Longitudinal measurements of bone density and biochemical indices in untreated primary hyperparathyroidism.

Abstract

A large number of patients with primary hyperparathyroidism today do not undergo parathyroidectomy. In this prospective study, we evaluated the effect of untreated disease on biochemical and bone densitometric indices. In 66 patients, seven annual measurements showed no change in serum calcium, phosphorus, PTH, vitamin D, or alkaline phosphatase; in urinary calcium, hydroxyproline or hydroxypyridinium cross-link excretion; or lumbar spine, femoral neck, and radial bone mineral density. The subset of postmenopausal women also showed no change in biochemical indices or bone density at any of the three sites. Twenty-four patients met guidelines for surgery as established by the NIH Consensus Conference, 1990. They differed from those who did not meet these guidelines only by being younger (50 +/- 3 vs. 62 +/- 2 yr; P = 0.0005) and by having higher urinary calcium excretion [7.7 +/- 0.9 vs. 5.4 +/- 0.3 mmol/L (310 +/- 37 vs. 215 +/- 14 mg/g creatinine); P < 0.01]. No longitudinal changes in biochemical profile or bone mineral density at any site were noted in this subgroup. Conservative management of patients with mild primary hyperparathyroidism does not lead to progression of disease, as reflected by biochemical indices. Bone density is maintained over 6 yr of observation at sites reflecting both cortical (radius) and cancellous (lumbar spine) bone.

Marked and sustained increase in bone mineral density after parathyroidectomy in patients with primary hyperparathyroidism; a six‐year longitudinal study with or without parathyroidectomy in a Japanese population

“…Similar results were obtained by previous studies (Silverberg et al, 1995aAbdelhadi & Nordenstrom, 1998). Similar results were obtained by previous studies (Silverberg et al, 1995aAbdelhadi & Nordenstrom, 1998).…”

“…A similar effect of PTX on BMD in pHPT patients was found in a long-term study (Martin et al ., 1990;Silverberg et al ., 1995b). Most pHPT patients without PTX have been reported to be clinically stable over the long-term (Silverberg et al ., 1995a;Abdelhadi & Nordenstrom, 1998). (1999) subsequently reported that successful surgery led to sustained increases in BMD at trabecular but not cortical sites during 10 years of follow-up after PTX and that cortical bone loss was irreversible at the time of diagnosis.…”

Bone mineral density analysis in patients with primary hyperparathyroidism associated with multiple endocrine neoplasia type 1 after total parathyroidectomy

“…[2][3][4][5] Compared with s-HPT, HPT/MEN1 presents as a multiglandular parathyroid neoplasia (hyperplasia vs. adenoma); has an earlier disease onset (20 vs. 40 years of age); is frequently less aggressive; harbours a germline mutation in the MEN1 gene that is not found in s-HPT; has a higher recurrence rate after a parathyroidectomy (PTx) and the recommended surgical approach in HPT/MEN1 is subtotal or total PTx, whereas adenomectomy is indicated for s-HPT. 7,11,12 BMD values in the LS are either slightly diminished or even normal in s-HPT, [11][12][13] which clearly contrasts with the vertebral demineralization so far reported in HPT/MEN1. Excess of PTH in HPT increases bone turnover, leading to a reversible loss of cortical and trabecular bone caused by an expansion of the remodelling space, and an irreversible loss of cortical bone caused by increased endocortical resorption.…”

Anabolic Therapy for Osteoporosis

“…The work of Silverberg and her colleagues have demonstrated that in the mild asymptomatic form of the disease seen today, a particular pattern occurs in terms of bone density (49). The work of Silverberg and her colleagues have demonstrated that in the mild asymptomatic form of the disease seen today, a particular pattern occurs in terms of bone density (49).…”