<0.05). Conclusions: Urinary NGAL measurement represents a suitable readout for monitoring the degree of cholemic nephropathy in CBDL mice and reflects the therapeutic effects of norUDCA. Future studies should determine urinary NGAL levels in patients with cholemic nephropathy. Disclosures: The Medical University of Graz has filed a patent for the use of norUDCA in the treatment of liver diseases, and P.F. and M.T. are listed as co-inventors (publication number WO2006119803) and P.F. received a research grant and norUDCA from Dr. Falk Pharma GmbH for this project. Disclosures: Michael Trauner - Advisory Committees or Review Panels: MSD, Janssen, Gilead, Abbvie; Consulting: Phenex; Grant/Research Support: Intercept, Falk Pharma, Albireo; Patent Held/Filed: Med Uni Graz (norUDCA);

Speaking and Teaching: Falk Foundation, Roche, Gilead Peter Fickert – Consulting: Falk Foundation, Falk Foundation, MCE Falk Foundation, Falk Foundation; Speaking and Teaching: Roche Austria, Gilead Austria, MSD Austria, MERCK Austria, Roche Austria, Gilead Austria, MSD Austria, MERCK Austria, Roche Austria, Gilead Austria, MSD Austria, MERCK Austria, Roche Austria, Gilead Austria, MSD Austria, MERCK Austria The following people have nothing to disclose: Elisabeth Krones, Dietmar Glaenzer, Franziska Durchschein, Alexander Kirsch, Kathrin Eller, Alexander R. Rosenkranz Patients with cirrhosis develop hyperdynamic circulation with an increase in cardiac output (CO) and a decrease in systemic vascular resistance (SVR). Patients with hyperdynamic circulation can develop circulatory dysfunction(CD) when this compensatory mechanism is insufficient. Although this takes place theoretically in decompensated patients, namely in patients with ascites, its prevalence has never been specifically analysed.

Furthermore, we also assessed the expression levels of MMP2 in the stable PTEN-knockdown clones of SMMC-7721, BEL-7402, and PTEN−/− MEFs. Endogenous MMP2 mRNA expression was markedly up-regulated

in these cell lines. This finding suggests that, in our HCC knockdown cells and knockout MEF models, the enhanced cell invasion mediated by loss of PTEN involved MMP2 up-regulation. Our results were consistent Carfilzomib solubility dmso with those from studies on murine cardiac fibroblasts cells.20 It has been reported that MMP9 is another factor playing important roles in cell invasiveness in HCC via the PI3K pathway.8 Surprisingly, in our study, MMP9 was not detected in gelatin zymography in both wild-type and PTEN knockout MEF cells, even when MM9 transcripts were abundantly expressed in both MEF cell lines (data not shown), suggesting that secretion of MMP9 might not be PTEN-dependent in the MEF model. We further delineated the molecular pathway by which PTEN knockdown enhanced cell invasion.

Previous reports have suggested that SP1 is one of the key regulators of the MMP2 promoter,13, 21, 22 and activation of AKT leads to phosphorylation of SP1, resulting in enhanced transcriptional activity of SP1.14, 23-25 Therefore, we speculated that SP1 might contribute to MMP2 activation in PTEN-deficient cells. Consistent results of enhanced SP1 endogenous protein expression selleck compound and its binding affinity with the MMP2 promoter were observed in PTEN-knockdown BEL-7402 and SMMC-7721

cells. Furthermore, there was a significant but negative association of both SP1 and MMP2 protein expression by immunohistochemistry with PTEN underexpression in human HCCs. Thus, our data provide the first evidence that MMP2 up-regulation upon PTEN loss is SP1-dependent and suggest that the PTEN/AKT/SP1/MMP2 pathway plays an important role in regulating the cell invasive ability in HCC cells. In this study, we documented that PTEN protein was frequently (47.5%) underexpressed in human HCCs. Its underexpression was significantly associated with larger tumor size and tumor microsatellite formation. Significantly, PTEN underexpression was associated with shorter overall survival of patients. Our findings are consistent with those of a number of previous studies showing underexpression of PTEN at both MCE公司 mRNA and protein levels in human HCCs.4, 5, 26-28 The significant association of PTEN underexpression with HCC progression, metastasis, and poorer prognosis in our study was in line with those from previous studies. As we aimed to focus on the relationship between PTEN and HCC invasion in this study, we did not examine the causes of underexpression. Indeed, PTEN is frequently lost or mutated in sporadic cancers and heritable diseases,3, 27, 29 and this may be attributed to chromosomal or allelic losses, mutations, or epigenetic silencing due to DNA methylation or histone deacetylation.

