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Eosinophilic enteritis localized to tunica muscu-laris
AGAA1365
April 2000
the presence of H. pylori IgG-antibodies using the HeloriIgG® ELISA. Positive sera were additionally tested for CagA status by the HeloriCTXIgG® ELISA. The primary outcome parameter of the ECCDS VI was clinical relapse as defined by an increase in CDAI >250 or CDAI >200 with a minimum increase of 60 over the lowest postoperative value for 2 consecutive weeks, by reoperation, a septic complication, or a new fistula within 18 months after resective CD surgery. We used a proportional hazard model to determine whether H. pylori infection, upon other variables, is a risk factor for postsurgical relapse. Results: 30/155 patients (19.4%) reached the primary endpoint. At study entry 36/155 (23.2%) were positive for H. pylori. Only 2 patients became H. pylori negative during follow up. CagA Status could be determined in 33 of these patients and was found positive in 13 (39.4%). Within the observation period 22 (18.5%) of the H. pylori negative patients and 8 (22.2%) of the H. pylori positive relapsed (p=0.63). 3/20 (15%) Cag A negative and 3/13 (23.1 %) Cag A positive patients relapsed (p=0.66). Independent risk factors for relapse identified were: duration of disease (p<0.006), smoking (p<0.025) and chronic activity (p<0.05) but not H. pylori (p=0.71) or CagA status (p=0.35). Conclusion: Despite H. pylori infection increases the operation frequency of infected CD patients, it does not seem to have an impact on the occurence of a clinical relapse within 18 months after surgery. 6210 NEUROENDOCRINE CHANGES IN COLON OF MICE WITH A DISRUPTED INTERLEUKIN·2 GENE. Bi-Feng Qian, Magdy EI-Salhy, Silvia Melgar, Marie-Louise Hammarstr6m, Ake Danielsson, Dept of Medicine, UmeCE Univ, UmeCE, Sweden; Dept of Immunology, UmeCE Univ, UmeCE, Sweden. Neuroendocrine peptides have a variety of physiological functions in the gastrointestinal tract. This study was carried out to investigate the impact of IL-2 deficiency on the neuroendocrine system in normal colon, and the neuroendocrine changes during colonic inflammation. Mice with homozygous disrupted interleukin- 2 gene (lL- 2-1-) spontaneously developed a bowel disease with similarities to human ulcerative colitis. Different types of colonic endocrine cells and myenteric nerves were analyzed in the IL-2-1mice using immunomorphometry. The neuropeptide contents in the colonic tissues were determined by radioimmunoassay. Age matched healthy IL2+1- and IL-2+ 1+ mice served as controls and the colonic IL-2 levels were compared between these two groups of mice by ELISA. Our data showed that only about half amount of IL-2 was synthesized in the colon oflL-2+ 1mice as compared to the IL-2+ 1+ wild type mice. Two major differences in the neuroendocrine colon were found between the mice with an intact and disrupted IL-2 gene. One was age related. The frequencies of various endocrine cells and myenteric nerves increased with age in the IL-2+ 1+ mice. However, no such increases were seen in the mice with a disrupted IL-2 gene. Instead, the volume densities of enteroglucagon, serotonin cells and substance P (SP), vasoactive intestinal polypeptide (VIP) or total myenteric nerves were lower in the older IL-2+ 1- and IL-2-1- mice as compared to the wild type. The other was disease related. Polypeptide YY (PYY) cells and tissue levels of PYY, SP and VIP were significantly decreased in the IL-2-1- mice during the course of bowel inflammation as compared to the healthy IL-2+ 1- and IL-2+ 1+ controls. These findings indicated that colonic neuroendocrine alterations did occur in the mice with a disrupted IL-2 gene and diminished local IL-2 level, suggesting a role of IL-2 in the regulation of the neuroendocrine system and a prevalent interaction between the immune and neuroendocrine systems in normal colon. On the other hand, there were some changes that seemed to correlate with the bowel inflammatory process. They might be associated with the impaired function in inflamed gut and contribute to the development and/or prolongation of of disease. 