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Change from oral antidiabetic therapy to insulin and risk of urinary tract infections in Type 2 diabetic patients: a population-based prescription study☆☆

Anne Katrine Sandenab, Martin B. Johansenb, Lars Pedersenb, Hans-Henrik Lervanga, Henrik C. Schønheyderc, Reimar W. ThomsenbCorresponding Author Informationemail address

Received 26 June 2009; received in revised form 19 December 2009; accepted 27 January 2010. published online 02 March 2010.
Corrected Proof

Abstract 

Background

Diabetes is a risk factor for urinary tract infections (UTI), but the impact of insulin treatment and glycaemic control on UTI risk is not clear.

Methods

We determined the risk of antibiotic-treated UTI episodes in a population-based cohort of 2737 Type 2 diabetic patients who switched from oral antidiabetic drug (OAD) to insulin therapy. Each patient was observed for 365 days before and after the switch date, excluding a 120-day time window around this date. Episodes of UTI were defined as filled prescriptions for a UTI-specific antibiotic. We used conditional logistic regression to estimate the relative risk (odds ratio) of having one or more UTIs in the insulin vs. OAD period overall and stratified by glycaemic change.

Results

After the switch to insulin, 53% of all patients experienced a decrease in individual mean hemoglobin A1c (median decrease=1.5%, interquartile range 0.9%-2.3%). Episodes of treated UTIs occurred in 446 (16.3%) Type 2 diabetic patients in the insulin period and 437 (16.0%) in the OAD period (relative risk 1.04, 95% CI 0.86–1.26). Stratified analyses showed no consistent association between levels of glycaemic improvement and decreased UTI risk during insulin treatment.

Conclusions

Among patients with Type 2 diabetes, no evidence was found that switch to insulin therapy with or without tightened glycaemic control decreased their high annual risk of antibiotic-treated UTI episodes.

a Department of Endocrinology, Aalborg Hospital, Aarhus University Hospital, Forskningens Hus, Sdr. Skovvej 15, DK-9000 Aalborg, Denmark

b Department of Clinical Epidemiology, Aarhus University Hospital, Forskningens Hus, Sdr. Skovvej 15, DK-9000 Aalborg, Denmark

c Department of Clinical Microbiology, Aalborg Hospital, Aarhus University Hospital, Forskningens Hus, Sdr. Skovvej 15, DK-9000 Aalborg, Denmark

Corresponding Author InformationCorresponding author. Department of Clinical Epidemiology, Aarhus University Hospital, Forskningens Hus, Sdr. Skovvej 15, DK-9000 Aalborg, Denmark. Tel.: +45 9932 6905; fax: +45 9932 6914.

 This study was supported by grants from the Afdelingen for Universitetshospitalsanliggender, Aalborg Hospital, Aarhus University Hospital; Forskningsinitiativet, Aarhus University; and Klinisk epidemiologisk forskningsfond, Aarhus University.

☆☆ Preliminary results in abstract form were presented at the 18th European Congress of Clinical Microbiology and Infectious Diseases, Barcelona, Spain 19-22 April 2008, abstract P1623.

 Deceased.

PII: S1056-8727(10)00003-6

doi:10.1016/j.jdiacomp.2010.01.002

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