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Michael Fromm - One of the best experts on this subject based on the ideXlab platform.
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Epithelial barrier dysfunction in Lymphocytic Colitis through cytokine-dependent internalization of claudin-5 and -8
Journal of Gastroenterology, 2017Co-Authors: Christian Barmeyer, Irene Erko, Karem Awad, Anja Fromm, Christian Bojarski, Svenja Meissner, Christoph Loddenkemper, Martin Kerick, Britta Siegmund, Michael FrommAbstract:Background Watery diarrhea is the cardinal symptom of Lymphocytic Colitis (LC). We have previously shown that colonic Na malabsorption is one of the major pathologic alterations of LC and found evidence for an epithelial barrier defect. On these grounds, this study aimed to identify the inherent mechanisms of this epithelial barrier dysfunction and its regulatory features. Methods Epithelial resistance ( R ^epi) was determined by one-path impedance spectroscopy and ^3H-mannitol fluxes were performed on biopsies from sigmoid colon in miniaturized Ussing chambers. Tight junction proteins were analyzed by Western blot and confocal microscopy. Inflammatory signaling was characterized in HT-29/B6 cells. Apoptosis and mucosal surface parameters were quantified morphologically. Results R ^epi was reduced to 53% and ^3H-mannitol fluxes increased 1.7-fold in LC due to lower expression of claudin-4, -5, and -8 and altered subcellular claudin-5 and -8 distributions off the tight junction. TNFα and IFNγ could mimic subcellular redistribution in HT-29/B6 cells, a process which was independent on MLCK activation. Epithelial apoptosis did not contribute to barrier dysfunction in LC and mucosal surface area was unchanged. Conclusions Epithelial barrier dysfunction in LC occurs through downregulation of claudin-4, -5, and -8, and redistribution of claudin-5 and -8 off the tight junction, which contributes to diarrhea by a leak-flux mechanism. The key effector cytokines TNFα and IFNγ turned out to be the trigger for redistribution of claudin-5 and -8. Thus, alongside sodium malabsorption, leak-flux is yet another important diarrheal mechanism in LC.
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epithelial barrier dysfunction in Lymphocytic Colitis through cytokine dependent internalization of claudin 5 and 8
Journal of Gastroenterology, 2017Co-Authors: Christian Barmeyer, Irene Erko, Karem Awad, Anja Fromm, Christian Bojarski, Svenja Meissner, Christoph Loddenkemper, Martin Kerick, Britta Siegmund, Michael FrommAbstract:Background Watery diarrhea is the cardinal symptom of Lymphocytic Colitis (LC). We have previously shown that colonic Na malabsorption is one of the major pathologic alterations of LC and found evidence for an epithelial barrier defect. On these grounds, this study aimed to identify the inherent mechanisms of this epithelial barrier dysfunction and its regulatory features.
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enac dysregulation through activation of mek1 2 contributes to impaired na absorption in Lymphocytic Colitis
Inflammatory Bowel Diseases, 2016Co-Authors: Christian Barmeyer, Irene Erko, Anja Fromm, Christian Bojarski, Christoph Loddenkemper, Martin Kerick, Britta Siegmund, Petra Dames, Michael FrommAbstract:BACKGROUND: Lymphocytic Colitis (LC) causes watery diarrhea. We aimed to identify mechanisms of altered Na absorption and regulatory inputs in patients with LC by examining the epithelial Na channel (ENaC) function as the predominant Na transport system in human distal colon. METHODS: Epithelial Na channel function and regulation was analyzed in biopsies from sigmoid colon of patients with LC and in rat distal colon in Ussing chambers. ENaC-subunit expression was measured by real-time PCR and RNA sequencing. Correction factors for subepithelial resistance contributions were determined by impedance spectroscopy. Upstream regulators in LC were determined by RNA sequencing. RESULTS: Epithelial Na channel-mediated electrogenic Na transport was inhibited despite aldosterone stimulation in human sigmoid colon of patients with LC. The increase in γ-ENaC mRNA expression in response to aldosterone was MEK1/2-dependently reduced in LC, since it could be restored toward normal by MEK1/2 inhibition through U0126. Parallel experiments for identification of signaling in rat distal colon established MEK1/2 to be activated by a cytokine cocktail of TNFα, IFNγ, and IL-15, which were identified as the most important regulators in the upstream regulator analysis in LC. CONCLUSIONS: In the sigmoid colon of patients with LC, the key effector cytokines TNFα, IFNγ, and IL-15 inhibited γ-ENaC upregulation in response to aldosterone through a MEK1/2-mediated pathway. This prevents ENaC to reach its maximum transport capacity and results in Na malabsorption which contributes to diarrhea.
