Peptic Ulcer

In uncomplicated cases of peptic ulcer disease, the clinical findings are few and non-specific with the following often recorded:

• Succussion splash as a result of partial or complete gastric outlet obstruction
• Mild epigastric tenderness 
• Right upper quadrant tenderness which may suggest a biliary etiolog
• Guaiac-positive stool as a result of occult blood loss
• Melena as a result of acute or subacute gastrointestinal bleeding

In patients with perforated peptic ulcer disease, onset of severe, sharp, abdominal pain is a common presentation [7]. In some other patients, generalised pain is described while epigastric pain is seen in rare cases. Since slight movement can bring about worsening of pains, a common presentation among peptic ulcer patients is the assumption of fetal position most of the time.

Abdominal examination also shows general tenderness, rigidity, rebound tenderness and guarding.

In diagnosis of ulcers, patients are subjected to diagnostic tests such as:

• Tests for Helicobacter pylori (stool, blood or breath depending on condition)
• Endoscopy (biopsy used in identification of Helicobacter pylori in the stomach lining)
• X-ray of the upper digestive system 

Treatment for peptic ulcers is dependent on the cause of the condition. Antibiotic medications taken over a period of two weeks can eradicate Helicobacter pylori [8]. Antibiotics are often used with additional medications to reduce stomach acid.

In the case of excessive acid production, protein pump inhibitors that block the production and promote healing can be used. Other treatment agents are histamine blockers, and antacids. Antacids are used to provide relief but they do not heal ulcers [9].

As long as the underlying cause is addressed, prognosis is positive. Majority of patients are successfully treated with eradication of Helicobacter pylori, adequate use of antisecretory therapy and the avoidance of drugs that are etiologic factors [6]. When Helicobacter pylori is eradicated, the natural history of the disease is altered and this leads to reduction of the recurrence rate from 60-90% to around 10-20%.

Mortality rate for peptic ulcer disease has decreased a great deal over the last three decades to approximately 1 death for every 100,000 cases.

Ulcers are caused by a variety of factors but in most cases, they arise as a result of Helicobacter pylori infection [3]. Other main causes of ulcer are drug use, unfavourable life style choices, severe physiologic stress, hypersecretory states and genetics.

Other lesser etiologic factors include:

• Hepatic cirrhosis
• Bile gastropathy
• Chronic obstructive pulmonary disease
• Graft versus host disease 
• Cytomegalovirus infection
• Allergic gastritis and eosinophilic gastritis
• Uremic gastropathy
• Celiac disease
• Henoch-Schönlein gastritis
• Corrosive gastropathy
• Crohn disease
• Autoimmune disease
• Other granulomatous gastritides such as sarcoidosis, histiocytosis X, tuberculosis
• Phlegmonous gastritis and emphysematous gastritis
• Use of crack cocaine, which causes localized vasoconstriction, resulting in reduced blood flow and may also lead to mucosal damage.
• Infections such as Epstein-Barr virus, HIV, Helicobacter heilmannii, herpes simplex, influenza, syphilis, Candida albicans, histoplasmosis, mucormycosis, and anisakiasis.
• Local radiation resulting in mucosal damage, which may lead to the development of duodenal ulcers.
• Chemotherapeutic agents

Peptic ulcer affects around 4.5 million people each year in the US. In other countries, the figures are variable and incidence is determined majorly on association with the major causes of peptic ulcer [4].

In the past, peptic ulcer was seen more in males than in females but now it occurs similarly in both males and females. Age statistics show that ulcer occurrence is declining in younger men especially for duodenal ulcer, while rates continue to increase in older women.

Peptic ulcers signify a defect in the gastric or duodenal mucosa which extends through the muscularis mucosa [5]. In a healthy individual, there is a physiologic balance between gastric acid secretion and gastroduodenal mucosal defense.

Mucosal injury and peptic ulcer set in when the balance between the aggressive factors and defensive mechanisms of the stomach become disrupted. Aggressive factors like Helicobacter pylori infection, alcohol pepsin and bile salts can alter the mucosal defense by allowing hydrogen ion diffusion and ensuing injury to the epithelial cell. Again, Helicobacter pylori colonisation often results in inflammation.

