Issue: April 2012
March 07, 2012
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Diabetic polyneuropathies, retinopathy and nephropathy increased in newly diagnosed diabetes

Dyck PJ. Diabetes Care. 2012:35;584-591.

Issue: April 2012
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Prevalence of diabetic polyneuropathies, retinopathy and nephropathy was increased in patients with new-onset diabetes, but not in those with impaired glycemia as defined by the American Diabetes Association, according to study results.

Researchers tested the occurrence of diabetic polyneuropathies, retinopathy or nephropathy of patients with impaired glycemia compared with otherwise healthy participants without impaired glycemia. Impaired glycemia consisted of abnormality of fasting glucose, impaired glucose tolerance and impaired HbA1c.

They used prospective, population-based diagnostic and laboratory registries in Olmstead County, Minn., to randomly identify 150 healthy participants without impaired glycemia, 174 with impaired glycemia and 218 patients with new diabetes.

Results showed that frequency of diabetic polyneuropathies occurred in 2% of healthy participants, 1.7% of those with impaired glycemia and 7.8% of patients with newly diagnosed diabetes.

In patients with new diabetes, frequency of retinopathy and nephropathy was significantly increased. However, secondary analysis showed small increases in retinopathy and nephropathy among those with IGT, impaired fasting glucose and combined groups.

In addition, the frequency of diabetic retinopathy was 3.4% in healthy participants, 4.7% in those with impaired glycemia and 9.4% in those with new diabetes.

An increase was not observed for atypical diabetic polyneuropathies in any groups.

“In medical practice, explanations other than impaired glycemia should be sought for patients with atypical diabetic polyneuropathies (chronic idiopathic axonal polyneuropathy) who have impaired glycemia,” the researchers concluded.

Disclosure: The researchers report no relevant financial disclosures.

PERSPECTIVE

The article by Dyck et al explores the prevalence of DPN and other microvascular complications in patients with normal glucose tolerance, impaired glucose tolerance and new-onset diabetes. They demonstrated that typical DPN is more prevalent in the category of patients with newly diagnosed diabetes, and that the prevalence of peripheral diabetic neuropathy is not different between the impaired group and the group with normal glucose tolerance. This study adds to our overall knowledge about these complications but is too small to prove that there is no association between impaired glucose tolerance and DPN. It does not address possible covariates such as age, obesity and inflammation. While it is comforting to know that impaired glucose tolerance does not impose an increased risk of DPN, it is clear that neuropathy can develop very early in patients with new onset type 2 diabetes. The study confirms that efforts to prevent diabetes are not misguided. Preventing diabetes may also prevent some of the early complications such as DPN.

Janet McGill, MD
Endocrine Today Editorial Board member