Ankylosing spondylitis medical therapy: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Ankylosing spondylitis}} | {{Ankylosing spondylitis}} | ||
{{CMG}} | {{CMG}}; {{AE}} {{VKG}} | ||
==Overview== | ==Overview== | ||
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** Assessment of SpondyloArthritis international Society (ASAS) | ** Assessment of SpondyloArthritis international Society (ASAS) | ||
** European League Against Rheumatism (EULAR) | ** European League Against Rheumatism (EULAR) | ||
** American College of | ** [[American College of Rheumatology]] (ACR)/[[Spondylitis Association of America]] (SAA)/Spondyloarthritis Research and Treatment Network (SPARTAN) collaboration | ||
* Pharmacologic medical therapies for ankylosing spondylitis(AS) include Nonsteroidal anti-inflammatory drugs (NSAIDs), tumor necrosis factor (TNF) blocker, analgesics, | * Pharmacologic medical therapies for [[ankylosing spondylitis]](AS) include Nonsteroidal anti-inflammatory drugs ([[NSAIDs]]), tumor necrosis factor ([[Tumor necrosis factors|TNF]]) blocker, [[Analgesic|analgesics]], [[sulfasalazine]],[[intraarticular]] injections and [[interleukin]] 17 (IL-17) inhibitors. | ||
===== Nonsteroidal antiinflammatory drugs(NSAIDs)'''<ref name="pmid16582683">{{cite journal |vauthors=Ardoin SP, Sundy JS |title=Update on nonsteriodal anti-inflammatory drugs |journal=Curr Opin Rheumatol |volume=18 |issue=3 |pages=221–6 |date=May 2006 |pmid=16582683 |doi=10.1097/01.bor.0000218940.04613.cc |url=}}</ref>'''<ref name="pmid16126792">{{cite journal |vauthors=Zochling J, van der Heijde D, Dougados M, Braun J |title=Current evidence for the management of ankylosing spondylitis: a systematic literature review for the ASAS/EULAR management recommendations in ankylosing spondylitis |journal=Ann. Rheum. Dis. |volume=65 |issue=4 |pages=423–32 |date=April 2006 |pmid=16126792 |pmc=1798100 |doi=10.1136/ard.2005.041129 |url=}}</ref><ref name="pmid22513148">{{cite journal |vauthors=van den Berg R, Baraliakos X, Braun J, van der Heijde D |title=First update of the current evidence for the management of ankylosing spondylitis with non-pharmacological treatment and non-biologic drugs: a systematic literature review for the ASAS/EULAR management recommendations in ankylosing spondylitis |journal=Rheumatology (Oxford) |volume=51 |issue=8 |pages=1388–96 |date=August 2012 |pmid=22513148 |doi=10.1093/rheumatology/kes066 |url=}}</ref><ref name="pmid2182853">{{cite journal |vauthors=Lequesne M |title=Methodology issues in the evaluation of NSAID in inflammatory rheumatic diseases |journal=J Rheumatol Suppl |volume=20 |issue= |pages=25–8 |date=February 1990 |pmid=2182853 |doi= |url=}}</ref><ref name="pmid26186173">{{cite journal |vauthors=Kroon FP, van der Burg LR, Ramiro S, Landewé RB, Buchbinder R, Falzon L, van der Heijde D |title=Non-steroidal anti-inflammatory drugs (NSAIDs) for axial spondyloarthritis (ankylosing spondylitis and non-radiographic axial spondyloarthritis) |journal=Cochrane Database Syst Rev |volume= |issue=7 |pages=CD010952 |date=July 2015 |pmid=26186173 |doi=10.1002/14651858.CD010952.pub2 |url=}}</ref><ref name="pmid15934081">{{cite journal |vauthors=Wanders A, Heijde Dv, Landewé R, Béhier JM, Calin A, Olivieri I, Zeidler H, Dougados M |title=Nonsteroidal antiinflammatory drugs reduce radiographic progression in patients with ankylosing spondylitis: a randomized clinical trial |journal=Arthritis Rheum. |volume=52 |issue=6 |pages=1756–65 |date=June 2005 |pmid=15934081 |doi=10.1002/art.21054 |url=}}</ref> ===== | ===== Nonsteroidal antiinflammatory drugs(NSAIDs)'''<ref name="pmid16582683">{{cite journal |vauthors=Ardoin SP, Sundy JS |title=Update on nonsteriodal anti-inflammatory drugs |journal=Curr Opin Rheumatol |volume=18 |issue=3 |pages=221–6 |date=May 2006 |pmid=16582683 |doi=10.1097/01.bor.0000218940.04613.cc |url=}}</ref>'''<ref name="pmid16126792">{{cite journal |vauthors=Zochling J, van der Heijde D, Dougados M, Braun J |title=Current evidence for the management of ankylosing spondylitis: a systematic literature review for the ASAS/EULAR management recommendations in ankylosing spondylitis |journal=Ann. Rheum. Dis. |volume=65 |issue=4 |pages=423–32 |date=April 2006 |pmid=16126792 |pmc=1798100 |doi=10.1136/ard.2005.041129 |url=}}</ref><ref name="pmid22513148">{{cite journal |vauthors=van den Berg R, Baraliakos X, Braun J, van der Heijde D |title=First update of the current evidence for the management of ankylosing spondylitis with non-pharmacological treatment and non-biologic drugs: a systematic literature review for the ASAS/EULAR management recommendations in ankylosing spondylitis |journal=Rheumatology (Oxford) |volume=51 |issue=8 |pages=1388–96 |date=August 2012 |pmid=22513148 |doi=10.1093/rheumatology/kes066 |url=}}</ref><ref name="pmid2182853">{{cite journal |vauthors=Lequesne M |title=Methodology issues in the evaluation of NSAID in inflammatory rheumatic diseases |journal=J Rheumatol Suppl |volume=20 |issue= |pages=25–8 |date=February 1990 |pmid=2182853 |doi= |url=}}</ref><ref name="pmid26186173">{{cite journal |vauthors=Kroon FP, van der Burg LR, Ramiro S, Landewé RB, Buchbinder R, Falzon L, van der Heijde D |title=Non-steroidal anti-inflammatory drugs (NSAIDs) for axial spondyloarthritis (ankylosing spondylitis and non-radiographic axial spondyloarthritis) |journal=Cochrane Database Syst Rev |volume= |issue=7 |pages=CD010952 |date=July 2015 |pmid=26186173 |doi=10.1002/14651858.CD010952.pub2 |url=}}</ref><ref name="pmid15934081">{{cite journal |vauthors=Wanders A, Heijde Dv, Landewé R, Béhier JM, Calin A, Olivieri I, Zeidler H, Dougados M |title=Nonsteroidal antiinflammatory drugs reduce radiographic progression in patients with ankylosing spondylitis: a randomized clinical trial |journal=Arthritis Rheum. |volume=52 |issue=6 |pages=1756–65 |date=June 2005 |pmid=15934081 |doi=10.1002/art.21054 |url=}}</ref> ===== | ||
* The first line treatment for all the patients who are having symptomatic ankylosing spondylitis (AS) are with Nonsteroidal antiinflammatory drugs(NSAIDs). | * The first line treatment for all the patients who are having symptomatic [[ankylosing spondylitis]] (AS) are with [[Non-steroidal anti-inflammatory drug|Nonsteroidal antiinflammatory drugs]](NSAIDs). | ||
