TRENDS OF PEPTIC ULCER DISEASES AND HELICOBACTER PYLORI INFECTION IN NORTHERN THAILAND

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1 Chiang Mai Med J 2010;49(2): Original article TRENDS OF PEPTIC ULCER DISEASES AND HELICOBACTER PYLORI INFECTION IN NORTHERN THAILAND Ong-ard Praisontarangkul, M.D., Pises Pisespongsa, M.D., Sith Hongsongkiat, M.D. Department of Medicine, Faculty of Medicine, Chiang Mai University Abstract Background The decline in global prevalence of Helicobacter pylori (Hp) and peptic ulcer disease (PUD) has been recognized, while the prevalence of non-hp PUD is increasing. This study aimed to determine the trends of PUD and Hp infection, and exposure to nonsteroid anti-inflammatory drugs and aspirin (NSAIDs/ASA), their association with upper gastrointestinal (UGI) bleeding, and comparison to previous data. Methods All PUD patients with complete records of Hp status and NSAIDs/ASA exposure in 2008 were included for analysis of prevalence and their association with UGI bleeding. We compared present data of PUD and Hp infection to previous data of 1992 to show their trends. Results A total of 98 cases were included; gastric ulcer (GU) in 55, duodenal ulcer (DU) in 28, and 15 cases of combined ulcers. The Hp infection in each group was 38.18%, 42.86%, and 33.33%, respectively. Hp related ulcers had less UGI bleeding than NSAIDs/ASA related. When compared to previous data, the proportion of DU had decreased, GU and combined ulcers had increased, and the Hp infection rate in all 3 groups had decreased. Conclusions While the prevalence of PUD and Hp was decreasing, more NSAIDs/ASA related and non-hp, non-nsaids/asa related ulcers were diagnosed. NSAIDs/ASA related ulcers have more chances of bleeding. Chiang Mai Medical Journal 2010;49(2): Keywords: Helicobacter pylori, peptic ulcer disease, NSAIDs/ASA related ulcer Helicobacter pylori (Hp) infection has been demonstrated as associated with peptic ulcer disease (PUD). (1) Hp infection has been found in % of patients with duodenal ulcer (DU) and % of those with gastric ulcer (GU). (2-7) During this decade, there have been some reports showing a decline in global prevalence of Hp infection and PUD. (8-10) This phenomenon also was seen in many Asian countries. (11-14) However, nonsteroid anti-inflammatory drugs (NSAIDs), which have been used for various rheumatic conditions, and aspirin (ASA) for prevention of thrombotic events in cardiovascular and cerebrovascular diseases, or protection against colorectal cancer, are still prescribed widely by physicians, and easily available as over-the-counter drugs. These medications have been found as major risk factors in non-hp associated PUD, especially regarding their complications in GU. (15-18) Methods This was a retrospective observational study of all upper gastrointestinal endoscopic reports from May to August 2008 at the Endoscopic Unit, Address requests for reprints: Ong-ard Praisontarangkul, M.D., Department of Medicine, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand: ongard@mail.med.cmu.ac.th Received 23 July 2010, and in revised form 11, Agust 2010.