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ENaC Dysregulation Through Activation of MEK1/2 Contributes to Impaired Na+ Absorption in Lymphocytic Colitis.
Inflammatory Bowel Diseases, 2016Co-Authors: Christian Barmeyer, Irene Erko, Anja Fromm, Christian Bojarski, Christoph Loddenkemper, Martin Kerick, Britta Siegmund, Michael Fromm, Petra Dames, Michal R. SchweigerAbstract:BACKGROUND: Lymphocytic Colitis (LC) causes watery diarrhea. We aimed to identify mechanisms of altered Na absorption and regulatory inputs in patients with LC by examining the epithelial Na channel (ENaC) function as the predominant Na transport system in human distal colon. METHODS: Epithelial Na channel function and regulation was analyzed in biopsies from sigmoid colon of patients with LC and in rat distal colon in Ussing chambers. ENaC-subunit expression was measured by real-time PCR and RNA sequencing. Correction factors for subepithelial resistance contributions were determined by impedance spectroscopy. Upstream regulators in LC were determined by RNA sequencing. RESULTS: Epithelial Na channel-mediated electrogenic Na transport was inhibited despite aldosterone stimulation in human sigmoid colon of patients with LC. The increase in γ-ENaC mRNA expression in response to aldosterone was MEK1/2-dependently reduced in LC, since it could be restored toward normal by MEK1/2 inhibition through U0126. Parallel experiments for identification of signaling in rat distal colon established MEK1/2 to be activated by a cytokine cocktail of TNFα, IFNγ, and IL-15, which were identified as the most important regulators in the upstream regulator analysis in LC. CONCLUSIONS: In the sigmoid colon of patients with LC, the key effector cytokines TNFα, IFNγ, and IL-15 inhibited γ-ENaC upregulation in response to aldosterone through a MEK1/2-mediated pathway. This prevents ENaC to reach its maximum transport capacity and results in Na malabsorption which contributes to diarrhea.
Martin Kerick - One of the best experts on this subject based on the ideXlab platform.
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Epithelial barrier dysfunction in Lymphocytic Colitis through cytokine-dependent internalization of claudin-5 and -8
Journal of Gastroenterology, 2017Co-Authors: Christian Barmeyer, Irene Erko, Karem Awad, Anja Fromm, Christian Bojarski, Svenja Meissner, Christoph Loddenkemper, Martin Kerick, Britta Siegmund, Michael FrommAbstract:Background Watery diarrhea is the cardinal symptom of Lymphocytic Colitis (LC). We have previously shown that colonic Na malabsorption is one of the major pathologic alterations of LC and found evidence for an epithelial barrier defect. On these grounds, this study aimed to identify the inherent mechanisms of this epithelial barrier dysfunction and its regulatory features. Methods Epithelial resistance ( R ^epi) was determined by one-path impedance spectroscopy and ^3H-mannitol fluxes were performed on biopsies from sigmoid colon in miniaturized Ussing chambers. Tight junction proteins were analyzed by Western blot and confocal microscopy. Inflammatory signaling was characterized in HT-29/B6 cells. Apoptosis and mucosal surface parameters were quantified morphologically. Results R ^epi was reduced to 53% and ^3H-mannitol fluxes increased 1.7-fold in LC due to lower expression of claudin-4, -5, and -8 and altered subcellular claudin-5 and -8 distributions off the tight junction. TNFα and IFNγ could mimic subcellular redistribution in HT-29/B6 cells, a process which was independent on MLCK activation. Epithelial apoptosis did not contribute to barrier dysfunction in LC and mucosal surface area was unchanged. Conclusions Epithelial barrier dysfunction in LC occurs through downregulation of claudin-4, -5, and -8, and redistribution of claudin-5 and -8 off the tight junction, which contributes to diarrhea by a leak-flux mechanism. The key effector cytokines TNFα and IFNγ turned out to be the trigger for redistribution of claudin-5 and -8. Thus, alongside sodium malabsorption, leak-flux is yet another important diarrheal mechanism in LC.
