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Acute Respiratory Viral Infections Aggravate Arterial Endothelial Dysfunction in Children With Type 1 Diabetes

¹ Division of Pediatric Cardiology, Lund University Hospital, Lund, Sweden
² A.I. Virtanen Institute, University of Kuopio, Kuopio, Finland
³ Division of Pediatric Metabolism, Endocrinology, and Diabetology, Lund University Hospital, Lund, Sweden

Address correspondence and reprint requests to Petru Liuba, PhD, MD, Pediatric Cardiology, Lund University Hospital, 221 85 Lund, Sweden. E-mail: petru.liuba@pedi.lu.se

Abbreviations: CRP, C-reactive protein • FMD, flow-mediated dilatation • GTN, glyceryl-trinitrate • vWF, von Willebrand antigen

The first 20% of the full text of this article appears below.

	INTRODUCTION

 
Despite improvements in therapy for children with type 1 diabetes, the prevalence of cardiovascular morbidity in adulthood due to accelerated atherosclerosis remains significant (1). Similar to other cardiovascular risk factors, the diabetic state facilitates arterial endothelial injury, a primary event in the pathogenesis of atherosclerosis (2). Although several pediatric studies have reported an association of diabetes with arterial endothelial dysfunction (3,4), pathogenic animal studies have suggested that even though this disease predisposes to endothelial dysfunction and atherosclerosis, it might not be sufficient to cause them (5).

Notably, type 1 diabetes increases the propensity for both chronic and acute infections in part by weakening the immune mechanisms (6). The risk is particularly increased for respiratory tract infections, but other infections have also been associated with diabetes (7). Furthermore, diabetic patients are at greater risk for infection-related mortality (8), and the excess risk appears to be linked to cardiovascular diseases (9). In the present study, we investigated whether viral respiratory tract infections in children with type 1 diabetes might impose an additional burden on the arterial endothelial function.

	RESEARCH DESIGN AND METHODS

 
A total of 26 children (aged 6–18 years, mean [±SD] age 14 ± 3 years) with type 1 diabetes (duration 6 ± 3 years) were recruited. Of these, 11 . . . [Full Text of this Article]

Blood analyses
Endothelium-dependent and -independent reactivity of the brachial artery
Statistical analyses

	RESULTS

 
Clinical and metabolic profile
Baseline diameter and GTN-induced and flow-mediated dilatation of brachial artery

	CONCLUSIONS

 

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