BLEEDING PEPTIC ULCER, NONSTEROIDAL ANTIINFLAMMATORY DRUGS AND HELICOBACTER PYLORI INFECTION – A PROSPECTIVE, CONTROLLED, RANDOMIZED STUDY

  • Pavel Skok Oddelek za gastroenterologijo in endoskopijo Klinični oddelek za interno medicino Splošna bolnišnica Maribor Ljubljanska ul. 5 2000 Maribor
  • Igor Križman Na jami 7 1000 Ljubljana
  • Marija Skok Zdravstveni dom Maribor Ulica talcev 2 2000 Maribor
Keywords: peptic ulcer, complications, hemorrhage, nonsteroidal antiinflammatory drugs, Helicobacter pylori

Abstract

Background. The explanation of peptic ulcer etiology has changed significantly in the past decade after the clarification of the significance of Helicobacter pylori infection.

Aim. To evaluate the effectiveness of Helicobacter pylori eradication in patients with hemorrhaging peptic ulcer and patients with peptic ulcer without complications.

Study ethics. The study was approved in 1998 by the Medical Ethics Committee of the Republic of Slovenia (No. 90/09/98).

Type of study. Prospective, controlled and randomized study, carried out between 1998–2000.

Patients and methods. The study included 80 patients (50 male and 30 female, av.age 57.5 years, SD ± 17.1, range 22– 80) in which endoscopy confirmed hemorrhage from peptic ulcer of stomach or duodenum and Helicobacter pylori infection. In all cases endoscopic hemostasis was performed: injection sclerotherapy with diluted adrenalin 1:10,000 and 1% polidocanol or argon plasma coagulation. The control group was made up of 80 patients (50 male and 30 female, av.age 56.8 years, SD ± 16.8, range 19–80) with peptic ulcer of stomach or duodenum and Helicobacter pylori infection. Infection was confirmed by a rapid urease test and histologic investigation of the gastric mucosa. In all cases the recommended drug combinations were used in the treatment of the infection: a proton pump inhibitor, omeprazol (4 weeks), and combination of antibiotics, claritromycin and metronidazole or with regard to the antibiogram (1 week). The therapeutic success was ascertained endoscopically four weeks after inclusion in the study. Infection eradication was confirmed by the rapid urease test and histologic investigation of the gastric mucosa.

Results. Four weeks after inclusion in the study the success of infection eradication was 92.5% in the study group, in the control group it was 91.3% (p > 0.05). In 6 patients (7.5%, 6/ 80) from the study group and in 7 (8.8%, 7/80) from the control group we introduced a replacement treatment for the infection. Final treatment of the infection according to the antibiogram was required in two patients (2/80, 2.5%) from the study group and in 3 (3/80, 3.8%) from the control group. Control endoscopy showed the peptic ulcer had healed in 71/ 80 patients (88.8%) from the study group and in 68/80 patients (85%) from the control group (p > 0.05). Endoscopic investigation performed one year after inclusion in the study revealed a recurrence of Helicobacter pylori infection in 4 patients (5%, 4/80) from the study group and in 5 (6.3%, 5/80) from the control group (p > 0.05). Of these 9 patients we found peptic ulcer recurrence in only one patient (1.3%, 1/80) from the study group and in one (1.3%, 1/80) from the control group. Both patients has used preparations of acetylsalycilic acid prior to endoscopic investigation.

Conclusions. The findings of our study confirm that during the observed period of time, one year, the reinfection rate with Helicobacter pylori was 5.6%. In this period we did not observed rebleeding due to peptic ulcer and only two patients had a recurrence of ulcer disease.

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References

NIH Consensus conference. Helicobacter pylori in peptic ulcer disease. JAMA 1994; 272: 65–9.

Jorgensen T, Binder V. Epidemiology in gastroenterology. Scand J Gastroenterol 1996; 31: Suppl 216: 197–207.

Sonnenberg A, Everhart JE. Health impact of peptic ulcer in the United States. Am J Gastroenterol 1997; 92: 614–20.

Fock KM. Peptic ulcer disease in the 1990s: an Asian perspective. J Gastroenterol Hepatol 1997; 12: S23–S28.

Andersen IB, Bonnevie O, Jorgensen T, Sorensen TI. Time trends for peptic ulcer disease in Denmark, 1981–1993. Analysis of hospitalization register and mortality data. Scand J Gastroenterol 1998; 33: 260–6.