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epithelial barrier dysfunction in Lymphocytic Colitis through cytokine dependent internalization of claudin 5 and 8
Journal of Gastroenterology, 2017Co-Authors: Christian Barmeyer, Irene Erko, Karem Awad, Anja Fromm, Christian Bojarski, Svenja Meissner, Christoph Loddenkemper, Martin Kerick, Britta Siegmund, Michael FrommAbstract:Background Watery diarrhea is the cardinal symptom of Lymphocytic Colitis (LC). We have previously shown that colonic Na malabsorption is one of the major pathologic alterations of LC and found evidence for an epithelial barrier defect. On these grounds, this study aimed to identify the inherent mechanisms of this epithelial barrier dysfunction and its regulatory features.
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enac dysregulation through activation of mek1 2 contributes to impaired na absorption in Lymphocytic Colitis
Inflammatory Bowel Diseases, 2016Co-Authors: Christian Barmeyer, Irene Erko, Anja Fromm, Christian Bojarski, Christoph Loddenkemper, Martin Kerick, Britta Siegmund, Petra Dames, Michael FrommAbstract:BACKGROUND: Lymphocytic Colitis (LC) causes watery diarrhea. We aimed to identify mechanisms of altered Na absorption and regulatory inputs in patients with LC by examining the epithelial Na channel (ENaC) function as the predominant Na transport system in human distal colon. METHODS: Epithelial Na channel function and regulation was analyzed in biopsies from sigmoid colon of patients with LC and in rat distal colon in Ussing chambers. ENaC-subunit expression was measured by real-time PCR and RNA sequencing. Correction factors for subepithelial resistance contributions were determined by impedance spectroscopy. Upstream regulators in LC were determined by RNA sequencing. RESULTS: Epithelial Na channel-mediated electrogenic Na transport was inhibited despite aldosterone stimulation in human sigmoid colon of patients with LC. The increase in γ-ENaC mRNA expression in response to aldosterone was MEK1/2-dependently reduced in LC, since it could be restored toward normal by MEK1/2 inhibition through U0126. Parallel experiments for identification of signaling in rat distal colon established MEK1/2 to be activated by a cytokine cocktail of TNFα, IFNγ, and IL-15, which were identified as the most important regulators in the upstream regulator analysis in LC. CONCLUSIONS: In the sigmoid colon of patients with LC, the key effector cytokines TNFα, IFNγ, and IL-15 inhibited γ-ENaC upregulation in response to aldosterone through a MEK1/2-mediated pathway. This prevents ENaC to reach its maximum transport capacity and results in Na malabsorption which contributes to diarrhea.
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ENaC Dysregulation Through Activation of MEK1/2 Contributes to Impaired Na+ Absorption in Lymphocytic Colitis.
Inflammatory Bowel Diseases, 2016Co-Authors: Christian Barmeyer, Irene Erko, Anja Fromm, Christian Bojarski, Christoph Loddenkemper, Martin Kerick, Britta Siegmund, Michael Fromm, Petra Dames, Michal R. SchweigerAbstract:BACKGROUND: Lymphocytic Colitis (LC) causes watery diarrhea. We aimed to identify mechanisms of altered Na absorption and regulatory inputs in patients with LC by examining the epithelial Na channel (ENaC) function as the predominant Na transport system in human distal colon. METHODS: Epithelial Na channel function and regulation was analyzed in biopsies from sigmoid colon of patients with LC and in rat distal colon in Ussing chambers. ENaC-subunit expression was measured by real-time PCR and RNA sequencing. Correction factors for subepithelial resistance contributions were determined by impedance spectroscopy. Upstream regulators in LC were determined by RNA sequencing. RESULTS: Epithelial Na channel-mediated electrogenic Na transport was inhibited despite aldosterone stimulation in human sigmoid colon of patients with LC. The increase in γ-ENaC mRNA expression in response to aldosterone was MEK1/2-dependently reduced in LC, since it could be restored toward normal by MEK1/2 inhibition through U0126. Parallel experiments for identification of signaling in rat distal colon established MEK1/2 to be activated by a cytokine cocktail of TNFα, IFNγ, and IL-15, which were identified as the most important regulators in the upstream regulator analysis in LC. CONCLUSIONS: In the sigmoid colon of patients with LC, the key effector cytokines TNFα, IFNγ, and IL-15 inhibited γ-ENaC upregulation in response to aldosterone through a MEK1/2-mediated pathway. This prevents ENaC to reach its maximum transport capacity and results in Na malabsorption which contributes to diarrhea.
