LONGITUDINAL CHANGES IN BONE-MINERAL DENSITY AND BONE TURNOVER IN POSTMENOPAUSAL WOMEN WITH PRIMARY HYPERPARATHYROIDISM

The aims of this study were to determine 1) whether primary hyperparat hroidism (PHPT) is associated with accelerated bone loss in postmenopa usal women, 2) whether bone mineral density (BMD) and bone turnover ch ange to a similar extent with surgery and hormone replacement therapy (HRT) in these patients, and 3) whether biochemical markers of bone tu rnover measured at baseline can be used to predict the change in BMD i n these patients after different therapies. We studied 33 postmenopaus al women with PHPT; their ages at the time of study ranged from 48-80 yr (mean +/- SD, 63 +/- 10). Total body (TB), lumbar spine (LS), and f emoral neck (FN) BMD and biochemical markers of bone turnover were mea sured at baseline and 10-30 months (19 +/- 5) after parathyroid surger y, HRT, or no treatment. BMD was measured in 33 age-matched healthy co ntrols at baseline and at a mean of 24 months. Baseline biochemical ma rkers of bone turnover were measured in controls. In PHPT at baseline, the mean z-score of BMD was -1.25 at TB (95% confidence interval, -1. 64 to -0.86), -0.95 at LS (-1.37 to -0.53), and -1.30 at FN (-1.65 to -0.95), whereas the mean z score was 0.45 for serum carboxy-terminal p ropeptide of human type I procollagen (0.02-0.89), 1.05 for bone alkal ine phosphatase (0.38-1.71), 2.38 for 24-h urinary excretion of cross- linked N-terminal telopeptide of type I collagen (NTx; 1.63-3.13), and 2.36 for 24-h urinary excretion of galactosyl hydroxylysine (1.97-2.7 4). After surgery and HRT, BMD increased and bone turnover decreased d uring the follow-up. In the untreated group, BMD decreased at TB and F N, and levels of bone alkaline phosphatase, NTx/creatinine, and galact osyl hydroxylysine/creatinine increased. When the rate of change in BM D (percentage per yr) was compared with that in the control group, bon e gain was significant at all three skeletal sites after surgery and H RT, and bone loss was significant at TB and FN, but not at LS, in the untreated group. There was a weak, but significant, correlation betwee n baseline urinary NTx and the change in femoral neck BMD in the untre ated group (r = -0.36; P = 0.05). We conclude that untreated postmenop ausal women with PHPT have low BMD resulting from accelerated bone los s at the TB and FN. Surgery and HRT both restore BMD and bone turnover toward normal in postmenopausal women with PHPT. A single measurement of bone turnover is insufficient to predict BMD changes in individual patients with PHPT.