閉経後の骨粗鬆症におけるデノスマブ治療後の副甲状腺ホルモンは変化します

目的：デノスマブは、副甲状腺ホルモン（PTH）レベルの代償性増加を潜在的に誘導する可能性のある骨粗鬆症の新しい強力な抗吸収治療です。さまざまなカルシウムとビタミンD（CA/D）補給のレジメンを使用したデノスマブの投与後のPTH 1および6か月後のPTHの変化を評価することを目指しました。 DESIGN: Prospective, multicenter, study in a relatively small, heterogeneous sample of postmenopausal women followed for 6 months. PATIENTS: Forty seven postmenopausal women followed in 2 outpatient clinics, requiring onset or continuation of osteoporosis treatment.1 gの炭酸カルシウムと800 iuコレカルシフェロールを毎日6か月間投与し（グループA）、最初の月の二重用量を、それに続いて次の5か月間1 g/800 Iu CA/Dレジメン（グループB）を投与しました。 MEASUREMENTS: Parathyroid hormone (PTH) alterations between and within groups, and their associations with serum Ca and bone markers. RESULTS: Parathyroid hormone (PTH) levels were significantly higher at month 1 and 6 only in Group A;Ca levels were significantly decreased at month 1 and returned to baseline values at month 6 within the same Group.PTH [Δ（PTH1-0）]の1か月目とベースラインの平均パーセントの変化は、グループAでBよりも有意に高かった（63・5％±28・2％対-3・0％±4・7％、P = 0・029）。Δ（PTH1-0）は、Ca（rs = -0・610; p = 0・002）およびコラーゲン型I C末端テロペプチド（rs = -0・697; p = 0・003）のca（rs = -0・610; p = 0・002）の相互Δ変化と相関していました。 CONCLUSIONS: An increase in PTH should be expected, at least following the first administration of denosumab in common clinical practice.The effect of this compensatory onsequence in bone metabolism warrants further investigation.

OBJECTIVE: Denosumab is a new potent antiresorptive treatment of osteoporosis that can potentially induce a compensatory increase in parathyroid hormone (PTH) levels. We aimed to evaluate the alteration of PTH 1 and 6 months after denosumab's administration with different regimens of calcium and vitamin D (Ca/D) supplementation. DESIGN: Prospective, multicenter, study in a relatively small, heterogeneous sample of postmenopausal women followed for 6 months. PATIENTS: Forty seven postmenopausal women followed in 2 outpatient clinics, requiring onset or continuation of osteoporosis treatment. We administered 1 g calcium carbonate and 800 IU cholecalciferol daily for 6 months (Group A) or the double dose for the first month followed by the 1 g/800 IU Ca/D regimen for the next 5 months (Group B). MEASUREMENTS: Parathyroid hormone (PTH) alterations between and within groups, and their associations with serum Ca and bone markers. RESULTS: Parathyroid hormone (PTH) levels were significantly higher at month 1 and 6 only in Group A; Ca levels were significantly decreased at month 1 and returned to baseline values at month 6 within the same Group. The mean per cent change between month 1 and baseline for PTH [Δ(PTH1-0 )] was significantly higher in Group A than B (63·5% ± 28·2% vs -3·0% ± 4·7%, P = 0·029). Δ(PTH1-0 ) was correlated with the reciprocal Δ-changes of Ca (rs  = -0·610; P = 0·002) and collagen type I C-terminal telopeptide (rs  = -0·697; P = 0·003) only in Group A. CONCLUSIONS: An increase in PTH should be expected, at least following the first administration of denosumab in common clinical practice. The effect of this compensatory onsequence in bone metabolism warrants further investigation.