| Sumario: | Objectives: Helicobacter pylori (H. pylori) infection is a risk factor for the development of gastric and duodenal ulcers and may also lead to cancer. Studies have reported that H. pylori infection may also be implicated in chronic immune thrombocytopenia (cITP) which is characterised by the immune-mediated destruction of circulating platelets. In Japan, H. pylori eradication is a treatment used for cITP in patients with H. pylori. The effect of H. pylori on the platelet count of non-cITP individuals has not been previously investigated in New Zealand (NZ). This study sought to establish if H. pylori infection decreased the platelet count among patients attending endoscopy clinic at Middlemore Hospital (MMH) and the Manukau Surgical Centre (MSC) in the South Auckland region of NZ. The study also investigated whether infection with cytotoxin-associated gene product A (cagA) positive strains of H. pylori had a greater effect on the platelet count compared to cagA negative infections and whether eradication therapy was associated with an increase in the platelet count. Methods: Patients referred for gastro-endoscopy to MMH and the MSC were recruited for this study. Those who were bleeding, pregnant or had been diagnosed with a disorder likely to affect the platelet count were excluded. Gastric biopsy samples were screened using the Campylobacter-like organism test (CLO-test) for H. pylori infection and examined histologically for infection. Full blood counts (FBC) were performed on all patients and cagA serology on H. pylori confirmed cases. Biopsy positive, H. pylori infected patients were treated with antibiotics and followed up with stool sample screening using the H. pylori stool antigen test. The platelet counts from both infected and non-infected groups, and from patients post eradication therapy, were evaluated using the Kolmogorov-Smirnov test (KS-test). Results: Of the 165 patients enrolled in the study, 24 were CLO-test positive for H. pylori infection. The mean platelet counts for the H. pylori infected and uninfected groups were 247 and 282 x 109/L respectively. Of the infected group, cagA positive and cagA negative infections gave a mean platelet count of 237 and 261 x 109 /L respectively. The mean platelet count for those undergoing eradication treatment was 258 x 109 /L which increased to a mean of 268 x 109 /L post treatment. Conclusions: This study showed some difference between the mean platelet counts of H. pylori infected and uninfected patients (p = 0.0473). Patients infected with cagA positive strains, tended to have a lower mean platelet count compared to those with cagA negative strains. Eradication of H. pylori infection failed to make a significant difference to the platelet count in this study.
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