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Su1268 Serum Vitamin D Binding Protein Concentration Is Associated With Disease Flare in a Cohort of Patients in Crohn's Disease Remission
AGA Abstracts
the 130 IBD-K patients, cancer involved: the gastrointestinal (GI) (41%;n=53) or genitourinary tract (21%;n=27;urinary n=17), the lung (9.2%;n=12),skin (9.2%;n=12: 4 NMSC, 6 melanoma, 2 Kaposi), breast (6.1%;n=8), lymphoma (4.6%,n=6 only in CD: 4 NHL, IS in 4/6, IS+anti-TNFs 1/6), others (8.4%; n=11). The 53 GI tract cancers included: 35 (66%) colorectal (CRC),6 ileal (11%), 11 (23%) others. GI and genitourinary tract cancers were the first and, respectively, the second more frequent cancer in IBD (p<0.0001 vs others). Cancer sites were comparable in UC vs CD: GI (51% vs 34%), genitourinary tract (17% vs 23%), skin (7% vs 10%), lung (11% vs 8%), breast (6% vs 6%), lymphoma (0 vs 10%;p= ns all), respectively. CRC, including 35/53 (66%) GI cancers,were more frequent in UC vs CD (63% vs 37%;p<0.0001). In CD, the percentage of patients with perforating CD was higher in those developing any cancer (CD-K vs CD-C:29% vs 16%;p=0.01). In UC, the percentage of patients with pancolitis was higher in patients developing any cancer (UC-K vs UC-C: 60% vs 34%;p=0.006). Risk factors for any cancer included perforating behavior in CD (OR 2.94; 95% CI 1.25-7.11), pancolitis in UC (2.95;95% CI 1.35-6.71), but not IS and/or anti-TNFs use (CD:OR 1.77;95% CI 0.95-3.36;UC:OR 0.91; 95% CI 0.31-2.80) in IBD. Age, active smoking, IBD duration, IS and/or anti-TNFs use did not increase the overall cancer risk. CONCLUSIONS. In a prospective multicenter study, clinical characteristics, severity and phenotype of IBD appeared to significantly influence the overall cancer risk in IBD. Pancolitis in UC and penetrating behavior in CD were significant risk factors for any cancer.
1.656, 95%CI 1.092-2.512, p=0.0175). After adjusting for age, surgical remission, medication use and smoking history VDBP remained significantly associated with disease flare with adjusted hazard ratio 1.533, 95% CI 1.002-2.347, p=0.049. Using Kaplan-meier survival analysis the time to flare was significantly shorter in those with VDBP ≥6.26 compared to those with VDBP<6.26, log-rank = 0.0148. Conclusion: In a cohort of CD patients in remission, vitamin D deficiency is uncommon and the serum 25(OH)D3 did not predict subsequent disease flare. In contrast, the vitamin D binding protein concentration was associated with disease flare, which may reflect its function in mediating the inflammatory response. Further investigations to explore the possible mechanisms for this association are warranted.
