Background There is little information on the incidence andnatural history of neuropathy in patients with non-insulin-dependentdiabetes mellitus (NIDDM).
Methods We studied patients with newly diagnosed NIDDM and controlsubjects both at base line and 5 and 10 years later. Polyneuropathywas diagnosed on the basis of clinical criteria (pain and paresthesias)and electrodiagnostic studies (nerve conduction velocity andresponse-amplitude values). We investigated the relation betweenmetabolic variables (results of oral glucose-tolerance tests,serum lipid and insulin concentrations, and glycosylated hemoglobinvalues) and the development of polyneuropathy.
Results In 10 years, 36 patients with NIDDM and 8 control subjectsdied; 86 patients and 121 control subjects completed the study.When the study ended, 18 percent of the patients were beingtreated only with diet, 59 percent with oral hypoglycemic drugsalone, 12 percent with insulin alone, and 11 percent with bothinsulin and oral hypoglycemic agents. At base line the prevalenceof definite or probable polyneuropathy among the patients withNIDDM was 8.3 percent, as compared with 2.1 percent among thecontrol subjects. These values 10 years later were 41.9 percentand 5.8 percent, respectively. The number of patients with NIDDMwho had nerve-conduction abnormalities in the legs and feetincreased from 8.3 percent at base line to 16.7 percent after5 years and to 41.9 percent after 10 years. The decrease insensory and motor amplitudes, indicating axonal destruction,was more pronounced than the slowing of the nerve conductionvelocities, which indicates demyelination. Among the patientswith NIDDM, those with polyneuropathy had poorer glycemic controlthan those without. Low serum insulin concentrations beforeand after the oral administration of glucose were associatedwith the development of polyneuropathy, regardless of the degreeof glycemia.
Conclusions The prevalence of polyneuropathy among patientswith NIDDM increases with time, and the increase may be greaterin patients with hypoinsulinemia.
Source Information
From the Departments of Clinical Neurophysiology (J.P., J.L., E.M.), Clinical Nutrition (L.N., M.U.), and Internal Medicine (L.N., O.S.), University Hospital and University of Kuopio, Kuopio, Finland.
Address reprint requests to Dr. Partanen at the Department of Clinical Neurophysiology, Kuopio University Hospital, P.O. Box 1777, FIN-70211 Kuopio, Finland.
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