Journals / Turkish Journal of Gastroenterology / 2012 / Cilt: 23 - Sayı: 2

Duodenal ve gastrik ülserin etyolojisi

Etiological factors of duodenal and gastric ulcers

Pages
99–103
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

In about one-tenth of the patients, nonsteroidal antiinflammatory drug use was the cause of ulcer alone, and about one-tenth of the ulcers were classified as idiopathic.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Background/aims: We aimed to determine the etiology of patients with duodenal and gastric ulcers.
📊
Key Findings & Data:Methods: 140 patients diagnosed with peptic ulcer between April 2002-2009 were enrolled in this prospective study.
💡
Conclusion & Impact:In about one-tenth of the patients, nonsteroidal antiinflammatory drug use was the cause of ulcer alone, and about one-tenth of the ulcers were classified as idiopathic.
🔬Design:Research Article
📍Scope:2002-2009 Verileri
⚙️Variables:Domain Parameters

Abstract

Background/aims: We aimed to determine the etiology of patients with duodenal and gastric ulcers. Methods: 140 patients diagnosed with peptic ulcer between April 2002-2009 were enrolled in this prospective study. Two biopsy specimens were collected from the antrum and corpus for histology and one for rapid urease testing, and stool samples were analyzed for Helicobacter pylori antigen. Serum calcium and gastrin levels were also analyzed. Results: 82 (58%) patients were male, with a median age of 47.70±15.03 years (range: 16-92). The ulcer was located in the duodenum in 96 patients, stomach in 40, and both duodenum and stomach in 4. The rates of patients positive for Helicobacter pylori antigen in stool, positive in urease testing and positive for Helicobacter pylori presence in antral and corpus samples were 48%, 52%, 67%, and 60%, respectively. 107 (76%) patients were positive for Helicobacter pylori in one of the test methods. 64 (46%) patients had a history of nonsteroidal antiinflammatory drug use within the last month. Mean levels of calcium and gastrin were 9.29±0.40 (7.90-10.20) and 73.96±89.88 (12.86-562.50), respectively. Gastrin level was correlated to inflammatory activity (p<0.05). 19 (13.6%) of the patients were negative for Helicobacter pylori, nonsteroidal antiinflammatory drug use and hypersecretory illness, and were classified as idiopathic. Conclusions: The most common cause of duodenal and gastric ulcer was Helicobacter pylori, and it was responsible for three-fourths of the cases. About half of the patients had a history of nonsteroidal antiinflammatory drug use, and nonsteroidal antiinflammatory drug and Helicobacter pylori were both responsible for the ulcer in three-fourths of these patients. In about one-tenth of the patients, nonsteroidal antiinflammatory drug use was the cause of ulcer alone, and about one-tenth of the ulcers were classified as idiopathic.

Özet

Amaç: Duodenum ve mide ülserli hastaların etyolojisini tesbit etmek. Yöntem: Nisan 2002-2009 tarihleri arasında Endoskopi Ünitesine gastroskopi için başvuran ve peptik ülser saptanan 140 hasta prospektif olarak çalışmaya alındı. Hastalardan histolojik inceleme için antrumdan ve korpustan ikişer, üreaz için birer biyopsi alındı, gaitada Helikobakter pilori antijeni bakıldı. Her iiç yöntemden herhangi birinde Helikobakter pilori pozitifliği varsa etyolojik neden olarak Helikobakter pilori kabul edildi. Hiatopatolo-jik olarak inflamasyon aktivitesi, intestinal metaplazi, atrofı ve Helikobakter pilori bakıldı. Serumda kalsiyum ve gastrin seviyeleri bakıldı. Bulgular: Hastaların 82'si (%58) erkek, yaş ortalması 47.70±15.03 yaş (dağılım 16-92), 62'si (%44) sigara, 18'i (%13) alkol kullanıyor idi. Ülser 96 hastada duodenumda, 40 hastada midede. 4 hastada mide ve duodenumda yerleşmiş idi. Gaitada Helikobakter pilori antijen pozitifliği, üreaz pozitifliği, antrumda ve korpusta histolojik Helikobakter pilori varlığı sırasıyla: %48. %52, %67 ve %60 idi. Helikobakter pilori 107 hastada (%'76) yöntemlerden herhangi birinde pozitif idi. Son 1 ay içerisinde nonsteroid antiinflamatuar ilaç kullanım hikayesi olan 64 hastanın (%46), 48'inde (%75) Helikobakter pilori pozitif, 16 hastada (25) negatif idi. Antrum biyopsilerinde inflamatuvar aktivite varlığı, atrofı, intestinal metaplazi sıklığı sırasıyla %S5, %17.5, %11; korpusta ise %66, %6.5 ve %15 idi. Ortalama kalsiyum düzeyi 9.29+0.40 (7.90-10.20), gastrin düzeyi 73.96±89.88 (12.86-562.50) idi. Gastrin düzeyi yüksek olan hastaların histolojik incelemelerinde hipersekretuar durum tesbit edilmedi. Gastrin yüksekliği inflamasyon aktivitesi ile korele idi (p<0.05). 17 hastada Helikobakter pilori, nonsteroid antiinflamatuar ilaç kullanımı ve hipersekretuar hastalık tesbit edilmedi ve idiyopatik kabul edildi. Sonuç: Duotlerıum ve mide ülserinin en sık nedeni Helikobakter pilori olup hastaların dörtte üçünden sorumludur. Hastaların yaklaşık yarısında nonsteroid antiinflamatuar ilaç kullanımı öyküsü vardır ve bunların da dörtte üçünde ülserden nonsteroid antiinflamatuar ilaç ve Helikobakter pilori birlikte sorumludur. Hastaların yaklaşık onda birinde nonsteroid antiinflamatuar ilaç tek başına etyolojik neden olarak saptanırken, yaklaşık onda biri idiyopatiktir.