Christian Barmeyer - One of the best experts on this subject based on the ideXlab platform.
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Epithelial barrier dysfunction in Lymphocytic Colitis through cytokine-dependent internalization of claudin-5 and -8
Journal of Gastroenterology, 2017Co-Authors: Christian Barmeyer, Irene Erko, Karem Awad, Anja Fromm, Christian Bojarski, Svenja Meissner, Christoph Loddenkemper, Martin Kerick, Britta Siegmund, Michael FrommAbstract:Background Watery diarrhea is the cardinal symptom of Lymphocytic Colitis (LC). We have previously shown that colonic Na malabsorption is one of the major pathologic alterations of LC and found evidence for an epithelial barrier defect. On these grounds, this study aimed to identify the inherent mechanisms of this epithelial barrier dysfunction and its regulatory features. Methods Epithelial resistance ( R ^epi) was determined by one-path impedance spectroscopy and ^3H-mannitol fluxes were performed on biopsies from sigmoid colon in miniaturized Ussing chambers. Tight junction proteins were analyzed by Western blot and confocal microscopy. Inflammatory signaling was characterized in HT-29/B6 cells. Apoptosis and mucosal surface parameters were quantified morphologically. Results R ^epi was reduced to 53% and ^3H-mannitol fluxes increased 1.7-fold in LC due to lower expression of claudin-4, -5, and -8 and altered subcellular claudin-5 and -8 distributions off the tight junction. TNFα and IFNγ could mimic subcellular redistribution in HT-29/B6 cells, a process which was independent on MLCK activation. Epithelial apoptosis did not contribute to barrier dysfunction in LC and mucosal surface area was unchanged. Conclusions Epithelial barrier dysfunction in LC occurs through downregulation of claudin-4, -5, and -8, and redistribution of claudin-5 and -8 off the tight junction, which contributes to diarrhea by a leak-flux mechanism. The key effector cytokines TNFα and IFNγ turned out to be the trigger for redistribution of claudin-5 and -8. Thus, alongside sodium malabsorption, leak-flux is yet another important diarrheal mechanism in LC.
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epithelial barrier dysfunction in Lymphocytic Colitis through cytokine dependent internalization of claudin 5 and 8
Journal of Gastroenterology, 2017Co-Authors: Christian Barmeyer, Irene Erko, Karem Awad, Anja Fromm, Christian Bojarski, Svenja Meissner, Christoph Loddenkemper, Martin Kerick, Britta Siegmund, Michael FrommAbstract:Background Watery diarrhea is the cardinal symptom of Lymphocytic Colitis (LC). We have previously shown that colonic Na malabsorption is one of the major pathologic alterations of LC and found evidence for an epithelial barrier defect. On these grounds, this study aimed to identify the inherent mechanisms of this epithelial barrier dysfunction and its regulatory features.
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enac dysregulation through activation of mek1 2 contributes to impaired na absorption in Lymphocytic Colitis
Inflammatory Bowel Diseases, 2016Co-Authors: Christian Barmeyer, Irene Erko, Anja Fromm, Christian Bojarski, Christoph Loddenkemper, Martin Kerick, Britta Siegmund, Petra Dames, Michael FrommAbstract:BACKGROUND: Lymphocytic Colitis (LC) causes watery diarrhea. We aimed to identify mechanisms of altered Na absorption and regulatory inputs in patients with LC by examining the epithelial Na channel (ENaC) function as the predominant Na transport system in human distal colon. METHODS: Epithelial Na channel function and regulation was analyzed in biopsies from sigmoid colon of patients with LC and in rat distal colon in Ussing chambers. ENaC-subunit expression was measured by real-time PCR and RNA sequencing. Correction factors for subepithelial resistance contributions were determined by impedance spectroscopy. Upstream regulators in LC were determined by RNA sequencing. RESULTS: Epithelial Na channel-mediated electrogenic Na transport was inhibited despite aldosterone stimulation in human sigmoid colon of patients with LC. The increase in γ-ENaC mRNA expression in response to aldosterone was MEK1/2-dependently reduced in LC, since it could be restored toward normal by MEK1/2 inhibition through U0126. Parallel experiments for identification of signaling in rat distal colon established MEK1/2 to be activated by a cytokine cocktail of TNFα, IFNγ, and IL-15, which were identified as the most important regulators in the upstream regulator analysis in LC. CONCLUSIONS: In the sigmoid colon of patients with LC, the key effector cytokines TNFα, IFNγ, and IL-15 inhibited γ-ENaC upregulation in response to aldosterone through a MEK1/2-mediated pathway. This prevents ENaC to reach its maximum transport capacity and results in Na malabsorption which contributes to diarrhea.
