Measure of the Rate at which Mortality in Type 2 Diabetes Mellitus Occurs: Protocol for a Systematic Review.

Introduction: Type 2 diabetes is the third largest cause of mortality in the United Kingdom, with about 50% of patients’ having developed complications at time of diagnosis. We consider that the evidence which explores the actual hazard ratios of mortality has not been consistent. n this paper we discuss methodology and review the most recent accurate data on mortality in type 2 diabetes. Methods: A systematic review will be undertaken aimed at synthesis of evidence of relative risk of mortality in type 2 diabetes, using the Centre for Reviews and Dissemination guidelines. We will explore conflicting and unanswered questions in relation to mortality. The primary outcome is all-cause, overall-cause or total mortality expressed as hazard ratios. Sub-groups will also be explored; age, gender, socio-economic factors and causes of death. We will review abstracts published after 1990 in the English language. Our data source will include electronic databases; the Cochrane library, the Centre for Reviews and Dissemination, Medline/PubMed, and other grey literature. The study populations are type 2 diabetes patients whose mortality outcome, expressed as hazard ratio, has been evaluated. Data extraction will be undertaken by one reviewer and triangulated by the second and third reviewer. The quality of the included studies will be evaluated in accordance with the inclusion/exclusion criteria; methodological quality that meets the critical appraisal framework and the relevance to the research questions. Evidence from data will be synthesised through a descriptive epidemiological review from included studies; meta-analysis will be used if appropriate. Result & Conclusion: We expect to pool homogenous studies of large population cohorts which explore the hazard ratio of mortality, and to summarise the evidence of the actual mortality risk in type 2 diabetes, with limited bias. This will help direct future research in areas of unanswered questions and may influence healthcare policy decisions.

The effect of sulphasalazine on the in vitro activation of human peripheral blood mononuclear cells by phytohemagglutinin P

The in vitro action of sulphaslazine, BW 755-C and indomethacin on phytohemaglutinin P-induced human peripheral brood mononuclear cell activation was studied. Sulphasalazine increased, while indomethacin and BW 755-C decreased, prostaglandin E2 (PGE2) accumulation in activated cultures. When used together with indomethacin or BW 755-C, sulpjasalazine did not counteract the inhibiton of PGE2 caused by the other two. Sulphasalazine inhibited phytohemagglutinin P-induced cell activation in a concentration-dependent manner even when used together with indomethacin or BW 755-C. BW 755-C inhibited cell activation at 350 micronM, wehreas at 11, whereas at 11 micronM only increased sulphasalazine-induced inhibition. The implications of these findings on the etiopathology of inflammatory bowel disease are discussed