- Email: [email protected]
112 Concomitant Adenoma Rates in Patients with Microscopic Colitis
AGA Abstracts
- 57.8, p=0.002) with a statistically significant trend across quartiles (OR for trend = 1.9, 95% CI 1.3 - 2.8, p=0.001) in the univariate analysis. Adjustment for co-variates did not affect the magnitude of the findings. Conclusion Initially well participants, who have higher adipose tissue concentrations of AA, which represent dietary intake, have a significantly higher risk of developing ulcerative colitis compared to those with lower levels. These findings support previous data from dietary questionnaire-based epidemiological studies showing n-6 PUFAs may be involved in the aetiology of this condition. Lowering the dietary intake of AA may prevent the development of UC. 113
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Subclinical Inflammation Due to Environmental Exposure in Healthy Co-Twins to Twins with Inflammatory Bowel Disease Yaroslava Zhulina, Marie Carlson, Christer G. Peterson, Curt Tysk, Anders Gustavsson, Johan Bohr, Lennart Bodin, Jonas Halfvarson
Low Frequency of IBD-Related Colorectal Carcinoma in Non-Tertiary Centers: Final Results of a Nation Wide Long-Term Survey Judith E. Baars, Ernst J. Kuipers, Ruud Beukers, Adriaan C. Tan, Bas L. Weusten, M. K. Casparie, Christien J. van der Woude
Background and aim: Fecal calprotectin (FC) is a marker of neutrophil and monocyte activity and is elevated in infections, inflammation and malignancies in the gut. Elevated FC has also been observed in first-degree relatives of patients with inflammatory bowel disease. Whether elevated FC is a familial trait due to genetic predisposition or due to shared environmental factors is unknown. Twin studies could be of great help in this respect. Monozygotic twins are genetically identical and share environmental factors during childhood and adolescence, while dizygotic twins share environment to the same extent but only half of the genes. Material and Methods: Twins born 1936-1986 from a Swedish population based cohort of twins with inflammatory bowel disease were clinically phenotyped using the Montreal classification. FC was measured by ELISA kit (EK-CAL, Bühlmann Lab. AG, Switzerland), using <50 μg/g feces as cut off. Logistic regression was used, and odds ratios (OR) with corresponding 95% confidence intervals (95% CI) were calculated. Results: 109 twins, who had not undergone extensive Crohn's disease (CD) or ulcerative colitis (UC) related resections, participated. 33 twin pairs with CD (concordant monozygotic n=6, discordant monozygotic n=13, concordant dizygotic n=l and discordant dizygotic n=13), 16 twin pairs with UC (concordant monozygotic n=1, discordant monozygotic n=10 and discordant dizygotic n=5) as well as 11 single twins (CD n=3, UC n=3, healthy co-twins to twins with CD n=3 and healthy co-twins to twins with UC n=2) participated. A previously described control group (n=31) was used as reference population (Peterson C et al. Am J Gastro 2002). Elevated FC was detected in 36/43 twins (84%) with CD [OR 21.43 (6.43-71.40)] and in 14/20 twins (70%) with UC [OR 9.72 (2.63-35.93)]. Whereas 12/29 (41%) healthy cotwins to twins with CD had increased FC [OR 2.94 (0.92-9.36)] and 12/17 (71%) healthy twin siblings to twins with UC had elevated FC [OR 10.00 (2.54-39.43)]. FC was increased in both monozygotic and dizygotic healthy co-twins to twins with UC, OR 9.72 (1.9349.11) and OR 10.42 (1.61-67.33), respectively. Furthermore, FC seemed to be increased in monozygotic and dizygotic healthy co-twins to twins with CD, OR 3.57 (0.87-14.60) and OR 2.50 (0.65-9.63), respectively. Conclusion: Our preliminary data shows that elevated FC in first-degree relatives of patients with UC is due to shared environment rather than genetic predisposition, this might also be true for CD. These data suggest that environmental exposure cause subclinical inflammation in first-degree relatives. Why these relatives do not developed UC or CD needs to be addressed.