Furthermore, we also assessed the expression levels of MMP2 in the stable PTEN-knockdown clones of SMMC-7721, BEL-7402, and PTEN−/− MEFs. Endogenous MMP2 mRNA expression was markedly up-regulated

in these cell lines. This finding suggests that, in our HCC knockdown cells and knockout MEF models, the enhanced cell invasion mediated by loss of PTEN involved MMP2 up-regulation. Our results were consistent signaling pathway with those from studies on murine cardiac fibroblasts cells.20 It has been reported that MMP9 is another factor playing important roles in cell invasiveness in HCC via the PI3K pathway.8 Surprisingly, in our study, MMP9 was not detected in gelatin zymography in both wild-type and PTEN knockout MEF cells, even when MM9 transcripts were abundantly expressed in both MEF cell lines (data not shown), suggesting that secretion of MMP9 might not be PTEN-dependent in the MEF model. We further delineated the molecular pathway by which PTEN knockdown enhanced cell invasion.

Previous reports have suggested that SP1 is one of the key regulators of the MMP2 promoter,13, 21, 22 and activation of AKT leads to phosphorylation of SP1, resulting in enhanced transcriptional activity of SP1.14, 23-25 Therefore, we speculated that SP1 might contribute to MMP2 activation in PTEN-deficient cells. Consistent results of enhanced SP1 endogenous protein expression Barasertib in vivo and its binding affinity with the MMP2 promoter were observed in PTEN-knockdown BEL-7402 and SMMC-7721

cells. Furthermore, there was a significant but negative association of both SP1 and MMP2 protein expression by immunohistochemistry with PTEN underexpression in human HCCs. Thus, our data provide the first evidence that MMP2 up-regulation upon PTEN loss is SP1-dependent and suggest that the PTEN/AKT/SP1/MMP2 pathway plays an important role in regulating the cell invasive ability in HCC cells. In this study, we documented that PTEN protein was frequently (47.5%) underexpressed in human HCCs. Its underexpression was significantly associated with larger tumor size and tumor microsatellite formation. Significantly, PTEN underexpression was associated with shorter overall survival of patients. Our findings are consistent with those of a number of previous studies showing underexpression of PTEN at both MCE公司 mRNA and protein levels in human HCCs.4, 5, 26-28 The significant association of PTEN underexpression with HCC progression, metastasis, and poorer prognosis in our study was in line with those from previous studies. As we aimed to focus on the relationship between PTEN and HCC invasion in this study, we did not examine the causes of underexpression. Indeed, PTEN is frequently lost or mutated in sporadic cancers and heritable diseases,3, 27, 29 and this may be attributed to chromosomal or allelic losses, mutations, or epigenetic silencing due to DNA methylation or histone deacetylation.

Therefore, pathogens could be introduced by the procedure itself. Although bile was not obtained by ERCP in the study by Olsson et al., they reported previous ERCP as a risk factor for positive bile cultures.[6] After having shown the presence of pathogens in bile and portal tracts of patients with PSC, we investigated whether