2 42 Praisontarangkul O, Pisespongsa P, Hongsongkiat S. Department of Medicine, Faculty of Medicine, Maharaj Nakorn Chiang Mai Hospital, which is a university hospital providing tertiary care as well as referral center in northern Thailand. Patients with peptic ulcer diseases were examined in detail for the presence of Hp infection, and their history of exposure to NSAIDs/ASA was taken from medical records. Only patients with gastric and duodenal lesions and complete records on either rapid urease test (RUT) or histology staining to identify Hp by Giemsa stain were enrolled for analysis. Those who had malignant gastric or duodenal lesions were excluded from the analysis. The test for Hp infection by RUT was performed by taking one corpus and one antral biopsy for testing with the commercial testing urea kit, using the Pronto Dry test (Gastrex, Warsaw, Poland). Changing color from yellow to pink-red was interpreted as positive RUT for the presence of Hh. Histology with the use of Giemsa stain for Hp infection was based on identification of the bacteria on at least one of the specimens, which was taken from the corpus or antrum. A patient with a positive result either from RUT or histology was diagnosed as Hp positive. Additional biopsies were taken from the ulcer edges or other areas to rule out malignant diseases if endoscopic appearance was unfavorable for benign lesion. An ulcer was defined as a breach of mucosa >5 mm in depth. Malignant ulcers were differentiated from benign ones by the histologic appearance in the biopsy specimens. The presentation of upper gastrointestinal (UGI) bleeding from reports on both endoscopic findings of recent stigmata bleeding and medical records of patient history, physical examination and indication for endoscopic examination of each patient were reviewed. The patients were categorized into 2 groups: UGI bleeding and non-ugi bleeding. There were 57 cases in the UGI bleeding group, who were scheduled for endoscopy to find the causes of bleeding. All were examined within 24 to 48 hours after their presentations. The 41 cases in the non-ugi bleeding group were scheduled for endoscopic examination, due to symptoms other than those for upper gastrointestinal bleeding, namely, dyspeptic symptoms or abdominal pain. The association of Hp infection with NSAIDs/ASA usage was investigated in all of these patients. This study was compared with our previous data on PUD, which were collected from December 1991 to August 1992, comprising 80 consecutive cases of PUD tested for Hp infection and prevalence trends of Hp infection and PUD. (19) Statistical analysis The characteristics of ulcers were presented as descriptive statistics. Fisher s exact test was used to compare categorical data and odds ratio (OR) with 95% confidence interval (95% CI). Results A total of 119 patients with upper gastrointestinal ulcerative lesions was endoscopically diagnosed. Five cases of gastric cancer and 2 with lymphoma were identified by histology and excluded from the analysis, leaving 112 cases of benign peptic ulcer diseases. Sixty-three patients were found to have GU (56.25%), 33 DU (29.46%), and 16 combined GU and DU (14.28%). The data for Hp tests were not complete in 14 cases of PUD patients, and they were excluded from the analysis. Therefore, the 98 remaining cases had complete results of the test for Hp infection, either by RUT or histology, which fulfilled the criteria of inclusion. Seventy-nine cases were tested by RUT, and 26 showed a positive reaction (32.91%); 40 cases had biopsies taken for histologic staining for Hp, and 19 showed Hp organisms on a Giemsa stain (47.50%); and a total of 38 cases from the 98 tested patients were positive for Hp by either RUT or histology stain for Hp (38.78%). Of the 98 cases analyzed for the presence of Hp infection, by testing with at least one of the two methods, 55 had GU, 28 had DU, and 15 cases were found to have combined ulcers. Positive results for Hp infection were found in 21 of the 55 cases with GU (38.18%), 12 of the 28 cases with DU (42.86%), and 5 of the 15 cases with combined ulcers (33.33%), making a total of 38 positive Hp infection cases in 98 patients (38.78%). Medical records showed that of 42 patients with a history of NSAIDs/ASA usage in a recent period, 26 were of the 55 GU cases (47.27%), 11 were of the 28 DU cases (39.29%) and 5 were of

