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Sökning: onr:"swepub:oai:DiVA.org:uu-210193" > Early Electrophysio...

Early Electrophysiological Abnormalities and Clinical Neuropathy : A prospective study in patients with type 1 diabetes

Hyllienmark, Lars (författare)
Section of Neurology, Department of Clinical Neuroscience, Karolinska Institutet, Karolinska Hospital, Stockholm, Sweden
Alstrand, Nils (författare)
Department of Medical and Health Sciences, Linköping University and Östergötland County Council, Linköping, Sweden
Jonsson, Björn, 1939- (författare)
Uppsala universitet,Institutionen för kvinnors och barns hälsa,Barnendokrinologisk forskning/Gustafsson
visa fler...
Ludvigsson, Johnny (författare)
Division of Paediatrics, Department of Clinical and Experimental Medicine, Linköping University and Östergötland County Council, Linköping, Sweden
Cooray, Gerald (författare)
Section of Clinical Neurophysiology, Department of Clinical Neuroscience, Karolinska Institutet, Karolinska Hospital, Stockholm, Sweden
Wahlberg-Topp, Jeanette (författare)
Department of Medical and Health Sciences, Linköping University and Östergötland County Council, Linköping, Sweden
Alstrand, N (författare)
Ludvigsson, J (författare)
Jonsson, B (författare)
Hyllienmark, L (författare)
Karolinska Institutet
Wahlberg-Topp, J (författare)
Cooray, G (författare)
Karolinska Institutet
visa färre...
 (creator_code:org_t)
2013
2013
Engelska.
Ingår i: Diabetes Care. - 0149-5992 .- 1935-5548. ; 36:10, s. 3187-3194
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • OBJECTIVEThe aim of this study was to elucidate whether subclinical nerve dysfunction as reflected by neurophysiological testing predicts the development of clinical neuropathy in patients with type 1 diabetes.RESEARCH DESIGN AND METHODSFifty-nine patients were studied twice with neurophysiological measurements at baseline and at follow-up. At baseline, patients were 15.5 3.22 years (range 7-22 years) of age, and duration of diabetes was 6.8 3.3 years. At follow-up, patients were 20-35 years of age, and disease duration was 20 +/- 5.3 years (range 10-31 years).RESULTSAt baseline, patients showed modestly reduced nerve conduction velocities and amplitudes compared with healthy subjects, but all were free of clinical neuropathy. At follow-up, clinical neuropathy was present in nine (15%) patients. These patients had a more pronounced reduction in peroneal motor nerve conduction velocity (MCV), median MCV, and sural sensory nerve action potential at baseline (P < 0.010-0.003). In simple logistic regression analyses, the predictor with the strongest association with clinical neuropathy was baseline HbA(1c) (R-2 = 48%, odds ratio 7.9, P < 0.002) followed by peroneal MCV at baseline (R-2 = 38%, odds ratio 0.6, P < 0.006). With the use of a stepwise forward analysis that included all predictors, first baseline HbA(1c) and then only peroneal MCV at baseline entered significantly (R-2 = 61%). Neuropathy impairment assessment showed a stronger correlation with baseline HbA(1c) ( = 0.40, P < 0.002) than with follow-up HbA(1c) ( = 0.034, P < 0.007).CONCLUSIONSEarly defects in nerve conduction velocity predict the development of diabetic neuropathy. However, the strongest predictor was HbA(1c) during the first years of the disease.

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