Andrea Morgner
Research Subjects
Andrea Morgner has a total of 52 co-authors. Here are the top co-authors by number of shared publications:
- Stephan Miehlke
Medical Department I, Technical University Hospital, Dresden, Germany
10 shared publications Manfred Stolte
7 shared publications- Ahmed Madisch
Medical Department I, Technical University Hospital, Dresden, Germany
6 shared publications Eberhard Kuhlisch
4 shared publications- Christian Thiede
Department of Internal Medicine I, University Hospital Carl Gustav Carus University of Technology Dresden Germany
3 shared publications Gerhard Ehninger
Medical Department I
3 shared publications
Latest Publications
- 1 May 2011
- Published by Elsevier in Gastroenterology
- Vol. 140 (5)
Relevance of Yersinia Outer Membrane Proteins in Collagenous and Lymphocytic Colitis
- 1 May 2011
- Published by Elsevier in Gastroenterology
- Vol. 140 (5)
Relevance of Yersinia Outer Membrane Proteins in Collagenous and Lymphocytic Colitis
- 31 May 2009
- Published by Elsevier in Gastroenterology
- Vol. 136 (5) , A-442-442
M1901 Intragastric Acidity During Treatment with Generic Omeprazole 20 Mg Once Daily or Esomeprazole 20 Mg Once Daily- a Randomized, Two-Way Crossover Study
- 31 May 2009
- Published by Elsevier in Gastroenterology
- Vol. 136 (5) , A-442-442
M1901 Intragastric Acidity During Treatment with Generic Omeprazole 20 Mg Once Daily or Esomeprazole 20 Mg Once Daily- a Randomized, Two-Way Crossover Study
- 31 May 2009
- Published by Elsevier in Gastroenterology
- Vol. 136 (5) , A-519-519
T1191 Budesonide Treatment of Collagenous Colitis: Posthoc Analysis of 3 Randomized Placebo-Controlled Trials
- 31 May 2009
- Published by Elsevier in Gastroenterology
- Vol. 136 (5) , A-519-519
T1191 Budesonide Treatment of Collagenous Colitis: Posthoc Analysis of 3 Randomized Placebo-Controlled Trials
- 31 May 2009
- Published by Elsevier in Gastroenterology
- Vol. 136 (5) , A-150-150
979 Randomized Multicenter Study of Esomeprazole, Moxifloxacin and Amoxicillin for Second-Line or Rescue Treatment of Helicobacter pylori Infection – Impact of Treatment Duration
- 31 May 2009
- Published by Elsevier in Gastroenterology
- Vol. 136 (5) , A-150-150
979 Randomized Multicenter Study of Esomeprazole, Moxifloxacin and Amoxicillin for Second-Line or Rescue Treatment of Helicobacter pylori Infection – Impact of Treatment Duration
- 30 April 2008
- Published by Elsevier in Gastroenterology
- Vol. 134 (4) , A-488-488
T1123 Oral Budesonide for Maintenance Treatment of Collagenous Colitis: A Randomised, Placebo-Controlled, Double-Blind Trial
- 30 April 2008
- Published by Elsevier in Gastroenterology
- Vol. 134 (4) , A-488-488
T1123 Oral Budesonide for Maintenance Treatment of Collagenous Colitis: A Randomised, Placebo-Controlled, Double-Blind Trial
- 1 March 2006
- Published by Bentham Science Publishers Ltd. in Current Pharmacogenomics
- Vol. 4 (1) , 47-56
Relevance of Cytochrome P450 Polymorphisms in the Treatment of Helicobacter pylori Infection and Gastroesophageal Reflux Disease
Proton pump inhibitors (PPI) are widely used for the treatment of gastroesophageal reflux disease (GERD), and in combination with antibiotics for the treatment of Helicobacter pylori infection. PPI are mainly metabolized by the polymorphic cytochromes P450 2C19 and 3A4. Genetic polymorphisms of these genes with resulting different enzyme activities may have an impact on the clinical efficacy of PPI-based therapies. There is increasing evidence that in Asian patient populations the efficacy of PPI-based eradication therapies is influenced by the patients CYP2C19 metabolizer status. Also two European studies report on CYP2C19-dependent eradication rates of H. pylori. In slow metabolizers, the AUC of oral PPI are higher in comparison to extensive metabolizers resulting in a stronger suppression of intragastric acid secretion. Recent studies suggest that the healing rate of erosive GERD is also influenced by the CYP2C19 metabolizer status. This review focuses on the relationship between CYP2C19 polymorphisms and clinical outcome after PPI based therapies in H. pylori eradication and GERD.
