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The Prevalence of Peptic Ulcer Disease and Helicobacter Pylori Infection in Sickle Cell Disease Patients

87

Laiyemo, Adeyinka O., M.D.; Chava, Samyukta, M.D.; Smoot, Duane T., M.D.

American Journal of Gastroenterology: September 2005 - Volume 100 - Issue - p S52
Supplement Abstracts Submitted for the 70th Annual Scientific Meeting of the American College of Gastroenterology: STOMACH
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Medicine, Howard University Hospital, Washington, DC.

Purpose: There have been case reports suggesting Helicobacter pylori infection, and peptic ulcer disease as causes of abdominal pain in sickle cell disease patients. The common practice is to treat sickle cell patients with narcotics and hydration and endoscopic evaluation is seldom performed. Our aim was to determine the prevalence of peptic ulcer disease and helicobacter pylori infection in patients with sickle cell trait, and sickle cell disease as compared to those without the genetic abnormality.

Methods: We conducted a retrospective case controlled study of African American patients with sickle cell disease and sickle cell trait who had upper endoscopy, and compared them to age and sex matched African American controls.

Results: Sixty-one patients were identified. There were 16 (26.2%), 7 (11.5%), and 38 (62.3%) patients with genotype AS (trait), SC and SS, respectively. Fifty-nine patients (96.7%) were in-patients at the time of the upper endoscopy with 30 of the patients (50.8%) being hospitalized for vaso-occlusive crises. Fifty-six patients (91.8%) were born in the USA. The procedure was generally performed after pancreatitis, and gall bladder disease had been excluded. In fact, 18 patients (29.5%) already had had a cholecystectomy. There was no significant difference in endoscopic findings between sickle cell patients and controls, with normal endoscopy found in 21.3% vs 9.8% (p = 0.22). Peptic ulcer disease was found in 19.7% vs 16.4% (p = 0.29). H. pylori infection was found in 30.6% vs 20% (p = 0.11) when all the sickle cell patients (including traits) were considered, and 32% vs 20% (p = 0.105) in patients with sickle cell disease (SS and SC genotype only) as compared to the controls.

Conclusions: Our study did not show any significant difference in the prevalence of H. pylori infection, nor in the occurrence of peptic ulcer disease between sickle cell disease patients and African American controls. We advocate evaluating sickle cell disease patients with abdominal pain as one would for any patient without the genetic abnormality, including endoscopic evaluation, rather than the common practice which is to administer narcotics and hydrate patients with sickle cell disease who present with abdominal pain with the assumption that the etiology is probably just due to sickle cell abdominal crises.

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