🔖

Cite This Article

UYANIKOĞLU, A., DANALIOĞLU, A., AKYÜZ, F., ERMİŞ, M. F., GÜLLÜOĞLU, M., KAPRAN, Y., DEMİR, K., ÖZDİL, S., BEŞIŞIK, F., BOZTAŞ, G., MUNGAN, Z., KAYMAKOĞLU, S. (2012). Duodenal ve gastrik ülserin etyolojisi. Turkish Journal of Gastroenterology, Cilt: 23 - Sayı: 2, 99–103. https://ajindex.com/articles/410293

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (15)

  1. Malfertheiner P, Chan FK, McColl KE. Peptic ulcer disease. Lancet 2009; 374: 1449-61
  2. Wang YR, Richter JE, Dempsey DT. Trends and outcomes of hospitalizations for peptic ulcer disease in the United States, 1993 to 2006. Ann Surg 2010; 251: 51-8
  3. Zapata-Colindres JC, Zepeda-Gómez S, Montaño-Loza A, et al. The association of Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs in peptic ulcer disease. Can J Gastroenterol 2006; 20: 277-80
  4. 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: 628-32
  5. Arents NL, Thijs JC, van Zwet AA, Kleibeuker JH. Does the declining prevalence of Helicobacter pylori unmask patients with idiopathic peptic ulcer disease? Trends over an 8 year period. Eur J Gastroenterol Hepatol 2004; 16: 779- 83
  6. Lassen A, Hallas J, Schaffalitzky de Muckadell OB. Complicated and uncomplicated peptic ulcers in a Danish county 1993-2002: a population-based cohort study. Am J Gastroenterol 2006; 101: 945-53
  7. 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: 1527-31
  8. Arroyo MT, Forne M, de Argila CM, et al. The prevalence of peptic ulcer not related to Helicobacter pylori or non-steroidal anti-inflammatory drug use is negligible in southern Europe. Helicobacter 2004; 9: 249-54
  9. Kachintorn U, Luengrojanakul P, Atisook K, et al. Helicobacter pylori and peptic ulcer diseases: prevalence and association with antral gastritis in 210 patients. J Med Assoc Thai 1992; 75: 386-92
  10. Itoh T, Seno H, Kita T, et al. The response to Helicobacter pylori differs between patients with gastric ulcer and duodenal ulcer. Scand J Gastroenterol 2005; 40: 641-7
  11. Sari YS, Sander E, Erkan E, Tunali V. Endoscopic diagnoses and CLO test results in 9239 cases, prevalence of Helicobacter pylori in Istanbul, Turkey. J Gastroenterol Hepatol 2007; 22: 1706-11
  12. Takao T, Ishikawa T, Ando T, et al. Multifaceted Assessment of Chronic Gastritis: A Study of Correlations between Serological, Endoscopic, and Histological Diagnostics. Gastroenterol Res Pract 2011; 2011: 631461
  13. Xia HH, Phung N, Kalantar JS, Talley NJ. D. Med J Aust 2000; 173(10): 508-9
  14. Costa AC, Figueiredo C, Touati E. Pathogenesis of Helicobacter pylori infection. Helicobacter 2009; 14 (Suppl 1): 15- 20
  15. Satoh K, Sugano