2010 ACR/ARHP Abstract Supplement

1038 Pages·2010·16.8 MB·English

AN OFFICIAL JOURNAL OF THE AMERICAN COLLEGE OF RHEUMATOLOGY
Arthritis & Rheumatism
VOLUME 62, NUMBER 10 (SUPPLEMENT) OCTOBER 2010
ABSTRACT SUPPLEMENT
2010 ANNUAL SCIENTIFIC MEETING
November 6–11, 2010
Atlanta, Georgia
AMERICAN COLLEGE OF RHEUMATOLOGY
ABSTRACT SUPPLEMENT
American College of Rheumatology
74th Annual Scientific Meeting
Association of Rheumatology Health Professionals
45th Annual Scientific Meeting
November 6 -11, 2010 · Atlanta, Georgia
Copyright © 2010 by the American College of Rheumatology, Atlanta, GA
The printing of the 2010 ACR Annual Scientific Meeting Abstract Supplement was supported by Pfizer Inc.
• Formal presentations of new practice guidelines provided
ACR/ARHP 2010 Annual
to alert the membership and explain, in an open forum, the
Scientific Meeting Overall Needs data supporting the guidelines and propose approaches for
implementation
Assessment/Practice Gaps
• Over 40 workshops designed to provide hands-on skills training
The American College of Rheumatology and the Association of
Rheumatology Health Professionals are committed to providing
About ACR/ARHP Education
comprehensive education to improve the knowledge and
performance of physicians, health professionals and scientists. ACR/ARHP Program Objectives
Through evidence-based educational programs, the organization The American College of Rheumatology and the Association of
strives to enhance practice performance and improve the quality Rheumatology Health Professionals, a division of the ACR, are
of care in those with or at risk for arthritis, rheumatic and organizations of physicians, health professionals and scientists
musculoskeletal diseases. The 2010 ACR/ARHP Annual Scientific serving members through programs, including education and
Meeting program has been developed independent of commercial research. Through these programs, the ACR and the ARHP
influence. The following groups were involved in the planning foster excellence in the care of people with rheumatic and
process: the ACR Committee on Education; the ACR Annual musculoskeletal diseases.
Meeting Planning Committee; the ARHP Education Committee and
The 2010 ACR/ARHP Annual Scientific Meeting programs have
the ARHP Annual Meeting Program Planning Committee.
been independently planned by the ACR Committee on Education,
The program is the result of a planning process that identified the ACR Annual Meeting Planning Committee, the ARHP Annual
educational needs to change or enhance the knowledge, Meeting Program Committee, and the ARHP Clinical Focus Course
competence or performance of rheumatology professionals. The Task Force.
program’s content was derived from both needs assessment and
This program is sponsored by the American College of
practice gap analysis based on professional activities, practice
Rheumatology for educational purposes only. The material
setting, ABIM recertification requirements and physician attributes.
presented is not intended to represent the only or the best
methods appropriate for the medical conditions being discussed,
but rather are intended to present the opinions of the authors/
Program Highlights
presenters, which may be helpful to other healthcare professionals.
• Educational tracks to help attendees identify content targeted
Attendees participating in this medical education program do so
to them. Tracks include: business of rheumatology, clinical,
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reviewed and selected clinical and scientific abstracts, and
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focused content
At the conclusion of the 2010 ACR/ARHP Annual Scientific Meeting,
• Diverse formats of education delivery, including: didactic
participants should be able to:
lectures, debates, and interactive sessions, such as poster
• identify recent developments in the diagnosis and
tours, Meet the Professors and Workshop sessions
management of patients with rheumatic diseases
• A larger forum for discussion of practical management issues
• outline new technologies for the treatment of rheumatologic
such as the Curbside Consults – Ask the Professors session and
problems
Medical Aspects lectures
• describe potential challenges in the delivery of care to
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patients with rheumatic diseases and to specify possible
rheumatology, an area of the program developed by a
solutions
subcommittee of U.S. and internationally prominent basic
• utilize new research data to improve the quality of care of
scientists. Offerings include: the Basic Science Symposia,
patients with rheumatic diseases
State-of-the-Art Lectures, a series of Immunology Updates for
the Clinicians, and a Basic Science pre-meeting course
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• Clinical management sessions, including the Thieves’ Market
and basic management of difficult issues
of Participation
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Table of Contents
Monday, noveMber 8, 2010 2:30 - 4:00 pm
ACR/ARHP Combined Abstract Session
9:00 am - 6:00 pm
ACR/ARHP Combined Epidemiology and Health Services
ACR Poster Session A
Research: Impact on Osteoarthritis
Poster presenters will be available from 9:00 – 11:00 am.
