Increased Prevalence of Impaired Glucose Tolerance in Patients With Painful Sensory Neuropathy

  1. J. Robinson Singleton, MD,
  2. A. Gordon Smith, MD and
  3. Mark B. Bromberg, MD, PHD
  1. Division of Neuromuscular Disease, Department of Neurology, University of Utah, Salt Lake City, Utah

    Abstract

    OBJECTIVE—To characterize a cohort of patients with neuropathy and impaired glucose tolerance (IGT) but no other identifiable cause of neuropathy. Of patients with diabetes, 10% have peripheral neuropathy at the time of their diagnosis, suggesting that axonal injury may occur early in the course of glucose intolerance. The American Diabetes Association (ADA) revised diagnostic criteria to recognize IGT (a serum glucose between 140 and 200 mg/dl in a 2-h oral glucose tolerance test [OGTT]) as a risk factor for cardiovascular disease independent of development of diabetes.

    RESEARCH DESIGN AND METHODS—Using revised ADA criteria for diabetes and IGT, we prospectively evaluated 107 sequential patients with idiopathic neuropathy.

    RESULTS—A total of 13 of the 107 patients had diabetes, whereas 36 (34%) had IGT, nearly three times the prevalence in age-matched control subjects (P < 0.01). OGTT was often elevated, whereas both fasting plasma glucose and HbA1c were normal. Comparing patients with diabetes, IGT, or normal OGTT, age and BMI were similar. However, painful sensory symptoms were more common in patients with IGT and diabetes, and family history of neuropathy was significantly more common in normoglycemic patients. Electrodiagnostic findings of axonal injury were less severe in patients with IGT and were more likely to be confined to sensory fibers than in patients with diabetes.

    CONCLUSIONS—Our results suggest that IGT may cause or contribute to small-fiber neuropathy, which is similar in phenotype to the painful sensory neuropathy commonly encountered in diabetes. Two-hour OGTT is more sensitive than other measures of glucose handling in screening these patients.

    Footnotes

    • Address correspondence and reprint requests to Rob Singleton, MD, University of Utah, Department of Neurology, Room 3R-152, 50 N. Medical Dr., Salt Lake City, UT 84132. E-mail: rob.singleton{at}hsc.utah.edu.

      Received for publication 28 December 2000 and accepted in revised form 17 April 2001.

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