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Tectable levels of C-peptide has initiated the idea that C-peptide deficiency may have a pathogenic role in diabetic vascular dysfunction. An increasing number of experimental and clinical studies, published over the last decade, have indicated that C-peptide administration has effects on blood flow in various tissues in diabetes. C-peptide administration in type 1 diabetic patients has been shown to improve renal hyperfiltration [5], ameliorate sensory nerve dysfunction [6] and increase blood flow in various tissues, e.g. skeletal muscle, at rest and during exercise [7, 8]. In the study by Hansen et al. the effect of acute C-peptide infusion on myocardial dysfunction in type 1 diabetic patients was examined. During infusion, physiological levels of Cpeptide were obtained and systolic and diastolic velocities, SImax Fig. 2 ; and MBFI were increased to levels comparable to values obtained in non-diabetic controls. Although an increasing number of studies indicate beneficial effects of C-peptide on vascular dysfunction in type 1 diabetes, it is interesting that the mechanisms by which C-peptide exerts its effect on blood flow are still largely unknown. However, it has been shown that C-peptide in nanomolar concentrations binds specifically to cell surfaces, probably through a receptor system that may involve G-proteins, which subsequently activates Ca2 + -dependent intracellular signalling pathways and stimulation of Na-K-ATPase activity [9, 10]. Further, C-peptide has been shown to stimulate endothelial nitric oxide synthase in arterioles and nerves [8, 11], for instance, avapro 50 mg.
15 H pyloripositive patients treated in this study, all had chronic ITP with a platelet count less than 55 109 L 7 were 30 109 L ; and all have been previously treated for their ITP by 2 to different treatments including splenectomy in 5 cases 33% ; . Therefore, these patients had a very low likelihood of spontaneous improvement and the effectiveness of H pylori eradication on ITP outcome was easier to assess. The eradication rate was 93% since alternative treatment was pursued when the initial regimen was ineffective. However, despite this good rate of eradication and unlike previous studies, 2-8 only one of our H pyloripositive patients achieved a significant response 3 months after eradication and this response did not last. In this study, 3 months was chosen as the time limit for seeing an effect of H pylori eradication. If no response was seen at that time, other therapies were initiated if necessary. Previous studies that provided time frames all demonstrated platelet recovery within 60 days after H pylori eradication.2, 6, 8 In this study, extending the time beyond 3 months following H pylori eradication did not seem to affect the response since the only platelet changes observed were in those patients who had initiated other therapies. To explain the high rates of response reported by others Table 5 ; , a nonspecific effect of the drugs used to eradicate the bacteria seems unlikely since in this present study none of the 10 H pylorinegative patients who received the Prevpac experienced a significant improvement in their platelet count. The striking discrepancies between this report and those from Italy and Japan suggest several hypotheses. One hypothesis is that the response to H pylori infection could be influenced by the host's immunogenetic background.20, 21 However, the contradictory findings reported in patients of similar European origin ie, Spain, France, and Italy ; 2, 3, 4, Table 5 ; do not support this hypothesis. Another possibility is that different strains of H pylori, namely those with different cag or vag cytotoxicity virulence-associated genes ; proteins, 20 could exert different immunologic effects on the host T and B cells and hence on ITP. A third hypothesis is that the expression of various Lewis Le ; antigens by H pylori isolates22 and the subsequent production of anti-Le antibodies could play a role in ITP pathogenesis since platelets may adsorb Lewis antigens from the serum. The management of ITP in adults is complex and may require immunosuppressive therapies and or splenectomy. One of the challenges for physicians caring for patients with ITP is to find less toxic and more effective approaches. The expectation at the beginning of this study was that a percentage of patients could be "cured" by administration of the Prevpac for 2 weeks. Unexpectedly, in this study there was not a greater prevalence of H pylori in ITP patients. Furthermore, and unlike most of the previous studies, none of the patients substantially improved their platelet count as a result of H pylori eradication. Therefore, even if the success of treatment of the H pyloriinfected patients could be predicted by age and questionnaire, it is not obvious from this study that one would choose to test and eradicate infection in them. Future studies performed in this setting should be randomized and controlled and should include large numbers of patients requiring therapy. In addition to tracking the platelet count, other parameters that might be important determinants of response as suggested in the hypotheses considered above should also be studied.
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