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  1. Kang JY
    Singapore Med J, 1992 Oct;33(5):468-71.
    PMID: 1455270
    Several lines of evidence suggest that, of the three main races of Singapore, peptic ulcers are more common among the Chinese and Indians when compared to the Malays. These include studies on hospital series of patients with or without appropriate control groups, studies on the incidence of surgery for perforated ulcer as well as mortality statistics. A reduction in the Chinese:Malay difference in the incidence of perforated ulcer over three decades suggests that environmental factors are involved in producing these racial differences. However, we have to date been unable to determine the factor(s) responsible. The incidence of perforated ulcer in Singapore is increasing while ulcer mortality is declining. This is similar to the situation in Hong Kong but different from that in the western countries.
    Matched MeSH terms: Peptic Ulcer/epidemiology*
  2. Lee YY, Mahendra Raj S, Graham DY
    Helicobacter, 2013 Oct;18(5):338-46.
    PMID: 23607896 DOI: 10.1111/hel.12058
    Helicobacter pylori (H. pylori) infection is etiologically associated with gastric cancer and peptic ulcer diseases which are both important public health burdens which could be largely eliminated by H. pylori eradication. However, some investigators urge caution based on the hypothesis that eradication of H. pylori may result in an increase in the incidence of gastroesophageal reflux disease, esophageal adenocarcinoma, and childhood asthma. The ethnic Malays of northeastern Peninsular Malaysia have long had a low prevalence of H. pylori infection and, as expected, the incidence of gastric cancer and its precursor lesions is exceptionally low. The availability of a population with a low H. pylori prevalence and generally poor sanitation allows separation of H. pylori from the hygiene hypothesis and direct testing of whether absence of H. pylori is associated with untoward consequence. Contrary to predictions, in Malays, erosive esophagitis, Barrett's esophagus, distal esophageal cancers, and childhood asthma are all of low incidence. This suggests that H. pylori is not protective rather the presence of H. pylori infection is likely a surrogate for poor hygiene and not an important source of antigens involved in the hygiene hypothesis. Helicobacter pylori in Malays is related to transmission from H. pylori-infected non-Malay immigrants. The factors responsible for low H. pylori acquisition, transmission, and burden of H. pylori infection in Malays remain unclear and likely involves a combination of environmental, host (gene polymorphisms), and strain virulence factors. Based on evidence from this population, absence of H. pylori infection is more likely to be boon than a bane.
    Matched MeSH terms: Peptic Ulcer/epidemiology*
  3. Goh KL, Chan WK
    Aliment Pharmacol Ther, 2012 Aug;36(3):291-2; discussion 292-3.
    PMID: 22747451 DOI: 10.1111/j.1365-2036.2012.05164.x
    Matched MeSH terms: Peptic Ulcer/epidemiology*
  4. Goh KL
    Med J Malaysia, 2009 Sep;64(3):187-92.
    PMID: 20527265
    Observations of racial differences in the prevalence of Helicobacter pylori in Malaysia have been intriguing. The Indians and Chinese consistently have a higher prevalence compared to the Malays. The racial cohort theory has been proposed to explain these differences where transmission and perpetuation of infection takes place within a racial group rather than between races, races being separate owing to the low rate of interracial marriages. Studies have demonstrated distinctive bacterial strains between races. Phylogenetic studies have shown that H. pylori isolates amongst Chinese and Indians are distinctive while Malays have Indian and other strains suggesting a more recent acquisition of the bacterium from Indians. H. pylori is recognized as the major causative factor in peptic ulcer disease and gastric cancer. Despite the high prevalence of H. pylori, Indians have a relatively low prevalence of peptic ulcer disease and a low incidence of gastric cancer. This paradox with regards to gastric cancer has been termed the "Indian enigma". Bacterial strain differences between races may be putative but this observation may also indicate gastroprotective environmental factors or a lower genetic susceptibility to develop cancer in the Indians.
