Endocrine Abstracts

Introduction: Recent data suggest a reciprocal influence between bone and energy metabolism. Mediators have been identified as osteocalcin (OC), which stimulates insulin (IRI) secretion and activity and IRI as bone anabolic factor. Primary hyperparathyroidism (PHPT) stimulates bone turnover, induces osteoporosis and is associated with increased IRI resistance. A positive relationship between OC and IRI sensitivity has been found in PHPT, but no data exist on the relationship between IRI and bone mineral density (BMD).

Aim: To evaluate in a series of PHPT patients without known diabetes mellitus (DM), the relationship between IRI levels or sensitivity and BMD.

Subjects and methods: We studied 267 patients with PHPT (age, mean±S.D., 58.5±13.8 years; F/M 198/69; BMI 25.2±4.6 kg/m²; PTH 228.4±269.3 pg/ml; calcium 11.2±1.2 mg/dl) without known DM. Fasting blood glucose and IRI as well as BMD at lumbar spine, femur and forearm were measured. IRI sensitivity was assessed by the quantitative insulin sensitivity check index (QUICKI).

Results: In univariate analysis a positive relationship between IRI levels and BMD (R=0.19, P<0.03) or T score (R=0.23, P<0.005) at femoral site was found, but not at lumbar spine nor at forearm. A negative relationship between QUICKI and BMD (R=−0.20, P<0.015) or T score (R=−0.23, P<0.004) at femoral site was found. In multivariate analysis, we found that age (β=−0.35, P<0.000004), BMI (β=0.39, P<0.000001), PTH (β=−0.18, P<0.013) and QUICKI (R=−0.15, P<0.048) exerted an independent effect (R²=0.29) on femoral T score.

Conclusions: Our data show a relationship between insulin levels and/or sensitivity and BMD at femur in PHPT, as found in other diseases associated with insulin resistance. This finding suggest a link between bone and energy metabolism in PHPT. However, the clinical influence of this relationship on the PHPT-related bone damage is to be established.