Resolution of gastrointestinal protein loss after Helicobacter pylori eradication in a patient with hypertrophic lymphocytic gastritis

Research output: Contribution to journalResearch articleContributedpeer-review

Contributors

  • Ahmed Madisch - , University Hospital Carl Gustav Carus Dresden, Department of internal Medicine I (Author)
  • Daniela Aust - , Institute of Pathology, University Hospital Carl Gustav Carus Dresden (Author)
  • Andrea Morgner - , University Hospital Carl Gustav Carus Dresden, Department of internal Medicine I (Author)
  • Dana Grossmann - , University Hospital Carl Gustav Carus Dresden, Department of internal Medicine I (Author)
  • Renate Schmelz - , Department of internal Medicine I, University Hospital Carl Gustav Carus Dresden (Author)
  • Joachim Kropp - , University Hospital Carl Gustav Carus Dresden, Department of Nuclear Medicine (Author)
  • Gerhard Ehninger - , University Hospital Carl Gustav Carus Dresden, Department of internal Medicine I (Author)
  • Gustavo Baretton - , Institute of Pathology, University Hospital Carl Gustav Carus Dresden (Author)
  • Stephan Miehlke - , University Hospital Carl Gustav Carus Dresden, Department of internal Medicine I (Author)

Abstract

Background. 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. Case Report. 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. Conclusion. Protein-losing gastropathy caused by H. pylori-associated hypertrophic lymphocytic gastritis can be cured solely by H. pylori eradication therapy.

Details

Original languageEnglish
Pages (from-to)629-631
Number of pages3
JournalHelicobacter
Volume9
Issue number6
Publication statusPublished - 2004
Peer-reviewedYes

External IDs

PubMed 15610076

Keywords

Sustainable Development Goals

ASJC Scopus subject areas

Keywords

  • Helicobacter pylori, Hypertrophic lymphocytic gastritis, Protein-losing gastropathy