- 1 March 2006
- Published by Bentham Science Publishers Ltd. in Current Pharmacogenomics
- Vol. 4 (1) , 47-56
Relevance of Cytochrome P450 Polymorphisms in the Treatment of Helicobacter pylori Infection and Gastroesophageal Reflux Disease
Proton pump inhibitors (PPI) are widely used for the treatment of gastroesophageal reflux disease (GERD), and in combination with antibiotics for the treatment of Helicobacter pylori infection. PPI are mainly metabolized by the polymorphic cytochromes P450 2C19 and 3A4. Genetic polymorphisms of these genes with resulting different enzyme activities may have an impact on the clinical efficacy of PPI-based therapies. There is increasing evidence that in Asian patient populations the efficacy of PPI-based eradication therapies is influenced by the patients CYP2C19 metabolizer status. Also two European studies report on CYP2C19-dependent eradication rates of H. pylori. In slow metabolizers, the AUC of oral PPI are higher in comparison to extensive metabolizers resulting in a stronger suppression of intragastric acid secretion. Recent studies suggest that the healing rate of erosive GERD is also influenced by the CYP2C19 metabolizer status. This review focuses on the relationship between CYP2C19 polymorphisms and clinical outcome after PPI based therapies in H. pylori eradication and GERD.
- 1 December 2004
- Published by Wiley in Helicobacter
- Vol. 9 (6) , 629-631
Resolution of Gastrointestinal Protein Loss after Helicobacter pylori Eradication in a Patient with Hypertrophic Lymphocytic Gastritis
Lymphocytic gastritis is a rare condition found in approximately 1% of dyspeptic patients. An association with Helicobacter pylori infection has been described. Hypertrophic lymphocytic gastritis is a rare cause of gastrointestinal protein loss. Here, we describe a patient with hypertrophic lymphocytic gastritis, in whom gastrointestinal protein loss resolved completely following H. pylori eradication. A 38-year old obese man without gastrointestinal symptoms showed a markedly decreased serum protein (53 g/l, normal 66-85 g/l), a decreased serum albumin (33 g/l, normal 35-52 g/l) and decreased serum immunoglobulin G and immunoglobulin M levels. A renal cause for protein loss was excluded, liver function was normal. Endoscopy of the upper gastrointestinal tract revealed enlarged rigid gastric folds, and an H. pylori-associated lymphocytic gastritis. 99mTc-labelled albumin scintigraphy showed an increased activity in the upper left abdomen compatible with protein secretion in the stomach, and tracer pooling in the upper small bowel. Push enteroscopy with histology demonstrated a normal upper small bowel. Two months after eradication therapy, cure of H. pylori infection was documented and serum protein (71 g/l) and albumin (41 g/l) had returned to normal, while lymphocytic gastritis was still present. One year after eradication therapy endoscopy of the upper gastrointestinal tract and histology and laboratory values were normal. Protein-losing gastropathy caused by H. pylori-associated hypertrophic lymphocytic gastritis can be cured solely by H. pylori eradication therapy.
- 1 December 2004
- Published by Wiley in Helicobacter
- Vol. 9 (6) , 629-631
Resolution of Gastrointestinal Protein Loss after Helicobacter pylori Eradication in a Patient with Hypertrophic Lymphocytic Gastritis
Lymphocytic gastritis is a rare condition found in approximately 1% of dyspeptic patients. An association with Helicobacter pylori infection has been described. Hypertrophic lymphocytic gastritis is a rare cause of gastrointestinal protein loss. Here, we describe a patient with hypertrophic lymphocytic gastritis, in whom gastrointestinal protein loss resolved completely following H. pylori eradication. A 38-year old obese man without gastrointestinal symptoms showed a markedly decreased serum protein (53 g/l, normal 66-85 g/l), a decreased serum albumin (33 g/l, normal 35-52 g/l) and decreased serum immunoglobulin G and immunoglobulin M levels. A renal cause for protein loss was excluded, liver function was normal. Endoscopy of the upper gastrointestinal tract revealed enlarged rigid gastric folds, and an H. pylori-associated lymphocytic gastritis. 99mTc-labelled albumin scintigraphy showed an increased activity in the upper left abdomen compatible with protein secretion in the stomach, and tracer pooling in the upper small bowel. Push enteroscopy with histology demonstrated a normal upper small bowel. Two months after eradication therapy, cure of H. pylori infection was documented and serum protein (71 g/l) and albumin (41 g/l) had returned to normal, while lymphocytic gastritis was still present. One year after eradication therapy endoscopy of the upper gastrointestinal tract and histology and laboratory values were normal. Protein-losing gastropathy caused by H. pylori-associated hypertrophic lymphocytic gastritis can be cured solely by H. pylori eradication therapy.
