The prevalence of peripheral neuropathy in a population-based study of patients with type 2 diabetes in Sweden Lars Kärvestedt a, , Eva Mårtensson b , Valdemar Grill a,c , Stig Elofsson d , Gunvor von Wendt e , Anders Hamsten f , Kerstin Brismar a a Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden b Kronan Primary Health Care Centre, Sundbyberg, Sweden c Cancer Research and Molecular Medicine, Norwegian University of Science and Technology and St Olof Hospital, Trondheim, Norway d Institution for Social Work, University of Stockholm, Stockholm, Sweden e Department of Vitreoretinal Diseases, St. Erik's Eye Hospital, Stockholm, Sweden f Atherosclerosis Research Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden Received 9 November 2009; received in revised form 31 March 2010; accepted 14 April 2010 Abstract Aims: To assess peripheral neuropathy following a standardized foot examination protocol in a representative population-based cohort of subjects with type 2 diabetes. Methods: In a geographically defined population, aged 4070 years with diabetes prevalence of 3.5% according to medical records, we investigated 156 type 2 diabetic subjects, 95% Caucasian, mean age 61.7±7.2 years, duration of diabetes 7.0±5.7 years, and HbA 1c 7.3 ±2.4% (6.4% Mono-S), by questionnaires, clinical examinations, blood sampling, and review of medical records. Foot examination included clinical signs of peripheral neuropathy and tests of sensibility with monofilament, tuning fork, and assessments of the vibration perception thresholds (VPT). Results: Peripheral autonomic neuropathy (PAN) as judged by two or more signs of dysfunction was the most common and affected 43%. The prevalence of peripheral sensory neuropathy (PSN) was 15% by monofilament, 24% by tuning fork, and 28% by VPT expressed as ZscoreVPT 2.0 S.D. Twenty-nine percent had a VPT 25 V. Signs of peripheral motor neuropathy (PMN) affected 15%. Peripheral neuropathy, at least one variable, affected 67%, whereas 25% were affected by more than one variable of neuropathy, i.e., polyneuropathy. Exclusion of other identified causes for neuropathy than diabetes reduced the prevalence of diabetic polyneuropathy to 23%. Concurrent diabetic complications were 29% for retinopathy, 14% for incipient nephropathy, and 8% for overt nephropathy. The prevalence of macrovascular complications was 62% for CVD, 26% for PVD, and 11% for cerebrovascular lesion (CVL). Conclusion: Peripheral neuropathy was common in this representative type 2 diabetes population. Clinical signs of PAN were the most frequent followed by diminished perception of vibration and touch. © 2011 Elsevier Inc. All rights reserved. Keywords: Type 2 diabetes; Epidemiology; Population based; Peripheral neuropathy; Diabetes complications 1. Introduction Peripheral nerve function deteriorates naturally with age (Maser, Laudadio, & DeCherney, 1993; Wiles, Pearce, Rice, & Mitchell, 1991) and more rapidly in the presence of different diseases, intoxications, and states of deficiencies (Gorson & Ropper, 2006). Diabetes is a major cause for peripheral neuropathy. Diabetic neuropathy is defined as symptoms and/or signs of peripheral nerve dysfunction in people with diabetes after exclusion of other causes. Both somatic and autonomic nerves can be affected (Boulton, Malik, Arezzo, & Sosenko, 2004; Boulton et al., 2005; Vinik, Maser, Mitchell, & Freeman, 2003). Reported prevalence of diabetic peripheral neuropathy varies greatly depending on different selection of study population, methods of examination, differences in defini- tions (Cabezas-Cerrato, 1998; Dyck et al., 1993; Young, Journal of Diabetes and Its Complications 25 (2011) 97 106 WWW.JDCJOURNAL.COM The study was supported by grants from Solstickan Foundation, Heart-Lung Foundation, Familjen Erling-Persson Foundation, Swedish Diabetes Association, and Stockholms Sjukhem Foundation, and by funding from Stockholm County Council (ALF). Corresponding author. Stockholms Sjukhem Foundation, Mariebergs- gatan 22, S-112 19 Stockholm, Sweden. Tel.: +468 617 12 00; fax: +468 617 93 00. E-mail addresses: lars.karvestedt@ki.se, lars.karvestedt@stockholmssjukhem.se (L. Kärvestedt). 1056-8727/$ see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.jdiacomp.2010.04.001