Background & Aim:Guidelines for inflammatory bowel disease (IBD) recommend initiating surveillance after 8-10 yrs of extensive disease and 15-20 yrs of left-sided colitis. We investigated whether these guidelines reflect the natural history of IBD-related colorectal cancer (CRC) in non-tertiary centers. Methods:IBD-related CRC patients (pts) in all nontertiary centers in the Netherlands were identified using a nation-wide automated pathology database (PALGA). Pts with IBD+CRC diagnosed synchronously or metachronously in pathology-reports from 1990-2005 were included. In a 2nd search we included pts ≦65 yrs old to minimize interference with sporadic CRC. Further clinical data were obtained to assess the IBD population and verify diagnosis of IBD-associated CRC. Of selected pts clinical data were collected from pts-charts. Statistical analysis was performed using descriptive statistics, Kaplan-Meier & log-rank tests and cox-regression analysis. Results:In total, 78 of all 93 Dutch non-academic centers participated. We assessed 430 pts-charts and pathology reports. In 197 pts ≦65 yrs old, diagnosis of IBD-related CRC was confirmed: 125 had ulcerative colitis (UC), 69 Crohn's disease (CD) and 3 Indeterminate Colitis. Sixty-four percent were males (126/197), 20 pts had PSC (10%), mean age of diagnosis of IBD was 35 yrs (±15) and of CRC 50 yrs (±11). Eighty-four pts (44%) had T3 tumors and 31(16%) already had metastases at diagnosis. Mean time from IBD-diagnosis to CRC-diagnosis was 15.3 yrs (±12). Type of IBD, gender, concomitant PSC and/or pseudopolyps, and gravity- and extension of inflammation were not significantly associated with time to CRC-diagnosis. Although the latter was not significant (p=0.063), contrary to surveillance guidelines, there was a trend for pts with extensive UC to develop CRC at later stage (mean 16.7 yrs) than pts with leftsided colitis (mean 11 years). Diagnosis of IBD at older age was associated with earlier development of CRC (HR 1.09; 95%CI 1.07-1.10). Forty-eight percent of tumors were located in rectum or sigmoid and 73% occurred in previous inflamed areas. Location of inflammation was not predictive for tumor-location, but UC pts developed more left-sided tumors than CD pts (p=0.022). In 58 hospitals the size of the IBD population could be assessed: 26,855 pts in total, of whom only 163 developed CRC during 15 yrs follow-up. Conclusion:The risk of IBD-associated CRC is limited in a regular, secondary IBD population. Current surveillance strategies need to be adjusted, including equalisation of strategies for left-sided and pancolitis. A nested case-control is being performed, of which the results are expected early 2009.
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The Changing Pattern of Crohn's Disease Incidence According to Age in Northern France: A Constant Increase in the 0-19 Year's Age Group (19882005) Vincent Chouraki, Luc Dauchet, Gwenola Vernier-Massouille, Veronique Merle, Jean-Louis Dupas, Eric Lerebours, Jean-Eric Laberenne, jean-Louis Salomez, Guillaume Savoye, Antoine Cortot, Corinne Gower-Rousseau, Jean-Frederic Colombel
Concomitant Adenoma Rates in Patients with Microscopic Colitis Eugene F. Yen, Bhupesh Pokhrel, Laura K. Bianchi, Hemant K. Roy, Curtis R. Hall, Benjamin Witt Introduction and aims: Microscopic colitis is a chronic inflammatory bowel disease that is currently considered to harbor no increased risk for colon cancer, unlike ulcerative colitis or Crohn's disease of the colon. However, colorectal adenoma, a precursor to colon carcinogenesis, has not been rigorously studied in this setting. Our aim was to identify patients with a diagnosis of microscopic colitis, and to compare the prevalence of adenoma or advanced neoplasia to a reference group of patients without microscopic colitis. Methods: We reviewed the records of patients with a histologic diagnosis of microscopic colitis (MC), lymphocytic colitis (LC), or collagenous colitis (CC), as identified in our pathology database from January 2000 to August 2008. Demographic, endoscopic, and histologic factors were recorded, particularly concomitant adenoma or incident adenocarcinoma. Age and gendermatched patients without diarrhea, presenting for outpatient colonoscopy from July 2005March 2007, served as the reference population in a 1:1 fashion. Results: A total of 745 patients (176 male: 569 female) were identified with a diagnosis of microscopic colitis. Median age was 70 (24-101) and the mean age 67.4 years. Microscopic colitis cases were categorized as lymphocytic colitis (n=418), collagenous colitis (n=284), and “features of both lymphocytic and collagenous colitis” (n=43). Overall, concomitant adenoma was seen 64/418 (15.3%) of lymphocytic colitis, 22/284 (7.75%) of collagenous colitis, and 85/745 (11.4%) of all patients with microscopic colitis, compared to 173/745 (23.2%) of controls (Table). Incident colon cancer was seen in 2/745 cases of microscopic colitis and 5/745 controls. Conclusion: At diagnosis, patients with microscopic colitis are not at increased risk for colon adenoma or adenocarcinoma. The lower rates of concomitant adenoma in MC patients may be attributed to prior colonoscopy with removal of polyps, although both the MC group and the reference group could have had previous colonoscopy. Further investigation and long-term follow-up on this very large cohort of patients is currently being undertaken to determine other disease associations and if a true risk or of colorectal cancer exists. Adenoma or advanced neoplasia
AGA Abstracts
Introduction and aim of the study: Crohn's disease (CD) incidence rates are stable or increase in industrialized countries since the 1980's. In Northern France, we previously reported a 25% increase of CD incidence between 1988 and 1999 (1). The aim of our study was to assess the trends in CD incidence according to age over an 18 years period (1988-2005) in a population-based study. Patients and methods: All patients living in Northern France (Nord, Pas-de-Calais, Somme and Seine-Maritime departments - total of 5 834 574 inhabitants representing 9.5% of the whole French population) between 1988 and 2005 were included in the study. Case ascertainment was established according to a methodology previously described (2). Trends in incidence adjusted for age at diagnosis and sex were studied using a Poisson regression model in six three-year periods (1988-90, 1991-93, 1994-96, 199799, 2000-02, 2003-05). Evolution of CD location at diagnosis and of median diagnosis delay was also studied. Results: 6467 incident CD cases were recorded including 3634 females (F) and 2833 males (M) with a stable sex-ratio (F/M) at 1.3. Median age at diagnosis (27 years, interquartile range (IQR) 20-38) and median diagnosis delay (3 months, IQR: 18) remained unchanged during that period. CD overall incidence rates increased from 5.3/ 105 person-years in 1988-1990 to 6.4 in 2003-2005 (+20.7%), stabilizing after a peak of 7.0 in 1997-1999. CD incidence rates in the 0-19 year's age category increased linearly by 48.5%, from 3.5 in 1988-1990 to 5.2 in 2003-2005. Proportion of patients with initial ileocolonic location increased from 51% in 1988-1990 to 65% in 2002-2005 (p<0.0001) whereas proportion of those with pure colonic location decreased from 27% to 16% (p<0.0001). Conclusions: During the period 1988 to 2005, CD incidence rates increased by 20.7% in the whole population of Northern France and increased two more fold in the 0-19 year's age group. Consequently, studies of CD risk factors should focus on the population aged less than 20. 1-Molinié et al. Gut 2004; 2-Gower-Rousseau et al. Gut 1994.
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- 57.8, p=0.002) with a statistically significant trend across quartiles (OR for trend = 1.9, 95% CI 1.3 - 2.8, p=0.001) in the univariate analysis. Adjustment for co-variates did not affect the magnitude of the findings. Conclusion Initially well participants, who have higher adipose tissue concentrations of AA, which represent dietary intake, have a significantly higher risk of developing ulcerative colitis compared to those with lower levels. These findings support previous data from dietary questionnaire-based epidemiological studies showing n-6 PUFAs may be involved in the aetiology of this condition. Lowering the dietary intake of AA may prevent the development of UC. 113
111
Subclinical Inflammation Due to Environmental Exposure in Healthy Co-Twins to Twins with Inflammatory Bowel Disease Yaroslava Zhulina, Marie Carlson, Christer G. Peterson, Curt Tysk, Anders Gustavsson, Johan Bohr, Lennart Bodin, Jonas Halfvarson
Low Frequency of IBD-Related Colorectal Carcinoma in Non-Tertiary Centers: Final Results of a Nation Wide Long-Term Survey Judith E. Baars, Ernst J. Kuipers, Ruud Beukers, Adriaan C. Tan, Bas L. Weusten, M. K. Casparie, Christien J. van der Woude