Su1267 Poor Recognition and Management of Iron Deficiency Anemia in Inflammatory Bowel Disease: A Missed Opportunity Sharmila Subramaniam, Kalpesh Besherdas Introduction: Iron deficiency anaemia (IDA) is a common complication of inflammatory bowel disease (IBD) that has an impact on the patient's quality of life. IDA is caused by inadequate dietary intake, malabsorption of iron and iron loss through intestinal bleeding. Current guidelines recommend that all patients with IBD should be assessed for IDA and that iron supplementation be given as indicated. The aim of this study was to ascertain the prevalence of IDA in our IBD cohort, to look at whether iron replacement therapy (and in what form) was given and to assess treatment response. Methods: A single centre, retrospective analysis of IBD patients from a large district general NHS trust in North London was performed. The database of patients was collated by the IBD Clinical Nurse Specialist. Electronic patient records (blood results and outpatient clinic letters) were used to collect data on patient demographics, diagnosis, screening parameters for IDA (Hb, Ferritin/transferrin saturation, CRP) and iron replacement therapy. The WHO definitions of anaemia were used (Hb<13g/dL in men and Hb<12g/dL in non pregnant women). Iron deficiency was diagnosed if ferritin <30 ug/L in quiescent IBD or <100ug/L in active IBD (CRP elevated) or transferrin saturation <16%. Results: 333 IBD patients were identified in the database. 3 patients were excluded because of insufficient data as their care was transferred. 293/330 (88.8%) were checked for IDA using the screening parameters. 146/293 (49.8%) of this group were found to be anaemic. 101/146 (69.2%) had evidence of iron deficiency. 61/101 (60.4%) were treated using oral and/or intravenous (IV) iron preparations or blood transfusions. Most patients (50/61) received oral iron while 10 patients had IV iron (4 had failed oral therapy) and 6 had a transfusion. The recurrence rate of IDA was 21/50 with oral iron, 4/10 with IV iron and 4/6 with transfusions. We also noted that there were 39/184 patients (21.2%) with iron deficiency in the absence of anaemia. Only 3 of these patients were treated for iron deficiency. Conclusion: The prevalence of IDA in our IBD group was close to 50%. Current practice in our trust does not comply with guidelines as only 60.4% of IDA patients were treated. Iron replacement therapy was mostly administered in the oral form. Recurrence of IDA was similar (about 40%) with both oral and IV iron therapy. There is little guidance on management of iron deficiency in the absence of anaemia and supplementation was not widespread in this group. Barriers to appropriate recognition of IDA including lack of routine monitoring and knowledge on iron data interpretation will need to be addressed to improve practice.
Su1269 Preoperative Anti TNF α Therapy in Ulcerative Colitis Patients Is Not Associated With an Increased Risk of Post Operative Ileal Pouch-Anal Anastomosis (IPAA) Leaks and Infectious Complications Eran Zittan, Raquel Milgrom, Harden Huang, Andrea D. Tyler, Brenda I. O'Connor, Joanne M. Stempak, Robin S. McLeod, Helen M. MacRae, Salah A Metwaly, Richard Kirsch, Robert H. Riddell, Gordon R. Greenberg, Geoffrey C. Nguyen, Kenneth Croitoru, A. Hillary Steinhart, Mark S. Silverberg, Zane Cohen Background: Previous studies of short-term outcomes after preoperative exposure to anti TNF-α therapy in ulcerative colitis (UC) patients who have undergone IPAA have been controversial. By querying our IPAA pouch database, we sought to determine the rate of postoperative pouch leaks and the rate of infectious complications including pelvic abscesses, in anti TNF-α treated UC patient who underwent IPAA surgery versus those who were not treated with anti TNF-α. Methods: A retrospective matched cohort study was performed for subjects with UC who underwent IPAA between 2003 and 2013. Individuals with documented preoperative exposure to infliximab and/or adalimumab from our IBD database were identified. Anti-TNF -α exposure was verified by reviewing both the inpatient and outpatient charts of each individual patient. Control who was not exposed to anti TNF-α therapy pre-operatively was matched to each subject with anti-TNF exposure by age (±10y), diagnosis, BMI, gender, disease duration and albumin. For each patient, we collected the time from the last infusion date to surgery (0-15 days, 15-30 days, 31-180 days and more than 180 days). In addition we collected the cumulative dosage data for each patient. (1, 2, 3, 4 and greater than 4 doses of anti TNF-α therapy pre-operatively). Pouch leaks were documented by clinical and radiologic means. Early leak was defined as occurring within 30 day of the IPAA construction and late post operative leak was defined as within 12 month post ileostomy closure. Comparison between two groups was presented by Pearson Chi-square test and Wilcoxon rank sum test for categorical and continuous variables, respectively Results: 768 UC IPAA patients were reviewed. 20 patients were excluded from the analysis due to missing information. There were 164 patients who were exposure to anti TNF-α therapy and 584 matched patients who were not exposed to anti TNF-α therapy pre-operatively. 79 patients had an IPAA leak. 17 of those 79 patients were exposed to anti TNF-α therapy preoperatively. There were no significant differences in the postoperative IPAA leak rate in those who had been operated upon within 15 days from last anti TNFα dose (n=36), within 15-30 days (n=34) or 31-180 days (n=75) (8.3%,11.7%, 10.6% respectively, p=0.91). There were no significant differences in other secondary outcomes such as pelvic abscesses. (17% vs 11.4%, respectively, P=0.13). There were no significant differences in the postoperative IPAA leak rates in those who had been exposed to more than 4 doses of anti TNF-α preoperatively compared to the matched control group (11.7% vs 10.6% respectively, p=0.49). Conclusion: Preoperative treatment with anti TNF-α therapy in patients with UC having undergone IPAA surgery is not associated with early and or late postoperative IPAA leaks or with infectious complications including pelvic abscesses.
