Published by BioScientifica
British Endocrine Societies Joint Meeting 2003

British Endocrine Societies Joint Meeting 2003

Glasgow, UK
24 March 2003 - 26 March 2003
British Endocrine Societies

Endocrine Abstracts (2003) 5 P11

Effects of growth hormone replacement on parathyroid gland responsiveness to hypo- and hypercalcaemic stimuli in adult growth hormone deficiency

AM Ahmad1, J Thomas1, HD White1, MT Hopkins1, BH Durham2, JP Vora1 & WD Fraser2

1Department of Diabetes and Endocrinology, Royal Liverpool University Hospital, Liverpool, UK; 2Department of Clinical Chemistry, Royal Liverpool University Hospital, Liverpool, UK.


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.


Endocrine Abstracts (2003) 5 P11