Peptic ulcer disease(PUD): Symptoms, Pathogenesis, Diagnosis & Treatments
Peptic ulcer disease (PUD) is a lesion that can invade from the mucous membrane of the digestive tract to the muscularis mucosa. PUD can range from natural remission without any treatment to severe complications such as bleeding or perforation.
The stomach acts to decompose the protein by the action of the acidic environment and enzymes. The stomach itself has the ability to protect the stomach wall, so this PUD is not good. Most PUDs are caused by an infection of Helicobacter pylori (H. pylori) or by the ingestion of nonsteroidal anti-inflammatory drugs (NSAIDs) that interfere with normal protective function.
Pathogenesis
The mechanism of ulcer formation by H. pylori is not clear, but it is thought to affect the gastrointestinal tract and its mucous membrane in four aspects. First, it increases the secretion of gastric acid. H. pylori infection increases secretion of Gastrin, a hormone that increases the secretion of gastric acid. This is because H. pylori stimulates enterochromaffin-like (ECL) cells that secrete parietal cells and histamine.
NSAIDs mostly block the action of systemic cyclooxygenase (COX). There are two types of COX: COX-1 and COX-2. Normal mucosa of the stomach or duodenum produces prostaglandin (PG) that protects the mucous membrane steadily with COX-1, and COX-2 acts when inflammation occurs. However, since NSAIDs do not act on either COX-1 or COX-2, the protective effect of the gastrointestinal mucosa is deteriorated by the action of COX-1 as well as COX-2.
Symptoms
In patients with PUD, dyspepsia is the main symptom. PUD patients are often accompanied by gastroesophageal reflux disease (GERD). In this case, the patient may complain of burning pain, and eating habits such as eating and lying down may be associated with pain. However, asymptomatic cases of PUD patients account for nearly 70 percent. These patients are more likely to develop PUD complications later because they do not feel the disease.
Diagnosis
Diagnosis of PUD is based on endoscopic findings and biopsy without symptom-based diagnosis. Therefore, esophagogastroduodenoscopy (EGD) is essential for accurate diagnosis, but it can not be done for all patients with epigastric pain. Therefore, it is most important to suspicion of PUD by screening patients with H. pylori infection or NSAIDs that cause PUD.
Treatments
First, all patients with PUD need to know if they have H. pylori infection and if they are infected, treatment to eliminate H. pylori should be preceded. Helicobacter pylori eradication therapy is a two-week treatment with PPI (lansoprazole, omeprazole, etc.), amoxicillin and clarithromycin as a triple therapy using proton pump inhibitor (PPI) and antibiotics. In addition, H. pylori-associated or unrelated ulcers are treated with PPI to inhibit gastric acid secretion.
Approximately 60 percent of PUDs heal and disappear by themselves, but in combination with H. pylori eradication therapy, over 90 percent of ulcers are cured. 5 to 10 percent of PUDs continue to develop without chronic hearing, even if the PPI inhibits gastric acid secretion.
The stomach acts to decompose the protein by the action of the acidic environment and enzymes. The stomach itself has the ability to protect the stomach wall, so this PUD is not good. Most PUDs are caused by an infection of Helicobacter pylori (H. pylori) or by the ingestion of nonsteroidal anti-inflammatory drugs (NSAIDs) that interfere with normal protective function.
Pathogenesis
The mechanism of ulcer formation by H. pylori is not clear, but it is thought to affect the gastrointestinal tract and its mucous membrane in four aspects. First, it increases the secretion of gastric acid. H. pylori infection increases secretion of Gastrin, a hormone that increases the secretion of gastric acid. This is because H. pylori stimulates enterochromaffin-like (ECL) cells that secrete parietal cells and histamine.
NSAIDs mostly block the action of systemic cyclooxygenase (COX). There are two types of COX: COX-1 and COX-2. Normal mucosa of the stomach or duodenum produces prostaglandin (PG) that protects the mucous membrane steadily with COX-1, and COX-2 acts when inflammation occurs. However, since NSAIDs do not act on either COX-1 or COX-2, the protective effect of the gastrointestinal mucosa is deteriorated by the action of COX-1 as well as COX-2.
Symptoms
In patients with PUD, dyspepsia is the main symptom. PUD patients are often accompanied by gastroesophageal reflux disease (GERD). In this case, the patient may complain of burning pain, and eating habits such as eating and lying down may be associated with pain. However, asymptomatic cases of PUD patients account for nearly 70 percent. These patients are more likely to develop PUD complications later because they do not feel the disease.
Diagnosis
Diagnosis of PUD is based on endoscopic findings and biopsy without symptom-based diagnosis. Therefore, esophagogastroduodenoscopy (EGD) is essential for accurate diagnosis, but it can not be done for all patients with epigastric pain. Therefore, it is most important to suspicion of PUD by screening patients with H. pylori infection or NSAIDs that cause PUD.
Treatments
First, all patients with PUD need to know if they have H. pylori infection and if they are infected, treatment to eliminate H. pylori should be preceded. Helicobacter pylori eradication therapy is a two-week treatment with PPI (lansoprazole, omeprazole, etc.), amoxicillin and clarithromycin as a triple therapy using proton pump inhibitor (PPI) and antibiotics. In addition, H. pylori-associated or unrelated ulcers are treated with PPI to inhibit gastric acid secretion.
Approximately 60 percent of PUDs heal and disappear by themselves, but in combination with H. pylori eradication therapy, over 90 percent of ulcers are cured. 5 to 10 percent of PUDs continue to develop without chronic hearing, even if the PPI inhibits gastric acid secretion.