* 70 to 80 percent patients who are taking NSAIDs report substantial relief of back pain and stiffness. | * 70 to 80 percent patients who are taking [[Non-steroidal anti-inflammatory drug|NSAIDs]] report substantial relief of back pain and [[stiffness]]. | ||
* Play a crucial role in delaying the progression of ankylosing spondylitis. | * Play a crucial role in delaying the progression of [[ankylosing spondylitis]]. | ||
* Regardless of which NSAID used, the maximum dose is usually required to manage AS. | * Regardless of which [[Non-steroidal anti-inflammatory drug|NSAID]] used, the maximum [[dose]] is usually required to manage AS. | ||
* Treating with NSAIDs in AS especially in patients with increased erythrocyte sedimentation rate (ESR) shows especially effective in decreasing the ESR.<ref name="pmid22532639">{{cite journal |vauthors=Kroon F, Landewé R, Dougados M, van der Heijde D |title=Continuous NSAID use reverts the effects of inflammation on radiographic progression in patients with ankylosing spondylitis |journal=Ann. Rheum. Dis. |volume=71 |issue=10 |pages=1623–9 |date=October 2012 |pmid=22532639 |doi=10.1136/annrheumdis-2012-201370 |url=}}</ref> | * Treating with [[Non-steroidal anti-inflammatory drug|NSAIDs]] in AS especially in patients with increased erythrocyte sedimentation rate ([[Erythrocyte sedimentation rate|ESR]]) shows especially effective in decreasing the [[Erythrocyte sedimentation rate|ESR]].<ref name="pmid22532639">{{cite journal |vauthors=Kroon F, Landewé R, Dougados M, van der Heijde D |title=Continuous NSAID use reverts the effects of inflammation on radiographic progression in patients with ankylosing spondylitis |journal=Ann. Rheum. Dis. |volume=71 |issue=10 |pages=1623–9 |date=October 2012 |pmid=22532639 |doi=10.1136/annrheumdis-2012-201370 |url=}}</ref> | ||
'''Adult''' | '''Adult''' | ||
* Preferred regimen (1): | * Preferred regimen (1): [[Indomethacin]]: Initial: 75 mg once daily, may increase to 75 mg twice daily (maximum dose: 150 mg/day) for at least 4 weeks.<ref name="pmid1974927">{{cite journal |vauthors=Calin A, Elswood J |title=A prospective nationwide cross-sectional study of NSAID usage in 1331 patients with ankylosing spondylitis |journal=J. Rheumatol. |volume=17 |issue=6 |pages=801–3 |date=June 1990 |pmid=1974927 |doi= |url=}}</ref> | ||
* Preferred regimen (2): | * Preferred regimen (2): [[Celecoxib]] or [[Etoricoxib]]: Oral: 200 mg once daily or 100 mg twice daily.<ref name="pmid15818702">{{cite journal |vauthors=van der Heijde D, Baraf HS, Ramos-Remus C, Calin A, Weaver AL, Schiff M, James M, Markind JE, Reicin AS, Melian A, Dougados M |title=Evaluation of the efficacy of etoricoxib in ankylosing spondylitis: results of a fifty-two-week, randomized, controlled study |journal=Arthritis Rheum. |volume=52 |issue=4 |pages=1205–15 |date=April 2005 |pmid=15818702 |doi=10.1002/art.20985 |url=}}</ref><ref name="pmid16960941">{{cite journal |vauthors=Barkhuizen A, Steinfeld S, Robbins J, West C, Coombs J, Zwillich S |title=Celecoxib is efficacious and well tolerated in treating signs and symptoms of ankylosing spondylitis |journal=J. Rheumatol. |volume=33 |issue=9 |pages=1805–12 |date=September 2006 |pmid=16960941 |doi= |url=}}</ref><ref name="pmid11212158">{{cite journal |vauthors=Dougados M, Béhier JM, Jolchine I, Calin A, van der Heijde D, Olivieri I, Zeidler H, Herman H |title=Efficacy of celecoxib, a cyclooxygenase 2-specific inhibitor, in the treatment of ankylosing spondylitis: a six-week controlled study with comparison against placebo and against a conventional nonsteroidal antiinflammatory drug |journal=Arthritis Rheum. |volume=44 |issue=1 |pages=180–5 |date=January 2001 |pmid=11212158 |doi=10.1002/1529-0131(200101)44:1<180::AID-ANR24>3.0.CO;2-K |url=}}</ref><ref name="pmid12180720">{{cite journal |vauthors=Matsumoto AK, Melian A, Mandel DR, McIlwain HH, Borenstein D, Zhao PL, Lines CR, Gertz BJ, Curtis S |title=A randomized, controlled, clinical trial of etoricoxib in the treatment of rheumatoid arthritis |journal=J. Rheumatol. |volume=29 |issue=8 |pages=1623–30 |date=August 2002 |pmid=12180720 |doi= |url=}}</ref><ref name="pmid23126318">{{cite journal |vauthors=Lories RJ |title=Etoricoxib and the treatment of ankylosing spondylitis |journal=Expert Opin Drug Metab Toxicol |volume=8 |issue=12 |pages=1599–608 |date=December 2012 |pmid=23126318 |doi=10.1517/17425255.2012.741120 |url=}}</ref><ref name="pmid17616556">{{cite journal |vauthors=Sieper J, Klopsch T, Richter M, Kapelle A, Rudwaleit M, Schwank S, Regourd E, May M |title=Comparison of two different dosages of celecoxib with diclofenac for the treatment of active ankylosing spondylitis: results of a 12-week randomised, double-blind, controlled study |journal=Ann. Rheum. Dis. |volume=67 |issue=3 |pages=323–9 |date=March 2008 |pmid=17616556 |doi=10.1136/ard.2007.075309 |url=}}</ref> | ||
==== Tumor necrosis factor alpha antagonists(TNF-alpha)<ref name="pmid19232062">{{cite journal |vauthors=Sieper J |title=Developments in the scientific and clinical understanding of the spondyloarthritides |journal=Arthritis Res. Ther. |volume=11 |issue=1 |pages=208 |date=2009 |pmid=19232062 |pmc=2688219 |doi=10.1186/ar2562 |url=}}</ref><ref name="pmid18163509">{{cite journal |vauthors=Breban M, Ravaud P, Claudepierre P, Baron G, Henry YD, Hudry C, Euller-Ziegler L, Pham T, Solau-Gervais E, Chary-Valckenaere I, Marcelli C, Perdriger A, Le Loët X, Wendling D, Fautrel B, Fournié B, Combe B, Gaudin P, Jousse S, Mariette X, Baleydier A, Trape G, Dougados M |title=Maintenance of infliximab treatment in ankylosing spondylitis: results of a one-year randomized controlled trial comparing systematic versus on-demand treatment |journal=Arthritis Rheum. |volume=58 |issue=1 |pages=88–97 |date=January 2008 |pmid=18163509 |doi=10.1002/art.23167 |url=}}</ref><ref name="pmid24832835">{{cite journal |vauthors=Baji P, Péntek M, Szántó S, Géher P, Gulácsi L, Balogh O, Brodszky V |title=Comparative efficacy and safety of biosimilar infliximab and other biological treatments in ankylosing spondylitis: systematic literature