6211 EPIDEMIOLOGY AND CLINICAL PROFILE OF GASTROINTES· TINAL TUBERCULOSIS IN THE PAST 10 YEARS. Maria Margaret L. Quiblat, Jose D. Sollano, Univ of Santo Tomas, Manila, Philippines. Background and Objectives: Tuberculosis remains a global problem and is a major cause of morbidity and mortality in developing countries. The study aims to determine the prevalence and to describe the clinical profile of patients with gastrointestinal tuberculosis. Methodology: This is a 10 year review of all patients admitted at our institution with a discharge diagnosis of tuberculosis. Charts of all patients with diagnosis of tuberculosis were reviewed. The diagnosis of TB was based on clinical manifestations, AFB stain, culture, biopsy, or a combination of any of these. Results: A total of 1229 patients admitted at Santo Tomas University Hospital from 1989-1998. There were 988 patients (80.4%) diagnosed with pulmonary tuberculosis and 241 (19.6%) with extrapulmonary tuberculosis. The following forms of extrapulmonary tuberculosis were encountered: TB meningitis, 94 (39%); tuberculous pleural effusion, 79 (33%); gastrointestinal tuberculosis, 30 (12.5%); TB adenitis, II (4.1%); TB arthritis, 10 (4.1 %), renal TB , 5 (2.8%); tuberculous pericardial effusion, I (0.4%); Pott s disease, II (4.1). The forms of gastrointestinal tuberculosis was hepatobiliary tuberculosis (n= 16), ileo-cecal tuberculosis (n=3), TB peritonitis (n = 10), and a combination of ileo-cecal tuberculosis and TB peritonitis (n = 1). Out of these 30 patients, only 17 (56.7%) were biopsy-proven Mycobacterium tuberculosis. The age was 33.5 + 11.7 years and 19 (65%) were female. The most common concomitant disease was pulmonary tuberculosis, 18 (59%). A family history of tuberculosis
was seen in 14 (47%). Previous diagnosis of pulmonary tuberculosis was seen in 9 (35%). Of these 9 patients, only 5 had a history of previous anti-tuberculous treatment. The most common clinical manifestations were fever, night sweats, abdominal pain, icteresia, and weightloss. Chest X-ray evidence of tuberculosis were seen in 20 (65%). Haematologic examination revealed a hemoglobin of 106 + 32.9, hematocrit of 32.8 + 10.1; albumin of 24.7 + 11.9. Caseation necrosis was seen in 15 (50%) while chronic granulomatous inflammation was seen in 2 (7%). A positive AFB stain of the peritoneal fluid was demonstrated in only I patient with TB peritonitis. Conclusion: Gastrointestinal tuberculosis is the third most common form of extrapulmonary tuberculosis. Hepatobiliary TB is the most common form of GI tuberculosis. 6212 EOSINOPHILIC ENTERITIS LOCALIZED TO TUNICA MUSCU· LARIS. Sten N. Rasmussen, Peter Gjersoe, Birgit F. Hansen, Hvidovre Univ Hosp, Copenhagen, Denmark. Since the first description of eosiniphilic enteritis by Kaijser in 1937 a little more than 100 cases have been published. We present a case of this disorder in a 45 year old male with clinical and radiological symptoms and signs of inflammatory and stenosing small bowel disease. He also suffered from IDDM and epilepsia due to measles encephalitis during infancy. A diagnosis of Crohn' s disease was considered. He was treated with mesalazine and prednisolone. He improved. However, his diabetes and epilepsia were dysregulated during the period of prednisolone treatment. After cessation of this treatment he detiorated. He developed small bowel obstruction and was operated upon. Sixty em of small bowel was resected. The operation specimen shoved no mucosal ulcerations at all. Histopathological examination revealed the diagnosis of eosinophilic enteritis primarily localized to the tunica muscularis. He was postoperatively extensively investigated for parasitic disease which was not revealed. One year postoperatively he relapsed and small bowel x-ray demonstrated I m narrow and irregular ileum. Due to earlier severe side effects during prednisolone treatment he refused that kind of treatment. He had been on relapse preventing mesalazine and now also azathioprine and cromoglicate were instituted. He went into clinical remission. A small bowel x-ray one year later was normal and he fares well one and a half year after this latest relapse. 