A review of 82 (68 male) Kelantanese patients with non-alcoholic cirrhosis who underwent gastroduodenal endoscopy revealed duodenal and gastric ulcers in 4.9% and 7.3% of patients respectively. Comparing with prevalence rates of peptic ulcer disease reported in the literature, there was no evidence to suggest that duodenal ulcers occur more frequently in patients with non-alcoholic cirrhosis. There is a suggestion, albeit a tenuous one, that non-alcoholic cirrhosis may be associated with gastric ulceration.
The influence of the age of onset of symptoms on various clinical features of peptic ulcer was studied in a personal series of 492 patients (duodenal ulcer 363, gastric ulcer 98, combined gastric and duodenal ulcer 31). Duodenal ulcer patients whose age of onset of symptoms was within the first three decades (n = 166) were more likely to be men (77%) and to have a positive family history of dyspepsia (45%) and a history of haemorrhage (46%) when compared with late onset patients (n = 197, men 57%, positive family history 23%, history of haemorrhage 36%). Early onset duodenal ulcer patients also secreted more gastric acid than late onset patients. In contrast, while early onset gastric ulcer patients were more likely to be men, when compared to late onset patients, the two groups were similar in their family history of dyspepsia, their history of haemorrhage, and their gastric acid output. The age of onset of Malay duodenal ulcer patients (mean (SD) 43.6 (16.0] was higher than those for Chinese patients (33.7 (16.1].
A total of 1,688 non-repeat upper gastrointestinal endoscopies performed over a 33-month period from April 1985 to December 1987 at a University Medical Unit in Kuala Lumpur was analysed for a profile of peptic ulcer disease amongst Malaysians. There was a total of 360 peptic ulcer patients with a gastric ulcer to duodenal ulcer ratio of 1:1. The male: female ratio was 2.8: 1 for duodenal ulcer and 1.8:1 for gastric ulcer, and 2.3:1 for peptic ulcer overall. In both sexes, gastric ulcers were seen at an older age group compared to duodenal ulcers.
Of the three main Malaysian ethnic groups of Malays, Chinese and Indians, Chinese of both sexes had the highest frequency of gastric ulcers. Chinese females had the highest frequency of duodenal ulcers.
The Helicobacter pylori infection rate was determined in 124 consecutive patients with duodenal ulcers (DU), gastric ulcers (GU), duodenal erosions or gastric erosions diagnosed by endoscopy at a single institution in north-eastern peninsular Malaysia in 1996-97. Biopsies of the gastric antrum and body were subjected to the urease test, Gram staining of impression smears, culture and histopathological examination. Serology was undertaken on all patients using a locally validated commercial kit. Infection was defined as a positive result in at least one test. The infection rates were 20% (10/50), 21.2% (7/33), 16.7% (1/6) and 17.1% (6/35) in DU, GU, duodenal erosion and gastric erosion patients, respectively. The infection rate among Malays [7.0%, (6/86)] was lower than in non-Malays [47.4% (18/38)] (P < 0.001). There was a higher infection rate among males, who constituted 62.1% (77/124) of the sample. Seventy-eight patients (62.9%) were receiving non-steroidal anti-inflammatory drugs (NSAIDs) and 33 patients (26.6%) were neither receiving NSAIDs nor were infected with H. pylori. The H. pylori infection rate among peptic ulcer patients in this predominantly Malay rural population appears to be the lowest reported in the world thus far. Empirical H. pylori eradication therapy in peptic ulcer patients is clearly not indicated in this community. The possible reasons for the low prevalence of H. pylori infection are discussed.
A proton pump inhibitor (PPI) is often co-prescribed with clopidogrel to reduce the gastrointestinal risk of bleeding ulcers in patients following acute coronary syndrome or a stent implant. However, the safety issue of such practice has been scrutinized after some studies reporting an increased incidence of cardiovascular events and mortality, although there have also been contrary research reports. This has lead to a warning statement from the US Food and Drug Administration cautioning the concomitant use of PPI and clopidogrel. This review examines the evidence of PPI as gastroprotective agent, histamine H(2) antagonists as an alternative therapy, the influence of PPI on the antiplatelet effect of clopidogrel, and the controversies of various studies.
In recent years, infection of the stomach with the organism Helicobacter Pylori has been found to be the main cause of gastric ulcers, one of the common ailments afflicting humans. Excessive acid secretion in the stomach, reduction in gastric mucosal blood flow, constant intake of non-steroid anti-inflammatory drugs (NSAIDS), ethanol, smoking, stress etc. are also considered responsible for ulcer formation. The prevalent notion among sections of population in this country and perhaps in others is that "red pepper" popularly known as "Chilli," a common spice consumed in excessive amounts leads to "gastric ulcers" in view of its irritant and likely acid secreting nature. Persons with ulcers are advised either to limit or avoid its use. However, investigations carried out in recent years have revealed that chilli or its active principle "capsaicin" is not the cause for ulcer formation but a "benefactor." Capsaicin does not stimulate but inhibits acid secretion, stimulates alkali, mucus secretions and particularly gastric mucosal blood flow which help in prevention and healing of ulcers. Capsaicin acts by stimulating afferent neurons in the stomach and signals for protection against injury causing agents. Epidemiologic surveys in Singapore have shown that gastric ulcers are three times more common in the "Chinese" than among Malaysians and Indians who are in the habit of consuming more chillis. Ulcers are common among people who are in the habit of taking NSAIDS and are infected with the organism "Helicobacter Pylori," responsible for excessive acid secretion and erosion of the mucosal layer. Eradication of the bacteria by antibiotic treatment and avoiding the NSAIDS eliminates ulcers and restores normal acid secretion.