    Matched MeSH terms: Peptic Ulcer/epidemiology
  5. Goh KL, Wong HT, Lim CH, Rosaida MS
    Aliment Pharmacol Ther, 2009 Apr 1;29(7):774-80.
    PMID: 19183160 DOI: 10.1111/j.1365-2036.2009.03930.x
    Dramatic changes in the prevalence and pattern of gastrointestinal disease has taken place in Asia in recent years.
    Matched MeSH terms: Peptic Ulcer/epidemiology*
  6. Tan HJ, Goh KL
    J Dig Dis, 2008 Nov;9(4):186-9.
    PMID: 18959588 DOI: 10.1111/j.1751-2980.2008.00344.x
    As in developed societies, the prevalence of Helicobacter pylori has declined rapidly in Asia. This has been shown in both seroprevalence-based and endoscopy-based studies. While the decline in the incidence of gastric cancer has now been observed, a decrease in peptic ulcer disease has not been so clearly evident. This apparent paradox can be explained by an increase in non-H. pylori associated ulcers - such as those related to non-steroidal anti-inflammatory drugs or idiopathic ulcers. The increase of gastroesophageal reflux disease in Asia has been widely observed and commented on and its relationship to the decline in H. pylori speculated upon. However there have been few conclusive studies from Asia on this subject. While the improved diagnosis and elimination of H. pylori has contributed to its decline, a more basic change involving large segments of the Asian population must be responsible. An improvement in hygiene and living conditions that results from more affluent Asian societies is thought to be a possible cause.
    Matched MeSH terms: Peptic Ulcer/epidemiology*
  7. Goh KL, Peh SC, Wong NW, Parasakthi N, Puthucheary SD
    J Gastroenterol Hepatol, 1990 5 1;5(3):277-80.
    PMID: 2103410
    Over a 15-month period, 399 patients with dyspepsia were investigated for the presence of Campylobacter pylori infection. Half of the patients (50.6%) had Campylobacter organisms in the antrum of the stomach. C. pylori was found in 96.1% of patients with histological changes of chronic active gastritis in the antrum. Of patients with duodenal and gastric ulcers, 87.8% and 87.5%, respectively, had Campylobacter organisms, as did 39.3% of patients with non-ulcer dyspepsia. C. pylori infection was most commonly found in Chinese and Indians. Although the prevalence of infection appeared to increase with age, there was an equal distribution amongst the sexes.
    Matched MeSH terms: Peptic Ulcer/epidemiology
  8. Raj SM
    Med J Malaysia, 1991 Jun;46(2):183-6.
    PMID: 1839424
    A review of the records at a teaching hospital in Kelantan revealed that 175 new cases of peptic ulcer disease were diagnosed endoscopically over a period of 5 years. The ratio of duodenal to gastric ulcers was 2:1. Male patients outnumbered females by 2.7:1. There was a disproportionately high number of Chinese patients. A striking observation was that an unusually large proportion (45%) of patients had presented with acute gastrointestinal bleeding. The implication is that peptic ulcer disease in this region may be underdetected; the diagnosis often coming to light only after a serious complication has supervened.
    Matched MeSH terms: Peptic Ulcer/epidemiology*
  9. Uyub AM, Raj SM, Visvanathan R, Nazim M, Aiyar S, Anuar AK, et al.
    Scand. J. Gastroenterol., 1994 Mar;29(3):209-13.
    PMID: 8209178
    The prevalence of Helicobacter pylori infection was determined in peptic ulcer patients, in non-ulcer dyspepsia (NUD) patients, and in the general adult population. The H. pylori infection rate ascertained by microbiologic examination of multiple gastric antral biopsy specimens was 50% (17 of 34) in duodenal ulcer (DU), 5% (1 of 22) in gastric ulcer, and 9% (15 of 159) in NUD patients. A seroepidemiologic survey showed a prevalence of only 4.2% among 496 blood donors and 4.8% among 921 subjects who attended health screening clinics. H. pylori infection is relatively uncommon and does not appear to be the predominant factor in the pathogenesis of peptic ulcer disease in the area. The incidence of peptic ulcer perforations in the area in 1991-92 was 1.5 per 100,000 person-years, reflecting a relatively low frequency of peptic ulcers, which might be due to the low prevalence of H. pylori infection in the population.