6213 PROINFLAMMATORY EFFECT OF LYSOPHOSPHATIC ACID ON CHRONIC COLITIS IN TWO ANIMAL MODELS OF IN· FLAMMATORY BOWEL DISEASE. Heiko C. Rath, Andreas Sturm, Ines Melchner, Juergen Schoelmerich, Axel U. Dignass, Dept of Internal Medicine I, Univ of Regensburg, Regensburg, Germany; Div of Medicine, Univ of Essen, Essen, Germany; Dept of Medicine, Univ Clin Charite, Berlin, Germany. Background: Lysophosphatic acid (LPA) has demonstrated beneficial effect on intestinal epithelial wound repair in vitro and in vivo by enhancement of epithelial cell migration and proliferation through TGF-13 independent pathways. We characterized the effect of LPA on chronic T-cell dependant colitis in two different animal models. Methods: I. HLA-B27 transgenic (TG) rats (N=3), at the age of 3 1/2 months, when chronic colitis is established, were rectally treated with 500 t-tlLPA (5 mmolll) BID for 5 days. Controls (TG; N=3; and non TG; N=3) received 500 t-tl PBS BID for 5 days. Rats were killed 2 days after the last application of LPA. Rectal tissue was taken for biochemical assays and histology. 2. Chronic colitis in Balb/c mice was induced with 8 cycles 5% dextran sulphate sodium (DSS) in tap water (one cycle: 7 days DSS, 10 days water). 15 days after the last DSS application mice were treated rectally with 200 t-tl LPA (5 mmolll) BID for 5 days (N=4). DSS-controls received water (N=4). Balb/c mice without DSS-colitis served as negative controls and received LPA (N=4) or water (N=3). Two days after the last application ofLPA all mice were killed. Rectal tissues were taken for histology. Results: TG rats treated with LPA had significantly more weight loss than TG water controls (28.3 ± 3.4 g vs. 17.3 ± 1.8 g in TG water controls; p<0.05). Colonic inflammation was more evident in the LPA treated TG rats than in water controls, as shown by validated histology score (2.67 ± 0.17 vs. 1.67 ± 0.17 in TG water controls; p<0.015). This was confirmed by rectal tissue IL-113 (718 ± 22.7 pglmg total protein vs. 409 ± 49 pglmg in the TG water controls; p<0.005). Rectal tissue MPO was also increased in LPA treated TG rats compared with TG water controls, but did not reach significance. LPA also induced significant acceleration of intestinal inflammation in chronic DSS (histology: 3.6 ± 0.2 vs. 2.5 ± 0.4 in DSS water controls; p<0.05). Conclusion: Although effective in intestinal epithelial wound repair in vitro and in vivo the phospholipid LPA aggravates chronic colitis in two IBD animal models. This might be due to activation of proinflammatory mediators in the arachidonic pathway.
April 2000
the presence of H. pylori IgG-antibodies using the HeloriIgG® ELISA. Positive sera were additionally tested for CagA status by the HeloriCTXIgG® ELISA. The primary outcome parameter of the ECCDS VI was clinical relapse as defined by an increase in CDAI >250 or CDAI >200 with a minimum increase of 60 over the lowest postoperative value for 2 consecutive weeks, by reoperation, a septic complication, or a new fistula within 18 months after resective CD surgery. We used a proportional hazard model to determine whether H. pylori infection, upon other variables, is a risk factor for postsurgical relapse. Results: 30/155 patients (19.4%) reached the primary endpoint. At study entry 36/155 (23.2%) were positive for H. pylori. Only 2 patients became H. pylori negative during follow up. CagA Status could be determined in 33 of these patients and was found positive in 13 (39.4%). Within the observation period 22 (18.5%) of the H. pylori negative patients and 8 (22.2%) of the H. pylori positive relapsed (p=0.63). 3/20 (15%) Cag A negative and 3/13 (23.1 %) Cag A positive patients relapsed (p=0.66). Independent risk factors for relapse identified were: duration of disease (p<0.006), smoking (p<0.025) and chronic activity (p<0.05) but not H. pylori (p=0.71) or CagA status (p=0.35). Conclusion: Despite H. pylori infection increases the operation frequency of infected CD patients, it does not seem to have an impact on the occurence of a clinical relapse within 18 months after surgery. 