Cardiac transplantation exposes recipients to
osteoporosis and increased risk of consequent fractures. The purpose of the present study was to examine the magnitude, timing and mechanism of bone loss following
cardiac transplantation, and to establish whether bone loss can be prevented by
calcium with or without
calcitonin. Thirty patients (29 men, 1 woman), aged 26-68 years (mean 48 years), were randomized into three groups of 10 to receive either no additional treatment, oral
calcium 1 g twice daily for 12 months or the same dose of
calcium plus intranasal
calcitonin 400 IU/day for the first month and then 200 IU/day for 11 months. Bone mineral density (BMD) at the lumbar spine and three femoral sites (femoral neck, trochanter, Ward's triangle) was measured by dual-energy X-ray absorptiometry (DXA) at the time of
transplantation and 6 and 12 months later. Markers of bone formation [serum bone-specific
alkaline phosphatase (B-ALP),
type I procollagen carboxyterminal propeptide (
PICP) and aminoterminal propeptide (PINP)] and resorption [serum
type I collagen carboxyterminal telopeptide (ICTP)], as well as serum
testosterone in men, were assayed before
transplantation and at 1 week and 1, 3, 6 and 12 months after
transplantation. During the first 6 post-transplant months BMD calculated as a percent change from baseline decreased in the control group by 6.4% (p = 0.014) in the lumbar spine, by 6.0% (p = 0.003) in the femoral neck, by 5.0% (p = 0.003) in the trochanter and by 5.5% (p = 0.130) in Ward's triangle. Between 6 and 12 months a further decline in BMD occurred only at the three femoral sites, ranging from 2.2% to 9.8% (p = 0.004-0.079). In comparison with the control group, the group receiving
calcium alone lost less bone in the trochanter between 0 and 6 months (p = 0.019), and the group receiving
calcium together with
calcitonin lost less bone in the femoral neck (p = 0.068) and Ward's triangle (p = 0.076) between 0 and 12 months. Seven (28%) of 25 assessable patients experienced vertebral
compression fractures.
Calcium with or without
calcitonin had no effect on changes in biochemical parameters; consequently, the three study groups were combined. The markers of bone formation increased, the elevations in mean values being 59% for B-ALP at 1 month (p = 0.009), 152% for
PICP at 1 week (p < 0. 0001) and 27% for PINP at 1 week (p = 0.021). After a temporary decline at 3 months B-ALP (p = 0.0002) and PINP (p < 0.0001) at 1 year were nearly doubled compared with baseline values. Throughout the study the marker of
bone resorption, serum ICTP, was above normal, with a peak (mean values 67-69% above baseline) at 1 week (p = 0.0002) to 1 month (p < 0.0001). The mean concentration of total
testosterone was decreased by 48% (p < 0.0001) 1 week and by 28% (p = 0.0005) 1 month after
transplantation, but this was mainly explained by the concomitant drop in
serum albumin. High bone turnover underlies bone loss after
cardiac transplantation. Bone loss is most rapid during the first 6 post-transplant months. In the upper femur this bone loss may be reduced by treatment with
calcium and
calcitonin.