Background. Until recently, Plasmodium knowlesi malaria in humans was misdiagnosed as Plasmodium malariae malaria. The objectives of the present stud

Specific defects in innate and adaptive immune function have been identified in diabetic patients in a range ofin vitrostudies. However, the relevance of these findings to the integrated response to infectionin vivoremains unclear, especially in patients with good glycaemic control. Vaccine efficacy seems adequate in most diabetic patients, but those with type 1 diabetes and high glycosylated haemoglobin levels are most likely to exhibit hypo‐responsiveness. While particular infections are closely associated with diabetes, this is usually in the context of extreme metabolic disturbances such as ketoacidosis. The link between glycaemic control and the risk of common community‐acquired infections is less well established but could be clarified if infection data from large community‐based observational or intervention studies were available. The relationship between hospital‐acquired infections and diabetes is well recognized, particularly among post‐operative cardiac and critically ill surgical patients in whom intensive insulin therapy improves clinical outcome independent of glycaemia. Nevertheless, further research is needed to improve our understanding of the role of diabetes and glycaemic control in the pathogenesis and management of community‐ and hospital‐acquired infections. Copyright © 2006 John Wiley & Sons, Ltd.

Background.Plasmodium knowlesi is increasingly recognized as a cause of human malaria in Southeast Asia but there are no detailed prospective clinical

The Malaria Genomic Epidemiology Network reports a large multicenter association study for severe malaria due to Plasmodium falciparum in 11,890 cases and 17,441 controls from 12 locations in Africa, Asia and Oceania. They examine 27 loci previously associated with severe malaria and replicate associations at the HBB, ABO, ATP2B4, G6PD and CD40LG loci, but they fail to replicate other previously reported associations. Many human genetic associations with resistance to malaria have been reported, but few have been reliably replicated. We collected data on 11,890 cases of severe malaria due to Plasmodium falciparum and 17,441 controls from 12 locations in Africa, Asia and Oceania. We tested 55 SNPs in 27 loci previously reported to associate with severe malaria. There was evidence of association at P < 1 × 10−4 with the HBB, ABO, ATP2B4, G6PD and CD40LG loci, but previously reported associations at 22 other loci did not replicate in the multicenter analysis. The large sample size made it possible to identify authentic genetic effects that are heterogeneous across populations or phenotypes, with a striking example being the main African form of G6PD deficiency, which reduced the risk of cerebral malaria but increased the risk of severe malarial anemia. The finding that G6PD deficiency has opposing effects on different fatal complications of P. falciparum infection indicates that the evolutionary origins of this common human genetic disorder are more complex than previously supposed.

OBJECTIVE—To examine prospectively the relationship between diabetes, glycemic control, and spirometric measures. RESEARCH DESIGN AND METHODS—From a community-based cohort, 495 Europid (i.e., of European descent) patients with type 2 diabetes who had no history of pulmonary disease underwent baseline spirometry between 1993 and 1994. A subset of 125 patients was restudied a mean of 7.0 years later. The main outcome measures included forced vital capacity (FVC), forced expiratory volume in 1 s (FEV₁), vital capacity (VC), and peak expiratory flow (PEF) corrected for body temperature, air pressure, and water saturation and were expressed either in absolute terms or as percentage-predicted value for age, sex, and height. RESULTS—Mean percentage-predicted values of each spirometric measure were decreased >10% in the whole cohort at baseline and absolute measures continued to decline at an annual rate of 68, 71, and 84 ml/year and 17 l/min for FVC, FEV₁, VC, and PEF, respectively, in the 125 prospectively studied patients. Declining lung function measures were consistently predicted by poor glycemic control in the form of a higher updated mean HbA_1c, follow-up HbA_1c, or follow-up fasting plasma glucose. In a Cox proportional hazards model, decreased FEV₁ percentage-predicted value was an independent predictor of all-cause mortality. CONCLUSIONS—Reduced lung volumes and airflow limitation are likely to be chronic complications of type 2 diabetes, the severity of which relates to glycemic exposure. Airflow limitation is a predictor of death in type 2 diabetes after adjusting for other recognized risk factors.