6210 NEUROENDOCRINE CHANGES IN COLON OF MICE WITH A DISRUPTED INTERLEUKIN·2 GENE. Bi-Feng Qian, Magdy EI-Salhy, Silvia Melgar, Marie-Louise Hammarstr6m, Ake Danielsson, Dept of Medicine, UmeCE Univ, UmeCE, Sweden; Dept of Immunology, UmeCE Univ, UmeCE, Sweden. Neuroendocrine peptides have a variety of physiological functions in the gastrointestinal tract. This study was carried out to investigate the impact of IL-2 deficiency on the neuroendocrine system in normal colon, and the neuroendocrine changes during colonic inflammation. Mice with homozygous disrupted interleukin- 2 gene (lL- 2-1-) spontaneously developed a bowel disease with similarities to human ulcerative colitis. Different types of colonic endocrine cells and myenteric nerves were analyzed in the IL-2-1mice using immunomorphometry. The neuropeptide contents in the colonic tissues were determined by radioimmunoassay. Age matched healthy IL2+1- and IL-2+ 1+ mice served as controls and the colonic IL-2 levels were compared between these two groups of mice by ELISA. Our data showed that only about half amount of IL-2 was synthesized in the colon oflL-2+ 1mice as compared to the IL-2+ 1+ wild type mice. Two major differences in the neuroendocrine colon were found between the mice with an intact and disrupted IL-2 gene. One was age related. The frequencies of various endocrine cells and myenteric nerves increased with age in the IL-2+ 1+ mice. However, no such increases were seen in the mice with a disrupted IL-2 gene. Instead, the volume densities of enteroglucagon, serotonin cells and substance P (SP), vasoactive intestinal polypeptide (VIP) or total myenteric nerves were lower in the older IL-2+ 1- and IL-2-1- mice as compared to the wild type. The other was disease related. Polypeptide YY (PYY) cells and tissue levels of PYY, SP and VIP were significantly decreased in the IL-2-1- mice during the course of bowel inflammation as compared to the healthy IL-2+ 1- and IL-2+ 1+ controls. These findings indicated that colonic neuroendocrine alterations did occur in the mice with a disrupted IL-2 gene and diminished local IL-2 level, suggesting a role of IL-2 in the regulation of the neuroendocrine system and a prevalent interaction between the immune and neuroendocrine systems in normal colon. On the other hand, there were some changes that seemed to correlate with the bowel inflammatory process. They might be associated with the impaired function in inflamed gut and contribute to the development and/or prolongation of of disease. 6211 EPIDEMIOLOGY AND CLINICAL PROFILE OF GASTROINTES· TINAL TUBERCULOSIS IN THE PAST 10 YEARS. Maria Margaret L. Quiblat, Jose D. Sollano, Univ of Santo Tomas, Manila, Philippines. Background and Objectives: Tuberculosis remains a global problem and is a major cause of morbidity and mortality in developing countries. The study aims to determine the prevalence and to describe the clinical profile of patients with gastrointestinal tuberculosis. Methodology: This is a 10 year review of all patients admitted at our institution with a discharge diagnosis of tuberculosis. Charts of all patients with diagnosis of tuberculosis were reviewed. The diagnosis of TB was based on clinical manifestations, AFB stain, culture, biopsy, or a combination of any of these. Results: A total of 1229 patients admitted at Santo Tomas University Hospital from 1989-1998. There were 988 patients (80.4%) diagnosed with pulmonary tuberculosis and 241 (19.6%) with extrapulmonary tuberculosis. The following forms of extrapulmonary tuberculosis were encountered: TB meningitis, 94 (39%); tuberculous pleural effusion, 79 (33%); gastrointestinal tuberculosis, 30 (12.5%); TB adenitis, II (4.1%); TB arthritis, 10 (4.1 %), renal TB , 5 (2.8%); tuberculous pericardial effusion, I (0.4%); Pott s disease, II (4.1). The forms of gastrointestinal tuberculosis was hepatobiliary tuberculosis (n= 16), ileo-cecal tuberculosis (n=3), TB peritonitis (n = 10), and a combination of ileo-cecal tuberculosis and TB peritonitis (n = 1). Out of these 30 patients, only 17 (56.7%) were biopsy-proven Mycobacterium tuberculosis. The age was 33.5 + 11.7 years and 19 (65%) were female. The most common concomitant disease was pulmonary tuberculosis, 18 (59%). A family history of tuberculosis
was seen in 14 (47%). Previous diagnosis of pulmonary tuberculosis was seen in 9 (35%). Of these 9 patients, only 5 had a history of previous anti-tuberculous treatment. The most common clinical manifestations were fever, night sweats, abdominal pain, icteresia, and weightloss. Chest X-ray evidence of tuberculosis were seen in 20 (65%). Haematologic examination revealed a hemoglobin of 106 + 32.9, hematocrit of 32.8 + 10.1; albumin of 24.7 + 11.9. Caseation necrosis was seen in 15 (50%) while chronic granulomatous inflammation was seen in 2 (7%). A positive AFB stain of the peritoneal fluid was demonstrated in only I patient with TB peritonitis. Conclusion: Gastrointestinal tuberculosis is the third most common form of extrapulmonary tuberculosis. Hepatobiliary TB is the most common form of GI tuberculosis. 