Peptic Ulcer Disease

Abstract

Peptic ulcer disease (PUD) is one of the commonest diseases seen throughout the world. There are various risk factors for the development of peptic ulcer disease, but the most important ones are Helicobacter pylori infection and nonsteroidal antiinflammatory drugs (NSAIDs). Patients generally present with dyspepsia or peptic ulcer bleeding. Acid suppressant therapy, H. pylori eradication, and avoidance of nonsteroidal anti-inflammatory drugs are the cornerstones of treatment of peptic ulcer disease. Peptic ulcer bleeding could be life-threatening. It is managed by appropriate supportive care, intravenous proton pump inhibitor therapy, and endoscopic hemostasis. Transarterial embolization (TAE) and surgery are rarely required if endoscopic therapy fails.Keywords: peptic ulcer disease, dyspepsia, H. pylori infection, peptic ulcer bleeding, endoscopic treatment of peptic ulcer bleeding H. pylori infection and nonsteroidal anti-inflammatory drugs (NSAIDs) account for majority of the cases of PUD. More than 90% of duodenal ulcers and >70% of gastric ulcers are H. pylori positive [8]. A prospective study from Turkey found that H. pylori infection alone was responsible for PUD in 75% of cases, both H. pylori infection and NSAIDs in 50% of cases and NSAIDs alone in 10% of cases [9]. A Japanese study showed that the long-term use of low-dose aspirin could cause PUD in 6.2% of cases. The risk is increased in diabetic patients and in patients taking anticoagulants [9]. Both NSAIDs and aspirin inhibit the cyclooxygenase pathway and decrease the production of prostaglandin which is responsible for cytoprotection of gastric mucosa by stimulating mucus and bicarbonate secretion and increasing mucosal blood flow [10]. The chance of developing NSAID-induced PUD increases in the presence of certain risk factors which include age more than 65, heart disease, past history of PUD, and co-administration of corticosteroid, antiplatelets, and anticoagulants [11]. All NSAIDs can cause gastrointestinal injuries which include inflammation, erosions, ulcerations, and bleeding. The relative risk varies: the highest risk is associated with piroxicam and ketorolac; high risk with indomethacin and naproxen; intermediate risk with meloxicam, diclofenac, and ketoprofen; and low risk with ibuprofen and celecoxib [12]. About 11% of the US population take NSAIDs on a regular basis. 15-30% of them have PUD on endoscopy although clinical upper gastrointestinal events can occur in 1.5-4.5% of patients taking NSAIDs [13].H. pylori virulence factors are important in the pathogenesis of PUD. Cytotoxinassociated gene A (Cag A), vacuolating cytotoxin A (Vac A), and induced by contact with epithelium antigen (ice A) are associated with PUD. After entering the stomach, H. pylori utilizes its urease enzyme to neutralize the gastric acidity. H. pylori then moves toward the gastric epithelium where it binds to the gastric epithelial cell receptors by its adhesion molecule [14]. Cag A is a strong immunogenic protein and measures the virulence of H. pylori infecti...

Castor oil Induces Morphological Changes in Endometrium and Biochemical Parameters in Pregnant Wistar Rats

“…It has different parts, which are of importance and are used for the treatment of several diseases. The preliminary phytochemical screening of R. communis revealed the presence of steroids, saponins, alkaloids, flavonoids, and glycosides (7). The major constituent of castor oil which is suspected to have an abortifacient property is the protein ricin, and has also been associated with laxative effects.…”