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ENaC Dysregulation Through Activation of MEK1/2 Contributes to Impaired Na+ Absorption in Lymphocytic Colitis.
Inflammatory Bowel Diseases, 2016Co-Authors: Christian Barmeyer, Irene Erko, Anja Fromm, Christian Bojarski, Christoph Loddenkemper, Martin Kerick, Britta Siegmund, Michael Fromm, Petra Dames, Michal R. SchweigerAbstract:BACKGROUND: Lymphocytic Colitis (LC) causes watery diarrhea. We aimed to identify mechanisms of altered Na absorption and regulatory inputs in patients with LC by examining the epithelial Na channel (ENaC) function as the predominant Na transport system in human distal colon. METHODS: Epithelial Na channel function and regulation was analyzed in biopsies from sigmoid colon of patients with LC and in rat distal colon in Ussing chambers. ENaC-subunit expression was measured by real-time PCR and RNA sequencing. Correction factors for subepithelial resistance contributions were determined by impedance spectroscopy. Upstream regulators in LC were determined by RNA sequencing. RESULTS: Epithelial Na channel-mediated electrogenic Na transport was inhibited despite aldosterone stimulation in human sigmoid colon of patients with LC. The increase in γ-ENaC mRNA expression in response to aldosterone was MEK1/2-dependently reduced in LC, since it could be restored toward normal by MEK1/2 inhibition through U0126. Parallel experiments for identification of signaling in rat distal colon established MEK1/2 to be activated by a cytokine cocktail of TNFα, IFNγ, and IL-15, which were identified as the most important regulators in the upstream regulator analysis in LC. CONCLUSIONS: In the sigmoid colon of patients with LC, the key effector cytokines TNFα, IFNγ, and IL-15 inhibited γ-ENaC upregulation in response to aldosterone through a MEK1/2-mediated pathway. This prevents ENaC to reach its maximum transport capacity and results in Na malabsorption which contributes to diarrhea.
Curt Tysk - One of the best experts on this subject based on the ideXlab platform.
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Large intestine: Remission of Lymphocytic Colitis with budesonide.
Nature Reviews Gastroenterology & Hepatology, 2009Co-Authors: Curt TyskAbstract:Few randomized, controlled trials have investigated the efficacy of pharmacological treatment for Lymphocytic Colitis. data from a new randomized, placebo-controlled trial have demonstrated the efficacy of budesonide in inducing remission of this disease; this study is an important contribution to this field.
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Lymphocytic Colitis a retrospective clinical study of 199 swedish patients
Gut, 2004Co-Authors: Martin Olesen, Sune Eriksson, Johan Bohr, G Jarnerot, Curt TyskAbstract:Background: Lymphocytic Colitis is characterised by chronic diarrhoea and specific microscopic changes in a macroscopically normal colonic mucosa. We report clinical features and treatment outcome in a large patient cohort. Methods: Patients were searched for in 24 Swedish gastroenterology clinics. The biopsy material was reassessed using strict histopathological criteria. Clinical data were obtained from medical notes. Results: Lymphocytic Colitis was diagnosed in 199 cases. The female:male ratio was 2.4:1. Median age at diagnosis was 59 (48–70) years. The most frequent symptoms were diarrhoea (96%), abdominal pain (47%), and weight loss (41%). The course was chronic intermittent in 30% of patients, chronic continuous in 7%, and a single attack in 63%, and in these cases the disease duration was 6 (4–11) months. Seventy nine (40%) patients reported associated diseases, of which thyroid disorders, coeliac disease, and diabetes mellitus were the most common. In 34 first or second degree relatives of 24 (12%) patients, a family history of ulcerative Colitis, Crohn’s disease, collagenous Colitis, or coeliac disease was reported. Drug induced disease was suspected in 19 (10%) patients. A non-significant peak of disease onset was seen in December-January. More than 80% of treated patients improved on corticosteroids, including budesonide. Conclusions: A family history of other bowel disorders is a new finding. The sudden onset and single attack of limited duration may support a possible infectious cause in some cases. Drugs may cause Lymphocytic Colitis.