    Matched MeSH terms: Peptic Ulcer/epidemiology
  10. Kang JY, Yeoh KG, Ho KY, Guan R, Lim TP, Quak SH, et al.
    J Gastroenterol Hepatol, 1997 Oct;12(9-10):655-9.
    PMID: 9407329
    The aim of this study was to determine, first, whether racial differences exist in the seroprevalence of Helicobacter pylori infection in Singapore, and second, whether these differences correlate with racial differences in peptic ulcer frequency. A commercial serological test for immunoglobulin (Ig)G antibody to H. pylori which was 90% sensitive and 83% specific in our population was used to screen 403 adult blood donors of Chinese, Malay and Indian origin, aged between 15-60 years. Serum specimens from 84 paediatric patients admitted to the Paediatrics Department, National University of Singapore, with non-gastroenterological illnesses were also tested. In all three races, seroprevalence of H. pylori increased with age. Indians have the highest prevalence of infection followed by Chinese and Malays. Peptic ulcer prevalences are known to be highest in Chinese, followed by Indians and Malays. The Malays have the lowest prevalence of H. pylori and peptic ulcer among the three races in Singapore. Indians have a higher prevalence of H. pylori antibodies but a lower frequency of peptic ulcer than the Chinese. Racial differences in peptic ulcer frequency between Chinese and Indians are not explained by the prevalence of H. pylori infection; other environmental or genetic factors may be involved.
    Matched MeSH terms: Peptic Ulcer/epidemiology*
  11. Ross IN, Nair S, Jayakumar CR
    Singapore Med J, 1985 Jun;26(3):271-8.
    PMID: 4048988
    The results of 2449 investigations of the upper gastrointestinal tract were analysed to determine the incidence of disease. Abnormalities were detected in 53% of patients who had endoscopy, but were found in only 24% of patients who had barium studies (p <= 0.001). Altogether 916 patients had abnormal findings. Duodenal ulcer accounted for 42% of cases, gastric ulcer 16% and gastric cancer 9%. The prevalence of perforated ulcer was 13%. The annual incidence/1000 in males and females (>14 years) were respectively, for duodenal ulcer 1.66 and 0.42, for gastric ulcer 0.57 and 0.25, for perforated ulcer 0.36 and 0.05, and for gastric cancer 0.29 and 0.14. Most types of gastro-duodenal disease were less common in Malays than expected (p = <0.001). However oesophageal cancer and varices were more common in Indians compared to Malays and Chinese (p = <0.001). This study showed that the pallern of perforating ulcers was not the same as that of non-peforating ulcers, suggesting a differing pathogenesis. Identification of the factors causing a different prevalence of disease between the three ethnic groups would help in the understanding of the causes of upper gastrointestinal disease.
    Matched MeSH terms: Peptic Ulcer/epidemiology
  12. Ramelah M, Aminuddin A, Alfizah H, Isa MR, Jasmi AY, Tan HJ, et al.
    FEMS Immunol. Med. Microbiol., 2005 May 1;44(2):239-42.
    PMID: 15866222
    Helicobacter pylori infection of a distinct subtype of cagA may lead to different pathological manifestation. The aim of this study is to determine the presence of cagA gene and its variants in H. pylori infection among different ethnic groups and its effect on gastroduodenal diseases. Overall detection of cagA among the 205 clinical isolates of H. pylori was 94%. Variations in size of the 3' region of cagA gene were examined among 192 Malaysian H. pylori cagA-positive strains. Results showed that three cagA variants differing in fragment length of PCR products were detected and designated as type A (621-651bp), type B (732-735bp) and type C (525 bp). Although there was no association between any of the cagA subtypes with peptic ulcer disease (p>0.05), an association between cagA subtypes with a specific ethnic group was observed. Specific-cagA subtype A strains were predominantly isolated from Chinese compared to Malays and Indians (p<0.0005), and cagA subtype B strains were predominantly isolated from Malays and Indians compared to Chinese (p<0.05). The cagA type A strains of H. pylori is commonly found in the Chinese patients who have a higher risk of peptic ulcer disease, thus indicating that it could be used as an important clinical biomarker for a more severe infection.
