Thromb Haemost 2003; 89(04): 741-746
DOI: 10.1055/s-0037-1613581
Wound Healing and Inflammation/Infection
Schattauer GmbH

Helicobacter pylori causes gastrointestinal hemorrhage in patients with congenital bleeding disorders

Sam Schulman
1   The Division of Hematology and Department of Medicine, Karolinska Hospital, Stockholm, Sweden and Tartu University, Tartu, Estonia
,
Ann-Sofie Rehnberg
2   The Division of Gastroenterology and Hepatology, Department of Medicine, Karolinska Hospital, Stockholm, Sweden and Tartu University, Tartu, Estonia
,
Marju Hein
3   Department of Internal Medicine, Tartu University, Tartu, Estonia
,
Olga Hegedus
2   The Division of Gastroenterology and Hepatology, Department of Medicine, Karolinska Hospital, Stockholm, Sweden and Tartu University, Tartu, Estonia
,
Per Lindmarker
1   The Division of Hematology and Department of Medicine, Karolinska Hospital, Stockholm, Sweden and Tartu University, Tartu, Estonia
,
Per M. Hellström
2   The Division of Gastroenterology and Hepatology, Department of Medicine, Karolinska Hospital, Stockholm, Sweden and Tartu University, Tartu, Estonia
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Publikationsverlauf

Received 06. September 2002

Accepted after revision 27. Januar 2003

Publikationsdatum:
07. Dezember 2017 (online)

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Summary

Helicobacter pylori (H. pylori) infection is associated with peptic ulcer disease and gastric cancer. The eradication of H. pylori is of special interest in patients with congenital bleeding disorders, for whom treatment of gastrointestinal hemorrhage with factor concentrates is costly. The prevalence of H. pylori varies between different populations and identification of high-risk subgroups may allow for more targeted screening and eradication of the infection. We performed a 5-year retrospective study of gastrointestinal bleeding, combined with screening and treatment for H. pylori and a long-term prospective follow-up in 168 Swedish and 23 Estonian patients with hemophilia or von Willebrand disease. The prevalence of seropositivity was lower in Sweden than in Estonia (28 versus 48%, p = 0.03), lower in native Swedes than in non-Nordic immigrants to Sweden (20 versus 76%, p = 0.0001) and lower in patients less than 40 years of age than older patients (16 versus 38%, p = 0.002). The incidence of gastrointestinal hemorrhages among the 35 Swedish patients with active H. pylori infection, confirmed by a urea breath test, was 6.0 per 100 patient-years before eradication therapy versus 1.7 during the prospective followup. A negative urea breath test one month after therapy always remained negative after one year. Screening, followed by treatment of all infected patients, yielded a reduction of direct costs over a 5-year period of 130 US-$ per screened patient. We conclude that screening and eradication therapy for infection with H. pylori in patients with congenital bleeding disorders is an effective and economic strategy.