Su1268 Serum Vitamin D Binding Protein Concentration Is Associated With Disease Flare in a Cohort of Patients in Crohn's Disease Remission Simon Ghaly, Katherine Martin, Ruth Prosser, Justine Mill, Lisa A. Simms, Kevin Murray, Graham L. Radford-Smith, Peter A. Bampton, Ian C. Lawrance Introduction: Vitamin D deficiency has recently been associated with a more complicated course of Crohn's disease (CD), including the need for hospitalizations and surgery. This association may be due to a number of confounding factors including reduced sunlight exposure and reduced oral intake in patients with active disease. The vitamin D binding protein (VDBP) has important functions not only in vitamin D transport but also in the inflammatory response, particularly complement and macrophage activation. VDBP levels do not fluctuate with season or sunlight exposure, and thus may be more useful in exploring links between CD activity and vitamin D metabolism. Thus we aimed to examine a population of CD patients in remission to determine if there was an association between VDBP, serum 25(OH)D3 and the calculated free 25(OH)D3 concentrations with disease flare. Methods: Subjects were identified from a prospectively maintained IBD database at 3 teaching hospitals in Australia where serum is stored as part of an ongoing natural history study. Subjects were in steroid free clinical remission at the time of blood collection. Patients were followed up for a minimum of 12 months. Disease flare was defined as a change in symptoms warranting a change in medical therapy and a clinical opinion consistent with disease flare. The stored serum was retrieved and total and epimer-25(OH)D3 were analysed using LC/ MS/MS. The VDBP was analysed using immunonephelemetry. Results: A total of 310 CD patients meeting inclusion criteria were identified. Of these 47% were males and the mean age at diagnosis was 30±16. Disease flare was recorded in 99 (31.9%) over median follow up of 37 months (range 12-128). Serum 25(OH)D3 was in the deficient range (<50nmol/ L) in 37(11.9%), insufficient (50-75nmol/L) in 108 (34.8%) and sufficient (>75) in 165 (53.2%). While the serum total, free and epimer 25(OH)D3 did not predict subsequent disease flare, the VDBP concentration significantly increased the risk of disease flare (HR
AGA Abstracts
Su1270 Incidence of Avascular Necrosis of the Hip in a Large Well-Characterized Cohort of Patients With Inflammatory Bowel Disease Vineet Syan, Thomas J. Learch, Dmitry Karayev, Chadwick Williams, Dermot McGovern, Michael H. Weisman Background: Avascular necrosis of the femoral head affects patients with inflammatory bowel disease out of proportion to the general population. Signs and symptoms of AVN vary and AVN may be under diagnosed. Objective: To report the prevalence and clinical associations for avascular necrosis (AVN) of the femoral head in inflammatory bowel disease (IBD) patients at an IBD tertiary care referral center. A focus was placed on recognition of clinical signs and symptoms of AVN and whether this entity was recognized during the care of patients in this cohort. Methods: IBD patients recruited to the Cedars-Sinai MIRIAD biobank
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the 130 IBD-K patients, cancer involved: the gastrointestinal (GI) (41%;n=53) or genitourinary tract (21%;n=27;urinary n=17), the lung (9.2%;n=12),skin (9.2%;n=12: 4 NMSC, 6 melanoma, 2 Kaposi), breast (6.1%;n=8), lymphoma (4.6%,n=6 only in CD: 4 NHL, IS in 4/6, IS+anti-TNFs 1/6), others (8.4%; n=11). The 53 GI tract cancers included: 35 (66%) colorectal (CRC),6 ileal (11%), 11 (23%) others. GI and genitourinary tract cancers were the first and, respectively, the second more frequent cancer in IBD (p<0.0001 vs others). Cancer sites were comparable in UC vs CD: GI (51% vs 34%), genitourinary tract (17% vs 23%), skin (7% vs 10%), lung (11% vs 8%), breast (6% vs 6%), lymphoma (0 vs 10%;p= ns all), respectively. CRC, including 35/53 (66%) GI cancers,were more frequent in UC vs CD (63% vs 37%;p<0.0001). In CD, the percentage of patients with perforating CD was higher in those developing any cancer (CD-K vs CD-C:29% vs 16%;p=0.01). In UC, the percentage of patients with pancolitis was higher in patients developing any cancer (UC-K vs UC-C: 60% vs 34%;p=0.006). Risk factors for any cancer included perforating behavior in CD (OR 2.94; 95% CI 1.25-7.11), pancolitis in UC (2.95;95% CI 1.35-6.71), but not IS and/or anti-TNFs use (CD:OR 1.77;95% CI 0.95-3.36;UC:OR 0.91; 95% CI 0.31-2.80) in IBD. Age, active smoking, IBD duration, IS and/or anti-TNFs use did not increase the overall cancer risk. CONCLUSIONS. In a prospective multicenter study, clinical characteristics, severity and phenotype of IBD appeared to significantly influence the overall cancer risk in IBD. Pancolitis in UC and penetrating behavior in CD were significant risk factors for any cancer.
1.656, 95%CI 1.092-2.512, p=0.0175). After adjusting for age, surgical remission, medication use and smoking history VDBP remained significantly associated with disease flare with adjusted hazard ratio 1.533, 95% CI 1.002-2.347, p=0.049. Using Kaplan-meier survival analysis the time to flare was significantly shorter in those with VDBP ≥6.26 compared to those with VDBP<6.26, log-rank = 0.0148. Conclusion: In a cohort of CD patients in remission, vitamin D deficiency is uncommon and the serum 25(OH)D3 did not predict subsequent disease flare. In contrast, the vitamin D binding protein concentration was associated with disease flare, which may reflect its function in mediating the inflammatory response. Further investigations to explore the possible mechanisms for this association are warranted.