Everhart JE, Byrd Holt D, Sonnenberg A. Incidence and risk factors for selfreported peptic ulcer disease in the United States. Am J Epidemiol 1998; 147: 529–36.

Skok P. How efficient is endoscopic injection sclerotherapy in peptic ulcer hemorrhage? Hepatogastroenterology 1997; 15: 861–5.

Skok P. The epidemiology of hemorrhage from the upper gastrointestinal tract in the mid-nineties – has anything changed? Hepatogastroenterology 1998; 24: 2228–33.

Skok P. Peptična razjeda – najpogostejši vzrok krvavitve iz prebavne cevi. Zdrav Vestn 1999; 68: 415–9.

Malfertheiner P, Megraud F, O’Morain C et al. for the European Helicobacter pylori Study Group (EHPSG). Current European concepts in the management of Helicobacter pylori infection. The Maastricht Consensus Report. Eur J Gastroenterol Hepatol 1997; 9: 1–2.

Lee J, O’Morain CA. Consensus or confusion: a review of existing national guidelines and Helicobacter pylori related diseases. Eur J Gastroenterol Hepatol 1997; 9: 527–31.

Tepeš B, Križman I. Priporočila za zdravljenje okužbe z bakterijo Helicobacter pylori v Sloveniji. Zdrav Vestn 1998; 67: 159–62.

Grobovšek-Opara S, Vrhovec N, Šelb J. Epidemiologija ulkusne bolezni v Sloveniji. Krka Med Farm 1994; 15: 5–13.

Molj J, Ivanuša M, Drinovec J, Mrhar A. Nekateri epidemiološki vidiki ulkusne bolezni v Sloveniji. Zdrav Vestn 1998; 67: 697–701.

Skok P. Incidenca krvavitev iz zgornje prebavne cevi – petletna prospektivna študija. Zdrav Vestn 2000; 69: 727–31.

Tepeš B. Proučevanje sprememb pri ulkusnih bolnikih po eradikaciji bakterije Helicobacter pylori. Doktorska disertacija. Univerza v Ljubljani, Medicinska fakulteta, Ljubljana 1997: 1–146.

Gubina M, Newel DG, Hawthin PR, Avšič-Županc T, Križman I. Helicobacter IgG in our asymptomatic Slovenian population. Zdrav Vestn 1991; 60: 449– 52.

Moran AP, O’Morain CA. Pathogenesis and host response in Helicobacter pylori infections. Bad Homburg: Normed Verlag, 1997: 1–262.

Howden CW. For what conditions is there evidence-based justification for treatment of H.pylori infection? Gastroenterology 1997; 113: Suppl: S107– S112.

Lam SK, Talley NJ. Helicobacter pylori consensus: Report of the 1997 Asia Pacific Consensus Conference on the management of Helicobacter pylori infection. J Gastroenterol Hepatol 1998; 13: 1–12.

Tepeš B, Gubina M, Kavčič B, Košutič D, Križman I, Ihan A. Prospektivna kontrolirana študija zdravljenja bolnikov s Helicobacter pylori pozitivno ulkusno boleznijo dvanajstnika. Zdrav Vestn 1995; 64: 687–91.

Malfertheiner P, Leodolter A, Peitz U. Cure of Helicobacter pylori – associated ulcer disease through eradication. Bailliere’s Clinical Gastroenterology 2000; 14: 119–32.

Labenz J. Consequences of Helicobacter pylori cure in ulcer patients. Bailliere’s Clinical Gastroenterology 2000; 14: 133–45.

Porro GB, Lazzaroni M. The conflicting relationship between Helicobacter pylori and non-steroidal anti-inflammatory drugs in peptic ulcer bleeding. Scand J Gastroenterol 1999; 34: 225–8.

Chiba N, Lahaie R, Fedorak RN, Bailey R, Veldhuyzen van Zanten SJ, Bernucci B. Helicobacter pylori and peptic ulcer disease. Current evidence for management strategies. Can Fam Physician 1998; 44: 1481–8.

Everhart JE, Byrd Holt D, Sonnenberg A. Incidence and risk factors for selfreported peptic ulcer disease in the United States. Am J Epidemiol 1998; 147: 529–36.

Tytgat GNJ. Treatment of peptic ulcer. Digestion 1998; 59: 446–52.