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collagenous and Lymphocytic Colitis a clinical and histopathological review
Canadian Journal of Gastroenterology & Hepatology, 2000Co-Authors: Johan Bohr, Curt Tysk, Martin Olesen, G JarnerotAbstract:Collagenous Colitis and Lymphocytic Colitis are newly described colitides that are only diagnosable microscopically; therefore, both are known under the umbrella term ’microscopic Colitis’. This is a short review of the clinical findings, and epidemiological and basic observations of these relatively little described colitides belonging to the group of inflammatory bowel diseases.
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increased nitric oxide production in collagenous and Lymphocytic Colitis
European Journal of Clinical Investigation, 1997Co-Authors: Jon O Lundberg, Curt Tysk, Martin Olesen, Johan Bohr, M Herulf, N P Wiklund, Edward Morcos, Per M Hellstrom, Eddie Weitzberg, G JarnerotAbstract:The production of nitric oxide (NO) is increased in active ulcerative Colitis and in Crohn's disease. We have studied NO production in collagenous Colitis (CC) and Lymphocytic Colitis (LC), both of which are inflammatory bowel disorders of unknown aetiology. NO levels were measured directly in gas sampled from the colon during colonoscopy. Plasma levels of NO metabolites (nitrate/nitrite) were also measured. Luminal NO levels were more than 100 times higher in patients with CC compared with controls. In addition, plasma levels of nitrate/nitrite were increased in the patients as compared with controls. Measurements of NO directly in the colon or its oxidation products in plasma may be a helpful tool in further understanding the role of NO in the pathophysiology of CC and LC. Moreover, it is tempting to speculate that these measurements could be clinically useful in the diagnosis and therapy monitoring of these two inflammatory bowel diseases.
Fernando Fernandezbanares - One of the best experts on this subject based on the ideXlab platform.
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efficacy and safety of budesonide vs mesalazine or placebo as induction therapy for Lymphocytic Colitis
Gastroenterology, 2018Co-Authors: Stephan Miehlke, Fernando Fernandezbanares, Daniela Aust, Emese Mihaly, P Armerding, Gunther Bohm, Ole K Bonderup, Juozas Kupcinskas, Lars Kristian Munck, Kaiuwe RehbehnAbstract:Background & Aims Lymphocytic Colitis is a common cause of chronic, nonbloody diarrhea. However, the effects of treatment are unclear and randomized placebo-controlled trials were requested in a Cochrane review. We performed a randomized, placebo-controlled, multicenter study to evaluate budesonide and mesalazine as induction therapy for Lymphocytic Colitis. Methods Patients with active Lymphocytic Colitis were randomly assigned to groups given budesonide 9 mg once daily (Budenofalk granules), mesalazine 3 g once daily (Salofalk granules), or placebo for 8 weeks in a double-blind, double-dummy design. The primary endpoint was clinical remission, defined as ≤21 stools (including ≤6 watery stools), in the 7 days before week 8. Results The final analysis included 57 patients (19 per group). Most patients were female (72%) and the mean age was 59 years. The proportion of patients in clinical remission at week 8 was significantly higher in the budesonide group than in the placebo group (intention-to-treat analysis, 79% vs 42%; P = .01). The difference in proportions of patients in clinical remission at week 8 between the mesalazine (63%) and placebo groups was not significant (P = .09). The proportion of patients with histologic remission at week 8 was significantly higher in the budesonide group (68%) vs the mesalazine (26%; P = .02) or placebo (21%; P = .008) groups. The incidence of adverse events was 47.4% in the budesonide group, 68.4% in the mesalazine group, and 42.1% in the placebo group. Conclusions In a randomized multicenter study, we found oral budesonide 9 mg once daily to be effective and safe for induction of clinical and histologic remission in patients with Lymphocytic Colitis, compared with placebo. Oral mesalazine 3 g once daily was not significantly better than placebo. ClinicalTrials.gov no: NCT01209208 .