Su1267 Poor Recognition and Management of Iron Deficiency Anemia in Inflammatory Bowel Disease: A Missed Opportunity Sharmila Subramaniam, Kalpesh Besherdas Introduction: Iron deficiency anaemia (IDA) is a common complication of inflammatory bowel disease (IBD) that has an impact on the patient's quality of life. IDA is caused by inadequate dietary intake, malabsorption of iron and iron loss through intestinal bleeding. Current guidelines recommend that all patients with IBD should be assessed for IDA and that iron supplementation be given as indicated. The aim of this study was to ascertain the prevalence of IDA in our IBD cohort, to look at whether iron replacement therapy (and in what form) was given and to assess treatment response. Methods: A single centre, retrospective analysis of IBD patients from a large district general NHS trust in North London was performed. The database of patients was collated by the IBD Clinical Nurse Specialist. Electronic patient records (blood results and outpatient clinic letters) were used to collect data on patient demographics, diagnosis, screening parameters for IDA (Hb, Ferritin/transferrin saturation, CRP) and iron replacement therapy. The WHO definitions of anaemia were used (Hb<13g/dL in men and Hb<12g/dL in non pregnant women). Iron deficiency was diagnosed if ferritin <30 ug/L in quiescent IBD or <100ug/L in active IBD (CRP elevated) or transferrin saturation <16%. Results: 333 IBD patients were identified in the database. 3 patients were excluded because of insufficient data as their care was transferred. 293/330 (88.8%) were checked for IDA using the screening parameters. 146/293 (49.8%) of this group were found to be anaemic. 101/146 (69.2%) had evidence of iron deficiency. 61/101 (60.4%) were treated using oral and/or intravenous (IV) iron preparations or blood transfusions. Most patients (50/61) received oral iron while 10 patients had IV iron (4 had failed oral therapy) and 6 had a transfusion. The recurrence rate of IDA was 21/50 with oral iron, 4/10 with IV iron and 4/6 with transfusions. We also noted that there were 39/184 patients (21.2%) with iron deficiency in the absence of anaemia. Only 3 of these patients were treated for iron deficiency. Conclusion: The prevalence of IDA in our IBD group was close to 50%. Current practice in our trust does not comply with guidelines as only 60.4% of IDA patients were treated. Iron replacement therapy was mostly administered in the oral form. Recurrence of IDA was similar (about 40%) with both oral and IV iron therapy. There is little guidance on management of iron deficiency in the absence of anaemia and supplementation was not widespread in this group. Barriers to appropriate recognition of IDA including lack of routine monitoring and knowledge on iron data interpretation will need to be addressed to improve practice.
