Endocrine Abstracts

BACKGROUND: AGHD is associated with osteoporosis. Alterations in parathyroid gland responsiveness to changes in calcium concentration play a role in the genesis of osteoporosis.
OBJECTIVES: To investigate PTH response to hypo- and hypercalcaemic stimuli in AGHD.
METHODS: 12 patients with untreated AGHD were consented to the study. Venous cannulae were inserted in each arm and half-hourly blood samples collected between 0900-1800hours for PTH, calcium and albumin. After 5 basal samples, sodium EDTA infusion was commenced at 1100hours for 2hours to induce hypocalcaemia in 6 patients (group 1). Hypercalcaemia was induced in 6 patients (group 2) by calcium gluconate over 2hours. GHR was commenced after baseline visit. The protocol was repeated at 3 and 12 months on GHR. Local Ethical Committee approval was obtained.
RESULTS: In group 1, maximum PTH stimulation occurred at an ACa concentration (percentage drop) of 1.79 millimoles per litre (23.8%) at 0/12. Following GHR, maximum PTH stimulation occurred at an ACa concentration of 1.92 (17.2%) at 3/12 and 2.16 (12.9%) at 12/12 (p less than 0.05). The maximum PTH response was a 365% rise before and 326% rise after 12/12 (p=ns). In group 2, maximum PTH suppression occurred at an ACa concentration (percentage rise) of 2.79 (18.9%) at 0/12 compared to 2.92 (16.7%) at 3/12 (p=ns) and 2.84 (14.7%) at 12/12 (p less than 0.01). The maximum PTH suppression was 75% before and 82% after 12/12 (p=ns). The calcium set point (calcium concentration at which the rate of PTH secretion is half of its maximal value) progressively increased at 3 (p less than 0.01) and 12 months (p less than 0.001) in both groups following GHR.
CONCLUSIONS: These results suggest increased parathyroid gland sensitivity to significantly smaller changes in serum calcium following GHR. Our findings may help explain the genesis of osteoporosis in AGHD patients.