(Abstracts #682-687) ...........................S284
(Abstracts # 1-619)............................. S1
2:30 - 4:00 pm
11:00 am - 12:30 pm
ARHP Concurrent Abstract Session
ACR Plenary Session I
Physical Activity: Just “Move It”
Discovery 2010
S287
(Abstracts #688-693) ...........................
(Abstracts #620-624) ...........................S259
4:30 - 6:00 pm
11:15 am – 12:15 pm
ACR Concurrent Abstract Sessions
ARHP Concurrent Abstract Session
Infection-Related Rheumatic Disease
Issues in Lupus
(Abstracts #694-699) ...........................S290
(Abstracts #625-628) ...........................S261
Miscellaneous Rheumatic and Inflammatory Diseases
2:30 - 4:00 pm (Abstracts #700-705)...........................S292
ACR Concurrent Abstract Sessions
Osteoarthritis – Clinical Aspects: Genetics, Novel Approaches,
Biology and Pathology of Bone and Joint: and Therapy
Molecular Basis of Osteoarthritis
(Abstracts #706-711)...........................S294
S262
(Abstracts #629-634)...........................
Rheumatoid Arthritis – Animal Models: Insight in
Cytokines, Mediators, Gene Regulation Pathogenesis and Novel Therapeutic Targets
(Abstracts #635-639)...........................S264 (Abstracts #712-717)...........................S297
Epidemiology and Health Services Research: Rheumatoid Rheumatoid Arthritis Treatment – Small Molecules, Biologics
Arthritis and Gene Therapy: Safety and Efficacy
(Abstracts #640-645)...........................S266 (Abstracts #718-723)...........................S299
Fibromyalgia and Soft Tissue Disorders Systemic Sclerosis, Fibrosing Syndromes, and Raynaud’s –
S269
(Abstracts #646-651)........................... Clinical Aspects and Therapeutics
Pediatric Rheumatology – Pathogenesis and Genetics: (Abstracts #724-729)...........................S302
Biological Basis for Pediatric Rheumatic Disease
4:30 - 6:00 pm
(Abstracts #652-657)...........................S272
ACR REF Special Session
Rheumatoid Arthritis – Clinical Aspects: Preclinical RA and
REF Edmond L. Dubois, MD, Memorial Lectureship: The Path
Early RA
from Gene to Function: Analysis of a Lupus Susceptibility
S274
(Abstracts #658-663)...........................
Gene
Spondylarthropathies and Psoriatic Arthritis- Clinical Aspects (Abstracts #730-732) ...........................S305
and Treatment: Imaging

S277
(Abstracts #664-669)........................... Tuesday, noveMber 9, 2010
Systemic Sclerosis, Fibrosing Syndromes, and Raynaud’s:
9:00 am - 6:00 pm
Pathogenesis, Animal Models and Genetics
ACR/ARHP Poster Session B
S280
(Abstracts #670-675)...........................
Poster presenters will be available from 9:00 – 11:00 am.
ANCA- Associated Vasculitis
(Abstracts #733-1345) ..........................S307
(Abstracts #676-681)...........................S282
Table of Contents
9:15 - 10:15 am Cytokines, Mediators, Gene Regulation
ARHP Concurrent Abstract Session (Abstracts #1422-1427).........................S591
Physical and Psychosocial Challenges in Scleroderma Education
(Abstracts #1346-1349).........................S559 (Abstracts #1428-1433).........................S594
Pediatric Rheumatology – Clinical and Therapeutic Aspects –
11:00 am - 12:30 pm
Therapeutics
ACR Plenary Session II
(Abstracts #1434-1439).........................S596
Discovery 2010
Rheumatoid Arthritis – Clinical Aspects: Outcomes Associated
(Abstracts #1350-1355) .........................S560
with Biologic Therapy for RA
2:30 - 4:00 pm (Abstracts #1440-1445).........................S599
ACR Concurrent Abstract Sessions Spondylarthritis and Psoriatic Arthritis: Pathogenesis,
Antiphospholipid Syndrome Etiology, and Animal Models
(Abstracts # 1356-1361).........................S563 (Abstracts #1446-1451).........................S603
Epidemiology and Health Services: Gout Systemic Lupus Erythematosus – Clinical Aspects and
(Abstracts #1362-1367).........................S565 Treatment: New Therapies
Imaging of Rheumatic Disease: X-ray and MRI (Abstracts #1452-1457).........................S605
(Abstracts #1368-1373).........................S568
4:30 – 6:00 pm
Muscle Biology, Myositis and Myopathies: Insights into the
ACR REF Special Session
Pathogenesis and Outcomes of Myositis
REF Marshall J. Schiff, MD, Memorial Lectureship:
S571
(Abstracts #1374-1379).........................