Su1269 Preoperative Anti TNF α Therapy in Ulcerative Colitis Patients Is Not Associated With an Increased Risk of Post Operative Ileal Pouch-Anal Anastomosis (IPAA) Leaks and Infectious Complications Eran Zittan, Raquel Milgrom, Harden Huang, Andrea D. Tyler, Brenda I. O'Connor, Joanne M. Stempak, Robin S. McLeod, Helen M. MacRae, Salah A Metwaly, Richard Kirsch, Robert H. Riddell, Gordon R. Greenberg, Geoffrey C. Nguyen, Kenneth Croitoru, A. Hillary Steinhart, Mark S. Silverberg, Zane Cohen Background: Previous studies of short-term outcomes after preoperative exposure to anti TNF-α therapy in ulcerative colitis (UC) patients who have undergone IPAA have been controversial. By querying our IPAA pouch database, we sought to determine the rate of postoperative pouch leaks and the rate of infectious complications including pelvic abscesses, in anti TNF-α treated UC patient who underwent IPAA surgery versus those who were not treated with anti TNF-α. Methods: A retrospective matched cohort study was performed for subjects with UC who underwent IPAA between 2003 and 2013. Individuals with documented preoperative exposure to infliximab and/or adalimumab from our IBD database were identified. Anti-TNF -α exposure was verified by reviewing both the inpatient and outpatient charts of each individual patient. Control who was not exposed to anti TNF-α therapy pre-operatively was matched to each subject with anti-TNF exposure by age (±10y), diagnosis, BMI, gender, disease duration and albumin. For each patient, we collected the time from the last infusion date to surgery (0-15 days, 15-30 days, 31-180 days and more than 180 days). In addition we collected the cumulative dosage data for each patient. (1, 2, 3, 4 and greater than 4 doses of anti TNF-α therapy pre-operatively). Pouch leaks were documented by clinical and radiologic means. Early leak was defined as occurring within 30 day of the IPAA construction and late post operative leak was defined as within 12 month post ileostomy closure. Comparison between two groups was presented by Pearson Chi-square test and Wilcoxon rank sum test for categorical and continuous variables, respectively Results: 768 UC IPAA patients were reviewed. 20 patients were excluded from the analysis due to missing information. There were 164 patients who were exposure to anti TNF-α therapy and 584 matched patients who were not exposed to anti TNF-α therapy pre-operatively. 79 patients had an IPAA leak. 17 of those 79 patients were exposed to anti TNF-α therapy preoperatively. There were no significant differences in the postoperative IPAA leak rate in those who had been operated upon within 15 days from last anti TNFα dose (n=36), within 15-30 days (n=34) or 31-180 days (n=75) (8.3%,11.7%, 10.6% respectively, p=0.91). There were no significant differences in other secondary outcomes such as pelvic abscesses. (17% vs 11.4%, respectively, P=0.13). There were no significant differences in the postoperative IPAA leak rates in those who had been exposed to more than 4 doses of anti TNF-α preoperatively compared to the matched control group (11.7% vs 10.6% respectively, p=0.49). Conclusion: Preoperative treatment with anti TNF-α therapy in patients with UC having undergone IPAA surgery is not associated with early and or late postoperative IPAA leaks or with infectious complications including pelvic abscesses.