    Matched MeSH terms: Peptic Ulcer/epidemiology
  13. Yap PR, Goh KL
    Curr Pharm Des, 2015;21(35):5073-81.
    PMID: 26369685
    Non-steroidal anti-inflammatory drugs (NSAIDs) are the most prescribed group of drugs in the world. They are used primarily for pain relief in chronic inflammatory joint disease and act by inhibiting enzymes COX1 and COX2 and ultimately preventing the production of active prostanoids which are required for the innate inflammatory pathway. The use of NSAIDs have been associated with the development of gastrointestinal (GI) symptoms ranging from simple dyspepsia to life threatening GI bleeds and perforations. The definition of dyspepsia has evolved over the years and this has hampered accurate studies on the prevalence of dyspepsia as different studies used varying criteria to define dyspepsia. It is now known that NSAIDs significantly increase the risk of dyspepsia.The risk of developing peptic ulcer disease vary with specific NSAIDs and dosages but there is no correlation between the symptoms of dyspepsia and underlying peptic ulcers. The pathogenesis of dyspepsia with NSAIDs is not completely understood. Peptic ulceration alone is not able to account for the majority of dyspepsia symptoms encountered by NSAIDs users. Erosive oesophagitis secondary to NSAIDs may be contributing factor to the prevalence of dyspepsia in NSAIDs users. Altered gut permeability and changes in gastric mechanosensory function due to NSAIDs may also be a contributory factor. Management of NSAID induced dyspepsia is involves a multipronged approach. Drug avoidance if possible would be ideal. Other options include using the lowest effective dose, changing to an NSAIDs with a safer GI risk profile, avoiding concurrent use with other NSAIDs or if the patient has a previous history of peptic ulcer disease, and co-prescribing with anti-secretory medications such as proton pump inhibitors. Eradication of Helicobacter pylori has a protective role against developing peptic ulcers and may also improve symptoms of NSAIDs induced dyspepsia.
    Matched MeSH terms: Peptic Ulcer/epidemiology
  14. Goh KL
    J Gastroenterol Hepatol, 1997 Jun;12(6):S29-35.
    PMID: 9195409
    The aim of the present study was to determine the risk factors for Helicobacter pylori in a dyspeptic Malaysian population. A cross-sectional survey of 1060 consecutive patients presenting with dyspepsia at the Endoscopic Unit, University Hospital, Kuala Lumpur, Malaysia from January 1994 to July 1995 was undertaken. All patients answered a detailed questionnaire and underwent endoscopy, with two antral biopsies taken for diagnosis of H. pylori using a rapid urease test. An overall H. pylori prevalence of 49.0% was recorded. Helicobacter pylori prevalence in relation to the major endoscopic diagnoses were as follows: non-ulcer dyspepsia (NUD) 31.2%; duodenal ulcer (DU) 91.4%; and gastric ulcer (GU) 74.1%. The prevalence among the races were as follows: Malay 16.4%; Chinese 48.5%; and Indians 61.8%. Multiple logistic regression analysis identified the following as independent risk factors: > 45 years old 1.5 (1.1,2.0); male gender 1.6 (1.2,2.1); ethnic group: Chinese 2.5 (1.7,3.7); Indians 4.9 (3.2,7.5); level of education: low 2.3 (1.5,3.5); middle 1.7 (1.1,2.6); and smoking 1.6 (1.2,2.3). Analysis was also performed on DU, GU and non-UD patients separately; in both DU and GU patients, H. pylori prevalence was high regardless of age, sex, race or level of education. However, in DU patients, Indian race had an independent risk factor (Odds ratio = 7.8 (1.2,48.4)). The findings in the NUD group reflected the findings in the ¿all patients' group; > 45 years old, male gender, Indian and Chinese race, and low level of education were also significant, independent risk factors. The overall differences in H. pylori prevalence between the different subgroups were mainly due to differences in the NUD group. The increased risk of H. pylori infection in Chinese and Indians points to either an inherent ethnic genetic predisposition or to socio-cultural practices peculiar to the particular race which may be responsible for transmission of the infection.