Everything a Rheumatologist Should Know About Spine
Orthopedics, Low Back Pain and Rehabilitation Surgery but Was Afraid to Ask
(Abstracts #1380-1385).........................S574 (Abstracts #1458-1459).........................S608
Rheumatoid Arthritis – Human Etiology and Pathogenesis: RA
4:30 - 6:00 pm
Human Etiology and Pathogenesis
ARHP Concurrent Abstract Session
S576
(Abstracts #1386-1391).........................
Don’t Despair Over Health Disparities
Rheumatoid Arthritis Treatment – Small Molecules, Biologics
(Abstracts #1460-1465).........................S609
and Gene Therapy: Existing Non-Biologic DMARDs
S578
(Abstracts #1392-1397).........................
Wednesday, noveMber 10, 2010
Systemic Lupus Erythematosus – Clinical Aspects and
Treatment: Renal 9:00 am - 6:00 pm
S581
(Abstracts #1398-1403)......................... ACR/ARHP Poster Session C
2:30 - 4:00 pm Poster presenters will be available from 9:00 – 11:00 am.
(Abstracts #1466-2079 & 2089).................. S612
ACR /ARHP Combined Concurrent Abstract Session
ACR/ARHP Combined Pediatric Rheumatology – Clinical 9:15 - 10:15 am
and Therapeutic Aspects: Quality of Life in Children and ARHP Concurrent Abstract Session
Adolescents with Arthritis
Be Creative with Rheumatic Education: Where and How to Get It
(Abstracts #1404-1409) .........................S583 S869
(Abstracts #2080-2083).........................
4:30 - 6:00 pm 11:00 am - 12:30 pm
ACR Concurrent Abstract Sessions
ACR Plenary Session III
B-Cell Biology and Targets in Autoimmune Disease
Discovery 2010
(Abstracts #1410-1415).........................S587 S871
(Abstracts #2084-2088) .........................
Cell-Cell Adhesion, Cell Trafficking and Angiogenesis
(Abstracts #1416-1421).........................S589
Table of Contents
2:30 - 4:00 pm Rheumatoid Arthritis Treatment – Small Molecules, Biologics
ACR Concurrent Abstract Sessions and Gene Therapy: Novel Compounds
Epidemiology and Health Services Research: Osteoarthritis (Abstracts #2168-2173)........................ S909
(Abstracts #2090-2095)........................ S873 Sjögren’s Syndrome
S912
Osteoarthritis – Clinical Aspects: Pain and Biomechanics (Abstracts #2174-2179)........................
(Abstracts #2096-2101)........................ S876 Spondylarthropathies and Psoriatic Arthritis – Clinical Aspects
and Treatment: Biomarkers
Pediatric Rheumatology – Clinical and Therapeutic Aspects-
Outcomes (Abstracts #2180-2185)........................ S914
(Abstracts #2102-2107)........................ S879 Systemic Lupus Erythematosus – Animal Models
Quality Measures and Innovation in Practice Management and (Abstracts #2186-2191)........................ S917
Care Delivery Systemic Sclerosis, Fibrosing Syndromes, and Raynaud’s –
(Abstracts #2108-2113)........................ S882 Clinical Aspects and Therapeutics
Rheumatoid Arthritis – Human Etiology and Pathogenesis: (Abstracts #2192-2197)........................ S919
Anti – CCP in RA Etiology and Pathogenesis Vasculitis II
S884 S922
(Abstracts #2114-2119)........................ (Abstracts #2198-2203)........................
Systemic Lupus Erythematosus – Clinical Aspects and
Treatment: SLE and Cardiovascular Disease Thursday, noveMber 11, 2010
S887
(Abstracts #2120-2125)........................
7:45 - 8:45 am
T–Cell Biology and Targets in Autoimmune Disease
ARHP Concurrent Abstract Session
(Abstracts #2126-2131)........................ S890
Rheumatic Medications: More or Less?
2:30 - 4:00 pm (Abstracts #2204-2207)........................ S926
ACR/ARHP Combined Abstract Session
9:00 - 10:30 am
ACR/ARHP Combined Orthopedics, Low Back Pain and
ACR Concurrent Abstract Sessions
Rehabilitation: Hips and Knees- Focus on Function
Epidemiology and Health Services Research: General Interest
S892
(Abstracts #2132-2137)........................