6212 EOSINOPHILIC ENTERITIS LOCALIZED TO TUNICA MUSCU· LARIS. Sten N. Rasmussen, Peter Gjersoe, Birgit F. Hansen, Hvidovre Univ Hosp, Copenhagen, Denmark. Since the first description of eosiniphilic enteritis by Kaijser in 1937 a little more than 100 cases have been published. We present a case of this disorder in a 45 year old male with clinical and radiological symptoms and signs of inflammatory and stenosing small bowel disease. He also suffered from IDDM and epilepsia due to measles encephalitis during infancy. A diagnosis of Crohn' s disease was considered. He was treated with mesalazine and prednisolone. He improved. However, his diabetes and epilepsia were dysregulated during the period of prednisolone treatment. After cessation of this treatment he detiorated. He developed small bowel obstruction and was operated upon. Sixty em of small bowel was resected. The operation specimen shoved no mucosal ulcerations at all. Histopathological examination revealed the diagnosis of eosinophilic enteritis primarily localized to the tunica muscularis. He was postoperatively extensively investigated for parasitic disease which was not revealed. One year postoperatively he relapsed and small bowel x-ray demonstrated I m narrow and irregular ileum. Due to earlier severe side effects during prednisolone treatment he refused that kind of treatment. He had been on relapse preventing mesalazine and now also azathioprine and cromoglicate were instituted. He went into clinical remission. A small bowel x-ray one year later was normal and he fares well one and a half year after this latest relapse. 6213 PROINFLAMMATORY EFFECT OF LYSOPHOSPHATIC ACID ON CHRONIC COLITIS IN TWO ANIMAL MODELS OF IN· FLAMMATORY BOWEL DISEASE. Heiko C. Rath, Andreas Sturm, Ines Melchner, Juergen Schoelmerich, Axel U. Dignass, Dept of Internal Medicine I, Univ of Regensburg, Regensburg, Germany; Div of Medicine, Univ of Essen, Essen, Germany; Dept of Medicine, Univ Clin Charite, Berlin, Germany. Background: Lysophosphatic acid (LPA) has demonstrated beneficial effect on intestinal epithelial wound repair in vitro and in vivo by enhancement of epithelial cell migration and proliferation through TGF-13 independent pathways. We characterized the effect of LPA on chronic T-cell dependant colitis in two different animal models. Methods: I. HLA-B27 transgenic (TG) rats (N=3), at the age of 3 1/2 months, when chronic colitis is established, were rectally treated with 500 t-tlLPA (5 mmolll) BID for 5 days. Controls (TG; N=3; and non TG; N=3) received 500 t-tl PBS BID for 5 days. Rats were killed 2 days after the last application of LPA. Rectal tissue was taken for biochemical assays and histology. 2. Chronic colitis in Balb/c mice was induced with 8 cycles 5% dextran sulphate sodium (DSS) in tap water (one cycle: 7 days DSS, 10 days water). 15 days after the last DSS application mice were treated rectally with 200 t-tl LPA (5 mmolll) BID for 5 days (N=4). DSS-controls received water (N=4). Balb/c mice without DSS-colitis served as negative controls and received LPA (N=4) or water (N=3). Two days after the last application ofLPA all mice were killed. Rectal tissues were taken for histology. Results: TG rats treated with LPA had significantly more weight loss than TG water controls (28.3 ± 3.4 g vs. 17.3 ± 1.8 g in TG water controls; p<0.05). Colonic inflammation was more evident in the LPA treated TG rats than in water controls, as shown by validated histology score (2.67 ± 0.17 vs. 1.67 ± 0.17 in TG water controls; p<0.015). This was confirmed by rectal tissue IL-113 (718 ± 22.7 pglmg total protein vs. 409 ± 49 pglmg in the TG water controls; p<0.005). Rectal tissue MPO was also increased in LPA treated TG rats compared with TG water controls, but did not reach significance. LPA also induced significant acceleration of intestinal inflammation in chronic DSS (histology: 3.6 ± 0.2 vs. 2.5 ± 0.4 in DSS water controls; p<0.05). Conclusion: Although effective in intestinal epithelial wound repair in vitro and in vivo the phospholipid LPA aggravates chronic colitis in two IBD animal models. This might be due to activation of proinflammatory mediators in the arachidonic pathway.