ABSTRACT
The vaso-oculusive episode is the hallmark of sickle cell disease [SCD]. Abdominal pain is also a common presenting symptom in the sickle cell population. Careful evaluation is essential in distinguishing between pain secondary to vaso-occlusion and other intra-abdominal disease processes. Most cases of primary gastritis are now known to be caused by gastric infection with the organism Helicobacter pylori [H. pylori]. H. pylori has been described in association with recurrent abdominal pain in children. H. pylori induced peptic ulcer disease [PUD] has not previously been reported in children with SCD, [except one case]. The present study was designed to examine whether pain induced by H. pylori could imitate the recurrent abdominal pain in SCD. This is a cross sectional study, carried out in all of the patients with SCD [30 cases], who referred to Shiraz Motahari Clinic in 2004. At first 11 patients with recurrent abdominal pain [RAP] were selected and then by a questionnaire and an interview, 7 cases that had symptoms strongly suggestive of PUD were examined by upper gastroduodenoscopy with biopsy taken from gastric antrum. Six patients confirmed to be PUD induced by H. pylori were treated by quadriple therapy. All of them were followed for 9 months or more. Serum IgG titer against H. pylori was sent before and also 6 months after therapy.Endoscopic finding in 6 of the 11 patients with SCD and RAP was diagnosed as PUD. In all cases [6 cases] H. pylori serology [IgG] test was positive. After treatment for H. pylori infection, all of them had complete resolution of symptoms by 1 month, and H. pylori IgG [6 month after treatment] tests were negative.We conclude that careful evaluation is essential in distinguishing between pain secondary to vaso-occlusion in SCD and other intra-abdominal processes such as PUD. For differentiation of painful crises and H. pylori induced PUD, history and physical examination can be helpful. Episodic epigastric pain that was frequently associated with vomiting, nocturnal awakening and gastrointestinal bleeding is highly suggestive of presence of PUD. When definitive etiology of PUD is confirmed, appropriate treatment can be initiated and excess morbidity could be avoided