Patients with diabetes mellitus (DM) have infections more often than those without DM. The course of the infections is also more complicated in this patient group. One of the possible causes of this increased prevalence of infections is defects in immunity. Besides some decreased cellular responses in vitro, no disturbances in adaptive immunity in diabetic patients have been described. Different disturbances (low complement factor 4, decreased cytokine response after stimulation) in humoral innate immunity have been described in diabetic patients. However, the clinical relevance of these findings is not clear. Concerning cellular innate immunity most studies show decreased functions (chemotaxis, phagocytosis, killing) of diabetic polymorphonuclear cells and diabetic monocytes/macrophages compared to cells of controls. In general, a better regulation of the DM leads to an improvement of these cellular functions. Furthermore, some microorganisms become more virulent in a high glucose environment. Another mechanism which can lead to the increased prevalence of infections in diabetic patients is an increased adherence of microorganisms to diabetic compared to nondiabetic cells. This has been described for Candida albicans. Possibly the carbohydrate composition of the receptor plays a role in this phenomenon.

A n increased prevalence of urinary tract infections (UTIs) and asymptomatic bacteriuria (ASB) has been described in women with diabetes compared with women without diabetes (1-6). Because UTI complications (e.g., bacteremia, renal abscesses, and renal papillary necrosis) occur more often in diabetic patients, it is important to recognize UTIs in this patient group (1,2). However, the risk factors for developing a UTI have not been defined in women with diabetes, and it is unknown whether ASB precedes symptomatic bacteriuria in these patients. Therefore, we decided to investigate which risk factors (including ASB) are associated with an increased risk of symptomatic UTI development in a large group of women with either type 1 or type 2 diabetes during a period of 18 months. RESEARCH DESIGN AND METHODS -The recruitment of the patients has been described elsewhere (6). Briefly, all patients were interviewed, and data were obtained from the hospital files using a standardized questionnaire. We performed two urinary cultures to diagnose ASB in 417 of the 636 patients and did not find any significant differences between these 417 patients and the whole study group. At the moment of study entry (i.e., the initial clinical visit), all patients were given a standard form with a return envelope and were asked to mail the form to the investigator (S.E.G.) if they developed a symptomatic UTI (e.g., symptoms of dysuria, increased frequency of urination, and lower abdominal or flank pain) or used antimicrobial agents for any reason during the 18 months after inclusion. Furthermore, the treating physician asked the patient if she had developed a symptomatic UTI or had taken antimicrobials in the time between her inclusion into the study and the outpatient clinic visits for routine examination at 9 and 18 months after inclusion. Antimicrobial therapy was usually prescribed by a general practitioner after diagnosing a UTI in symptomatic women by means of urinary diagnostic tests (urine culture or microscopic analysis or leukocyte esterase on dipstick testing). The development of secondary complications (e.g., retinopathy, neuropathy, and macrovascular diseases) during this period was also recorded by the treating physician. Finally, the investigator phoned all patients (or the general practitioner of the patient, if the patient had moved) for whom these followup data were incomplete. HbA 1c , creatinine, and urinary albumin values were determined at baseline and at the end of the follow-up period. Follow-up results were available for 589 women (93% of the study population). Reasons for inadequate followup included the following: impossibility of reaching the patient (n = 41), known death (two by cardiovascular causes, one by breast carcinoma, and one by pneumonia), renalpancreatic transplantation (n = 1), and patient refusal (n = 1). Clinical characteris- A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances. Risk Factors for Symptomatic Urinary Tract ...

Women with type 2 DM and ASB have an increased risk of developing a symptomatic UTI than those without ASB.

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Background As women with diabetes mellitus (DM) have an increased prevalence of asymptomatic bacteriuria (ASB) and it is known that a correlation exists between the increased prevalence of genitourinary tract infection and impaired cytokine production in women infected with Human Immunodeficiency Virus (HIV), we studied urinary cytokine excretion in diabetic women and compared it with that of nondiabetic controls. Materials and methodsTo evaluate the cytokine secretion capacity of women with DM, both whole blood and isolated monocytes of women with and without DM were stimulated in vitro with lipopolysaccharide (LPS).Results Lower urinary interleukin-8 (IL-8) and interleukin-6 (IL-6) concentrations (P 0´1 and P , 0´001, respectively) were found in diabetic women than in nondiabetic controls. A lower urinary leukocyte cell count correlated with lower urinary IL-8 and IL-6 concentrations (P , 0´05). Lower tumour necrosis factor-alpha (TNF-a) and IL-6, but comparable interleukin-10 (IL-10) concentrations were found in whole blood (P , 0´04) and isolated monocytes (P 0´03) of women with DM type 1 compared to women without DM.Conclusions Diabetic women with ASB have lower urinary IL-6 concentrations than nondiabetic bacteriuric controls. In addition, monocytes of women with DM type 1 secrete lower pro-inflammatory cytokines after stimulation with LPS than monocytes of women without DM. This is not due to an inhibitory effect of the anti-inflammatory cytokine IL-10. This can have important consequences for both host defense, endothelial cell functioning and atherogenesis.