Necip TİYNAK, Fikret AKSOY, Gökhan DEMİRAL, Alp ÖZÇELİK, Burhan ŞABAN

Perfore peptik ülser olgularında Helikobakter pilori insidansı ve lansoprozol, klaritromisin, amoksisilin ile yapılan üçlü eradikasyon tedavi sonuçları

Giriş ve amaç: Helikobakter pilori peptik ülser hastalığının en sık sebebidir. Bu çalışmada perfore peptik ülser olgularında H. pilori insidansını ve ameliyat sonrası uygulanan üçlü eradikasyon tedavisi sonuçlarını inceledik. Gereç ve yöntem: Peptik ülser perforasyonu tanısıyla acil olarak opere edilen 80 hasta prospektif olarak incelendi. Ameliyatta perforasyon odağından alınan biyopsi materyali hızlı üreaz testi ile değerlendirildi. Sonuçlar negatif, hafif ve şidetli H. pilori enfeksiyonu şeklinde gruplandırıldı. Hastalara, ağızdan beslenmeye başladıkları günden itibaren H. pilori eradikasyonu amacıyla klaritromisin 2x500 mg 10 gün, amoksisilin 2x1000 mg 10 gün, lansoprozol 2x30 mg 28 gün süreyle verildi. Hastalar ameliyattan 45 gün sonra üst gastrointestinal sistem endoskopisi için kontrole çağrıldı ve sonuçlar histopatolojik olarak değerlendirildi. Bulgular: Çalışmaya 80 hasta alındı ancak 71 hasta ile çalışma tamamlandı. Perforasyon odağından alınan tam kat biyopsi materyallerinin hızlı üreaz testi ile yapılan değerlendirmesinde 7 (%8,75) hastada negatif, 10 (%12,5) hastada hafif, 63 (%78,75) hastada ise şiddetli H. pilori enfeksiyonu saptandı. Üçlü eradikasyon tedavisi uygulanan 71 hastanın kontrol endoskopilerinde alınan biyopsi materyalleri histolojik olarak değerlendirildiğinde 53 (%74,6) hastada negatif, 17 (%23,9) hastada hafif, 1 (%1,3) hastada şiddetli H. pilori enfeksiyonu saptandı. Sonuç: H. pilori, peptik ülser perforasyonu gelişiminde çok önemli bir rol oynamaktadır. Peptik ülser perforasyon ameliyatı sonrası üçlü eradikasyon tedavisi verilmeli ve 45 gün sonra üst gastrointestinal sistem endoskopisi ile eradikasyonun başarısı ve ülserin son durumu değerlendirilmelidir.

Anahtar Kelimeler:

Helikobakter pilori, peptik ülser, perforasyon, eradikasyon tedavisi

ncidence of Helicobacter pylori infection and the results of triple eradication therapy combining lansoprazole, clarithromycin, amoxicillin for perforated peptic ulcer

Background/aim: Helicobacter pylori (H. pylori) is the most common etiological factor in peptic ulcer. In this article, we review the incidence of H. pylori and the results of triple eradication therapy for perforated peptic ulcer. Materials and methods: 80 patients operated for peptic ulcer perforation were examined prospectively. Biopsies were taken from perforation site in order to perform rapid urease test. The results were grouped as negative, mild and severe H. pylori infection. The patients were treated with an eradication regimen consisting of a triple therapy of clarithromycin 2x500 mg 10 days, amoxicillin 2x1000 mg 10 days and lansoprazole 2x30 mg 28 days. Gastroscopy was performed 45 days postoperatively and histopathological investigations made. Results: The study was completed with 71 of the 80 patients. Full thickness mucosal biopsies were obtained from perforation site in all patients. The rapid urease test for H. pylori was severely positive in 63 (78.75%) and mildly positive in 10 (12.5%) patients. Seven (8.75%) of these patients had negative test results. After triple eradication therapy, biopsy materials of 71 patients were investigated histologically. In 53 (74.6%) patients, there was no H. pylori infection. Seventeen (23.9%) patients had mild and 1 (1.3%) patient had severe H. pylori infection. Conclusion: H. pylori plays an important role in the pathogenesis of peptic ulcer perforation. An appropriate triple H. pylori eradication therapy should be performed for peptic ulcer perforation and efficacy of treatment should be confirmed with gastroscopy 45 days postoperatively.

