H. pylori/NSAID--negative peptic ulcer--the mucin theory.
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.
Niv
Yaron
Y
Department of Gastroenterology, Rabin Medical Center, Tel Aviv University, Israel. yniv@clalit.org.il
D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D016480:Helicobacter pylori / Q000472:pathogenicity*; D006801:Humans; D009077:Mucins / Q000502:physiology*; D010437:Peptic Ulcer / Q000209:etiology* / Q000517:prevention & control
D000894:Anti-Inflammatory Agents, Non-Steroidal; D009077:Mucins