PSC patients may manifest an increased Th17 response after pathogen stimulation. Here, we report that in patients with PSC, but not in patients with PBC, stimulation of PBMCs with heat-inactivated bacteria led to a marked induction of Th17 responses. There was no difference click here between patients’ own pathogens and standard pathogens, but it should be noted that nonpathogenic E. coli strains were not able to elicit an increase in IL-17A expression. Of note, and in line with the deleterious effects of Candida cholangitis on the progression of disease, stimulation of PBMCs with inactivated C. albicans led to the highest expression of IL-17A in up to 30% of CD4+ T cells (Fig. 3C). In addition, more Th17 cells were found to coexpress IFN-γ (Th1/Th17 cells) after this website stimulation with E. faecalis or C. albicans (Fig. 5). These cells may be especially relevant for the development of autoimmune diseases[30, 31] and for memory functions involved in the defense

against S. aureus and C. albicans.[28] IL-17A-expressing lymphocytes could be detected around bile ducts of patients with PSC. Whereas these cells can be found in other inflammatory liver diseases as well,[32] 上海皓元医药股份有限公司 it is interesting to note that IL-17A receptors are expressed on biliary epithelial cells (BECs), and that upon stimulation with IL-17, BECs produce proinflammatory cytokines, such as IL-1β, IL-6, and IL-23.[33] These cytokines could, in turn, promote the

survival of Th17 cells. It is tempting to speculate that these cytokines could not only increase the survival of Th17 cells themselves,[34] but also stimulate fibroblasts to induce periductular fibrosis.[35, 36] Selective stimulation of the TLR-5 and −7 ligands, but not stimulation with other TLR ligands, also led to the induction of IL-17A in PSC, but not in the control groups. Further elucidation of signaling pathways involved may help to understand this aberrant response to pathogens. These results are reminiscent of data obtained in IBD patients, where the IL-23/Th17 axis has been reported to shape inflammatory response in the gut.[11] In children with IBD, an aberrant Th17 response to TLR stimulation and stimulation with Candida has been demonstrated previously.[37] Additionally, polymorphisms in genes relevant for the generation and maintenance of Th17 cells, such as the IL-23 receptor, were highly associated with IBD in GWAS.[38] Of note, in the patients reported on here, aberrant Th17 response was independent from the presence or absence of IBD, strongly suggesting that this is a feature of PSC itself and not the associated IBD.

Therefore, pathogens could be introduced by the procedure itself. Although bile was not obtained by ERCP in the study by Olsson et al., they reported previous ERCP as a risk factor for positive bile cultures.[6] After having shown the presence of pathogens in bile and portal tracts of patients with PSC, we investigated whether

PSC patients may manifest an increased Th17 response after pathogen stimulation. Here, we report that in patients with PSC, but not in patients with PBC, stimulation of PBMCs with heat-inactivated bacteria led to a marked induction of Th17 responses. There was no difference Ixazomib order between patients’ own pathogens and standard pathogens, but it should be noted that nonpathogenic E. coli strains were not able to elicit an increase in IL-17A expression. Of note, and in line with the deleterious effects of Candida cholangitis on the progression of disease, stimulation of PBMCs with inactivated C. albicans led to the highest expression of IL-17A in up to 30% of CD4+ T cells (Fig. 3C). In addition, more Th17 cells were found to coexpress IFN-γ (Th1/Th17 cells) after Selleck Roscovitine stimulation with E. faecalis or C. albicans (Fig. 5). These cells may be especially relevant for the development of autoimmune diseases[30, 31] and for memory functions involved in the defense

against S. aureus and C. albicans.[28] IL-17A-expressing lymphocytes could be detected around bile ducts of patients with PSC. Whereas these cells can be found in other inflammatory liver diseases as well,[32] MCE it is interesting to note that IL-17A receptors are expressed on biliary epithelial cells (BECs), and that upon stimulation with IL-17, BECs produce proinflammatory cytokines, such as IL-1β, IL-6, and IL-23.[33] These cytokines could, in turn, promote the

survival of Th17 cells. It is tempting to speculate that these cytokines could not only increase the survival of Th17 cells themselves,[34] but also stimulate fibroblasts to induce periductular fibrosis.[35, 36] Selective stimulation of the TLR-5 and −7 ligands, but not stimulation with other TLR ligands, also led to the induction of IL-17A in PSC, but not in the control groups. Further elucidation of signaling pathways involved may help to understand this aberrant response to pathogens. These results are reminiscent of data obtained in IBD patients, where the IL-23/Th17 axis has been reported to shape inflammatory response in the gut.[11] In children with IBD, an aberrant Th17 response to TLR stimulation and stimulation with Candida has been demonstrated previously.[37] Additionally, polymorphisms in genes relevant for the generation and maintenance of Th17 cells, such as the IL-23 receptor, were highly associated with IBD in GWAS.[38] Of note, in the patients reported on here, aberrant Th17 response was independent from the presence or absence of IBD, strongly suggesting that this is a feature of PSC itself and not the associated IBD.