review and meta-analysis |journal=Eur J Health Econ |volume=15 Suppl 1 |issue= |pages=S45–52 |date=May 2014 |pmid=24832835 |pmc=4046080 |doi=10.1007/s10198-014-0593-5 |url=}}</ref><ref name="pmid25887212">{{cite journal |vauthors=Maxwell LJ, Zochling J, Boonen A, Singh JA, Veras MM, Tanjong Ghogomu E, Benkhalti Jandu M, Tugwell P, Wells GA |title=TNF-alpha inhibitors for ankylosing spondylitis |journal=Cochrane Database Syst Rev |volume= |issue=4 |pages=CD005468 |date=April 2015 |pmid=25887212 |doi=10.1002/14651858.CD005468.pub2 |url=}}</ref><ref name="pmid26847392">{{cite journal |vauthors=Corbett M, Soares M, Jhuti G, Rice S, Spackman E, Sideris E, Moe-Byrne T, Fox D, Marzo-Ortega H, Kay L, Woolacott N, Palmer S |title=Tumour necrosis factor-α inhibitors for ankylosing spondylitis and non-radiographic axial spondyloarthritis: a systematic review and economic evaluation |journal=Health Technol Assess |volume=20 |issue=9 |pages=1–334, v–vi |date=February 2016 |pmid=26847392 |pmc=4781282 |doi=10.3310/hta20090 |url=}}</ref> ==== | ==== Tumor necrosis factor alpha antagonists(TNF-alpha)<ref name="pmid19232062">{{cite journal |vauthors=Sieper J |title=Developments in the scientific and clinical understanding of the spondyloarthritides |journal=Arthritis Res. Ther. |volume=11 |issue=1 |pages=208 |date=2009 |pmid=19232062 |pmc=2688219 |doi=10.1186/ar2562 |url=}}</ref><ref name="pmid18163509">{{cite journal |vauthors=Breban M, Ravaud P, Claudepierre P, Baron G, Henry YD, Hudry C, Euller-Ziegler L, Pham T, Solau-Gervais E, Chary-Valckenaere I, Marcelli C, Perdriger A, Le Loët X, Wendling D, Fautrel B, Fournié B, Combe B, Gaudin P, Jousse S, Mariette X, Baleydier A, Trape G, Dougados M |title=Maintenance of infliximab treatment in ankylosing spondylitis: results of a one-year randomized controlled trial comparing systematic versus on-demand treatment |journal=Arthritis Rheum. |volume=58 |issue=1 |pages=88–97 |date=January 2008 |pmid=18163509 |doi=10.1002/art.23167 |url=}}</ref><ref name="pmid24832835">{{cite journal |vauthors=Baji P, Péntek M, Szántó S, Géher P, Gulácsi L, Balogh O, Brodszky V |title=Comparative efficacy and safety of biosimilar infliximab and other biological treatments in ankylosing spondylitis: systematic literature review and meta-analysis |journal=Eur J Health Econ |volume=15 Suppl 1 |issue= |pages=S45–52 |date=May 2014 |pmid=24832835 |pmc=4046080 |doi=10.1007/s10198-014-0593-5 |url=}}</ref><ref name="pmid25887212">{{cite journal |vauthors=Maxwell LJ, Zochling J, Boonen A, Singh JA, Veras MM, Tanjong Ghogomu E, Benkhalti Jandu M, Tugwell P, Wells GA |title=TNF-alpha inhibitors for ankylosing spondylitis |journal=Cochrane Database Syst Rev |volume= |issue=4 |pages=CD005468 |date=April 2015 |pmid=25887212 |doi=10.1002/14651858.CD005468.pub2 |url=}}</ref><ref name="pmid26847392">{{cite journal |vauthors=Corbett M, Soares M, Jhuti G, Rice S, Spackman E, Sideris E, Moe-Byrne T, Fox D, Marzo-Ortega H, Kay L, Woolacott N, Palmer S |title=Tumour necrosis factor-α inhibitors for ankylosing spondylitis and non-radiographic axial spondyloarthritis: a systematic review and economic evaluation |journal=Health Technol Assess |volume=20 |issue=9 |pages=1–334, v–vi |date=February 2016 |pmid=26847392 |pmc=4781282 |doi=10.3310/hta20090 |url=}}</ref> ==== | ||
* | * [[Infliximab]], [[etanercept]], [[adalimumab]], [[certolizumab]], and [[golimumab]] are the available [[tumor necrosis factor alpha]] inhibitors(TNF-alpha) to treat AS. | ||
* In AS there is no much of a use in adding immunomodulatory drug, such | * In AS there is no much of a use in adding [[Immunomodulator|immunomodulatory]] drug, such as [[methotrexate]] (MTX) as the evidence shows no additional benefit but may increase the cost and the risk of adverse effects.<ref name="pmid18573802">{{cite journal |vauthors=Li EK, Griffith JF, Lee VW, Wang YX, Li TK, Lee KK, Tam LS |title=Short-term efficacy of combination methotrexate and infliximab in patients with ankylosing spondylitis: a clinical and magnetic resonance imaging correlation |journal=Rheumatology (Oxford) |volume=47 |issue=9 |pages=1358–63 |date=September 2008 |pmid=18573802 |doi=10.1093/rheumatology/ken207 |url=}}</ref><ref name="pmid15829577">{{cite journal |vauthors=Marzo-Ortega H, McGonagle D, Jarrett S, Haugeberg G, Hensor E, O'connor P, Tan AL, Conaghan PG, Greenstein A, Emery P |title=Infliximab in combination with methotrexate in active ankylosing spondylitis: a clinical and imaging study |journal=Ann. Rheum. Dis. |volume=64 |issue=11 |pages=1568–75 |date=November 2005 |pmid=15829577 |pmc=1755262 |doi=10.1136/ard.2004.022582 |url=}}</ref> | ||
* Treating patients in AS with tumor necrosis factor alpha inhibitors(TNF-alpha) shows significant improvements in disease progress and function such as at least 40 percent improvement from baseline were seen.<ref name="pmid247189592">{{cite journal |vauthors=Callhoff J, Sieper J, Weiß A, Zink A, Listing J |title=Efficacy of TNFα blockers in patients with ankylosing spondylitis and non-radiographic axial spondyloarthritis: a meta-analysis |journal=Ann. Rheum. Dis. |volume=74 |issue=6 |pages=1241–8 |date=June 2015 |pmid=24718959 |doi=10.1136/annrheumdis-2014-205322 |url=}}</ref> | * Treating patients in AS with [[tumor necrosis factor alpha]] inhibitors(TNF-alpha) shows significant improvements in disease progress and function such as at least 40 percent improvement from baseline were seen.<ref name="pmid247189592">{{cite journal |vauthors=Callhoff J, Sieper J, Weiß A, Zink A, Listing J |title=Efficacy of TNFα blockers in patients with ankylosing spondylitis and non-radiographic axial spondyloarthritis: a meta-analysis |journal=Ann. Rheum. Dis. |volume=74 |issue=6 |pages=1241–8 |date=June 2015 |pmid=24718959 |doi=10.1136/annrheumdis-2014-205322 |url=}}</ref> | ||
* Adalimumab, | * [[Adalimumab]], [[etanercept]], and [[infliximab]] have the same efficacy and potency in treating the AS patients.<ref name="pmid17651658">{{cite journal |vauthors=McLeod C, Bagust A, Boland A, Dagenais P, Dickson R, Dundar Y, Hill RA, Jones A, Mujica Mota R, Walley T |title=Adalimumab, etanercept and infliximab for the treatment of ankylosing spondylitis: a systematic review and economic evaluation |journal=Health Technol Assess |volume=11 |issue=28 |pages=1–158, iii–iv |date=August 2007 |pmid=17651658 |doi= |url=}}</ref> | ||
