Histomorphometric changes by teriparatide in alendronate-pretreated women with osteoporosis
Jazyk angličtina Země Velká Británie, Anglie Médium print-electronic
Typ dokumentu klinické zkoušky kontrolované, časopisecké články, multicentrická studie, práce podpořená grantem
- MeSH
- alendronát terapeutické užití MeSH
- bederní obratle patofyziologie MeSH
- biologické markery krev MeSH
- biopsie MeSH
- dospělí MeSH
- inhibitory kostní resorpce terapeutické užití MeSH
- kostní denzita účinky léků MeSH
- krček femuru patofyziologie MeSH
- lidé středního věku MeSH
- lidé MeSH
- náhrada léků MeSH
- osteogeneze účinky léků MeSH
- postmenopauzální osteoporóza farmakoterapie patologie patofyziologie MeSH
- remodelace kosti účinky léků MeSH
- senioři MeSH
- teriparatid terapeutické užití MeSH
- výsledek terapie MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- klinické zkoušky kontrolované MeSH
- multicentrická studie MeSH
- práce podpořená grantem MeSH
- Názvy látek
- alendronát MeSH
- biologické markery MeSH
- inhibitory kostní resorpce MeSH
- teriparatid MeSH
SUMMARY: The level of increased bone formation after 24 months of treatment with teriparatide (rhPTH (1-34), TPTD) is similar in patients who were either treatment-naïve (TN) or had lower bone turnover initially due to previous alendronate (ALN) therapy. INTRODUCTION: Bone anabolic effects of TPTD in postmenopausal women with osteoporosis may be blunted during the initial phase after switching from ALN to TPTD. To explore the long-term implications, we examined histomorphometric and biochemical markers of bone turnover of patients on TPTD therapy after long-term ALN treatment. METHODS: Paired biopsies were obtained after tetracycline double labeling at baseline and after 24 months of TPTD treatment from 29 ALN-pretreated (64.5 ± 16.4 months) and 16 TN patients. Biochemical markers were measured at baseline, during the treatment, or at study end. RESULTS: Compared with the baseline, after 24-month TPTD, activation frequency (Ac.F.) and osteoid surface (OS) increased in both groups: 0.11-0.34 cycles per year, 3.96-9.8% in the ALN-pretreated group and 0.19-0.33 cycles per year, 6.2-11.3% (p < 0.05) in the TN group, respectively. Biochemical and histomorphometric markers correlated positively both at baseline and endpoint. Serum amino terminal propeptide of type I procollagen (PINP) correlated with Ac.F. (r = 0.57, p < 0.001 and r = 0.48, p < 0.01) and OS (r = 0.51, p < 0.01 and r = 0.56, p < 0.01) at baseline and endpoint, respectively. Following 3 months of treatment, increases in biochemical markers like PINP predicted the increase in Ac.F. (r = 0.52, p < 0.01) and OS (r = 0.54, p < 0.01) after 24 months. CONCLUSIONS: The increased level of formation is similar in patients who were either TN or had lower bone turnover initially due to previous ALN therapy. Elevated bone formation in postmenopausal women with osteoporosis was sustained over a 24-month period by TPTD. Biochemical markers of bone formation are a good surrogate for the assessment of TPTD effects.
Zobrazit více v PubMed
Osteoporos Int. 2004 Mar;15(3):231-7 PubMed
J Bone Miner Res. 2005 Jun;20(6):962-70 PubMed
N Engl J Med. 2004 Mar 18;350(12):1189-99 PubMed
J Clin Endocrinol Metab. 2005 Jul;90(7):3970-7 PubMed
J Bone Miner Res. 1997 Oct;12(10):1700-7 PubMed
Mol Pharmacol. 2006 May;69(5):1624-32 PubMed
Bone. 2007 Sep;41(3):308-17 PubMed
J Bone Miner Res. 2005 Jul;20(7):1244-53 PubMed
Curr Med Res Opin. 2006 Jan;22(1):61-6 PubMed
J Bone Miner Res. 2004 Aug;19(8):1259-69 PubMed
J Bone Miner Res. 2007 Apr;22(4):495-502 PubMed
N Engl J Med. 2001 May 10;344(19):1434-41 PubMed
N Engl J Med. 2007 Aug 30;357(9):905-16 PubMed
J Clin Invest. 1997 Sep 15;100(6):1475-80 PubMed
J Bone Miner Res. 2008 Jan;23(1):6-16 PubMed
Bone. 2006 May;38(5):617-27 PubMed
N Engl J Med. 2007 Nov 15;357(20):2028-39 PubMed
J Clin Densitom. 2000 Fall;3(3):281-90 PubMed
Bone. 2007 Jun;40(6):1447-52 PubMed
J Bone Miner Res. 2003 Jan;18(1):9-17 PubMed
Endocr Rev. 2005 Aug;26(5):688-703 PubMed
J Bone Miner Res. 1991 Jun;6(6):639-44 PubMed
Bone. 1995 Aug;17(2):153-6 PubMed
J Clin Endocrinol Metab. 2008 Oct;93(10):3785-93 PubMed
J Bone Miner Res. 2009 Dec;24(12):1998-2006 PubMed
J Clin Endocrinol Metab. 1988 Oct;67(4):741-8 PubMed
J Bone Miner Res. 1987 Dec;2(6):595-610 PubMed
J Bone Miner Res. 2003 Nov;18(11):1932-41 PubMed
J Bone Miner Res. 2006 Mar;21(3):366-73 PubMed
J Clin Endocrinol Metab. 2006 Mar;91(3):870-7 PubMed
J Bone Miner Res. 2004 May;19(5):745-51 PubMed
Curr Osteoporos Rep. 2006 Mar;4(1):5-13 PubMed
Osteoporos Int. 2008 Jan;19(1):87-94 PubMed
Bone. 2002 Nov;31(5):620-5 PubMed
HSS J. 2007 Sep;3(2):169-72 PubMed
J Clin Invest. 1983 May;71(5):1316-21 PubMed
J Clin Endocrinol Metab. 2008 Mar;93(3):852-60 PubMed
J Bone Miner Res. 2008 Oct;23(10):1591-600 PubMed
Lancet. 1984 May 19;1(8386):1091-3 PubMed
J Bone Miner Res. 1987 Oct;2(5):427-36 PubMed
Nephrol Dial Transplant. 1995;10(1):52-8 PubMed
Calcif Tissue Int. 2008 Mar;82(3):191-201 PubMed
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