The Experts below are selected from a list of 15168 Experts worldwide ranked by ideXlab platform
Hasse Abrahamsson - One of the best experts on this subject based on the ideXlab platform.
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Long-term Course in Collagenous Colitis and the Impact of Bile Acid Malabsorption and Bile Acid Sequestrants on Histopathology and Clinical Features
2001Co-Authors: Kjell-arne Ung, Anders Kilander, Ola Nilsson, Hasse AbrahamssonAbstract:Background: Bile acid Malabsorption is common in collagenous colitis, although long-term follow-up data on the impact of bile acids are limited. The aim was to study whether bile acid Malabsorption is a permanent finding, with an impact on histopathology and clinical features in collagenous colitis. Methods:
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role of bile acids and bile acid binding agents in patients with collagenous colitis
2000Co-Authors: Richard Gillberg, Anders Kilander, Hasse AbrahamssonAbstract:BACKGROUND—In a retrospective study bile acid Malabsorption was observed in patients with collagenous colitis. AIMS—To study the occurrence of bile acid Malabsorption and the effect of bile acid binders prospectively in patients with chronic diarrhoea and collagenous colitis. METHODS—Over 36 months all patients referred because of chronic diarrhoea completed a diagnostic programme, including gastroscopy with duodenal biopsy, colonoscopy with biopsies, and the 75Se-homocholic acid taurine (75SeHCAT) test for bile acid Malabsorption. Treatment with a bile acid binder (cholestyramine in 24, colestipol in three) was given, irrespective of the results of the 75SeHCAT test. RESULTS—Collagenous colitis was found in 28 patients (six men, 22 women), 27 of whom had persistent symptoms and completed the programme. Four patients had had a previous cholecystectomy or a distal gastric resection. The 75SeHCAT test was abnormal in 12/27 (44%) of the collagenous colitis patients with 75SeHCAT values 0.5-9.7%, and normal in 15 patients (56%). Bile acid binding treatment was followed by a rapid, marked, or complete improvement in 21/27 (78%) of the collagenous colitis patients. Rapid improvement occurred in 11/12 (92%) of the patients with bile acid Malabsorption compared with 10/15 (67%) of the patients with normal 75SeHCAT tests. CONCLUSION—Bile acid Malabsorption is common in patients with collagenous colitis and is probably an important pathophysiological factor. Because of a high response rate without serious side effects, bile acid binding treatment should be considered for collagenous colitis, particularly patients with bile acid Malabsorption. Keywords: bile acid Malabsorption; collagenous colitis; diarrhoea; cholestyramine; colestipol
Virginia A Stallings - One of the best experts on this subject based on the ideXlab platform.
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pancreatic function in chronic pancreatitis a cohort study comparing 3 methods of detecting fat Malabsorption and the impact of short term pancreatic enzyme replacement therapy
2019Co-Authors: Jefferson N Brownell, Joan I Schall, Virginia A StallingsAbstract:ObjectivesReliable pancreatic function tests in patients with chronic pancreatitis (CP) are needed. This cohort study identified Malabsorption in people with CP compared with healthy people and then investigated short-term pancreatic enzyme replacement therapy (PERT) and fat Malabsorption, nutrition
M Raithel - One of the best experts on this subject based on the ideXlab platform.
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brown bowel syndrome a rare complication in diseases associated with long standing Malabsorption
2014Co-Authors: H Albrecht, A Hagel, Thomas M De Rossi, Tilman T Rau, Thomas Kirchner, Markus F Neurath, M RaithelAbstract:BACKGROUND/AIMS Longtime chronic Malabsorption may among other things cause a lack of liposoluble vitamins. Vitamin E deficiency can lead to formation of lipofuscin aggregates. Its deficiency is also associated with an increased lipofuscinosis of the bowel, i.e. brown bowel syndrome. METHODS Systematic research via Medline on brown bowel syndrome, lipofuscinosis, and vitamin E deficiency was performed. We combined our own clinical experience and a review of the literature for this paper. Its goal is to inform about the possible consequences of severe Malabsorption and brown bowel syndrome. RESULTS Systematic data about the occurrence of severe Malabsorption and brown bowel syndrome are rare. Only about 27 scientific reports can be found on this subject. Brown bowel syndrome is found mostly in conjunction with vitamin E deficiency and lipofuscinosis of the bowel. The clinical findings are caused by both Malabsorption and lipofuscinosis. Case reports show a therapeutic effect of vitamin E. CONCLUSION Vitamin deficiency caused by longtime chronic Malabsorption can lead to the development of brown bowel syndrome, which is seen as the expression of lipofuscinosis of the bowel, and can cause further clinical disorders. Patients with Malabsorption should therefore be monitored regarding their vitamin E levels.
