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Increased Bone Remodeling in First-Episode Major Depressive Disorder

 

作者: Andrés Herrán,   José Amado,   María García-Unzueta,   José Vázquez-Barquero,   Lorena Perera,   Jesús González-Macías,  

 

期刊: Psychosomatic Medicine  (OVID Available online 2000)
卷期: Volume 62, issue 6  

页码: 779-782

 

ISSN:0033-3174

 

年代: 2000

 

出版商: OVID

 

关键词: depressive disorder,;bone density,;bone remodeling markers,;osteoporosis.

 

数据来源: OVID

 

摘要:

ObjectiveBone mineral density is decreased in patients with depressive disorder. This study evaluated biochemical bone remodeling markers in patients having their first depressive episode who had not taken psychotropic medications to evaluate possible pathogenic mechanisms implicated in the loss of bone mineral density in early states of this illness.MethodsSerum osteocalcin, parathyroid hormone, bone alkaline phosphatase, telopeptide, collagen type I C-terminal propeptide, cross-laps, and 25-hydroxyvitamin D levels were measured in 19 depressive patients and 19 age-matched healthy women. In addition, serum cortisol and interleukin-6 were determined. Patients were assessed with the Schedules for Clinical Assessment in Neuropsychiatry interview and met criteria for a single depressive episode.ResultsDepressed patients had increased levels of osteocalcin (p= .003), an osteoblastic marker; telopeptide (p= .01), an osteoclastic marker; and cross-laps (p= .000), another osteoclastic marker. Parathyroid hormone was lower in patients (p= .02), whereas the rest of the markers were comparable between patients and healthy control subjects. Serum cortisol was higher in depressed patients than in control subjects (p= .003), but cortisolemia and interleukin-6 did not show any relationship with bone markers in patients. Clinical severity of the illness and weight loss due to depression in patients did not correlate with bone remodeling markers.ConclusionsThese data suggest that an increase in bone remodelingnotdue to vitamin D deficiency induces a release of calcium from bone and inhibition of parathyroid hormone secretion.

 

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