* Patients who are getting treated with tumor necrosis factor alpha inhibitors shows approximately 80% good response and at least 50% improvement from the baseline of the disease.<ref name="pmid11508441">{{cite journal |vauthors=Anderson JJ, Baron G, van der Heijde D, Felson DT, Dougados M |title=Ankylosing spondylitis assessment group preliminary definition of short-term improvement in ankylosing spondylitis |journal=Arthritis Rheum. |volume=44 |issue=8 |pages=1876–86 |date=August 2001 |pmid=11508441 |doi=10.1002/1529-0131(200108)44:8<1876::AID-ART326>3.0.CO;2-F |url=}}</ref> | * Patients who are getting treated with tumor necrosis factor alpha inhibitors shows approximately 80% good response and at least 50% improvement from the baseline of the disease.<ref name="pmid11508441">{{cite journal |vauthors=Anderson JJ, Baron G, van der Heijde D, Felson DT, Dougados M |title=Ankylosing spondylitis assessment group preliminary definition of short-term improvement in ankylosing spondylitis |journal=Arthritis Rheum. |volume=44 |issue=8 |pages=1876–86 |date=August 2001 |pmid=11508441 |doi=10.1002/1529-0131(200108)44:8<1876::AID-ART326>3.0.CO;2-F |url=}}</ref> | ||
* Response to TNF antagonists: The following parameters are sighs of a good response to TNF antagonists<ref name="pmid15037444">{{cite journal |vauthors=Rudwaleit M, Listing J, Brandt J, Braun J, Sieper J |title=Prediction of a major clinical response (BASDAI 50) to tumour necrosis factor alpha blockers in ankylosing spondylitis |journal=Ann. Rheum. Dis. |volume=63 |issue=6 |pages=665–70 |date=June 2004 |pmid=15037444 |pmc=1755042 |doi=10.1136/ard.2003.016386 |url=}}</ref><ref name="pmid19273449">{{cite journal |vauthors=Rudwaleit M, Claudepierre P, Wordsworth P, Cortina EL, Sieper J, Kron M, Carcereri-De-Prati R, Kupper H, Kary S |title=Effectiveness, safety, and predictors of good clinical response in 1250 patients treated with adalimumab for active ankylosing spondylitis |journal=J. Rheumatol. |volume=36 |issue=4 |pages=801–8 |date=April 2009 |pmid=19273449 |doi=10.3899/jrheum.081048 |url=}}</ref> | * Response to [[Tumor necrosis factors|TNF]] antagonists: The following parameters are sighs of a good response to TNF antagonists<ref name="pmid15037444">{{cite journal |vauthors=Rudwaleit M, Listing J, Brandt J, Braun J, Sieper J |title=Prediction of a major clinical response (BASDAI 50) to tumour necrosis factor alpha blockers in ankylosing spondylitis |journal=Ann. Rheum. Dis. |volume=63 |issue=6 |pages=665–70 |date=June 2004 |pmid=15037444 |pmc=1755042 |doi=10.1136/ard.2003.016386 |url=}}</ref><ref name="pmid19273449">{{cite journal |vauthors=Rudwaleit M, Claudepierre P, Wordsworth P, Cortina EL, Sieper J, Kron M, Carcereri-De-Prati R, Kupper H, Kary S |title=Effectiveness, safety, and predictors of good clinical response in 1250 patients treated with adalimumab for active ankylosing spondylitis |journal=J. Rheumatol. |volume=36 |issue=4 |pages=801–8 |date=April 2009 |pmid=19273449 |doi=10.3899/jrheum.081048 |url=}}</ref> | ||
** Age, especially young patients. | ** Age, especially young patients. | ||
** Elevated C-reactive protein ('''CRP'''). | ** Elevated [[C-reactive protein]] ('''CRP'''). | ||
** The best predictor is, Shorter disease duration. | ** The best predictor is, Shorter disease duration. | ||
* Treating with TNF alpha inhibitors in patients with AS shows beneficial effect in improving bone density.<ref name="pmid18585759">{{cite journal |vauthors=Barnabe C, Hanley DA |title=Effect of tumor necrosis factor alpha inhibition on bone density and turnover markers in patients with rheumatoid arthritis and spondyloarthropathy |journal=Semin. Arthritis Rheum. |volume=39 |issue=2 |pages=116–22 |date=October 2009 |pmid=18585759 |doi=10.1016/j.semarthrit.2008.04.004 |url=}}</ref><ref name="pmid23950191">{{cite journal |vauthors=Durnez A, Paternotte S, Fechtenbaum J, Landewé RB, Dougados M, Roux C, Briot K |title=Increase in bone density in patients with spondyloarthritis during anti-tumor necrosis factor therapy: 6-year followup study |journal=J. Rheumatol. |volume=40 |issue=10 |pages=1712–8 |date=October 2013 |pmid=23950191 |doi=10.3899/jrheum.121417 |url=}}</ref><ref name="pmid17644538">{{cite journal |vauthors=Chopin F, Garnero P, le Henanff A, Debiais F, Daragon A, Roux C, Sany J, Wendling D, Zarnitsky C, Ravaud P, Thomas T |title=Long-term effects of infliximab on bone and cartilage turnover markers in patients with rheumatoid arthritis |journal=Ann. Rheum. Dis. |volume=67 |issue=3 |pages=353–7 |date=March 2008 |pmid=17644538 |doi=10.1136/ard.2007.076604 |url=}}</ref> | * Treating with [[Tumor necrosis factors|TNF]] alpha inhibitors in patients with AS shows beneficial effect in improving [[bone density]].<ref name="pmid18585759">{{cite journal |vauthors=Barnabe C, Hanley DA |title=Effect of tumor necrosis factor alpha inhibition on bone density and turnover markers in patients with rheumatoid arthritis and spondyloarthropathy |journal=Semin. Arthritis Rheum. |volume=39 |issue=2 |pages=116–22 |date=October 2009 |pmid=18585759 |doi=10.1016/j.semarthrit.2008.04.004 |url=}}</ref><ref name="pmid23950191">{{cite journal |vauthors=Durnez A, Paternotte S, Fechtenbaum J, Landewé RB, Dougados M, Roux C, Briot K |title=Increase in bone density in patients with spondyloarthritis during anti-tumor necrosis factor therapy: 6-year followup study |journal=J. Rheumatol. |volume=40 |issue=10 |pages=1712–8 |date=October 2013 |pmid=23950191 |doi=10.3899/jrheum.121417 |url=}}</ref><ref name="pmid17644538">{{cite journal |vauthors=Chopin F, Garnero P, le Henanff A, Debiais F, Daragon A, Roux C, Sany J, Wendling D, Zarnitsky C, Ravaud P, Thomas T |title=Long-term effects of infliximab on bone and cartilage turnover markers in patients with rheumatoid arthritis |journal=Ann. Rheum. Dis. |volume=67 |issue=3 |pages=353–7 |date=March 2008 |pmid=17644538 |doi=10.1136/ard.2007.076604 |url=}}</ref> | ||
