PEPTIC ULCER DISEASE

PEPTIC ULCER DISEASE

Introduction

Peptic ulcer disease can be defined as a defect in the upper gastrointestinal mucosa, usually located in the stomach or proximal duodenum, whereby injury extends through the muscularis mucosa and into deep-lying layers of the gut wall. The ulcers also present themselves in the oesophagus or on Meckel’s diverticulum. Traditionally, a hypersectretory acidic environment, along with stress or dietary factors, was presumed to be the cause of most peptic ulcers. This perception was only changed when Helicobacter pylori infection was discovered recently as well as widespread, frequent use of non-steroidal anti-inflammatory drugs (NSAIDs) in the 20^th century. PUD affects 1 to 2 people per 1000 annually as per a systematic review with data from the USA, United Kingdom, and Europe. In the general population, it’s currently projected that the lifetime prevalence of peptic ulcer disease is about 5 – 10%, with an incidence rate of 0.1 to 0.3% every year. This may, however, be on the decline worldwide, especially in countries with high-income populations. It is also reported that mortalities associated with peptic ulcer disease were on an all-time high in generations born at the end of the 19^th century then fell in those born in the 20^th century.

Etiology and Risk Factors

Helicobacter pylori infection, along with the misuse of NSAIDs or aspirin, are considered to be the significant risk factors associated with both duodenal and gastric ulcers. Studies suggest that about 70% of gastric ulcers and 90% of duodenal ulcers can be related to H. pylori infection. Although these percentages are now considered to be lower, H. pylori is still an integral risk factor for gastric cancer, thus further emphasizing the need for its eradication.

It is, however, noteworthy that only a small number of people taking NSAIDs or aspirin or having an H. pylori infection actually develop peptic ulcers, which suggests that a couple of factors including individual susceptibility to bacterial virulence and drug toxicity are paramount to the initiation of mucosal damage. Other risk factors include cigarette smoking, physiological and psychological stress, gastric tumors mistaken for peptic ulcers, infections (mainly in immunocompromised patients), and Zollinger-Ellison syndrome, which is an uncommon, gastrin producing tumor usually located in the pancreas.

Pathophysiology

The manner exactly with which Helicobacter pylori brings about the development of the various lesions seen in the gastric and duodenal mucosa is not properly comprehended. However, the inflammatory response associated with H. pylori can result either in hypochlorhydria or hyperchlorhydria, thus determining the kind of peptic ulcer formed. About 10-15% of patients diagnosed with H. pylori infection have antral gastritis that is associated with ulcers and a heightened gastric secretion that is derived from hypergastrinemia and reduced antral somatostatin content. NSAIDs, on the other hand, cause damage to the gastroduodenal mucosa through either local or systemic mechanisms. However, the systemic inhibition of cyclooxygenase 1 (COX-1)- derived prostaglandins is considered as the primary mechanism. The decreased prostaglandin levels on mucous membranes is associated with low bicarbonate and mucus secretion, decreased mucosal blood flow, and inhibition of cell proliferation, which are quite paramount in the preservation of mucosal integrity. NSAIDs cause damage to mucous membranes in the cell through disruption of mucus phospholipids or the cell membrane as well as through uncoupling of mitochondrial oxidative phosphorylation. The loss of mucosal integrity is usually accompanied by the tissue reaction, which in turn is intensified by luminal content such as food, bile, pepsin, acid, and Helicobacter pylori infection.

Clinical Manifestations and Complications

Manifestations of peptic ulcers are highly non-specific, thus have limited predictive value. Patients having duodenal ulcers usually experience hunger or nocturnal abdominal pain, while those having gastric ulcers often experience postprandial abdominal pain, weight loss, nausea, and vomiting. Elderly patients having peptic ulcer disease typically are asymptomatic or only experience mild symptoms. Perforation, hemorrhage, gastric obstruction from fibrotic stricturing and penetration to a surrounding organ are some of the critical complications associated with peptic ulcer disease. Penetration can lead to secondary pancreatitis if the pancreas is involved. Obstruction, on the other hand, leads to nausea and vomiting.

Diagnostics

A “test and treat” strategy has been primarily recommended in individuals under the age of 50-55 years for H. pylori in patients with symptoms suggestive of peptic ulcer disease. Non-invasive tests used in the diagnosis of peptic ulcer disease include stool antigen test, urea breath test, or serology. The gold standard that is applied in the diagnosis of peptic ulcer disease, however, is endoscopy. In elderly patients, upper gastrointestinal endoscopy is the universally recommended test to confirm or exclude the condition.