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original contributionsincidence of collagenous and Lymphocytic Colitis a 5 year population based study
The American Journal of Gastroenterology, 1999Co-Authors: Fernando Fernandezbanares, Antonio Salas, Maria Esteve, Montserrat Forne, Jorge C Espinos, Josep Maria ViverAbstract:Objective: The incidence of collagenous and Lymphocytic Colitis is not well known. We sought to assess the incidence of collagenous and Lymphocytic Colitis in a well-defined population during a 5-yr study period. Methods: From January 1, 1993, to December 31, 1997, all new patients diagnosed with collagenous or Lymphocytic Colitis living in the catchment area of the Hospital Mutua de Terrassa (Barcelona, Spain) were identified. Since 1993 all patients with chronic diarrhea were referred for a diagnostic colonoscopy. Multiple biopsy sampling of the entire colon was performed when appearance of the colonic mucosa was grossly normal. Results: Twenty-three cases of collagenous Colitis and 37 of Lymphocytic Colitis were diagnosed. The female:male ratios were 4.75:1 and 2.7:1 for collagenous and Lymphocytic Colitis, respectively. The mean age at onset of symptoms was 53.4 ± 3.2 (range, 29–82) yr for collagenous Colitis, and 64.3 ± 2.7 (range, 28–87) yr for Lymphocytic Colitis (p = 0.012). The mean annual incidence per 100,000 inhabitants based on the year of onset of symptoms was 1.1 (95% confidence interval [CI], 0.4–1.7) for collagenous Colitis, and 3.1 (95% CI, 2.0–4.2) for Lymphocytic Colitis. A peak incidence was observed in older women in both diseases. A rate of microscopic Colitis of 9.5 per 100 normal-looking colonoscopies performed in patients with chronic watery diarrhea was observed. Normal rectal biopsies were found in 43% and 8% of patients with collagenous and Lymphocytic Colitis, respectively. Conclusions: The incidence of Lymphocytic Colitis is three times higher than that of collagenous Colitis. Microscopic Colitis should be considered as a major possibility in the work-up of chronic diarrhea in older women.
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incidence of collagenous and Lymphocytic Colitis a 5 year population based study
The American Journal of Gastroenterology, 1999Co-Authors: Fernando Fernandezbanares, Antonio Salas, Maria Esteve, Montserrat Forne, Jorge C Espinos, Josep Maria ViverAbstract:Objective: The incidence of collagenous and lympho- cytic Colitis is not well known. We sought to assess the incidence of collagenous and Lymphocytic Colitis in a well-defined population during a 5-yr study period. Methods: From January 1, 1993, to December 31, 1997, all new patients diagnosed with collagenous or lympho- cytic Colitis living in the catchment area of the Hospital Mutua de Terrassa (Barcelona, Spain) were identified. Since 1993 all patients with chronic diarrhea were re- ferred for a diagnostic colonoscopy. Multiple biopsy sampling of the entire colon was performed when ap- pearance of the colonic mucosa was grossly normal. Results: Twenty-three cases of collagenous Colitis and 37 of Lymphocytic Colitis were diagnosed. The female:male ratios were 4.75:1 and 2.7:1 for collagenous and lym- phocytic Colitis, respectively. The mean age at onset of symptoms was 53.4 6 3.2 (range, 29 - 82) yr for collag- enous Colitis, and 64.3 6 2.7 (range, 28 - 87) yr for lym- phocytic Colitis (p 5 0.012). The mean annual incidence per 100,000 inhabitants based on the year of onset of symptoms was 1.1 (95% confidence interval (CI), 0.4 - 1.7) for collagenous Colitis, and 3.1 (95% CI, 2.0 - 4.2) for Lymphocytic Colitis. A peak incidence was observed in older women in both diseases. A rate of microscopic Colitis of 9.5 per 100 normal-looking colonoscopies per- formed in patients with chronic watery diarrhea was observed. Normal rectal biopsies were found in 43% and 8% of patients with collagenous and Lymphocytic Colitis, respectively. Conclusions: The incidence of Lymphocytic Colitis is three times higher than that of collagenous Colitis. Microscopic Colitis should be considered as a major possibility in the work-up of chronic diarrhea in older women. (Am J Gastroenterol 1999;94:418 - 423. © 1999 by Am. Coll. of Gastroenterology)
