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Basal plasma immunoreactive calcitonin in postmenopausal osteoporosis
Metabolism: Clinical and Experimental
|June 1, 1980
Summary
Calcitonin (CT) deficiency is not a cause of postmenopausal osteoporosis (PM-OP). Studies show normal CT levels in PM-OP patients and no link between CT levels and bone mass changes during therapy.
Area of Science:
- Endocrinology
- Bone Metabolism
- Gerontology
Background:
- Postmenopausal osteoporosis (PM-OP) is a significant health concern.
- Calcitonin (CT) deficiency has been hypothesized as a potential cause of PM-OP.
Purpose of the Study:
- To investigate the role of calcitonin (CT) in the etiology and pathogenesis of postmenopausal osteoporosis (PM-OP).
- To determine if basal calcitonin levels are decreased in women with PM-OP.
- To assess the relationship between calcitonin levels and bone mass changes during CT therapy.
Main Methods:
- Measured basal immunoreactive calcitonin (iCT) using radioimmunoassay (RIA) in 62 PM-OP women and 28 controls.
- Assessed correlations between iCT levels and age, disease severity (compression fractures), serum biochemistry, and total body calcium (TBC).
- Evaluated the relationship between basal iCT and bone mass response (TBC) in 20 PM-OP patients treated with synthetic salmon CT.
Main Results:
- Mean basal iCT levels were not significantly different between PM-OP women and age-matched controls.
- No significant correlations were found between basal iCT and age, disease severity, serum markers, or total body calcium in PM-OP patients.
- Basal iCT levels did not correlate with improvements in bone mass during calcitonin therapy.
Conclusions:
- Basal calcitonin levels are not decreased in women with postmenopausal osteoporosis.
- Circulating calcitonin levels do not appear to influence therapeutic changes in bone mass during CT treatment.
- Calcitonin is unlikely to be a major etiologic or pathogenetic factor in postmenopausal osteoporosis.