Endocrine Abstracts

Parathyroid responsiveness to parathyroid hormone (1-34) infusion is altered in adult growth hormone deficiency following growth hormone replacement

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

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 increased prevalence of osteoporosis. Alterations in both parathyroid gland sensitivity to changes in calcium concentration and end-organ response to the effects of PTH play a role in the development of osteoporosis.
OBJECTIVES: To investigate the effects of PTH (1-34) infusion on end-organ and parathyroid gland responsiveness.
METHODS: 6 patients with severe AGHD were recruited. All patients were admitted, prior to commencement of GH replacement (GHR), at 1300hours. Venous cannulae were inserted in each arm and half-hourly blood sampling was commenced at 1400hours. hPTH (1-34) was infused over 24 hours. PTH, calcium and albumin were measured on all samples. GHR was commenced after the baseline visit. The protocol was repeated at 3 and 12 months on GHR. Local ethical committee approval was obtained.
RESULTS: Following hPTH (1-34) infusion, ACa concentration increased after 10 hours in untreated AGHD patients, whereas, after 12 months on GHR, ACa concentration increased within 5 hours. After 12 months on GHR, the percentage increase at 4 hours was 3.2 plus/minus 0.60% versus 0.83 plus/minus 0.66% in untreated AGHD patients (p less than 0.05) that remained significantly higher over the 24 hours (17.8 plus/minus 2.9% versus 12.6 plus/minus 2.2%, p less than 0.05).There was no significant difference in the maximum PTH (1-84) suppression between visits. There was a significant increase in the calcium set-point (calcium concentration at which the rate of PTH secretion is half its maximal value) after 3 (p less than 0.05) and 12 months (p less than 0.001) compared to baseline.
CONCLUSIONS: We have demonstrated increased end-organ responsiveness to the effects of PTH resulting in a significant increase in calcium concentration in response to PTH (1-34) infusion, following GHR. Together with the increase in calcium set-point these results may help understand the mechanisms underlying the genesis of osteoporosis in AGHD.

Endocrine Abstracts (2003) 5 P6