- 1 April 2001
- Published by American Society of Clinical Oncology (ASCO) in Journal of Clinical Oncology
- Vol. 19 (7) , 2041-2048
Complete Remission of Primary High-Grade B-Cell Gastric Lymphoma After Cure of Helicobacter pylori Infection
PURPOSE: Treatment of low-grade gastric mucosa-associated lymphoid tissue lymphoma by eradication of Helicobacter pylori is reported to result in complete lymphoma remission in approximately 75% of cases. The effect that cure of the infection has on the course of a primary high-grade gastric lymphoma is largely uncertain. The aim of this study was to report the effect of cure of H pylori infection exerted in patients with high-grade B-cell gastric lymphoma. PATIENTS AND METHODS: Eight patients (4 males and 4 females; age range, 26 to 85 years) with H pylori infection and high-grade lymphoma received eradication therapy before planned treatment. The effect of H pylori eradication on the course of high-grade lymphoma was assessed by analysis of surgical specimens (n = 2) or endoscopic biopsies (n = 6). RESULTS: H pylori eradication was successful in all patients and led to complete remission of the lymphoma in seven patients. One patient has experienced partial remission. Two patients were referred to surgery, one of whom (stage II1E) had lymph node involvement, and the histologic work-up of the resected stomach revealed residual infiltrates of a low-grade lymphoma, which prompted consolidation chemotherapy. In one patient (initially stage I1E), abdominal lymphoma developed 6 months after eradication therapy, which regressed completely after chemotherapy. In four patients, no further treatment was given. Six patients continue in complete remission (range, 6 to 66 months). CONCLUSION: Primary high-grade B-cell gastric lymphoma in stages IE through IIE1 associated with H pylori may regress completely after successful cure of the infection. Prospective trials are needed to investigate this treatment in larger numbers of patients.
- 1 April 2001
- Published by American Society of Clinical Oncology (ASCO) in Journal of Clinical Oncology
- Vol. 19 (7) , 2041-2048
Complete Remission of Primary High-Grade B-Cell Gastric Lymphoma After Cure of Helicobacter pylori Infection
PURPOSE: Treatment of low-grade gastric mucosa-associated lymphoid tissue lymphoma by eradication of Helicobacter pylori is reported to result in complete lymphoma remission in approximately 75% of cases. The effect that cure of the infection has on the course of a primary high-grade gastric lymphoma is largely uncertain. The aim of this study was to report the effect of cure of H pylori infection exerted in patients with high-grade B-cell gastric lymphoma. PATIENTS AND METHODS: Eight patients (4 males and 4 females; age range, 26 to 85 years) with H pylori infection and high-grade lymphoma received eradication therapy before planned treatment. The effect of H pylori eradication on the course of high-grade lymphoma was assessed by analysis of surgical specimens (n = 2) or endoscopic biopsies (n = 6). RESULTS: H pylori eradication was successful in all patients and led to complete remission of the lymphoma in seven patients. One patient has experienced partial remission. Two patients were referred to surgery, one of whom (stage II1E) had lymph node involvement, and the histologic work-up of the resected stomach revealed residual infiltrates of a low-grade lymphoma, which prompted consolidation chemotherapy. In one patient (initially stage I1E), abdominal lymphoma developed 6 months after eradication therapy, which regressed completely after chemotherapy. In four patients, no further treatment was given. Six patients continue in complete remission (range, 6 to 66 months). CONCLUSION: Primary high-grade B-cell gastric lymphoma in stages IE through IIE1 associated with H pylori may regress completely after successful cure of the infection. Prospective trials are needed to investigate this treatment in larger numbers of patients.