3 Prevalences of PUD and Hp, NSAIDs/ASA exposure 43 the 15 combined ulcer cases (33.33%) (Table 1). The percentages of patients were then examined in the aspects of Hp infection alone, history of NSAIDs/ASA exposure alone, combination of both Hp infection and NSAIDs/ASA exposure, and non-hp, non-nsaids/asa exposure, and the following findings were obtained: Of the 55 GU patients, 9 cases had both Hp infection and a history of NSAIDs/ASA usage (16.36%), 12 had only Hp infection without a history of NSAIDs/ASA usage (21.82%), 17 had only a history of NSAIDs/ASA usage without Hp infection (30.90%), and 17 showed no Hp infection and no history of NSAIDs/ASA exposure (30.90%). In the 28 DU patients, 4 cases had both Hp infection and a history of NSAIDs/ASA usage (14.49%), 8 had only Hp infection without a history of NSAIDs/ASA usage (28.57%), 7 had only a history of NSAIDs/ASA usage without Hp infection (25.00%), and 9 showed no Hp infection and no history of NSAIDs/ASA exposure (32.14%). Of the 15 combined GU & DU patients, there were 5 cases in each of the 3 groups: Hp infection alone, NSAIDs/ASA expsosure alone, and non- Hp, non-nsaids/asa exposure (Table 2). By grouping the patients into UGI bleeding and non-ugi bleeding, there were 57 UGI bleeding and 41 non-ugi bleeding patients. Of the UGI bleeding patients, 18 had Hp infection (31.58%), and 30 had a history of NSAIDs/ASA usage (52.63%). In the non-ugi bleeding patients, 20 cases had Hp infection (48.78%), and 12 had a history of NSAIDs/ASA usage. (29.27%). The history of NSAIDs/ASA exposure was significantly associated with the UGI bleeding group (OR 2.69, 95% CI ), while Hp infection was found more in the non-bleeding group (OR 0.49, 95% CI ) (Table 3). When analysed by grouping the patients into 4 subgroups, using non-hp, non-nsaids as a reference, it was found that an NSAIDs/ASA associated ulcer had more tendency towards UGI bleeding than Hp associated ulcers. However, a combination of Hp infection and exposure of NSAIDs did not show increased risk of UGI bleeding in our series (Table 4). From our previous data of PUD and Hp infection, which were collected from December 1991 to August 1992, (19) we had 80 consecutive cases with PUD and tested for Hp infection in every one using both RUT and histologic staining for Hp by Giemsa stain. For RUT, the CLO test (Ballard Medical Products, USA.) was used. There were 33 GU (41.25%), 40 DU (50%), and 7 combined ulcers (8.75%). The Hp infection was found by Table 1. Patients for Hp tests and history of NSAIDs/ASA exposure Type of PUD No RUT positive/tested (%) Histology positive/tested (%) RUT/ Histology positive/tested (%) Hx of NSAIDs positive/tested (%) GU 55 14/42 (33.33) 10/22 (45.46) 21/55 (38.18) 26/55 (47.27) DU 28 7/23 (30.43) 8/13 (61.54) 12/28 (42.86) 11/28 (39.29) GU + DU 15 5/14 (35.71) 1/5 (20) 5/51 (33.33) 5/15 (33.33) Total 98 26/79 (32.91) 19/40 (47.50) 38/98 (38.78) 42/98 (42.86) Table 2. Patients profile on association of Hp status and NSAIDs/ASA exposure No Hp+/NS + Hp+/NS- Hp-/NS+ Hp-/NS- GU 55 9 (16.36) 12 (21.82) 17 (30.9) 17 (30.9) DU 28 4 (14.29) 8 (28.57) 7 (25) 9 (32.14) GU + DU 15 0 (0) 5 (33.33) 5 (33.33) 5 (33.33) Total (13.27) 25 (25.51) 29 (29.59) 31 (31.63) Hp+ = positive Hp test; Hp- = negative Hp test; NS+ = exposure to NSAIDs NS- = non-exposure to NSAIDs

4 44 Praisontarangkul O, Pisespongsa P, Hongsongkiat S. Table 3. UGI bleeding vs non-bleeding on Hp status and history of NSAIDs exposure UGIB (57 patients) Non-UGIB (41 patients) OR (95% CI) p-value NS+ 30 (52.63) 12 (29.27) 2.69 ( ) Hp+ 18 (31.58) 20 (48.78) 0.49 ( ) Table 4. Risk of UGI bleeding in different status of Hp infection and NSAIDs/ASA exposure Status (No) OR SE p-value 95% CI Hp-ns- (31) Ref Ref Ref Ref Hp+ns- (25) Hp-ns+ (29) Hp+ns+ (13) Table 5. Comparison of PUD prevalences in 1992 vs p-value GU 33 (41.25) 55 (56.12) DU 40 (50) 28 (28.57) GU+DU 7 (8.75) 15 (15.31) Total 80 (100) 98 (100) positive results