To reduce the risk of peptic ulcer, the following is advised [10]:

• Protect yourself from Helicobacter pylori infection. There is no definite path on how it spreads but evidence suggest that it can be transmitted from person to person and via food and water. Prevention can therefore be achieved by adequate hygiene and consistent washing of hands with soap and water and also eating properly cooked foods.
• Exercise caution when using pain relievers as regular use only increases the risk of peptic ulcer. It is also advisable to take medications with meals at all times.

Peptic ulcer refers to the condition that arises when there is a clear breach in the mucosal lining of the stomach or the first part of the small intestine [1]. The former is known as gastric ulcer while the latter is known as duodenal ulcer. Peptic ulcers arise following the caustic effects of acid and pepsin in the lumen.

Peptic ulcer is defined histologically as a necrosis of the mucosa that leads to the production of lesions that are equal to or greater than 0.5 cm. It is also the most common ulcer of the gastrointestinal tract. The very painful nature of the condition is a result of the acidic nature of the gastrointestinal tract. Ulcers are often worsened by drugs like aspirin or ibuprofen.

Peptic ulcers occur four times more in the duodenum than in the stomach. 4% of gastric ulcers are as a result of a malignant tumor [2]. This is why biopsies are used in most cases to exclude the possibility of cancer. Duodenal ulcers are benign generally.

Peptic ulcers are sores that develop on the lining of the esophagus, stomach, and upper part of the small intestine. In patients with peptic ulcer the most common symptom is abdominal pain.

Ulcers that occur inside the stomach are known as gastric ulcers while those that occur in the throat and in the upper part of the small intestine are known as esophageal and duodenal ulcers respectively.

Treatment of ulcers in most cases is with the aid of antibiotics and medication to help reduce the pain and other symptoms that arise from it. Contrary to common opinion, eating spicy meals or working a stressful shift does not cause ulcer.

1. Chey WD, Wong BC. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol. Aug 2007;102(8):1808-25.
2. Javid G, Zargar SA, U-Saif R, Khan BA, Yatoo GN, Shah AH, et al. Comparison of p.o. or i.v. proton pump inhibitors on 72-h intragastric pH in bleeding peptic ulcer. J Gastroenterol Hepatol. Jul 2009;24(7):1236-43.
3. Lai KC, Lam SK, Chu KM, Wong BC, Hui WM, Hu WH, et al. Lansoprazole for the prevention of recurrences of ulcer complications from long-term low-dose aspirin use. N Engl J Med. Jun 27 2002;346(26):2033-8.
4. Lai KC, Lam SK, Chu KM, Hui WM, Kwok KF, Wong BC, et al. Lansoprazole reduces ulcer relapse after eradication of Helicobacter pylori in nonsteroidal anti-inflammatory drug users--a randomized trial. Aliment Pharmacol Ther. Oct 15 2003;18(8):829-36.
5. Sung JJ, Tsoi KK, Ma TK, Yung MY, Lau JY, Chiu PW. Causes of mortality in patients with peptic ulcer bleeding: a prospective cohort study of 10,428 cases. Am J Gastroenterol. Jan 2010;105(1):84-9. 
6. Bardhan KD, Cole DS, Hawkins BW, Franks CR. Does treatment with cimetidine extended beyond initial healing of duodenal ulcer reduce the subsequent relapse rate? Br Med J (Clin Res Ed) 1982; 284:621.
7. Gudmand-Høyer E, Jensen KB, Krag E, et al. Prophylactic effect of cimetidine in duodenal ulcer disease. Br Med J 1978; 1:1095.
8. Current status of maintenance therapy in peptic ulcer disease. The ACG Committee on FDA-Related Matters. Am J Gastroenterol 1988; 83:607.
9. Jorde R, Bostad L, Burhol PG. Asymptomatic gastric ulcer: a follow-up study in patients with previous gastric ulcer disease. Lancet 1986; 1:119.
10. Howden CW, Hunt RH. The relationship between suppression of acidity and gastric ulcer healing rates. Aliment Pharmacol Ther 1990; 4:25.

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