Albert De La Chapelle - One of the best experts on this subject based on the ideXlab platform.
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inherited cobalamin Malabsorption mutations in three genes reveal functional and ethnic patterns
2012Co-Authors: Stephan M Tanner, Amy C Sturm, Elizabeth C Baack, Sandya Liyanarachchi, Albert De La ChapelleAbstract:Inherited Malabsorption of cobalamin (Cbl) causes hematological and neurological abnormalities that can be fatal. Three genes have been implicated in Cbl Malabsorption; yet, only about 10% of ~400-500 reported cases have been molecularly studied to date. Recessive mutations in CUBN or AMN cause Imerslund-Grasbeck Syndrome (IGS), while recessive mutations in GIF cause Intrinsic Factor Deficiency (IFD). IGS and IFD differ in that IGS usually presents with proteinuria, which is not observed in IFD. The genetic heterogeneity and numerous differential diagnoses make clinical assessment difficult. We present a large genetic screening study of 154 families or patients with suspected hereditary Cbl Malabsorption. Patients and their families have been accrued over a period spanning >12 years. Systematic genetic testing of the three genes CUBN, AMN, and GIF was accomplished using a combination of single strand conformation polymorphism and DNA and RNA sequencing. In addition, six genes that were contenders for a role in inherited Cbl Malabsorption were studied in a subset of these patients. Our results revealed population-specific mutations, mutational hotspots, and functionally distinct regions in the three causal genes. We identified mutations in 126/154 unrelated cases (82%). Fifty-three of 126 cases (42%) were mutated in CUBN, 45/126 (36%) were mutated in AMN, and 28/126 (22%) had mutations in GIF. We found 26 undescribed mutations in CUBN, 19 in AMN, and 7 in GIF for a total of 52 novel defects described herein. We excluded six other candidate genes as culprits and concluded that additional genes might be involved. Cbl Malabsorption is found worldwide and genetically complex. However, our results indicate that population-specific founder mutations are quite common. Consequently, targeted genetic testing has become feasible if ethnic ancestry is considered. These results will facilitate clinical and molecular genetic testing of Cbl Malabsorption. Early diagnosis improves the lifelong care required by these patients and prevents potential neurological long-term complications. This study provides the first comprehensive overview of the genetics that underlies the inherited Cbl Malabsorption phenotype.
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inherited cobalamin Malabsorption mutations in three genes reveal functional and ethnic patterns
2012Co-Authors: Stephan M Tanner, Amy C Sturm, Elizabeth C Baack, Sandya Liyanarachchi, Albert De La ChapelleAbstract:Background Inherited Malabsorption of cobalamin (Cbl) causes hematological and neurological abnormalities that can be fatal. Three genes have been implicated in Cbl Malabsorption; yet, only about 10% of ~400-500 reported cases have been molecularly studied to date. Recessive mutations in CUBN or AMN cause Imerslund-Grasbeck Syndrome (IGS), while recessive mutations in GIF cause Intrinsic Factor Deficiency (IFD). IGS and IFD differ in that IGS usually presents with proteinuria, which is not observed in IFD. The genetic heterogeneity and numerous differential diagnoses make clinical assessment difficult.
Jost Langhorst - One of the best experts on this subject based on the ideXlab platform.
