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Long-term bone loss in insulin-dependent diabetic patients with microvascular complications
Affiliation:1. Grup de Recerca en Neurologia Pediàtrica, Institut de Recerca Vall d''Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain;2. First Department of Pediatrics, Agia Sofia Hospital, University of Athens, Athens, Greece;3. Departament de Genètica, Facultat de Biologia, Universitat de Barcelona, Spain;4. Institut de Biomedicina de la Universitat de Barcelona (IBUB), Barcelona, Spain;5. Center for Biomedical Network Research on Rare Diseases (CIBERER), Barcelona, Spain;6. Pediatric Neurology Department, Teknon Clinic, Barcelona, Spain
Abstract:Insulin-dependent diabetic patients have an approximately 10% decreased bone mineral content (BMC) when they are studied a few years after clinical onset of diabetes. After that time, patients without diabetic microvascular complications have no, or only very little, further bone loss. The aim of the present study was to investigate if any substantial long-term bone loss occurs in diabetic patients with microvascular complications. We studied 19 insulin-dependent diabetic patients with neither physiologic nor pathologic conditions known to interfere with bone metabolism, other than diabetes. BMC was determined twice, with an interval of 11 years. At initial examination, no patient had diabetic microangiopathy, but at final examination 7 patients had developed diabetic microvascular complications while 12 patients had not. As compared with gender- and age-matched controls, both subgroups had significantly decreased BMC at the initial examination. During the study period, the patients with complications showed further bone loss, whereas the subgroup without complications had unchanged decreased BMC. At final examination, BMC was significantly lower in patients with microvascular complications than in patients without them. The biochemistry of bone metabolism showed a significantly increased fasting urinary excretion of calcium and hydroxyproline in patients with complications, but not in the group without complications, and there was a negative correlation between plasma BGP (osteocalcin) and hemoglobin A1c for all patients. These findings indicate that, in addition to a decreased BMC (before or shortly after clinical onset of diabetes), patients who develop microvascular complications also develop ongoing bone loss. This loss may be caused by an increased bone resorption, but decreased bone formation during periods of poor diabetic control may be involved as well.
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