from either RUT or histologic proof of the organisms, and there was Hp infection in 22 cases of the 33 GU (66.7%), 29 of the 40 DU (72.5%), and 4 of the 7 combined GU & DU (57.2%) (Table 5, 6). It was noticeable that the proportion of GU and DU in this study changed in the opposite direction, when the proportion of GU significantly increased (41.25 % vs 56.12%, p = 0.034), while that of DU significantly decreased (50.00% vs 28.57%, p = 0.012) (Table 5). The prevalence of Hp infection in PUD significantly declined from 68.75% to 38.78% (p < 0.001) during this period. Also the prevalence of Hp infection in GU declined from 66.7% to 38.18%, and that in DU from 72.5% to 42.86% (Table 6). Discussion During the past three decades, the prevalence of PUD has decreased remarkably in the United States, Europe, Australia and Japan. (20-22) Many factors have been taken into consideration regarding this phenomenon, for example, the rapid change in the pattern of PUD is more likely due to changes in environmental factors rather than those in the gene of an affected patient. (23) The decline in Hp infection prevalence during this decade may be due to the global trend of improved socioeconomic status. One study from Japan showed that the decline of Hp infection was as much as 20% between 1986 and 1994, (24) while another study from South Korea showed that the prevalence of infection in young children was inversely related to the socioeconomic class of their family, (25) and a study from Italy showed that the prevalence of Hp infection was higher in rural areas when compared to that in industrial ones. (26) Besides socioeconomic status or environmental issues, part of the reasons for this decline might be increased awareness of Hp eradication from the test and treat strategy used by both general practitioners and specialists, (27) and also the effectiveness of organism eradication by antibiotics combined with proton pump inhibitors (28-29) as well as the low re-infection rate of Hp. (30) All these reasons have led to the decrease of Hp infection and low ulcer recurrence in patients, which in turn might be reflected by decreased peptic ulcer prevalence related Hp infection. The data from this study and the previous period also gave results that showed a significant Table 6. Comparison of Hp prevalences in 1992 vs Hp+/total (%) 2008 Hp+/total (%) p-value GU 22/33 (66.7) 21/55 (38.18) DU 29/40 (72.5) 12/28 (42.86) GU+ DU 4/7 (57.2) 5/15 (33.33) Total 55/80 (68.75) 38/98 (38.78) <0.001

5 Prevalences of PUD and Hp, NSAIDs/ASA exposure 45 decline in the prevalence of Hp infection and PUD, despite the RUT kits being different in each period. We used the CLO test in 1992, and Pronto Dry test in 2008, since each kit was commercially available at those times. However, both kits were tested and validated, and found to have equally and high accuracy for the diagnosis of Hp infection. (31) A selection bias in this study was unlikely since we included all patients who had gastroscopy and Hp status tested in both periods. Our present data showed that the percentage of non- Hp related PUD significantly increased. Interestingly, when an increasing prevalence of NSAIDs/ASA related PUD is found, it may be partly due to the decrease in Hp infection, which made NSAIDs/ASA related ulcers relatively increase in prevalence. However, it may be a real increase in this entity of disease, since NSAIDs/ ASA associated gastric ulcers do not require Hp for their development, (32) and easy access to this medication may be a contributing factor for the development of this type of ulcer. (33-34) The prevalence of non-hp, non-nsaids/asa related PUD differs from country to country, and studies from North America showed an incidence rise from 11-44%, (35-37) while the incidence rate was as low as 1.3% in Japan. (38) The study from South Korea showed a non-hp, non-nsaids/ ASA prevalence of 22.2%, (12) whereas, it was 18.8% in Hong Kong. (39) This study gave a figure of 31.63%. We still do not know exactly if this entity of PUD was just a relative increase while the prevalence of Hp related PUD decreased, or whether it was a real increasing prevalence. Whatever, the