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a prospective multicenter study on the prevalence of fructose Malabsorption in patients with chronic inflammatory bowel disease
2021Co-Authors: Ulf Helwig, Anna K Koch, C Reichel, Petra Jessen, J Buning, Stefan Schreiber, Jost LanghorstAbstract:Background and aims Patients with chronic inflammatory bowel disease (IBD) might have a higher prevalence of fructose Malabsorption than healthy controls. This study's aim was to determine the prevalence and symptom severity of fructose Malabsorption in patients with active and inactive IBD. Methods The present study was a multicenter noninterventional diagnostic pilot trial. Two hundred fifty-one participants were recruited from 12 outpatient clinics for internal medicine across Germany and from the University of Kiel. Fructose Malabsorption was diagnosed by hydrogen breath testing. Patients diagnosed with bacterial overgrowth, non-H2 producers, and patients who were tested positive for lactose Malabsorption were excluded. Gastrointestinal symptoms during breath testing were evaluated using four-point subjective items to determine severity of bloating, abdominal pain, and diarrhea. Results Two hundred five patients (45 with active IBD, 80 with IBD in remission, and 81 healthy controls) were analyzed. The number of patients diagnosed with fructose Malabsorption - 35/44 (79.6%) in patients with active IBD, 59/80 (73.8%) inactive IBD, and 66/81 (81.5%) in healthy controls - did not differ between the groups (χ2 [2, N = 205] = 1.48, p = 0.48). However, abdominal pain was more frequent in patients with active IBD than patients with IBD in remission (z = -2.936, p = 0.010), and diarrhea was more frequent in patients with active IBD than in healthy controls (z = 2.489, p = 0.038). Conclusions Fructose Malabsorption is not more common among patients with IBD than healthy subjects. However, the greater prevalence of patient-reported symptoms among patients with IBD may be of pathological and therapeutic relevance.
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the predictive value of the hydrogen breath test in the diagnosis of fructose Malabsorption
2019Co-Authors: Ulf Helwig, Anna K Koch, Nadine Koppka, Sylvia Holtmann, Jost LanghorstAbstract:BACKGROUND Fructose Malabsorption is commonly diagnosed by the hydrogen fructose (H2) breath test. However, the mechanisms behind fructose Malabsorption in humans are not well understood and the clinical relevance of this test is considered controversial. Hence, the main aim of this study is to evaluate the predictive value of the H2 breath test. METHODS Regarding exclusion criteria, the study enrolled 562 consecutive patients, enlisted to a gastroenterology clinic between 2009 and 2011 for testing Malabsorption. In the final data analysis, 246 patients were included. Ecotrophologists used 3 categories to rate dietary success: complete response, partial response and no response to the diet. They also rated the occurrence of abdominal pain, diarrhoea and bloating during the H2 breath test. Ordinal regression analysis using SPSS was performed to evaluate whether H2 breath test results - measured as the maximum H2 level, the maximum increase in H2, and the area under the curve (AUC) - predicted dietary success or failure. Correlation analyses were applied to test whether symptoms of fructose Malabsorption correlated with the H2 breath test measures. Finally, we evaluated whether cut-off-values of 40 or 60 parts per million (ppm) serve better than the test measure of 20 ppm to diagnose fructose Malabsorption. RESULTS When a fructose-free diet was administered it was found that 103 patients (41.9%) were complete responders, 116 (47.2%) were partial responders and 27 (11%) were non-responders. The H2 breath test with the 20 ppm cut-off-value, that is, the maximum H2 level, the maximum increase in H2, and the AUC did not predict dietary response (all 95% CI ns). This was also the case when using 40 or 60 ppm as cut-off-values (all 95% CI ns). Abdominal pain during the test correlated significantly with the AUC. Diarrhoea and bloating correlated significantly with the AUC, the maximum H2 level and the maximum increase in H2 (p < 0.05). CONCLUSIONS The H2 breath test produced no predictive value for the fructose-free diet outcomes; its value as a predictive test is therefore questionable. However, the symptoms of fructose Malabsorption correlated significantly with the H2 breath test measures, and this is an indication that there is at least a degree of validity of the H2 breath test beyond the simple detection or exclusion of fructose Malabsorption.