Background and aim: Fecal calprotectin (FC) is a marker of neutrophil and monocyte activity and is elevated in infections, inflammation and malignancies in the gut. Elevated FC has also been observed in first-degree relatives of patients with inflammatory bowel disease. Whether elevated FC is a familial trait due to genetic predisposition or due to shared environmental factors is unknown. Twin studies could be of great help in this respect. Monozygotic twins are genetically identical and share environmental factors during childhood and adolescence, while dizygotic twins share environment to the same extent but only half of the genes. Material and Methods: Twins born 1936-1986 from a Swedish population based cohort of twins with inflammatory bowel disease were clinically phenotyped using the Montreal classification. FC was measured by ELISA kit (EK-CAL, Bühlmann Lab. AG, Switzerland), using <50 μg/g feces as cut off. Logistic regression was used, and odds ratios (OR) with corresponding 95% confidence intervals (95% CI) were calculated. Results: 109 twins, who had not undergone extensive Crohn's disease (CD) or ulcerative colitis (UC) related resections, participated. 33 twin pairs with CD (concordant monozygotic n=6, discordant monozygotic n=13, concordant dizygotic n=l and discordant dizygotic n=13), 16 twin pairs with UC (concordant monozygotic n=1, discordant monozygotic n=10 and discordant dizygotic n=5) as well as 11 single twins (CD n=3, UC n=3, healthy co-twins to twins with CD n=3 and healthy co-twins to twins with UC n=2) participated. A previously described control group (n=31) was used as reference population (Peterson C et al. Am J Gastro 2002). Elevated FC was detected in 36/43 twins (84%) with CD [OR 21.43 (6.43-71.40)] and in 14/20 twins (70%) with UC [OR 9.72 (2.63-35.93)]. Whereas 12/29 (41%) healthy cotwins to twins with CD had increased FC [OR 2.94 (0.92-9.36)] and 12/17 (71%) healthy twin siblings to twins with UC had elevated FC [OR 10.00 (2.54-39.43)]. FC was increased in both monozygotic and dizygotic healthy co-twins to twins with UC, OR 9.72 (1.9349.11) and OR 10.42 (1.61-67.33), respectively. Furthermore, FC seemed to be increased in monozygotic and dizygotic healthy co-twins to twins with CD, OR 3.57 (0.87-14.60) and OR 2.50 (0.65-9.63), respectively. Conclusion: Our preliminary data shows that elevated FC in first-degree relatives of patients with UC is due to shared environment rather than genetic predisposition, this might also be true for CD. These data suggest that environmental exposure cause subclinical inflammation in first-degree relatives. Why these relatives do not developed UC or CD needs to be addressed.
Background & Aim:Guidelines for inflammatory bowel disease (IBD) recommend initiating surveillance after 8-10 yrs of extensive disease and 15-20 yrs of left-sided colitis. We investigated whether these guidelines reflect the natural history of IBD-related colorectal cancer (CRC) in non-tertiary centers. Methods:IBD-related CRC patients (pts) in all nontertiary centers in the Netherlands were identified using a nation-wide automated pathology database (PALGA). Pts with IBD+CRC diagnosed synchronously or metachronously in pathology-reports from 1990-2005 were included. In a 2nd search we included pts ≦65 yrs old to minimize interference with sporadic CRC. Further clinical data were obtained to assess the IBD population and verify diagnosis of IBD-associated CRC. Of selected pts clinical data were collected from pts-charts. Statistical analysis was performed using descriptive statistics, Kaplan-Meier & log-rank tests and cox-regression analysis. Results:In total, 78 of all 93 Dutch non-academic centers participated. We assessed 430 pts-charts and pathology reports. In 197 pts ≦65 yrs old, diagnosis of IBD-related CRC was confirmed: 125 had ulcerative colitis (UC), 69 Crohn's disease (CD) and 3 Indeterminate Colitis. Sixty-four percent were males (126/197), 20 pts had PSC (10%), mean age of diagnosis of IBD was 35 yrs (±15) and of CRC 50 yrs (±11). Eighty-four pts (44%) had T3 tumors and 31(16%) already had metastases at diagnosis. Mean time from IBD-diagnosis to CRC-diagnosis was 15.3 yrs (±12). Type of IBD, gender, concomitant PSC and/or pseudopolyps, and gravity- and extension of inflammation were not significantly associated with time to CRC-diagnosis. Although the latter was not significant (p=0.063), contrary to surveillance guidelines, there was a trend for pts with extensive UC to develop CRC at later stage (mean 16.7 yrs) than pts with leftsided colitis (mean 11 years). Diagnosis of IBD at older age was associated with earlier development of CRC (HR 1.09; 95%CI 1.07-1.10). Forty-eight percent of tumors were located in rectum or sigmoid and 73% occurred in previous inflamed areas. Location of inflammation was not predictive for tumor-location, but UC pts developed more left-sided tumors than CD pts (p=0.022). In 58 hospitals the size of the IBD population could be assessed: 26,855 pts in total, of whom only 163 developed CRC during 15 yrs follow-up. Conclusion:The risk of IBD-associated CRC is limited in a regular, secondary IBD population. Current surveillance strategies need to be adjusted, including equalisation of strategies for left-sided and pancolitis. A nested case-control is being performed, of which the results are expected early 2009.