prevalence appeared to be increasing. When looking into the detail of UGI bleeding in this study, Hp infection accounted for 31.58% of cases, and NSAIDs/ASA related patients were found at 52.63%. The Hp infection was found in 48.78% of UGI bleeding cases, while NSAIDs/ ASA exposure was found in 29.27%. These figures showed that NSAIDs/ASA associated PUD had more risk of bleeding when compared to the risk of bleeding from Hp infection. A meta-analysis by Huang et al (40) showed an additive effect on PUD bleeding rate combined Hp infection and exposure to NSAIDs (OR 6.13), while Hp infection alone and NSAIDs exposure alone showed a lower risk (OR 1.79 and 4.85 respectively). However, this study could not find this additive effect because the reference group had non-hp, non- NSAIDs/ASA related ulcers; not like the healthy control in Huang s study, and this was due partly to the small sample size. In conclusion, our studies from 2 periods showed the trends of decline in PUD and Hp infection, which were in accordance with the global incidence. At the same time, we found more NSAIDs/ASA associated cases and more non-hp, non-nsaids/asa associated ulcers, as well as NSAIDs/ASA related PUD having a greater percentage of UGI bleeding. We believe that effective eradication of Hp infection and more thoughtful decision making in prescribing NSAIDs/ASA to patients would reduce the prevalence of PUD in these entities. However, for non-hp, non-nsaids/asa related PUD, the prevalence would not decrease, and we need to know more about the natural history of this entity of ulcer before we can have effective management of it, which may be different from that used in Hp or NSAIDs/ASA associated ulcers. References 1. Marshall BJ, Warren JR. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet 1984;1: Ciociola AA, McSorley DJ, Turner K, Sykes D, Palmer JB. Helicobacter pylori infection rates in duodenal ulcer patients in the United States may be lower than previously estimated. Am J Gastroenterol 1999;94: Borody TJ, George LL, Brandl S, et al. Helicobacter pylori-negative duodenal ulcer. Am J Gastroenterol 1991;86: Kuipers EJ, Thijs JC, Festen HP. The prevalence of Helicobacter pylori in peptic ulcer disease. Aliment Pharmacol Ther 1995;9(Suppl 2): Vu C, Ng YY. Prevalence of Helicobacter pylori in peptic ulcer disease in a Singapore hospital. Singapore Med J 2000;41: Tsuji H, Kohli Y, Fukumitsu S, et al. Helicobacter pylori-negative gastric and duodenal ulcers. J Gastroenterol 1999;34: Meucci G, Di Battista R, Abbiati C, et al. Prevalence and risk factors of Helicobacter pylorinegative peptic ulcer: a multicenter study. J Clin Gastroenterol 2000;31: el-serag HB, Sonnenberg A. Opposing time

6 46 Praisontarangkul O, Pisespongsa P, Hongsongkiat S. trends of peptic ulcer and reflux disease. Gut 1998;43: Kang JY, Tinto A, Higham J, Majeed A. Peptic ulceration in general practice in England and Wales : period prevalence and drug management. Aliment Pharmacol Ther 2002;16: Xia HH, Phung N, Altiparmak E, Berry A, Matheson M, Talley NJ. Reduction of peptic ulcer disease and Helicobacter pylori infection but increase of reflux esophagitis in Western Sydney between 1990 and Dig Dis Sci 2001;46: Wong SN, Sollano JD, Chan MM, et al. Changing trends in peptic ulcer prevalence in a tertiary care setting in the Philippines: a seven-year study. J Gastroenterol Hepatol 2005;20: Jang HJ, Choi MH, Shin WG, et al. Has peptic ulcer disease changed during the past ten years in Korea? A prospective multi-center study. Dig Dis Sci 2008;53: Xia B, Xia HH, Ma CW, et al. Trends in the prevalence of peptic ulcer disease and Helicobacter pylori infection in family physician-referred uninvestigated dyspeptic patients in Hong Kong. Aliment Pharmacol Ther 2005;22: Ho KY, Chan YH, Kang JY. Increasing trend of reflux esophagitis and decreasing trend of Helicobacter pylori infection in patients from a multiethnic Asian country. Am J Gastroenterol 2005;100: Griffin MR. Epidemiology of nonsteroidal antiinflammatory drug-associated gastrointestinal injury. Am J Med 1998;104:23S-9S; discussion 41S-2S. 16. Hollander D. Gastrointestinal complications of nonsteroidal