All enrolled participants received comprehensive information about this study, and informed consent

was obtained before any study-related processes began. The study was conducted at Hanyang University Hospital in Korea between March 2011 and August 2011, and was approved by the Clinical Research Ethics Committee of the Hanyang University Hospital of Korea (2010-04-009). After a 2-week run-in period, enrolled patients were randomly assigned to receive either one capsule (500 mg) of LacClean Gold-S (Cell Biotech, Co. Ltd, Gimpo, Korea; a multispecies probiotics) Dabrafenib chemical structure or one capsule (500 mg) of a placebo twice daily (total dosage 1000 mg/day) for 4 weeks (Fig. 1). The patients were instructed to take the study product between meals because the increased gastric pH is more favorable for the ingested bacteria. LacClean Gold-S is a capsule-form probiotics containing six species beta-catenin inhibitor of live bacteria. The six strains of probiotics were Bifidobacterium bifidum (KCTC 12 199BP), Bifidobacterium lactis (KCTC 11 904BP), Bifidobacterium longum (KCTC 12 200BP), Lactobacillus acidophilus (KCTC 11 906BP), Lactobacillus rhamnosus (KCTC 12 202BP), and Streptococcus thermophilus (KCTC 11 870BP). A total of 5 × 109 viable cells in a lyophilized powder form were included in each

capsule and constituted 13.1% (w/w) of the total weight (500 mg/capsule). The amount of probiotics equally consisted in each of the six strains. The dose was determined based on previous studies where the daily doses were MCE公司 between 5 × 107 and 3.6 × 1011 colony forming units (CFUs)/day, and ≥ 5 × 109 CFUs/day has been suggested.[9-11] The placebo powder contained the same

“other ingredients” as the active medication and maltodextrin instead of bacteria. OY Lee and KN Lee enrolled the patients for this study. Patients were allocated to the probiotics or placebo group using a computer-generated randomization schedule with a 1 : 1 allocation ratio. Dr. Jun generated the random allocation sequence, and no one but him knew the allocation sequence. The practice nurse gave a questionnaire and explained the protocol to the patients. The nurse did not know the allocation sequence and met the patients in regular sequence. The patient received the medication from the clinical pharmacist. No one could differentiate the two drugs without the sequence information. Stool samples for fecal microflora analysis were obtained immediately before the start of treatment and at the end of the 4 weeks of treatment. Fecal microbiota was analyzed only from patients who agreed to the stool sample collection. IBS symptoms were assessed by examiners and patients at baseline and week 4 using a questionnaire. Global relief of IBS symptoms, drug compliance, and adverse events were evaluated by a questionnaire after the 4 weeks of treatment. The primary efficacy end-point was the proportion of patients who experienced global relief of IBS symptoms after the 4-week treatment.

All enrolled participants received comprehensive information about this study, and informed consent

was obtained before any study-related processes began. The study was conducted at Hanyang University Hospital in Korea between March 2011 and August 2011, and was approved by the Clinical Research Ethics Committee of the Hanyang University Hospital of Korea (2010-04-009). After a 2-week run-in period, enrolled patients were randomly assigned to receive either one capsule (500 mg) of LacClean Gold-S (Cell Biotech, Co. Ltd, Gimpo, Korea; a multispecies probiotics) AZD1208 or one capsule (500 mg) of a placebo twice daily (total dosage 1000 mg/day) for 4 weeks (Fig. 1). The patients were instructed to take the study product between meals because the increased gastric pH is more favorable for the ingested bacteria. LacClean Gold-S is a capsule-form probiotics containing six species see more of live bacteria. The six strains of probiotics were Bifidobacterium bifidum (KCTC 12 199BP), Bifidobacterium lactis (KCTC 11 904BP), Bifidobacterium longum (KCTC 12 200BP), Lactobacillus acidophilus (KCTC 11 906BP), Lactobacillus rhamnosus (KCTC 12 202BP), and Streptococcus thermophilus (KCTC 11 870BP). A total of 5 × 109 viable cells in a lyophilized powder form were included in each