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112
The Changing Pattern of Crohn's Disease Incidence According to Age in Northern France: A Constant Increase in the 0-19 Year's Age Group (19882005) Vincent Chouraki, Luc Dauchet, Gwenola Vernier-Massouille, Veronique Merle, Jean-Louis Dupas, Eric Lerebours, Jean-Eric Laberenne, jean-Louis Salomez, Guillaume Savoye, Antoine Cortot, Corinne Gower-Rousseau, Jean-Frederic Colombel
Concomitant Adenoma Rates in Patients with Microscopic Colitis Eugene F. Yen, Bhupesh Pokhrel, Laura K. Bianchi, Hemant K. Roy, Curtis R. Hall, Benjamin Witt Introduction and aims: Microscopic colitis is a chronic inflammatory bowel disease that is currently considered to harbor no increased risk for colon cancer, unlike ulcerative colitis or Crohn's disease of the colon. However, colorectal adenoma, a precursor to colon carcinogenesis, has not been rigorously studied in this setting. Our aim was to identify patients with a diagnosis of microscopic colitis, and to compare the prevalence of adenoma or advanced neoplasia to a reference group of patients without microscopic colitis. Methods: We reviewed the records of patients with a histologic diagnosis of microscopic colitis (MC), lymphocytic colitis (LC), or collagenous colitis (CC), as identified in our pathology database from January 2000 to August 2008. Demographic, endoscopic, and histologic factors were recorded, particularly concomitant adenoma or incident adenocarcinoma. Age and gendermatched patients without diarrhea, presenting for outpatient colonoscopy from July 2005March 2007, served as the reference population in a 1:1 fashion. Results: A total of 745 patients (176 male: 569 female) were identified with a diagnosis of microscopic colitis. Median age was 70 (24-101) and the mean age 67.4 years. Microscopic colitis cases were categorized as lymphocytic colitis (n=418), collagenous colitis (n=284), and “features of both lymphocytic and collagenous colitis” (n=43). Overall, concomitant adenoma was seen 64/418 (15.3%) of lymphocytic colitis, 22/284 (7.75%) of collagenous colitis, and 85/745 (11.4%) of all patients with microscopic colitis, compared to 173/745 (23.2%) of controls (Table). Incident colon cancer was seen in 2/745 cases of microscopic colitis and 5/745 controls. Conclusion: At diagnosis, patients with microscopic colitis are not at increased risk for colon adenoma or adenocarcinoma. The lower rates of concomitant adenoma in MC patients may be attributed to prior colonoscopy with removal of polyps, although both the MC group and the reference group could have had previous colonoscopy. Further investigation and long-term follow-up on this very large cohort of patients is currently being undertaken to determine other disease associations and if a true risk or of colorectal cancer exists. Adenoma or advanced neoplasia
AGA Abstracts
Introduction and aim of the study: Crohn's disease (CD) incidence rates are stable or increase in industrialized countries since the 1980's. In Northern France, we previously reported a 25% increase of CD incidence between 1988 and 1999 (1). The aim of our study was to assess the trends in CD incidence according to age over an 18 years period (1988-2005) in a population-based study. Patients and methods: All patients living in Northern France (Nord, Pas-de-Calais, Somme and Seine-Maritime departments - total of 5 834 574 inhabitants representing 9.5% of the whole French population) between 1988 and 2005 were included in the study. Case ascertainment was established according to a methodology previously described (2). Trends in incidence adjusted for age at diagnosis and sex were studied using a Poisson regression model in six three-year periods (1988-90, 1991-93, 1994-96, 199799, 2000-02, 2003-05). Evolution of CD location at diagnosis and of median diagnosis delay was also studied. Results: 6467 incident CD cases were recorded including 3634 females (F) and 2833 males (M) with a stable sex-ratio (F/M) at 1.3. Median age at diagnosis (27 years, interquartile range (IQR) 20-38) and median diagnosis delay (3 months, IQR: 18) remained unchanged during that period. CD overall incidence rates increased from 5.3/ 105 person-years in 1988-1990 to 6.4 in 2003-2005 (+20.7%), stabilizing after a peak of 7.0 in 1997-1999. CD incidence rates in the 0-19 year's age category increased linearly by 48.5%, from 3.5 in 1988-1990 to 5.2 in 2003-2005. Proportion of patients with initial ileocolonic location increased from 51% in 1988-1990 to 65% in 2002-2005 (p<0.0001) whereas proportion of those with pure colonic location decreased from 27% to 16% (p<0.0001). Conclusions: During the period 1988 to 2005, CD incidence rates increased by 20.7% in the whole population of Northern France and increased two more fold in the 0-19 year's age group. Consequently, studies of CD risk factors should focus on the population aged less than 20. 1-Molinié et al. Gut 2004; 2-Gower-Rousseau et al. Gut 1994.
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