Management of Peptic Ulcer Disease Not Related to Helicobacter pylori or NSAIDs

Abstract

Helicobacter pylori (H. pylori) infection is widely accepted as the most important factor in the pathogenesis of duodenal ulcer. However, in parallel with more effective eradication of H. pylori, the prevalence of H. pylori is changing, and H. pylori-negative peptic ulcer disease appears to be increasing. When making a diagnosis of H. pylori-negative peptic ulcer disease, it is essential to avoid misclassification because of inaccurate diagnosis. In addition, secondary causes may need to be excluded with appropriate investigations. In the absence of H. pylori, nonsteroidal anti-inflammatory drug usage is the most common cause of peptic ulcer; surreptitious nonsteroidal anti-inflammatory drug usage is a cause of unexplained ulcer disease in up to 60% of patients. Hypersecretory syndromes such as Zollinger-Ellison syndrome, although rare, need to be excluded. Once all known etiological factors are excluded, there remains a group of patients with so-called "idiopathic ulcers." The interplay of etiological factors in the pathogenesis of idiopathic peptic ulcer disease is poorly defined but may include a genetic predisposition, altered acid secretion, rapid gastric emptying, defective mucosal defense mechanisms, psychological stress, and smoking. The management of idiopathic peptic ulcers is not defined; they appear to be more resistant to standard therapy, can be associated with more frequent complications, and those that relapse may require long-term maintenance therapy.

ETIOPATHOGENESIS OF PEPTIC ULCER: back to the past?

“…A meta-analysis of seven double blind, randomized trials in North America found that 20% of patients with H. pylori-associated ulcers had ulcer recurrence within 6 months despite successful H. pylori eradication and no reported NSAID use (37)(38)(39) . No role could be proposed for the smoking habit on the basis of two studies, either on non-H. pylori and non-NSAID duodenal ulcers or on H. pylori-associated ulcers (49,63) . In developed countries there was wide variation in the rates of DUP and of infection by H. pylori.…”

“…Results from the USA suggest that the proportion of H. pylori-negative ulcer, while varying somewhat, appears to be rising (60) ; the prevalence of infection in some regions may be of only 30%, and about 20% of the PUD patients are not infected (45) . Quan and Talley (49) systematically reviewed the prevalence of unexplained ulceration in the period between 1995 and 2001, finding that a relevant proportion of PUD patients were not infected by H. pylori. Other studies in the USA showed that 20% to 50% of the peptic ulcers were not related to H. pylori infection or to the use of NSAID (14,15,23,25) .…”

Antioxidant and Gastric Ulcer Healing Effect of Orthosiphonstamineus (Benth.) Leaves Extract in Aspirin-Induced Rats

“…Gastric ulcer is believed to be due to an imbalance between aggressive and mucosal integrity factors. Increase of aggressive factors (gastric acid and pepsin secretion) and decrease of mucosal integrity factors (inhibition of prostaglandin, decrease of bicarbonate concentration, and diminished of blood flow in gastric) have potential against developed of gastric ulcer [2][3][4].…”

La úlcera Péptica : ¿Un trastorno gastrointestinal infeccioso o Biopsicosocial?

“…Múlti-ples estudios han demostrado que esta bacteria es un factor de riesgo fundamental en la UP. En este sentido, se ha hallado que cerca del 95% y 85% de las personas con UD y UG respectivamente están infectadas, y que la erradicación de la bacteria aumenta la tasa de curación de este problema de salud y reduce de forma significativa las recaídas (Quan y Talley, 2002). Así mismo, se ha podido determinar que hay una relación temporal entre la gastritis asociada a la H. pylori y el origen de la UP; que la probabilidad de desarrollar la UP aumenta a mayor exposición a la H. pylori, y que hay una serie de mecanismos fisiopatológicos asociados a la bacteria que explican su relación con esta condición médica (p.ej., la inflamación de la mucosa gástrica y las alteraciones en la actividad ácido-péptica) (Gisbert, Boixeda y Martín de Argila, 1996).…”