NATURAL-HISTORY OF PERIPHERAL NEUROPATHY IN PATIENTS WITH NON-INSULIN-DEPENDENT DIABETES-MELLITUS

Citation
J. Partanen et al., NATURAL-HISTORY OF PERIPHERAL NEUROPATHY IN PATIENTS WITH NON-INSULIN-DEPENDENT DIABETES-MELLITUS, The New England journal of medicine, 333(2), 1995, pp. 89-94
Citations number
20
Categorie Soggetti
Medicine, General & Internal
ISSN journal
00284793
Volume
333
Issue
2
Year of publication
1995
Pages
89 - 94
Database
ISI
SICI code
0028-4793(1995)333:2<89:NOPNIP>2.0.ZU;2-#
Abstract
Background. There is little information on the incidence and natural h istory of neuropathy in patients with non-insulin-dependent diabetes m ellitus (NIDDM).Methods. We studied patients with newly diagnosed NIDD M and control subjects both at base line and 5 and 10 years later. Pol yneuropathy was diagnosed on the basis of clinical criteria (pain and paresthesias) and electrodiagnostic studies (nerve conduction velocity and response-amplitude values). We investigated the relation between metabolic variables (results of oral glucose-tolerance tests, serum li pid and insulin concentrations, and glycosylated hemoglobin values) an d the development of polyneuropathy. Results. In 10 years, 36 patients with NIDDM and 8 control subjects died; 86 patients and 121 control s ubjects completed the study. When the study ended, 18 percent of the p atients were being treated only with diet, 59 percent with oral hypogl ycemic drugs alone, 12 percent with insulin alone, and 11 percent with both insulin and oral hypoglycemic agents. At base line the prevalenc e of definite or probable polyneuropathy among the patients with NIDDM was 8.3 percent, as compared with 2.1 percent among the control subje cts. These values 10 years later were 41.9 percent and 5.8 percent, re spectively. The number of patients with NIDDM who had nerve-conduction abnormalities in the legs and feet increased from 8.3 percent at base line to 16.7 percent after 5 years and to 41.9 percent after 10 years . The decrease in sensory and motor amplitudes, indicating axonal dest ruction, was more pronounced than the slowing of the nerve conduction velocities, which indicates demyelination. Among the patients with NID DM, those with polyneuropathy had poorer glycemic control than those w ithout. Low serum insulin concentrations before and after the oral adm inistration of glucose were associated with the development of polyneu ropathy, regardless of the degree of glycemia. Conclusions. The preval ence of polyneuropathy among patients with NIDDM increases with time, and the increase may be greater in patients with hypoinsulinemia.