===== Side Effects<ref name="pmid12922954">{{cite journal |vauthors=Baeten D, Kruithof E, Van den Bosch F, Van den Bossche N, Herssens A, Mielants H, De Keyser F, Veys EM |title=Systematic safety follow up in a cohort of 107 patients with spondyloarthropathy treated with infliximab: a new perspective on the role of host defence in the pathogenesis of the disease? |journal=Ann. Rheum. Dis. |volume=62 |issue=9 |pages=829–34 |date=September 2003 |pmid=12922954 |pmc=1754658 |doi= |url=}}</ref> ===== | ===== Side Effects<ref name="pmid12922954">{{cite journal |vauthors=Baeten D, Kruithof E, Van den Bosch F, Van den Bossche N, Herssens A, Mielants H, De Keyser F, Veys EM |title=Systematic safety follow up in a cohort of 107 patients with spondyloarthropathy treated with infliximab: a new perspective on the role of host defence in the pathogenesis of the disease? |journal=Ann. Rheum. Dis. |volume=62 |issue=9 |pages=829–34 |date=September 2003 |pmid=12922954 |pmc=1754658 |doi= |url=}}</ref> ===== | ||
* Using TNF-alpha inhibitors increases the risk of reactivation of latent tuberculosis and | * Using [[TNF-alpha]] inhibitors increases the risk of reactivation of [[latent tuberculosis]] and | ||
* Using TNF-alpha inhibitors increases the risk of exacerbation or development of demyelinating disease. | * Using [[TNF-alpha]] inhibitors increases the risk of exacerbation or development of [[demyelinating]] disease. | ||
'''Adult''' '''Dosage''' | '''Adult''' '''Dosage''' | ||
* Preferred regimen (1): | * Preferred regimen (1): [[Infliximab]] 5 mg/kg at 0, 2, and 6 weeks, followed by 5 mg/kg every 6 weeks thereafter. | ||
* Preferred regimen (2): | * Preferred regimen (2): [[Etanercept]] once-weekly dosing: 50 mg once weekly; maximum dose (rheumatoid arthritis): 50 mg/week. | ||
* Preferred regimen (3): | * Preferred regimen (3): [[Adalimumab]] IV: 2 mg/kg at weeks 0, 4, and then every 8 weeks thereafter. | ||
* Preferred regimen (4): | * Preferred regimen (4): [[Certolizumab]] Initial: 400 mg, repeat dose 2 and 4 weeks after initial dose; Maintenance: 200 mg every 2 weeks or 400 mg every 4 weeks. | ||
===== Disease-modifying antirheumatic drugs(DMARDs) ===== | ===== Disease-modifying antirheumatic drugs(DMARDs) ===== | ||
* The use of DMARDs regarded as useful but is limited in AS patients | * The use of [[DMARDs]] regarded as useful but is limited in AS patients with [[sulfasalazine]]. | ||
** Preferred regimen (1): Oral: Initial: 500 mg once daily; may increase up to 2 to 3 g/day in divided doses. | ** Preferred regimen (1): Oral: Initial: 500 mg once daily; may increase up to 2 to 3 g/day in divided doses. | ||
'''Other DMARDs''' | '''Other DMARDs''' | ||
* Methotrexate | * [[Methotrexate]] | ||
* Leflunomide | * [[Leflunomide]] | ||
===== Glucocorticoids ===== | ===== Glucocorticoids ===== | ||
* Pharmacologic medical therapies for [[Ankylosing spondylitis|Ankylosing spondylitis]] (AS) include Glucocorticoids but using them for long term basis for patients is not suggested, although high doses | * Pharmacologic medical therapies for [[Ankylosing spondylitis|Ankylosing spondylitis]] (AS) include Glucocorticoids but using them for long term basis for patients is not suggested, although high doses of [[prednisolone]] may have shown some benefit for very short-term therapy.<ref name="pmid23625982">{{cite journal |vauthors=Haibel H, Fendler C, Listing J, Callhoff J, Braun J, Sieper J |title=Efficacy of oral prednisolone in active ankylosing spondylitis: results of a double-blind, randomised, placebo-controlled short-term trial |journal=Ann. Rheum. Dis. |volume=73 |issue=1 |pages=243–6 |date=January 2014 |pmid=23625982 |doi=10.1136/annrheumdis-2012-203055 |url=}}</ref> | ||
* | * [[Prednisolone]] has dose-dependent therapeutic properties in AS.<ref name="pmid11920413">{{cite journal |vauthors=Maksymowych WP, Jhangri GS, Fitzgerald AA, LeClercq S, Chiu P, Yan A, Skeith KJ, Aaron SL, Homik J, Davis P, Sholter D, Russell AS |title=A six-month randomized, controlled, double-blind, dose-response comparison of intravenous pamidronate (60 mg versus 10 mg) in the treatment of nonsteroidal antiinflammatory drug-refractory ankylosing spondylitis |journal=Arthritis Rheum. |volume=46 |issue=3 |pages=766–73 |date=March 2002 |pmid=11920413 |doi=10.1002/art.10139 |url=}}</ref><ref name="pmid27881910">{{cite journal |vauthors=Bandinelli F, Scazzariello F, Pimenta da Fonseca E, Barreto Santiago M, Marcassa C, Nacci F, Matucci Cerinic M |title=Low-dose modified-release prednisone in axial spondyloarthritis: 3-month efficacy and tolerability |journal=Drug Des Devel Ther |volume=10 |issue= |pages=3717–3724 |date=2016 |pmid=27881910 |pmc=5115695 |doi=10.2147/DDDT.S115099 |url=}}</ref> | ||
** Preferred regimen (1): Prednisolone: oral: 0.1 to 2 mg/kg/day in 3 or 4 divided dose. | ** Preferred regimen (1): [[Prednisolone]]: oral: 0.1 to 2 mg/kg/day in 3 or 4 divided dose. | ||
===== Monoclonal antibody<ref name="pmid24035250">{{cite journal |vauthors=Baeten D, Baraliakos X, Braun J, Sieper J, Emery P, van der Heijde D, McInnes I, van Laar JM, Landewé R, Wordsworth P, Wollenhaupt J, Kellner H, Paramarta J, Wei J, Brachat A, Bek S, Laurent D, Li Y, Wang YA, Bertolino AP, Gsteiger S, Wright AM, Hueber W |title=Anti-interleukin-17A monoclonal antibody secukinumab in treatment of ankylosing spondylitis: a randomised, double-blind, placebo-controlled trial |journal=Lancet |volume=382 |issue=9906 |pages=1705–13 |date=November 2013 |pmid=24035250 |doi=10.1016/S0140-6736(13)61134-4 |url=}}</ref><ref name="pmid26699169">{{cite journal |vauthors=Baeten D, Sieper J, Braun J, Baraliakos X, Dougados M, Emery P, Deodhar A, Porter B, Martin R, Andersson M, Mpofu S, Richards HB |title=Secukinumab, an Interleukin-17A Inhibitor, in Ankylosing Spondylitis |journal=N. Engl. J. Med. |volume=373 |issue=26 |pages=2534–48 |date=December 2015 |pmid=26699169 |doi=10.1056/NEJMoa1505066 |url=}}</ref> ===== | ===== Monoclonal antibody<ref name="pmid24035250">{{cite journal |vauthors=Baeten D, Baraliakos X, Braun J, Sieper J, Emery P, van der Heijde D, McInnes I, van Laar JM, Landewé R, Wordsworth P, Wollenhaupt J, Kellner H, Paramarta J, Wei J, Brachat A, Bek S, Laurent D, Li Y, Wang YA, Bertolino AP, Gsteiger S, Wright AM, Hueber W |title=Anti-interleukin-17A monoclonal antibody secukinumab in treatment of ankylosing spondylitis: a randomised, double-blind, placebo-controlled trial |journal=Lancet |volume=382 |issue=9906 |pages=1705–13 |date=November 2013 |pmid=24035250 |doi=10.1016/S0140-6736(13)61134-4 |url=}}</ref><ref name="pmid26699169">{{cite journal |vauthors=Baeten D, Sieper J, Braun J, Baraliakos X, Dougados M, Emery P, Deodhar A, Porter B, Martin R, Andersson M, Mpofu S, Richards HB |title=Secukinumab, an Interleukin-17A Inhibitor, in Ankylosing Spondylitis |journal=N. Engl. J. Med. |volume=373 |issue=26 |pages=2534–48 |date=December 2015 |pmid=26699169 |doi=10.1056/NEJMoa1505066 |url=}}</ref> ===== | ||
