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Familial factors influence diabetic microvascular complications
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NEW YORK (Reuters Health) - Familial factors influence the risk of microvascular complications of type 1 diabetes, independent from the familial risk of diabetes itself, according to a report in the December issue of The Journal of Clinical Endocrinology & Metabolism.

"To the extent that glucose control is important, it may be even more critical in those patients potentially at higher risk for complications, those being type 1 diabetic-affected siblings of type 1 diabetes patients with complications, and also women, who appear to be at higher risk for complications," Dr. David A. Greenberg from Columbia University, New York told Reuters Health.

Dr. Greenberg, along with Dr. Maria C. Monti and colleagues, sought to identify familial risk factors for diabetic microvascular complications and to examine how these risk factors influence retinopathy, nephropathy, and neuropathy onset. They included a total of 8114 subjects in the study: 4935 probands with type 1 diabetes, 921 siblings, and 695 parents.

The presence of type 2 diabetes (but not type 1 diabetes) in a parent was significantly associated with the development of all three microvascular complications, the authors report.

Diabetic patients whose siblings had type 1 diabetes complications faced substantially higher risks of developing microvascular complications themselves, with odds ratios of 9.9 for retinopathy in patients whose siblings had retinopathy, 6.18 for nephropathy in patients whose siblings had nephropathy, and 2.2 for neuropathy in patients whose siblings had neuropathy.

Retinopathy and neuropathy were more common in female type 1 diabetes patients than in male type 1 diabetes patients, the researchers say, and the risk of second complications was higher in female patients than in male patients.

The risk of complications increased with increasing duration of type 1 diabetes, and diagnosis at a very young age (under 5 years) or past puberty (over 14 years) was associated with a lower likelihood of developing complications.

"These new findings tell us that the explanation for what causes complications must involve shared pathogenic mechanisms in the family (mechanisms that may be independent of the susceptibility to type 1 diabetes)," the authors conclude.

"Today, the emphasis is on whole-genome association studies and SNS," Dr. Greenberg pointed out. "One of the consequences of this emphasis is that family data, such as we used in our work, has been denigrated, and data collection in genetic studies focuses on subjects with the disease and their comparison with controls. Thus, the familial aspects of genetic studies are being lost, which will ultimately be detrimental to our overall understanding of how genes cause disease."

J Clin Endocrin Metab 2007.


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