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  1. Cheah JS, Chia BL, Tay HH, Tan BY
    Med J Aust, 1970 Nov 28;2(22):1029-30.
    PMID: 5494951
  2. Tay HH, Yap I, Guan R, Koh PS, LaBrooy SJ, Kang JY
    Med J Malaysia, 1988 Jun;43(2):181-5.
    PMID: 3070309
    Thirty-one patients with endoscopically proven chronic gastric ulcer completed a randomised double-blind trial comparing the effects of cimetidine and placebo on ulcer healing. Seventeen patients received cimetidine 400 mg bid and 14 patients received placebo. Repeat endoscopy at six weeks showed that the ulcer had healed in 12 patients (71%) receiving cimetidine and in four patients (29%) receiving placebo (p=O.032). Non-smokers healed their ulcers better than smokers (83% vs 35%, p=O.023). The use of cimetidine was not associated with any adverse effects.
  3. Kang JY, Wee A, Math MV, Guan R, Tay HH, Yap I, et al.
    Gut, 1990 Aug;31(8):850-3.
    PMID: 2387503
    Peptic ulcer occurs with different frequencies in the three main racial groups in Singapore. This study aimed firstly to determine the prevalence of Helicobacter pylori in peptic ulcer and non-ulcer dyspepsia patients of the different races and secondly, to assess the relation between H pylori, histological gastritis, patient diagnosis, and race. Gastric antral biopsy specimens from 1502 patients undergoing gastroduodenoscopy were studied and 892 (59%) were positive for H pylori. H pylori was strongly associated with gastritis: 873 of 1197 (73%) patients with gastritis were positive compared with 19 of 305 (6%) without gastritis (p less than 0.0001). The prevalences of H pylori and gastritis were similar in peptic ulcer patients of different races. Malay patients with non-ulcer dyspepsia, however, were less likely to be positive for H pylori (10 of 46 (22%] or to have antral gastritis (17 of 46 (37%] than Chinese (292 of 605 (48%) were positive for H pylori and 421 of 605 (70%) had gastritis) and Indians (35 of 61 (57%) were H pylori positive and 42 of 61 (69%) had gastritis). Patients with duodenal ulcer were more likely to be positive for H pylori than those with non-ulcer dyspepsia, even when subjects with gastritis were considered separately. While our results do not help to explain the observed racial differences in peptic ulcer frequency it may be that the pathophysiology of non-ulcer dyspepsia is different in the different races in Singapore.
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