Keywords:

Helicobacter pylori, peptic ulcer, perforation, eradication therapy,

PDF

___

Metzger J, Styger S, Sieber C, et al. Prevalence of Helicobacter pylori infection in peptic ulcer perforations. Swiss Med Wkly 2001; 131: 99-103.
Ng EK, Lam YH, Sung JJ, et al. Eradication of Helicobacter pylori prevents recurrence of ulcer after simple closure of duodenal ulcer perforation: randomized controlled trial. Ann Surg 2000; 231: 153-8.
Shiotani A, Nurgalivea ZZ, Yamaoka Y, et al. Helicobacter pylori. Med Clin North Am 2000; 84: 1125-36.
Beşışık F. Türkiye’de Helicobacter pylori sorunu. Editör; Göksoy E. Aktüel Gastroenteroloji ve Hepatoloji-I. 2. Edisyon. İstanbul, Bil- medya Grup 2003; 39-50.
Tovey FI, Hobsley M, Holton J. Helicobacter pylori virulence fac- tors in duodenal ulceration: A primary cause or a secondary infec- tion causing chronicity. World J Gastroenterol 2006; 12: 6-9.
Hamzaoğlu HÖ. Peptik ülser tedavisi sonrası karşılaşılan sorunlar. Editör; Göksoy E. Aktüel Gastroenteroloji ve Hepatoloji-I. 2. Edis- yon. İstanbul, Bilmedya Grup 2003; 95-9.
Tomassetti P, Campana D, Piscitelli L, et al. Treatment of Zollinger- Ellison Syndrome. World J Gastroenterol 2005; 11: 5423-32.
Kalafat H. 2000’li yıllarda peptik ülser cerrahisi. Editör; Göksoy E. Aktüel Gastroenteroloji ve Hepatoloji-I. 2. Edisyon. İstanbul, Bil- medya Grup 2003; 107-12.
Cave DR. Transmission and epidemiology of Helicobacter pylori. Am J Med 1996; 100: 12-7.
Pounder RE, Ng D. The prevalence of Helicobacter pylori infection in different countries. Aliment Pharmacol Ther 1995; 9: 33-9.
Wyle FA. Helicobacter pylori: Current perspectives. J Clin Gatro- enterol 1991; 13: 114-24.
Graham DY. A reliable cure for Helicobacter pylori infection. Gut 1995; 37: 154-6.
Savarino V. Vigneri S. How should we decide on the best regimen for eradicating Helicobacter pylori? BMJ 1995; 311: 581-82.
Malfertheiner P, Megraud F, et al. Current concepts in the manage- ment of Helicobacter pylori infection: Ther Maastricht 2000 con- census report. Aliment Pharmacol Ther 2002; 16: 167-80.
Önder GF, Aydın A. Helikobakter pilori infeksiyonunda pantopro- zol, amoksisilin, klaritromisin kombinasyonu ile 1 ve 2 haftalık teda- vilerin etkinliği. Turk J Gastroenterol 2003; 14: 149-53.
Güliter S, Keleş H ve ark. Lansoprozol + klaritromisin + amoksisi- lin tedavi rejimlerinin ilk basamak Helikobakter pilori eradikasyo- nundaki yeri. Turk J Gastroenterol 2003; 1: 887-92.
National Institutes of Health Concencus Development Conference. H. pylori in peptic ulcer disease. JAMA 1994; 272: 65-9.
Parsonnet J. Helicobacter pylori and gastric cancer. Gastroenterol Clin North Am. 1993; 22: 89-104.
Schutze K, Hentschel E. Duodenal ulcer healing after 7 day treat- ment: a pilot study with lansoprazole, amoxicillin and clarithromy- cin. Z Gastroenterol 1995; 33: 651-3.
Catalone F, Branciforte G, Catanzaro R, et al. Helicobacter pylori positive duodenal ulcer: three day antibiotic eradication regimen. Aliment Pharmacol Ther 2000; 14: 1329-34.
Gisbert JP, Marcos S, Gisbert JL, et al. High efficacy of ranitidine bismuth citrate, amoxicilline, chlarithromycin and metranidazole twice daily for only five days in H. pylori eradication. Helicobacter 2001; 6: 157-62.
Hurenkamp GJ, Van Der Ende A, Grundmeijer HG, et al. Equally high efficacy of 4, 7 and 10 day triple therapies to eradicate H. pylo- ri infection in patients with ulcer disease. Aliment Pharmacol Ther 2000; 14: 1065-70.
Bhasin DK, Sharma BC, Ray P, et al. Comparison of seven and fo- urteen days lansoprozole, amoxicilline and chlarithromycin therapy for eradication of Helicobacter pylori: a report from India. Helico- bacter 2000; 5: 84-7.
Maconi G, Parente F, Russo A, et al. Do some patients with Helico- bacter pylori infection benefit from an extension to 2 weeks of a pro- ton pump inhibitor –based triple eradication therapy? Am J Gastro- enterol 2001; 96: 359-66.