capsule and constituted 13.1% (w/w) of the total weight (500 mg/capsule). The amount of probiotics equally consisted in each of the six strains. The dose was determined based on previous studies where the daily doses were MCE公司 between 5 × 107 and 3.6 × 1011 colony forming units (CFUs)/day, and ≥ 5 × 109 CFUs/day has been suggested.[9-11] The placebo powder contained the same

“other ingredients” as the active medication and maltodextrin instead of bacteria. OY Lee and KN Lee enrolled the patients for this study. Patients were allocated to the probiotics or placebo group using a computer-generated randomization schedule with a 1 : 1 allocation ratio. Dr. Jun generated the random allocation sequence, and no one but him knew the allocation sequence. The practice nurse gave a questionnaire and explained the protocol to the patients. The nurse did not know the allocation sequence and met the patients in regular sequence. The patient received the medication from the clinical pharmacist. No one could differentiate the two drugs without the sequence information. Stool samples for fecal microflora analysis were obtained immediately before the start of treatment and at the end of the 4 weeks of treatment. Fecal microbiota was analyzed only from patients who agreed to the stool sample collection. IBS symptoms were assessed by examiners and patients at baseline and week 4 using a questionnaire. Global relief of IBS symptoms, drug compliance, and adverse events were evaluated by a questionnaire after the 4 weeks of treatment. The primary efficacy end-point was the proportion of patients who experienced global relief of IBS symptoms after the 4-week treatment.

The mean age was 57 years with male predominance. Adenoma was detected in 102 patients (48.1%). Adenocarcinoma was documented in 17 patients (8%).

In all groups, most patients were non-smokers (p-value 0.035). Left-sided involvement is most frequent (p-value BMN 673 mw 0.000). Adenomas and non-neoplastic polyps were diminutive in size while adenocarcinomas were >1.0 cm (p-value 0.000). Multiple lesions were seen (p-value 0.001). BMI and age did not show any significant difference among patient groups (p-value 0.144 and 0.618). Logistic regression modeling was not statistically significant. Conclusion: Colorectal adenoma has a calculated prevalence of 48.1%. Most patients have left-sided involvement. No significant association was shown between male gender, age ≥50 years, obesity, family history of colorectal cancer, presence of diabetes, smoking and alcohol intake in the development of colorectal adenoma. Key Word(s): 1. colorectal polyp; PLX4032 nmr 2. colorectal

neoplasia; Table 3. Logistic Regression of Risk Factors tor Colorectal Neoplasia Risk Factors Colorectal Adenoma Colorectal Cancer Odds Ratio p-value Odds Ratio p-value 1. Age ≥50 0.477 0.125 0.696 0.598 2. Male Gender 0.554 0.212 0.868 0.833 3. Obesity (BMI ≥ 30) 0.270 0.223 0.298 0.343 4. Smoking history 0.327 0.081 0.697 0.683 5. Alcohol intake 0.905 0.879 1.286 0.781 6. Family history of CRC 1.131 0.830 1.016 0.985 7. Diabetes melitus 1.349 0.661 2.309 0.330 Presenting Author: SOPHIA ZAMORA ZAMORA Additional Authors: EULENIA NOLASCO NOLASCO, VENANCIO GLORIA

