Subcutaneous administration of the amino-terminal fragment of human parathyroid hormone-(1-34): kinetics and biochemical response in estrogenized osteoporotic …

R Lindsay, J Nieves, E Henneman… - The Journal of …, 1993 - academic.oup.com
R Lindsay, J Nieves, E Henneman, V Shen, F Cosman
The Journal of Clinical Endocrinology & Metabolism, 1993academic.oup.com
A standard dose (400 U or 25 micrograms) of human (h) PTH-(1-34) was administered sc in
11 estrogen-treated patients with postmenopausal osteoporosis. Increments in circulating
hPTH-(1-34) were brisk, peaking at 30 min, with variable peak levels averaging 10 times
normal. Clearance of the peptide from the circulation followed an expontential pattern, with a
mean t1/2 of 75 min. Peptide administration was followed by an immediate decline in serum
concentrations of PTH-(1-84), which remained suppressed at about 65% of the basal value …
Abstract
A standard dose (400 U or 25 micrograms) of human (h) PTH-(1-34) was administered sc in 11 estrogen-treated patients with postmenopausal osteoporosis. Increments in circulating hPTH-(1-34) were brisk, peaking at 30 min, with variable peak levels averaging 10 times normal. Clearance of the peptide from the circulation followed an expontential pattern, with a mean t1/2 of 75 min. Peptide administration was followed by an immediate decline in serum concentrations of PTH-(1-84), which remained suppressed at about 65% of the basal value for the duration of the study (4 h). Serum calcium did not increase until 120 min, thus occurring after the diminution in PTH-(1-84). Serum phosphorus declined promptly as urinary phosphate excretion increased. There were no clear changes in urinary calcium excretion, but urinary cAMP excretion increased within 120 min. In 9 of 11 patients, the serum concentration of 1,25-dihydroxyvitamin D increased, with mean levels increasing progressively after 90 min to approximately 30% above baseline (P < 0.05). In conclusion, sc administration of 25 micrograms hPTH-(1-34) produces significant short term changes in mineral homeostasis that appear to be mediated by the kidney, parathyroid gland, and skeleton, with the latter displaying the most delayed response.
Oxford University Press