Su1268 Serum Vitamin D Binding Protein Concentration Is Associated With Disease Flare in a Cohort of Patients in Crohn's Disease Remission Simon Ghaly, Katherine Martin, Ruth Prosser, Justine Mill, Lisa A. Simms, Kevin Murray, Graham L. Radford-Smith, Peter A. Bampton, Ian C. Lawrance Introduction: Vitamin D deficiency has recently been associated with a more complicated course of Crohn's disease (CD), including the need for hospitalizations and surgery. This association may be due to a number of confounding factors including reduced sunlight exposure and reduced oral intake in patients with active disease. The vitamin D binding protein (VDBP) has important functions not only in vitamin D transport but also in the inflammatory response, particularly complement and macrophage activation. VDBP levels do not fluctuate with season or sunlight exposure, and thus may be more useful in exploring links between CD activity and vitamin D metabolism. Thus we aimed to examine a population of CD patients in remission to determine if there was an association between VDBP, serum 25(OH)D3 and the calculated free 25(OH)D3 concentrations with disease flare. Methods: Subjects were identified from a prospectively maintained IBD database at 3 teaching hospitals in Australia where serum is stored as part of an ongoing natural history study. Subjects were in steroid free clinical remission at the time of blood collection. Patients were followed up for a minimum of 12 months. Disease flare was defined as a change in symptoms warranting a change in medical therapy and a clinical opinion consistent with disease flare. The stored serum was retrieved and total and epimer-25(OH)D3 were analysed using LC/ MS/MS. The VDBP was analysed using immunonephelemetry. Results: A total of 310 CD patients meeting inclusion criteria were identified. Of these 47% were males and the mean age at diagnosis was 30±16. Disease flare was recorded in 99 (31.9%) over median follow up of 37 months (range 12-128). Serum 25(OH)D3 was in the deficient range (<50nmol/ L) in 37(11.9%), insufficient (50-75nmol/L) in 108 (34.8%) and sufficient (>75) in 165 (53.2%). While the serum total, free and epimer 25(OH)D3 did not predict subsequent disease flare, the VDBP concentration significantly increased the risk of disease flare (HR
AGA Abstracts
Su1270 Incidence of Avascular Necrosis of the Hip in a Large Well-Characterized Cohort of Patients With Inflammatory Bowel Disease Vineet Syan, Thomas J. Learch, Dmitry Karayev, Chadwick Williams, Dermot McGovern, Michael H. Weisman Background: Avascular necrosis of the femoral head affects patients with inflammatory bowel disease out of proportion to the general population. Signs and symptoms of AVN vary and AVN may be under diagnosed. Objective: To report the prevalence and clinical associations for avascular necrosis (AVN) of the femoral head in inflammatory bowel disease (IBD) patients at an IBD tertiary care referral center. A focus was placed on recognition of clinical signs and symptoms of AVN and whether this entity was recognized during the care of patients in this cohort. Methods: IBD patients recruited to the Cedars-Sinai MIRIAD biobank
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