GLORIA Corresponding Author: SOPHIA ZAMORA ZAMORA Affiliations: Manila Doctors Hospital Objective: Intestinal tuberculosis 上海皓元 (ITB) is still a major health concern in the Philippines. This study aims to evaluate the clinicopathologic and endoscopic features of intestinal TB in Manila Doctors Hospital (MDH) a tertiary hospital in the Philippines from August 2010 to August 2012. Methods: This is a descriptive study, involving patients diagnosed with ITB who satisfy at least two of the following criteria: (1) histopathology findings of chronic granulomatous colitis with Langhan’s giant cells (2) positive TB-PCR or (3) positive response to treatment. Results: Twenty–two patients were included in the study. There was an equal distribution of ITB in both males and females. More than 50% belonged to the 21 to 40 years age group. The most common presenting symptoms were abdominal pain, 40.91% and hematochezia, 36.36%. Ulcerative pattern was noted in 40.91% of patients. Ileum was the most common location. Only 31.82% of patients have histopathology findings consistent with ITB. Five of these patients had positive TB-PCR while the other two patients had negative TB-PCR. Majority of patients, 68.18%, has histopathology findings of chronic ileitis and positive for TB-PCR. Conclusion: In this study, the presenting symptoms of ITB were protean and can be seen in other conditions.

The mean age was 57 years with male predominance. Adenoma was detected in 102 patients (48.1%). Adenocarcinoma was documented in 17 patients (8%).

In all groups, most patients were non-smokers (p-value 0.035). Left-sided involvement is most frequent (p-value Selleckchem PF-01367338 0.000). Adenomas and non-neoplastic polyps were diminutive in size while adenocarcinomas were >1.0 cm (p-value 0.000). Multiple lesions were seen (p-value 0.001). BMI and age did not show any significant difference among patient groups (p-value 0.144 and 0.618). Logistic regression modeling was not statistically significant. Conclusion: Colorectal adenoma has a calculated prevalence of 48.1%. Most patients have left-sided involvement. No significant association was shown between male gender, age ≥50 years, obesity, family history of colorectal cancer, presence of diabetes, smoking and alcohol intake in the development of colorectal adenoma. Key Word(s): 1. colorectal polyp; EX527 2. colorectal

neoplasia; Table 3. Logistic Regression of Risk Factors tor Colorectal Neoplasia Risk Factors Colorectal Adenoma Colorectal Cancer Odds Ratio p-value Odds Ratio p-value 1. Age ≥50 0.477 0.125 0.696 0.598 2. Male Gender 0.554 0.212 0.868 0.833 3. Obesity (BMI ≥ 30) 0.270 0.223 0.298 0.343 4. Smoking history 0.327 0.081 0.697 0.683 5. Alcohol intake 0.905 0.879 1.286 0.781 6. Family history of CRC 1.131 0.830 1.016 0.985 7. Diabetes melitus 1.349 0.661 2.309 0.330 Presenting Author: SOPHIA ZAMORA ZAMORA Additional Authors: EULENIA NOLASCO NOLASCO, VENANCIO GLORIA

GLORIA Corresponding Author: SOPHIA ZAMORA ZAMORA Affiliations: Manila Doctors Hospital Objective: Intestinal tuberculosis 上海皓元 (ITB) is still a major health concern in the Philippines. This study aims to evaluate the clinicopathologic and endoscopic features of intestinal TB in Manila Doctors Hospital (MDH) a tertiary hospital in the Philippines from August 2010 to August 2012. Methods: This is a descriptive study, involving patients diagnosed with ITB who satisfy at least two of the following criteria: (1) histopathology findings of chronic granulomatous colitis with Langhan’s giant cells (2) positive TB-PCR or (3) positive response to treatment. Results: Twenty–two patients were included in the study. There was an equal distribution of ITB in both males and females. More than 50% belonged to the 21 to 40 years age group. The most common presenting symptoms were abdominal pain, 40.91% and hematochezia, 36.36%. Ulcerative pattern was noted in 40.91% of patients. Ileum was the most common location. Only 31.82% of patients have histopathology findings consistent with ITB. Five of these patients had positive TB-PCR while the other two patients had negative TB-PCR. Majority of patients, 68.18%, has histopathology findings of chronic ileitis and positive for TB-PCR. Conclusion: In this study, the presenting symptoms of ITB were protean and can be seen in other conditions.