Langtry HD, Wilde MI. Omeprazole. A review of its use in Helicobacter pylori infection, gastro-oesophageal reflux disease and peptic ulcers induced by nonsteroidal anti-inflammatory drugs. Drugs 1998; 56: 447–86.

Lee J, O’Morain C. Who should be treated for Helicobacter pylori infection? A review of consensus conferences and guidelines. Gastroenterology 1997; 113: Suppl 6: S99–S106.

Lin HJ, Tseng GY, Hsieh YH et al. Will Helicobacter pylori affect short-term reebleding rate in peptic ulcer bleeding patients after successful endoscopic therapy? Am J Gastroenterol 1999; 94: 3184–9.

Santolaria S, Lanas A, Benito R et al. Helicobacter pylori infection is a protective factor for bleeding gastric ulcers but not for bleeding duodenal ulcers in NSAID user. Aliment Pharmacol Ther 1999; 13: 1511–8.

Kuyvenhoven JP, Veenendal RA, Vandebroucke JP. Peptic ulcer bleeding: Interaction between non-steroidal antiinflammatory drugs, Helicobacter pylori infection and the ABO blood group system. Scand J Gastroenterol 1999; 34: 1082–6.

Martino G, Paoletti M, Marcheggiano A, D’Ambra G, DelleFava G, Annibale B. Duodenal ulcer relapse is not always associated with recurrence of H. pylori infection. A prospective three-year follow-up study. Helicobacter 1999; 4: 243–8.

Gisbert JP, Blanco M, Mateos JM et al. H-pylori negative duodenal ulcer prevalence and causes in 744 patients. Dig Dis Sci 1999; 44: 2295–302.

McColl KE, Dickson A, El-Nujumi A, El-Omar E, Kelman A. Symptomatic benefit 1–3 years after H. pylori eradication in ulcer patients: impact of gastroesophageal reflux disease. Am J Gastroenterol 2000; 95: 101–5.

DiMario, Dal Bo N, Salandin S et al. The appearance of GORD in patients with duodenal ulcer after eradication of Helicobacter pylori infection: a 4 year prospective study. Gastroenterology 1998; 114: A105–5.

Barr M, Buckley M, O’Morain C. Review article: non-steroidal anti-inflammatory drugs and Helicobacter pylori. Aliment Pharmacol Ther 2000; 14: Suppl 3: 43–7.

Lee J, O’Morain C. Who should be treated for Helicobacter pylori infection? A review of consensus conferences and guidelines. Gastroenterology 1997; 113: Suppl 6: S99–S106.

Newton M, Bryan R, Buraham WR, Kamm MA. Evaluation of Helicobacter pylori in reflux oesophagitis and Barrett’s oesophagus. Gut 1997; 40: 9–13.

Metz DC, Kroser JA. Helicobacter pylori and gastroesophageal reflux disease. Gastroenterol Clin North Am 1999; 28: 971–85.

Labenz J, Malfertheiner P. Helicobacter pylori in gastro-oesophageal reflux disease: causal agent, independent or protective factor? Gut 1997; 41: 277–80.

Labenz J, Blum AL, Bayerdörfer E, Meining A, Stolte M, Börsch G. Curing Helicobacter pylori infection in patients with duodenal ulcer may provoke reflux esophagitis. Gastroenterology 1997; 112: 1442–7.

Tepeš B. Primerjava dveh trotirnih antimikrobnih shem zdravljenja okužbe z bakterijo Helicobacter pylori. Zdrav Vestn 2000; 69: 505–8.

Schütze K, Hentschel E, Dragosics B et al. Helicobacter pylori reinfection with identical organism: transmission by the patients’ spouses. Gut 1995; 36: 831–3.

Vigneri S, Termini R, Savarino V, Pace F. Review article: is Helicobacter pylori status relevant in the management of GORD? Aliment Pharmacol Ther 2000; 14: Suppl 3: 31–42.

How to Cite
1.
Skok P, Križman I, Skok M. BLEEDING PEPTIC ULCER, NONSTEROIDAL ANTIINFLAMMATORY DRUGS AND HELICOBACTER PYLORI INFECTION – A PROSPECTIVE, CONTROLLED, RANDOMIZED STUDY. ZdravVestn [Internet]. 1 [cited 18Jun.2019];71(6). Available from: https://vestnik.szd.si/index.php/ZdravVest/article/view/1598
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