Vaira D, Menegatti M, Miglioli M. What is the role of Helicobacter pylori in complicated ulcer disease? Gastroenterology 1997; 113; 78-84.
Kuipers EJ, Thijs JC, Festen HP. The prevalence of H. pylori in pep- tic ulcer disease. Aliment Pharmacol Ther 1995; 9: 59-69.
Gispert JP, Blanco M, Mateos JM, et al. H. pylori negative duode- nal ulcer prevalance and causes in 774 patients. Dig Dis Sci 1999; 44: 2295-302.
Khanna AK, Pandey S, Jain AK, et al. H. pylori infection in patients with perforated chronic duodenal ulcer. Indian J Gastroenterol 2001; 20: 204-7.
Oncel M, Kurt N, Kucuk HF, et al. H. pylori eradication after duode- nal ulcer perforation . Indian J Gastroenterol 2001; 20: 251-4.
Kumar D, Sinha AN. H. pylori infection delays ulcer healing in pa- tients operated on for perforated duodenal ulcer. Indian J Gastro- enterol 2002: 21: 19-22.
Wara P. Effect of HP eradication on the ulcer recurrence rate after simple closure of perforated duodenal ulcer: retrospective and pros- pective randomised controlled studies. Br J Surg 2002; 89: 493-94.
Tran TT, Quandalle P. Treatment of perforated gastroduodenal ul- cer by simple sutur followed by HP eradication. Ann Chir 2002; 127: 32-4.
Gonchar MG, Del'tsova EI, Kuchirka IaM, et al. HP in patients with complicated peptic ulcer. Khirurgiia(Mosk) 1999; 6: 25-6.
Kate V, Ananthakrishnan N, Badrinadth S. Effect of HP eradication on the ulcer recurrence rate after simple closure of perforated du- odenal ulcer: retrospective and prospective randomized controlled studies. British J Surg 2001; 88: 1054-8.
Stabile BE. Redefining the role of surgery for perforated duodenal ulcer in the H. pylori era. Ann Surg 2000; 231: 159-60.
Veldhuyzen Van Zanten S, Lauritsen K, Deltchier JC, et al. One we- ek triple thrapy with esomeprazole provides effective eradication of H. pylori in duodenal ulcer disease. Aliment Pharmacol Ther 2000; 14: 1605-11.
Scott LJ, Dunn CJ, Mallarkey G, et al. Esomeprazole: A view of its use in the management of acid-related disorders. Drugs 2002; 62: 1503-38.
Watanabe Y, Aoyama N, Shirasaka D, et al. Levofloxacin based trip- le therapy as a second line treatment after failure of H. pylori era- dication with standart triple therapy. Dig Liver Dis 2003; 35: 711- 5.
Graham DY, Lew GM, Malaty HM, et al. Factors influencing the eradication of H. pylori with triple therapy. Gastroenterolgy 1992; 102: 493-6.
Boey J, Lee NW, Wong J, et al. Perforations in acute abdominal ul- cers. Surg Gynecol Obstet 1982; 155: 193-6.
Jordan GL Jr, Angel RT, De Bakey ME. Acute gastroduodenal per- foration: comparative study of treatment with simple closure, subto- tal gastrectomy and hemigastrectomy and vagotomy. Arch Surg 1966; 92: 449-55.
Pierandozzi JS, Hinshaw DB. Vagotomy and pyloroplasty for acute perforated duodenal ulcer: a report of 75 patients. Am J Surg 1960; 100: 245-50.
Jordan PH, Thornby J. Perforated pyloroduodenal ulcers: long term results with omental patch closure and parietal cell vagotomy. Ann Surg 1995; 221: 479-86.
Hermansson M, Stael VH. Peptic ulcer perforation before and after the introduction of H2 receptor blockers and proton pump inhibi- tors. Scand J Gastroenterol 1977; 32: 523-9.
Macintyre IM, Millar A. Impact of H2 receptor antagonists on the outcome of treatment of perforated duodenal ulcer. J R Coll Surg Edinb 1990; 35: 348-52.
Van Der Hulst RW, Rauws EA, Koycu B, et al. Prevention of ulcer recurrence after eradication of H. pylori: a prospective long term follow up study. Gastroenterology 1997; 113: 1082-6.
Higham J, Kang JY, Majeed A, et al. Recent trends in admissions and mortality due to peptic ulcer in England: increasing frequency of haemorrhage among older subjects. Gut 2002; 50: 460-4.