F. Cosman et al., PARATHYROID RESPONSIVITY IN POSTMENOPAUSAL WOMEN WITH OSTEOPOROSIS DURING TREATMENT WITH PARATHYROID-HORMONE, The Journal of clinical endocrinology and metabolism, 83(3), 1998, pp. 788-790
Endocrine systems maybe affected permanently by administration of supr
aphysiologic doses of hormone. This is a well known complication of gl
ucocorticoid treatment where the pituitary/adrenal axis may never full
y recover, especially when large doses of steroids are needed during s
ignificant physical stress. The goal of this investigation was to dete
rmine whether responsivity of the parathyroid gland was normal after u
se of (1-34)PTH daily as an investigational therapy for osteoporosis.
Patients were all postmenopausal osteoporotic women treated with estro
gen and enrolled in a 3-yr trial of(1-34)PTH by daily subcutaneous inj
ection (400 IU/day) in addition to their estrogen therapy. A volunteer
subgroup (n = 10) of this population was recruited for this investiga
tion. All patients had an EDTA-provoked hypocalcemic challenge before
beginning PTH treatment. The same patients had repeat EDTA-challenge t
ests at various times during the 3-yr PTH treatment trial. Three patie
nts had 2 infusions while on PTH treatment (interim and at the end of
3 yr). Ionized calcium declined identically before and during PTH trea
tment in response to the EDTA stimulus. PTH(1-84) responses were ident
ical before and during PTH therapy. Furthermore, there were no differe
nces in 1,25(OH)(2)D elevation or in phosphorus reduction over the cou
rse of the EDTA infusion during daily PTH treatment. Osteocalcin level
s were higher during PTH treatment, as expected, but responsivity to a
cute endogenous PTH elevations was the same after PTH treatment. We co
nclude that 1-34PTH therapy, at 400 IU/day for up to 3 yr, does not su
ppress parathyroid responsivity and should therefore (at least within
this period of treatment) have no permanent adverse effect on the abil
ity of the body to maintain calcium homeostasis. Additionally, there i
s no difference in target organ responsivity to acute endogenous eleva
tions of PTH after exogenous PTH therapy.