Article type
Year
Abstract
Introduction: Osteoporosis is a disease characterized by low bone mass, which leads to an increased risk of fracture. It is the most frequent metabolic disorder in Canada and has significant effects on quality of life. Exogenous calcitonin has been shown to be effective in arresting postmenopausal bone loss. Calcitonin is an antiresorptive agent, which acts by inhibiting osteoclastic activity. It has also been effective in treatment of pain secondary to compression fractures, a property, which is thought to be mediated, through release of beta-endorphins.
Objective: The purpose of this systematic overview was to: access the medical literature on the subject of calcitonin intervention in postmenopausal osteoporosis (PMO); and to determine whether treatment of PMO with calcitonin correlates with increased bone mineral density (BMD), decreased fracture rate, and reduction of pain.
Methods: Retrieval of randomized controlled trials (RCTs) of calcitonin treatment of PMO involved a computerised search of Medline (1984-95 Mesh headings: calcitonin, bone density, osteoporosis, RCTs) and a bibliographic search. The list of trials was reviewed by content experts. The quality of each trial was assessed. Outcome measures included BMD: vertebral and distal radius. Subgroup analysis compared different machines (DPA to DEXA) and different doses of calcitonin (50 IU to 400 IU per day).
Results: The percentage mean difference of BMD between treatment and control groups was derived using RevMan. Of the 30 published RCTs, eleven trials satisfied our inclusion criteria and data were extracted. The weighted mean difference for vertebral BMD was 5.81 (95% CI 5.40-6.22), and for cortical bone there was a less impressive difference of 1.9 (95% CI 0.8-3.0). Data to assess the effect on fracture rates were lacking. Pain control was assessed in two trials using a visual analogue scale and this resulted in a mean difference of -4.61 (95% CI -5.43 to -3.79). Vertebral BMD was not significantly different for DEXA versus DPA.
Discussion: There appears to be a positive effect of calcitonin in treatment of PMO on vertebral BMD, but there is not enough information to assess reduction of fractures.
Objective: The purpose of this systematic overview was to: access the medical literature on the subject of calcitonin intervention in postmenopausal osteoporosis (PMO); and to determine whether treatment of PMO with calcitonin correlates with increased bone mineral density (BMD), decreased fracture rate, and reduction of pain.
Methods: Retrieval of randomized controlled trials (RCTs) of calcitonin treatment of PMO involved a computerised search of Medline (1984-95 Mesh headings: calcitonin, bone density, osteoporosis, RCTs) and a bibliographic search. The list of trials was reviewed by content experts. The quality of each trial was assessed. Outcome measures included BMD: vertebral and distal radius. Subgroup analysis compared different machines (DPA to DEXA) and different doses of calcitonin (50 IU to 400 IU per day).
Results: The percentage mean difference of BMD between treatment and control groups was derived using RevMan. Of the 30 published RCTs, eleven trials satisfied our inclusion criteria and data were extracted. The weighted mean difference for vertebral BMD was 5.81 (95% CI 5.40-6.22), and for cortical bone there was a less impressive difference of 1.9 (95% CI 0.8-3.0). Data to assess the effect on fracture rates were lacking. Pain control was assessed in two trials using a visual analogue scale and this resulted in a mean difference of -4.61 (95% CI -5.43 to -3.79). Vertebral BMD was not significantly different for DEXA versus DPA.
Discussion: There appears to be a positive effect of calcitonin in treatment of PMO on vertebral BMD, but there is not enough information to assess reduction of fractures.