    Matched MeSH terms: Peptic Ulcer/epidemiology*
  15. Kang JY, Guan R, LaBrooy SJ, Lim KP, Yap I
    Ann Acad Med Singap, 1983 Oct;12(4):527-31.
    PMID: 6611105
    A consecutive series of 2,277 patients presenting for upper gastrointestinal endoscopy was analysed. The following groups of patients were studied with reference to sex, race and dialect groups: those presenting with dyspepsia but no haemorrhage, those presenting with upper gastrointestinal haemorrhage, those with non-ulcer dyspepsia, gastric ulcer and duodenal ulcer. Males out-numbered females in all diagnostic groups. Male and female Malays were under-represented in all diagnostic groups when compared to the Singapore population. Amongst female Chinese, there was an excess of Cantonese patients and an under-representation of Teochew patients in most diagnostic groups. These dialect differences were not remarkable amongst male Chinese. The possible reasons for these differences and their significance are discussed.
    Matched MeSH terms: Peptic Ulcer/epidemiology
  16. Moayyedi P, Eikelboom JW, Bosch J, Connolly SJ, Dyal L, Shestakovska O, et al.
    Gastroenterology, 2019 08;157(2):403-412.e5.
    PMID: 31054846 DOI: 10.1053/j.gastro.2019.04.041
    BACKGROUND & AIMS: Antiplatelets and anticoagulants are associated with increased upper gastrointestinal bleeding. We evaluated whether proton pump inhibitor therapy could reduce this risk.

    METHODS: We performed a 3 × 2 partial factorial double-blind trial of 17,598 participants with stable cardiovascular disease and peripheral artery disease. Participants were randomly assigned to groups given pantoprazole 40 mg daily or placebo, as well as rivaroxaban 2.5 mg twice daily with aspirin 100 mg once daily, rivaroxaban 5 mg twice daily, or aspirin 100 mg alone. The primary outcome was time to first upper gastrointestinal event, defined as a composite of overt bleeding, upper gastrointestinal bleeding from a gastroduodenal lesion or of unknown origin, occult bleeding, symptomatic gastroduodenal ulcer or ≥5 erosions, upper gastrointestinal obstruction, or perforation.

    RESULTS: There was no significant difference in upper gastrointestinal events between the pantoprazole group (102 of 8791 events) and the placebo group (116 of 8807 events) (hazard ratio, 0.88; 95% confidence interval [CI], 0.67-1.15). Pantoprazole significantly reduced bleeding of gastroduodenal lesions (hazard ratio, 0.52; 95% confidence interval, 0.28-0.94; P = .03); this reduction was greater when we used a post-hoc definition of bleeding gastroduodenal lesion (hazard ratio, 0.45; 95% confidence interval, 0.27-0.74), although the number needed to treat still was high (n = 982; 95% confidence interval, 609-2528).

    CONCLUSIONS: In a randomized placebo-controlled trial, we found that routine use of proton pump inhibitors in patients receiving low-dose anticoagulation and/or aspirin for stable cardiovascular disease does not reduce upper gastrointestinal events, but may reduce bleeding from gastroduodenal lesions. ClinicalTrials.gov ID: NCT01776424.

    Matched MeSH terms: Peptic Ulcer/epidemiology
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