anti-inflammatory drugs: prophylactic and therapeutic strategies. Am J Med 1994; 96: Singh G, Ramey DR, Morfeld D, Shi H, Hatoum HT, Fries JF. Gastrointestinal tract complications of nonsteroidal anti-inflammatory drug treatment in rheumatoid arthritis. A prospective observational cohort study. Arch Intern Med 1996; 156: Bjorkman DJ. Nonsteroidal anti-inflammatory drug-induced gastrointestinal injury. Am J Med 1996;101:25S-32S. 19. Praisontarangkul O, Thongsawat S. Comparative study of Helicobacter pylori infection in northern and other parts of Thailand. NMS & Fac. of Med. CMU Conference, Chiang Mai, August 1999 (abstract p. 7) 20. Vogt TM, Johnson RE. Recent changes in the incidence of duodenal and gastric ulcer. Am J Epidemiol 1980;111: Smith MP. Decline in duodenal ulcer surgery. JAMA 1977;237: Wylie CM. The complex wane of peptic ulcer. I. Recent national trends in deaths and hospital care in the United States. J Clin Gastroenterol 1981;3: Sonnenberg A, Muller H, Pace F. Birth-cohort analysis of peptic ulcer mortality in Europe. J Chronic Dis 1985;38: Kumagai T, Malaty HM, Graham DY, et al. Acquisition versus loss of Helicobacter pylori infection in Japan: results from an 8-year birth cohort study. J Infect Dis 1998;178: Malaty HM, Kim JG, Kim SD, Graham DY. Prevalence of Helicobacter pylori infection in Korean children: inverse relation to socioeconomic status despite a uniformly high prevalence in adults. Am J Epidemiol 1996;143: Dore MP, Malaty HM, Graham DY, Fanciulli G, Delitala G, Realdi G. Risk Factors Associated with Helicobacter pylori Infection among Children in a Defined Geographic Area. Clin Infect Dis 2002;35: Moayyedi P. Helicobacter pylori test and treat strategy for young dyspeptic patients: new data. Gut 2002;50 Suppl 4:iv Sung JJ, Chung SC, Ling TK, et al. Antibacterial treatment of gastric ulcers associated with Helicobacter pylori. N Engl J Med 1995;332: Sung JJ, Chung SC, Ling TK, et al. One-year follow-up of duodenal ulcers after 1-wk triple therapy for Helicobacter pylori. Am J Gastroenterol 1994;89: Adachi M, Mizuno M, Yokota K, et al. Reinfection rate following effective therapy against Helicobacter pylori infection in Japan. J Gastroenterol Hepatol 2002;17: Said RM, Cheah PL, Chin SC, Goh KL. Evaluation of a new biopsy urease test: Pronto Dry, for the diagnosis of Helicobacter pylori infection. Eur J Gastroenterol Hepatol 2004;16: Laine L, Marin-Sorensen M, Weinstein WM. Nonsteroidal antiinflammatory drug-associated gastric ulcers do not require Helicobacter pylori for their development. Am J Gastroenterol 1992;87:

7 Prevalences of PUD and Hp, NSAIDs/ASA exposure Ong TZ, Hawkey CJ, Ho KY. Nonsteroidal antiinflammatory drug use is a significant cause of peptic ulcer disease in a tertiary hospital in Singapore: a prospective study. J Clin Gastroenterol 2006;40: Manuel D, Cutler A, Goldstein J, Fennerty MB, Brown K. Decreasing prevalence combined with increasing eradication of Helicobacter pylori infection in the United States has not resulted in fewer hospital admissions for peptic ulcer disease-related complications. Aliment Pharmacol Ther 2007;25: Kurata JH, Nogawa AN. Meta-analysis of risk factors for peptic ulcer. Nonsteroidal antiinflammatory drugs, Helicobacter pylori, and smoking. J Clin Gastroenterol 1997;24: Jyotheeswaran S, Shah AN, Jin HO, Potter GD, Ona FV, Chey WY. Prevalence of Helicobacter pylori in peptic ulcer patients in greater Rochester, NY: is empirical triple therapy justified? Am J Gastroenterol 1998;93: Sprung DJ, Apter MN. What is the role of Helicobacter pylori in peptic ulcer and gastric cancer outside the big cities? J Clin Gastroenterol 1998;26: Nishikawa K, Sugiyama T, Kato M, et al. Non- Helicobacter pylori and non-nsaid peptic ulcer disease in the Japanese population. Eur J Gastroenterol Hepatol 2000;12: Hung LC, Ching JY, Sung JJ, et al. Long-term outcome of Helicobacter pylori-negative idiopathic bleeding ulcers: a prospective cohort study. Gastroenterology 2005;128: Huang JQ, Sridhar S, Hunt RH. Role of Helicobacter pylori infection and non-steroidal anti -inflammatory drugs in peptic-ulcer disease: a meta-analysis. Lancet 2002;359:14-22.

