H. pylori/NSAID - Negative peptic ulcer - The mucin theory

Research output: Contribution to journalArticlepeer-review

17 Scopus citations


The incidence of Helicobacter pylori (H. pylori) and non-steroidal anti inflammatory drug (NSAID) - negative peptic ulcer disease increases, especially in the Western world and in countries where H. pylori infection rate is low. For the diagnosis of " idiopathic ulcer" one should rule out, in addition to H. pylori infection and NSAID or aspirin therapy, also other drugs, other infectious agents, as well as malignant and benign rare diseases. The mucin unstirred layer keeps the pH above the mucosa stable, and prevents the enzymatic attack by pepsin. Inhibition of cyclo-oxygenase by NSAID and aspirin prevents mucin secretion and exposes the mucosa for toxic effect of acid and enzymes. There is also relationship between H. pylori and mucin that from one hand enables mucin invasion but on the other hand protects the gastric mucosa. Mucin genetic or epigenetic changes may be blamed for idiopathic peptic ulcer disease, but this hypothesis should be further investigated.

Original languageEnglish
Pages (from-to)433-435
Number of pages3
JournalMedical Hypotheses
Issue number5
StatePublished - Nov 2010
Externally publishedYes


Dive into the research topics of 'H. pylori/NSAID - Negative peptic ulcer - The mucin theory'. Together they form a unique fingerprint.

Cite this