* In the United | * In the United States [[Secukinumab]] has been approved for use in patients with AS.<ref name="pmid27255593">{{cite journal |vauthors=Blair HA, Dhillon S |title=Secukinumab: A Review in Ankylosing Spondylitis |journal=Drugs |volume=76 |issue=10 |pages=1023–30 |date=July 2016 |pmid=27255593 |doi=10.1007/s40265-016-0598-8 |url=}}</ref> | ||
* Secukinumab, is an anti-interleukin (IL)-17A monoclonal antibody.<ref name="pmid26982813">{{cite journal |vauthors=Braun J, Baraliakos X, Kiltz U |title=Secukinumab (AIN457) in the treatment of ankylosing spondylitis |journal=Expert Opin Biol Ther |volume=16 |issue=5 |pages=711–22 |date=2016 |pmid=26982813 |doi=10.1517/14712598.2016.1167183 |url=}}</ref> | * [[Secukinumab]], is an anti-interleukin (IL)-17A [[Monoclonal antibodies|monoclonal]] antibody.<ref name="pmid26982813">{{cite journal |vauthors=Braun J, Baraliakos X, Kiltz U |title=Secukinumab (AIN457) in the treatment of ankylosing spondylitis |journal=Expert Opin Biol Ther |volume=16 |issue=5 |pages=711–22 |date=2016 |pmid=26982813 |doi=10.1517/14712598.2016.1167183 |url=}}</ref> | ||
* IL-17A a proinflammatory cytokine which plays important role in the pathogenesis of AS.<ref name="pmid29511503">{{cite journal |vauthors=Dubash S, McGonagle D, Marzo-Ortega H |title=New advances in the understanding and treatment of axial spondyloarthritis: from chance to choice |journal=Ther Adv Chronic Dis |volume=9 |issue=3 |pages=77–87 |date=March 2018 |pmid=29511503 |pmc=5833172 |doi=10.1177/2040622317743486 |url=}}</ref> | * IL-17A a proinflammatory cytokine which plays important role in the pathogenesis of AS.<ref name="pmid29511503">{{cite journal |vauthors=Dubash S, McGonagle D, Marzo-Ortega H |title=New advances in the understanding and treatment of axial spondyloarthritis: from chance to choice |journal=Ther Adv Chronic Dis |volume=9 |issue=3 |pages=77–87 |date=March 2018 |pmid=29511503 |pmc=5833172 |doi=10.1177/2040622317743486 |url=}}</ref> | ||
** Preferred regimen (1): Secukinumab:150 mg administered subcutaneously weekly for four weeks, then every four weeks thereafter. | ** Preferred regimen (1): [[Secukinumab]]:150 mg administered subcutaneously weekly for four weeks, then every four weeks thereafter. | ||
** Preferred regimen (2): Ustekinumab: IV: Infuse over at least 1 hour; use of IV set with an in-line, low-protein binding filter (0.2 micrometer) required. | ** Preferred regimen (2): [[Ustekinumab]]: IV: Infuse over at least 1 hour; use of IV set with an in-line, low-protein binding filter (0.2 micrometer) required. | ||
** Preferred regimen (3): Pamidronate:30 mg/10 mL (10 mL); 90 mg/10 mL (10 mL).<ref name="pmid11196517">{{cite journal |vauthors=Maksymowych WP, Lambert R, Jhangri GS, Leclercq S, Chiu P, Wong B, Aaron S, Russell AS |title=Clinical and radiological amelioration of refractory peripheral spondyloarthritis by pulse intravenous pamidronate therapy |journal=J. Rheumatol. |volume=28 |issue=1 |pages=144–55 |date=January 2001 |pmid=11196517 |doi= |url=}}</ref> | ** Preferred regimen (3): [[Pamidronate]]:30 mg/10 mL (10 mL); 90 mg/10 mL (10 mL).<ref name="pmid11196517">{{cite journal |vauthors=Maksymowych WP, Lambert R, Jhangri GS, Leclercq S, Chiu P, Wong B, Aaron S, Russell AS |title=Clinical and radiological amelioration of refractory peripheral spondyloarthritis by pulse intravenous pamidronate therapy |journal=J. Rheumatol. |volume=28 |issue=1 |pages=144–55 |date=January 2001 |pmid=11196517 |doi= |url=}}</ref> | ||
** Preferred regimen (4): Rituximab IV: 1,000 mg on days 1 and 15.<ref name="pmid20461780">{{cite journal |vauthors=Song IH, Heldmann F, Rudwaleit M, Listing J, Appel H, Braun J, Sieper J |title=Different response to rituximab in tumor necrosis factor blocker-naive patients with active ankylosing spondylitis and in patients in whom tumor necrosis factor blockers have failed: a twenty-four-week clinical trial |journal=Arthritis Rheum. |volume=62 |issue=5 |pages=1290–7 |date=May 2010 |pmid=20461780 |doi=10.1002/art.27383 |url=}}</ref> | ** Preferred regimen (4): [[Rituximab]] IV: 1,000 mg on days 1 and 15.<ref name="pmid20461780">{{cite journal |vauthors=Song IH, Heldmann F, Rudwaleit M, Listing J, Appel H, Braun J, Sieper J |title=Different response to rituximab in tumor necrosis factor blocker-naive patients with active ankylosing spondylitis and in patients in whom tumor necrosis factor blockers have failed: a twenty-four-week clinical trial |journal=Arthritis Rheum. |volume=62 |issue=5 |pages=1290–7 |date=May 2010 |pmid=20461780 |doi=10.1002/art.27383 |url=}}</ref> | ||
===== Turmeric<ref name="pmid236259823">{{cite journal |vauthors=Haibel H, Fendler C, Listing J, Callhoff J, Braun J, Sieper J |title=Efficacy of oral prednisolone in active ankylosing spondylitis: results of a double-blind, randomised, placebo-controlled short-term trial |journal=Ann. Rheum. Dis. |volume=73 |issue=1 |pages=243–6 |date=January 2014 |pmid=23625982 |doi=10.1136/annrheumdis-2012-203055 |url=}}</ref><ref name="pmid23425071">{{cite journal |vauthors=Aggarwal BB, Gupta SC, Sung B |title=Curcumin: an orally bioavailable blocker of TNF and other pro-inflammatory biomarkers |journal=Br. J. Pharmacol. |volume=169 |issue=8 |pages=1672–92 |date=August 2013 |pmid=23425071 |pmc=3753829 |doi=10.1111/bph.12131 |url=}}</ref> ===== | ===== Turmeric<ref name="pmid236259823">{{cite journal |vauthors=Haibel H, Fendler C, Listing J, Callhoff J, Braun J, Sieper J |title=Efficacy of oral prednisolone in active ankylosing spondylitis: results of a double-blind, randomised, placebo-controlled short-term trial |journal=Ann. Rheum. Dis. |volume=73 |issue=1 |pages=243–6 |date=January 2014 |pmid=23625982 |doi=10.1136/annrheumdis-2012-203055 |url=}}</ref><ref name="pmid23425071">{{cite journal |vauthors=Aggarwal BB, Gupta SC, Sung B |title=Curcumin: an orally bioavailable blocker of TNF and other pro-inflammatory biomarkers |journal=Br. J. Pharmacol. |volume=169 |issue=8 |pages=1672–92 |date=August 2013 |pmid=23425071 |pmc=3753829 |doi=10.1111/bph.12131 |url=}}</ref> ===== | ||
