Bone status in adults with early-onset juvenile idiopathic arthritis following 1-year anti-TNFα therapy and discontinuation of glucocorticoids
Language English Country Germany Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Adalimumab MeSH
- Antirheumatic Agents pharmacology therapeutic use MeSH
- Biomarkers blood MeSH
- C-Reactive Protein metabolism MeSH
- Adult MeSH
- Etanercept MeSH
- Antibodies, Monoclonal, Humanized pharmacology therapeutic use MeSH
- Immunoglobulin G pharmacology therapeutic use MeSH
- Infliximab MeSH
- Arthritis, Juvenile blood diagnostic imaging drug therapy MeSH
- Collagen Type I blood MeSH
- Bone and Bones diagnostic imaging drug effects MeSH
- Bone Density drug effects MeSH
- Humans MeSH
- Adolescent MeSH
- Antibodies, Monoclonal pharmacology therapeutic use MeSH
- Osteocalcin blood MeSH
- Procollagen blood MeSH
- Radiography MeSH
- Receptors, Tumor Necrosis Factor therapeutic use MeSH
- Bone Remodeling drug effects MeSH
- Tumor Necrosis Factor-alpha antagonists & inhibitors MeSH
- Treatment Outcome MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Adolescent MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Adalimumab MeSH
- Antirheumatic Agents MeSH
- Biomarkers MeSH
- C-Reactive Protein MeSH
- Etanercept MeSH
- Antibodies, Monoclonal, Humanized MeSH
- Immunoglobulin G MeSH
- Infliximab MeSH
- Collagen Type I MeSH
- Antibodies, Monoclonal MeSH
- Osteocalcin MeSH
- Procollagen MeSH
- Receptors, Tumor Necrosis Factor MeSH
- Tumor Necrosis Factor-alpha MeSH
Juvenile idiopathic arthritis (JIA) is an inflammatory disease associated with bone loss and low bone mineral density (BMD). The treatment involves disease-modifying antirheumatic drugs, glucocorticoids (GCs) and biological agents. The aim of this study was to evaluate effects of 12-month therapy with the anti-tumor necrosis factor alpha (anti-TNFα) preparations on bone mineral density (BMD) and biochemical turnover markers (BTM) in adult patients with JIA who were previously either treated or not treated with glucocorticoids (GC) and to assess effects of the discontinuation of GCs on their bone status. Nineteen adult patients (12 women, 7 men) aged 18-33 years with active JIA were prospectively enrolled to receive the anti-TNFα therapy (infliximab, etanercept or adalimumab). BMD and BTMs were determined at baseline and 1-year follow-up. The anti-TNFα therapy resulted in a significant reduction in disease activity score 28 (DAS28) and C-reactive protein (CRP) and a significant increase in BMD at the lumbar spine and total body and in serum N-terminal propeptide of type I procollagen (PINP, marker of bone formation). No significant changes in serum beta C-terminal telopeptide of type I collagen (βCTX, marker of osteoclastic bone resorption) and osteocalcin (marker of bone remodeling) were found. A significant negative correlation was observed between the change in the DAS28, CRP and serum PINP. The change in serum PINP concentrations positively correlated with the change in lumbar spine BMD. A significant increase in serum PINP was observed only in patients discontinuing GCs during the anti-TNFα treatment. After the initiation of the anti-TNFα therapy in young adults with JIA, the increase in new bone formation can be explained by discontinuation of GCs administration as the patients with the largest reduction in DAS28 and CRP probably are the ones most likely to stop GC.
See more in PubMed
J Clin Densitom. 2008 Jan-Mar;11(1):75-91 PubMed
Arthritis Rheum. 1999 Apr;42(4):790-8 PubMed
Arthritis Rheum. 2003 Apr;48(4):1093-101 PubMed
Mol Endocrinol. 2009 Oct;23(10):1525-31 PubMed
Rheumatology (Oxford). 2003 May;42 Suppl 2:ii11-6 PubMed
Ann Rheum Dis. 2006 Aug;65(8):1044-9 PubMed
J Osteoporos. 2011 Feb 20;2011:569417 PubMed
N Engl J Med. 2000 Mar 16;342(11):763-9 PubMed
Gene. 2003 Dec 4;321:1-15 PubMed
J Bone Miner Res. 2011 Aug;26(8):1729-39 PubMed
J Rheumatol. 2002 Jun;29(6):1296-300 PubMed
Semin Arthritis Rheum. 2009 Oct;39(2):116-22 PubMed
Ann Rheum Dis. 2006 Aug;65(8):1074-9 PubMed
Cytokine Growth Factor Rev. 2004 Feb;15(1):49-60 PubMed
Adv Exp Med Biol. 2003;544:181-96 PubMed
Ann Rheum Dis. 2003 Mar;62(3):245-7 PubMed
Ann Rheum Dis. 2006 Nov;65(11):1495-9 PubMed
J Bone Miner Res. 2007 May;22(5):646-55 PubMed
Arthritis Rheum. 2000 Mar;43(3):531-40 PubMed
Arthritis Rheum. 1996 May;39(5):746-57 PubMed
Med Sci Monit. 2007 Jul;13(7):PI13-8 PubMed
Clin Gastroenterol Hepatol. 2008 Dec;6(12):1378-84 PubMed
J Rheumatol. 2007 Dec;34(12):2481-5 PubMed
Arthritis Rheum. 2006 Jun;54(6):1987-94 PubMed
Ann Intern Med. 1999 Mar 16;130(6):478-86 PubMed
Arthritis Rheum. 2003 Jan;48(1):218-26 PubMed
Arthritis Rheum. 2002 Mar;46(3):785-92 PubMed
Rheumatology (Oxford). 2005 Jun;44(6):777-80 PubMed
Arthritis Rheum. 2003 Aug;48(8):2214-23 PubMed
Bone. 2008 Apr;42(4):606-15 PubMed
J Pediatr Gastroenterol Nutr. 2011 Jan;52(1):31-7 PubMed
Rheumatology (Oxford). 2004 Jun;43 Suppl 3:iii10-iii16 PubMed
J Clin Invest. 1998 Jul 15;102(2):274-82 PubMed
J Rheumatol. 1993 Jul;20(7):1189-95 PubMed
Med Care. 1992 Jun;30(6):473-83 PubMed
J Clin Endocrinol Metab. 2006 Mar;91(3):870-7 PubMed
Lancet. 1994 Jul 2;344(8914):23-7 PubMed
Osteoporos Int. 2010 Apr;21(4):637-45 PubMed
Rev Endocr Metab Disord. 2008 Jun;9(2):107-22 PubMed
Rheumatology (Oxford). 2010 Aug;49(8):1550-8 PubMed
Lancet. 1994 Oct 22;344(8930):1105-10 PubMed
Osteoporos Int. 2000;11 Suppl 6:S2-17 PubMed
J Clin Invest. 2005 Feb;115(2):282-90 PubMed
Nat Med. 2007 Feb;13(2):156-63 PubMed
