Objective To quantify the association between diabetes and the risk of incident infections by conducting a systematic review and meta-analysis. Research design and methods Two reviewers independently screened articles identified from PubMed, EMBASE, Cochrane Library, IPA, and Web of Science databases. Cohort studies (CS) or case-control studies (CCS) evaluating the incidence of infections in adults with diabetes were included. Infections were classified as: skin and soft tissue, respiratory, blood, genitourinary, head and neck, gastrointestinal, bone, viral, and nonspecified infections. Study quality was assessed using the Newcastle-Ottawa Quality Assessment Scale. Summary crude and adjusted OR with 95% CIs were calculated using random effects models, stratified by study design. Heterogeneity was measured using the I 2 statistic and explored using subgroup analyses. Results A total of 345 (243 CS and 102 CCS) studies were included. Combining adjusted results from all CS, diabetes was associated with an increased incidence of skin (OR 1.94, 95% CI 1.78 to 2.12), respiratory (OR 1.35, 95% CI 1.28 to 1.43), blood (OR 1.72, 95% CI 1.48 to 2.00), genitourinary (OR 1.61, 95% CI 1.42 to 1.82), head and neck (OR 1.17, 95% CI 1.13 to 1.22), gastrointestinal (OR 1.48, 95% CI 1.40 to 1.57), viral (OR 1.29, 95% CI 1.13 to 1.46), and non-specified (OR 1.84, 95% CI 1.66 to 2.04) infections. A stronger association was observed among CCS: skin (OR 2.64, 95% CI 2.20 to 3.17), respiratory (OR 1.62, 95% CI 1.37 to 1.92), blood (OR 2.40, 95% CI 1.68 to 3.42), genitourinary (OR 2.59, 95% CI 1.60 to 4.17), gastrointestinal (OR 3.61, 95% CI 2.94 to 4.43), and nonspecified (OR 3.53, 95% CI 2.62 to 4.75). Conclusion Diabetes is associated with an increased risk of multiple types of infections. A high degree of heterogeneity was observed; however, subgroup analysis decreased the amount of heterogeneity within most groups. Results were generally consistent across types of infections. INTRODUCTIONThe International Diabetes Federation estimates that there were almost 400 million people living with diabetes throughout the world in 2014. The prevalence of diabetes is expected to increase to more than 590 million people by the year 2035.1 Well-known complications of diabetes include both microvascular (retinopathy, neuropathy, nephropathy) and macrovascular (coronary heart disease, cerebrovascular disease, and peripheral vascular disease) 2 ; however, there are numerous lesser known complications including effects on immunity.3-5 Immune system dysfunction in people with diabetes may be mediated through impaired migration, phagocytosis, intracellular killing, and chemotaxis. [4][5][6][7][8] Indeed, several studies have suggested that people with diabetes are at an increased risk of infection-related mortality 9 10 ; however, not all studies support such an association. 12Furthermore, patients with diabetes tend to be hospitalized for infections more frequently than those without.

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AimsWe have recently created an age-dependent hypertensive-mono-arthritic animal model from the stroke-resistant spontaneously hypertensive rat to model populations with autoimmune disease who are hypertensive and are prone to stroke. The model exhibits signs of hemorrhagic stroke (HS) subsequent to chronic inflammation and hypertension. HS is also associated with the inability of middle cerebral arteries to undergo pressure dependent constriction (PDC). We investigated alterations in the cerebrovasculature of our hypertensive mono-arthritic animals that develop stroke.Main MethodsAnimals were fed either a high salt diet (HSD) (4% NaCl) or Purina chow (0.58% NaCl) from weaning. Complete Freund’s Adjuvant (CFA) was injected into the left hind paw at 21–28 weeks; controls received saline and histological and functional studies were performed.ResultsBrain damage was more prominent with the high salt, with inflammation exacerbating the damage. High salt alone significantly decreased middle cerebral artery’s (MCA’s) ability to undergo PDC. Inflammation significantly decreased the ability of cerebrovasculature to respond to pressure step in the regular salt diet. The responses to vasoactive peptides were also significantly attenuated in both inflamed groups regardless of diet.ConclusionInduction of chronic systemic inflammation increases brain damage, and affect the MCA’s vasogenic function, decreasing its ability to respond to intraluminal pressure. HSD further exacerbates organ damage associated with chronic inflammation, further compromising cerebrovascular function, and likely increasing the incidence of intracerebral hemorrhage and injury.