8 48 Praisontarangkul O, Pisespongsa P, Hongsongkiat S. แนวโน มของอ บ ต การณ โรคแผลในกระเพาะอาหารและลำไส เล กส วนต น ก บการต ดเช อ Helicobacter pylori ในภาคเหน อ องอาจ ไพรสณฑรางก ร, พ.บ., พ เศษ พ เศษพงษา, พ.บ., ส ทธ หงส ทรงเก ยรต, พ.บ. ภาคว ชาอาย รศาสตร คณะแพทยศาสตร มหาว ทยาล ยเช ยงใหม บทค ดย อ บทนำ อ บ ต การณ ของแผลในทางเด นอาหารส วนต นและการต ดเช อเฮล โคแบคเตอร ไพลอไร (Hp) ม แนวโน มลดลงท วโลก ในขณะเด ยวก นอ บ ต การณ ของแผลจากการใช ยาต านการอ กเสบท ไม ใช สเต ยรอยด รวมท งแอสไพร น กล บพบเพ มข น ผ ว จ ยได ส บค นแนวโน มของอ บ ต การณ ด งกล าว รวมไปถ งแนวโน มการม เล อดออกจากแผลในทางเด นอาหารส วนต น ในแต ละกรณ ว ธ การ โดยการว เคราะห ข อม ลผลส องกล องทางเด นอาหารส วนต นในช วงเด อนพฤษภาคม ถ งเด อน ส งหาคม 2551 และเปร ยบเท ยบก บข อม ลท ทำไว เม อเด อนธ นวาคม 2534 ถ ง เด อนส งหาคม 2535 ผลการศ กษา ความส มพ นธ ก บการต ดเช อ Hp ใน GU, DU, combined ulcers ร อยละ 38.18, และร อยละ ตามลำด บ แผลจากการต ดเช อ Hp ม เล อดออกน อยกว าแผลส มพ นธ ก บการใช NSAIDs/ASA เม อเปร ยบเท ยบก บข อม ลเด ม อ ตราส วนของ DU ลดลง แต ของ GU และ combined ulcers กล บเพ มข น การต ดเช อ Hp ลดลงท ง 3 กล ม สร ป อ บ ต การณ ของแผลในทางเด นอาหารส วนต นส มพ นธ ก บการต ดเช อ Hp ลดลง แต ม แผลท เก ด จากการใช NSAIDs/ASA และแผลท ไม ส มพ นธ ก บป จจ ยท งสองต างม อ ตราส วนเพ มข น แผลท ส มพ นธ ก บการใช NSAIDs/ASA ม อ บ ต การณ ตกเล อดส งกว าแผลในกล มต ดเช อ Hp เช ยงใหม เวชสาร 2553;49(2): Keywords: เช อเฮล โคแบคเตอร ไพลอไร แผลกระเพาะอาหารและลำไส เล กส วนต น แผลจากยา ต านการอ กเสบท ไม ใช สเต ยรอยด