Primary hyperparathyroidism and osteoporosis.
Primary hyperparathyroidism (PHPT) is considered a cause of secondary osteoporosis as a consequence of its known catabolic effect promoting osteoclast activity and bone resorption. However, recent in vitro and in vivo studies have shown that parathyroid hormone (PTH) may also have an anabolic effect on the mammalian skeleton. These two paradoxical effects of parathyroid hormone are discussed in the light of recent results of basic research, and of bone densitometric and histomorphometric data collected in patients affected by PHPT. Review of the literature leads to the conclusion that in PHPT skeletal damage involves prevalently cortical bone, while the mineral content of trabecular bone is preserved or even increased. On the basis of bone mineral density (BMD) measurements, osteoporosis prevalence in the early postmenopausal period seems to be significantly higher in women affected by PHPT than in the general population. As age progresses, osteoporosis prevalence seems to decrease in PHPT, while it increases exponentially with age in the general population. Similarly in PHPT, vertebral and appendicular fractures occur prevalently in the earlier decades of life with a higher frequency than in normal subjects, while with advancing age the fracture incidence becomes equal to that of the general population. When bone density is measured in lateral projection at lumbar level, BMD values in patients with mild asymptomatic PHPT are significantly higher than in controls. We conclude that PTH hypersecretion may represent a risk factor for osteoporosis and fractures in the young and in the early postmenopausal period, while it may have a protective effect on trabecular bone in elderly postmenopausal women.
Mazzuoli
G F
GF
II Clinica Medica, Policlinico Umberto I, La Sapienza University, Roma, Italy.
D'Erasmo
E
E
Pisani
D
D
D000368:Aged; D005260:Female; D006801:Humans; D006961:Hyperparathyroidism / Q000150:complications*; D008875:Middle Aged; D015663:Osteoporosis, Postmenopausal / Q000209:etiology*