* Curcuma longa (turmeric) has a very long history of extensive use in Ayurvedic medicine as a treatment for inflammatory conditions in India.<ref name="pmid19594223">{{cite journal |vauthors=Jurenka JS |title=Anti-inflammatory properties of curcumin, a major constituent of Curcuma longa: a review of preclinical and clinical research |journal=Altern Med Rev |volume=14 |issue=2 |pages=141–53 |date=June 2009 |pmid=19594223 |doi= |url=}}</ref> | * Curcuma longa ([[turmeric]]) has a very long history of extensive use in [[Ayurveda|Ayurvedic]] medicine as a treatment for inflammatory conditions in India.<ref name="pmid19594223">{{cite journal |vauthors=Jurenka JS |title=Anti-inflammatory properties of curcumin, a major constituent of Curcuma longa: a review of preclinical and clinical research |journal=Altern Med Rev |volume=14 |issue=2 |pages=141–53 |date=June 2009 |pmid=19594223 |doi= |url=}}</ref> | ||
* Turmeric contains 3 active components called curcuminoids<ref name="pmid195942232">{{cite journal |vauthors=Jurenka JS |title=Anti-inflammatory properties of curcumin, a major constituent of Curcuma longa: a review of preclinical and clinical research |journal=Altern Med Rev |volume=14 |issue=2 |pages=141–53 |date=June 2009 |pmid=19594223 |doi= |url=}}</ref> | * [[Turmeric]] contains 3 active components called curcuminoids<ref name="pmid195942232">{{cite journal |vauthors=Jurenka JS |title=Anti-inflammatory properties of curcumin, a major constituent of Curcuma longa: a review of preclinical and clinical research |journal=Altern Med Rev |volume=14 |issue=2 |pages=141–53 |date=June 2009 |pmid=19594223 |doi= |url=}}</ref> | ||
** Curcumin(diferuloylmethane) | ** [[Curcumin]](diferuloylmethane) | ||
** Demethoxycurcumin | ** Demethoxycurcumin | ||
** Bisdemethoxycurcumin | ** Bisdemethoxycurcumin | ||
* | * [[Turmeric]] when administered orally in the diet improves both the wasting and histopathological signs of inflammation. | ||
* Curcumin also suppress the expression of inflammatory cytokines such as TNF-α. | * [[Curcumin]] also suppress the expression of inflammatory cytokines such as TNF-α. | ||
* Curcumin when combined with IL-10, curcumin inhibited NF-κB quite effectively.<ref name="pmid12454848">{{cite journal |vauthors=Sugimoto K, Hanai H, Tozawa K, Aoshi T, Uchijima M, Nagata T, Koide Y |title=Curcumin prevents and ameliorates trinitrobenzene sulfonic acid-induced colitis in mice |journal=Gastroenterology |volume=123 |issue=6 |pages=1912–22 |date=December 2002 |pmid=12454848 |doi=10.1053/gast.2002.37050 |url=}}</ref> | * [[Curcumin]] when combined with IL-10, curcumin inhibited NF-κB quite effectively.<ref name="pmid12454848">{{cite journal |vauthors=Sugimoto K, Hanai H, Tozawa K, Aoshi T, Uchijima M, Nagata T, Koide Y |title=Curcumin prevents and ameliorates trinitrobenzene sulfonic acid-induced colitis in mice |journal=Gastroenterology |volume=123 |issue=6 |pages=1912–22 |date=December 2002 |pmid=12454848 |doi=10.1053/gast.2002.37050 |url=}}</ref> | ||
** Preferred regimen(1): Turmeric :150 mg of curcumin twice daily, decreases the levels of expression of inflammatory cytokines such as TNF-α and IL-6 in serum. | ** Preferred regimen(1): [[Turmeric]] :150 mg of curcumin twice daily, decreases the levels of expression of [[inflammatory]] [[Cytokine|cytokines]] such as [[Tumor necrosis factors|TNF]]-α and [[Interleukin 6|IL-6]] in [[serum]].<ref name="pmid19958764">{{cite journal |vauthors=Tham CL, Liew CY, Lam KW, Mohamad AS, Kim MK, Cheah YK, Zakaria ZA, Sulaiman MR, Lajis NH, Israf DA |title=A synthetic curcuminoid derivative inhibits nitric oxide and proinflammatory cytokine synthesis |journal=Eur. J. Pharmacol. |volume=628 |issue=1-3 |pages=247–54 |date=February 2010 |pmid=19958764 |doi=10.1016/j.ejphar.2009.11.053 |url=}}</ref> | ||
** Preferred regimen(2):Turmeric: 2 gms/day of curcumin can suppress NF-κB activation.<ref name="pmid19372569">{{cite journal |vauthors=Sung B, Kunnumakkara AB, Sethi G, Anand P, Guha S, Aggarwal BB |title=Curcumin circumvents chemoresistance in vitro and potentiates the effect of thalidomide and bortezomib against human multiple myeloma in nude mice model |journal=Mol. Cancer Ther. |volume=8 |issue=4 |pages=959–70 |date=April 2009 |pmid=19372569 |pmc=2694943 |doi=10.1158/1535-7163.MCT-08-0905 |url=}}</ref> | ** Preferred regimen(2):[[Turmeric]]: 2 gms/day of curcumin can suppress [[NF-κB]] activation.<ref name="pmid19372569">{{cite journal |vauthors=Sung B, Kunnumakkara AB, Sethi G, Anand P, Guha S, Aggarwal BB |title=Curcumin circumvents chemoresistance in vitro and potentiates the effect of thalidomide and bortezomib against human multiple myeloma in nude mice model |journal=Mol. Cancer Ther. |volume=8 |issue=4 |pages=959–70 |date=April 2009 |pmid=19372569 |pmc=2694943 |doi=10.1158/1535-7163.MCT-08-0905 |url=}}</ref> | ||
==References== | ==References== |
Latest revision as of 20:44, 15 April 2018
Ankylosing spondylitis Microchapters |
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Ankylosing spondylitis medical therapy On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vamsikrishna Gunnam M.B.B.S [2]
Overview
Pharmacologic medical therapies for ankylosing spondylitis(AS) include Nonsteroidal anti-inflammatory drugs (NSAIDs), tumor necrosis factor (TNF) blocker, and interleukin 17 (IL-17) inhibitors.Ankylosing spondylitis (AS) is a chronic inflammatory disease which is manifested by back pain and gradually to spinal stiffness.While treating the AS patients the primary goal is to maximize long-term health-related quality of life.
