Electrophysiological Study and Glutamic Acid Decarboxylase 65 in Detection of Subclinical Neuropathy in Recently Diagnosed Type 1 Diabetes Mellitus

Faculty Medicine Year: 2009
Type of Publication: ZU Hosted Pages:
Authors:
Journal: Egyptian Rheumatology and Rehabilitation The Egyptian Society for Rheumatology and Rehabilitation Volume:
Keywords : Electrophysiological Study , Glutamic Acid Decarboxylase , , , Detection    
Abstract:
Background: The early detection of patients with subclinical neuropathy is essential to increase their motivation to improve diabetic control and prevention of diabetic neuropathy. The ideal method of diagnosis and follow-up includes a combination of clinical examination, laboratory investigation and electrophysiological study. Objectives: to evaluate the role of electrophysiological study and serum glutamic acid decarboxylase (GAD65Ab) in the detection of subclinical neuropathy, in addition to their correlations with glycaemic control in Type 1 diabetic patients within the first year of the disease, to help prevention of neuropathic complications. Subjects & Methods: This study was conducted on 30 patients of Type 1diabetes milletus within the first year of diagnosis, according to WHO criteria 1999 and 20 healthy volunteers subjects as a control group. All subjects were evaluated for subjective neuropathy symptoms, neurological examination, electrophysiological findings, GAD65Ab, glycosylated hemoglobin (HbA1), cholesterol and triglyceride in serum. Patients with symptoms of somatosensory neuropathy, other systemic illnesses, history of alcoholism, or psychiatric disease were excluded. At least two abnormal independent neurophysiological nerve parameters were accepted as the criteria of the peripheral nervous system involvement. Results:All patients were clinically asymptomatic. Electrophysiological study showed that peripheral nervous system involvement found in 93.3% of diabetic patients. The percentages of abnormal electrophysiological parameters in different motor and sensory nerves were 90% in sural nerve, 82.4% in peroneal motor nerve, 68.5% in posterior tibial motor nerve, 62.2% in median motor nerve, 59.9% in ulnar motor nerve, 65.2% in median sensory nerve, and 60.5% in ulnar sensory nerve. In all sensory nerve conduction studies, the most frequent abnormal parameter was distal latency. As regard motor nerves, distal motor latency (DML) was affected in the upper extremity, while the motor nerve conduction velocity (MCV) and minimum F latency were affected in lower extremities in the early stage of diabetes. In our results neither the duration of the disease nor the age of the subject correlated with nerve dysfunction. Antibodies to GAD65 were detected in 18 of 30 patients( 60%).After correction of data for effects of age and glycemia, patients with positive GAD65Ab had slower motor nerve conduction velocities in the median, ulnar, and peroneal nerves and prolonged sural nerve latency. There is a positive correlation between HbA1 levels and peripheral nerve dysfunction in the lower extremity. However, upper extremity nerve dysfunction was not correlated with HbA1 value. Highly significant correlation between HbA1 and GAD65 in patients group was noticed. Conclusion: In patients with recent onset Type I diabetes mellitus, subclinical diabetic peripheral neuropathy can be detected by electrophysiological tests, which are useful to verify the range and extent of the nerve lesion involved in the early stage of asymptomatic peripheral neuropathy. Also we may suggest that the most useful and practical nerves for electrophysiological study in diabetic patients were the motor and sensory nerves of lower extremity. The poor glycaemic control and GAD65Ab have an impact on peripheral nerve function.
   
     
 
       

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