Medical Therapy
- Medical therapy for AS is according to the guidelines proposed by [1][2][3]
- Assessment of SpondyloArthritis international Society (ASAS)
- European League Against Rheumatism (EULAR)
- American College of Rheumatology (ACR)/Spondylitis Association of America (SAA)/Spondyloarthritis Research and Treatment Network (SPARTAN) collaboration
- Pharmacologic medical therapies for ankylosing spondylitis(AS) include Nonsteroidal anti-inflammatory drugs (NSAIDs), tumor necrosis factor (TNF) blocker, analgesics, sulfasalazine,intraarticular injections and interleukin 17 (IL-17) inhibitors.
Nonsteroidal antiinflammatory drugs(NSAIDs)[4][5][6][7][8][9]
- The first line treatment for all the patients who are having symptomatic ankylosing spondylitis (AS) are with Nonsteroidal antiinflammatory drugs(NSAIDs).
- 70 to 80 percent patients who are taking NSAIDs report substantial relief of back pain and stiffness.
- Play a crucial role in delaying the progression of ankylosing spondylitis.
- Regardless of which NSAID used, the maximum dose is usually required to manage AS.
- Treating with NSAIDs in AS especially in patients with increased erythrocyte sedimentation rate (ESR) shows especially effective in decreasing the ESR.[10]
Adult
- Preferred regimen (1): Indomethacin: Initial: 75 mg once daily, may increase to 75 mg twice daily (maximum dose: 150 mg/day) for at least 4 weeks.[11]
- Preferred regimen (2): Celecoxib or Etoricoxib: Oral: 200 mg once daily or 100 mg twice daily.[12][13][14][15][16][17]
Tumor necrosis factor alpha antagonists(TNF-alpha)[18][19][20][21][22]
- Infliximab, etanercept, adalimumab, certolizumab, and golimumab are the available tumor necrosis factor alpha inhibitors(TNF-alpha) to treat AS.
- In AS there is no much of a use in adding immunomodulatory drug, such as methotrexate (MTX) as the evidence shows no additional benefit but may increase the cost and the risk of adverse effects.[23][24]
- Treating patients in AS with tumor necrosis factor alpha inhibitors(TNF-alpha) shows significant improvements in disease progress and function such as at least 40 percent improvement from baseline were seen.[25]
- Adalimumab, etanercept, and infliximab have the same efficacy and potency in treating the AS patients.[26]
- Patients who are getting treated with tumor necrosis factor alpha inhibitors shows approximately 80% good response and at least 50% improvement from the baseline of the disease.[27]
- Response to TNF antagonists: The following parameters are sighs of a good response to TNF antagonists[28][29]
- Age, especially young patients.
- Elevated C-reactive protein (CRP).
- The best predictor is, Shorter disease duration.
- Treating with TNF alpha inhibitors in patients with AS shows beneficial effect in improving bone density.[30][31][32]
Side Effects[33]
- Using TNF-alpha inhibitors increases the risk of reactivation of latent tuberculosis and
- Using TNF-alpha inhibitors increases the risk of exacerbation or development of demyelinating disease.
Adult Dosage
- Preferred regimen (1): Infliximab 5 mg/kg at 0, 2, and 6 weeks, followed by 5 mg/kg every 6 weeks thereafter.
- Preferred regimen (2): Etanercept once-weekly dosing: 50 mg once weekly; maximum dose (rheumatoid arthritis): 50 mg/week.
- Preferred regimen (3): Adalimumab IV: 2 mg/kg at weeks 0, 4, and then every 8 weeks thereafter.
- Preferred regimen (4): Certolizumab Initial: 400 mg, repeat dose 2 and 4 weeks after initial dose; Maintenance: 200 mg every 2 weeks or 400 mg every 4 weeks.
Disease-modifying antirheumatic drugs(DMARDs)
- The use of DMARDs regarded as useful but is limited in AS patients with sulfasalazine.
- Preferred regimen (1): Oral: Initial: 500 mg once daily; may increase up to 2 to 3 g/day in divided doses.
Other DMARDs
Glucocorticoids
- Pharmacologic medical therapies for Ankylosing spondylitis (AS) include Glucocorticoids but using them for long term basis for patients is not suggested, although high doses of prednisolone may have shown some benefit for very short-term therapy.[34]
- Prednisolone has dose-dependent therapeutic properties in AS.[35][36]
- Preferred regimen (1): Prednisolone: oral: 0.1 to 2 mg/kg/day in 3 or 4 divided dose.
Monoclonal antibody[37][38]
- In the United States Secukinumab has been approved for use in patients with AS.[39]
- Secukinumab, is an anti-interleukin (IL)-17A monoclonal antibody.[40]
- IL-17A a proinflammatory cytokine which plays important role in the pathogenesis of AS.[41]
- Preferred regimen (1): Secukinumab:150 mg administered subcutaneously weekly for four weeks, then every four weeks thereafter.
- Preferred regimen (2): Ustekinumab: IV: Infuse over at least 1 hour; use of IV set with an in-line, low-protein binding filter (0.2 micrometer) required.
- Preferred regimen (3): Pamidronate:30 mg/10 mL (10 mL); 90 mg/10 mL (10 mL).[42]
- Preferred regimen (4): Rituximab IV: 1,000 mg on days 1 and 15.[43]
Turmeric[44][45]
- Curcuma longa (turmeric) has a very long history of extensive use in Ayurvedic medicine as a treatment for inflammatory conditions in India.[46]
- Turmeric contains 3 active components called curcuminoids[47]
- Curcumin(diferuloylmethane)
- Demethoxycurcumin
- Bisdemethoxycurcumin
- Turmeric when administered orally in the diet improves both the wasting and histopathological signs of inflammation.
- Curcumin also suppress the expression of inflammatory cytokines such as TNF-α.
- Curcumin when combined with IL-10, curcumin inhibited NF-κB quite effectively.[48]
References
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