(Abstracts #2208-2213)........................ S927
2:30 - 4:00 pm Genetics, Genomics and Proteomics: RA and Other Rheumatic
ARHP Concurrent Abstract Session Diseases
Keep Working with Arthritis (Abstracts #2214-2219)........................ S930
(Abstracts #2138-2143)........................ S894 Imaging of Rheumatic Disease: Ultrasound
4:30 - 6:00 pm (Abstracts #2220-2225)....................... S933
ACR Concurrent Abstract Sessions Innate Immunity and Rheumatic Disease
Genetics, Genomics and Proteomics: SLE (Abstracts #2226-2231)........................ S935
(Abstracts #2144-2149)........................ S897 Rheumatoid Arthritis – Animal Models: T cell Pathogenesis
and Novel Therapeutic Targets
Metabolic and Crystal Arthropathies – Pathogenesis,
Prevalence, Imaging, and New Therapy (Abstracts #2232-2237)........................ S938
(Abstracts #2150-2155)........................ S900 Systemic Lupus Erythematosus – Clinical Aspects and Treatment
Osteoporosis and Metabolic Bone Disease: Clinical Aspects (Abstracts #2238-2243)........................ S940
and Pathogenesis
9:15 - 10:45 am
(Abstracts #2156-2161)........................ S902
ARHP Concurrent Abstract Session
Rheumatoid Arthritis – Clinical Aspects: RA and
What a Pain Rheumatic Disease Can Be!
Cardiovascular Disease
(Abstracts #2244-2249)........................ S943
(Abstracts #2162-2167)........................ S905
Table of Contents
11:00 am - 12:30 pm
ACR Concurrent Abstract Sessions
Antiphospholipid Syndrome
(Abstracts #2250-2255)........................ S945
Rheumatoid Arthritis – Clinical Aspects: Radiographic and
Other Outcomes in RA
(Abstracts #2256-2261)........................ S948
Rheumatoid Arthritis Treatment – Small Molecules, Biologics
and Gene Therapy: Existing Biologics
(Abstracts #2262-2267)........................ S951
Spondylarthropathies and Psoriatic Arthritis – Clinical Aspects
and Treatment – Therapy
(Abstracts #2268-2273)........................ S954
Systemic Lupus Erythematosus – Human Etiology and
Pathogenesis: Etiology and Pathogenesis
(Abstracts #2274-2278)........................ S957
11:00 am - 12:30 pm
ARHP Concurrent Abstract Session
Rheumatoid Arthritis: From Clinic to Home
S959
(Abstracts #2279-2284)........................
PatientsandMethods:GenomicDNAsampleswereobtainedfrom111
ACR Poster Session A
patientswithAPS(45primaryAPSand66secondlyAPS),296patientswith
AntiphospholipidSyndrome
systemiclupuserythematosus(SLE)intheabsenceofAPSand428healthy M
Monday,November8,2010,9:00AM–6:00PM controls. Among APS group, seventy nine patients (71%) had arterial or o
n
thrombosis,58(52%)arterialthrombosis,37(33%)venousthrombosisand d
a
52(47%)cerebralinfarction,respectively.AGTRL1SNP(rs9943582)was y,
genotyped using TaqMan SNP genotyping assay and PRKCH SNP N
1 o
(rs2230500) was genotyped using direct sequencing. Chi-square tests and v
e
Acquired Resistance to Activated Protein C Is a Feature of Both Odds ratio were used for statistical analysis after evaluation for Hardy- m
b
SystemicLupusErythematosus(SLE)andAntiphospholipidSyndrome Weinbergequilibrium.Inaddition,thestratificationanalysisbythrombotic e
r
(APS)andIsMoreMarkedinPatientswithSLEandAPS. DenisWahl3, eventswasperformed. 8
Ste´phane Zuily4, Agne`s Brunette2, Marie Prestat-Tilly4, Ve´ronique Reg- Results:BothAGTRL1rs9943582GalleleandPRKCHrs2230500A
nault2, Jean Devignes1 and Thomas Lecompte1.1Biological Haematology allele frequencies were significantly increased in patients with APS
Department, Nancy University Hospital, Vandoeuvre les Nancy, France, (OR(cid:2)1.43, 95%Cl:1.03–2.31 and OR(cid:2)1.89, 95%Cl: 1.17–3.05, respec-
2INSERMU961,NancyUniversite´,VandoeuvrelesNancy,France,3Vascu- tively). No association was found between these 2 SNPs and SLE in the
larMedicineUnit,VandoeuvrelesNancy,France,4VascularMedicineUnit, absence of APS. In the stratification analysis by clinical manifestations of
NancyUniversityHospital,VandoeuvrelesNancy,France APS, both AGTRL1 and PRKCH alleles were associated with arterial or
venousthromboticeventsinpatientswithAPS(OR(cid:2)1.69,95%Cl:1.15–2.49
Vascular manifestations of antiphospholipid syndrome (APS) include andOR(cid:2)1.58,95%Cl:1.04–2.38,respectively)
both venous (VTE) and arterial (ATE) thromboembolic events. However Conclusion:ThefunctionalSNPinanSp1-bindingsiteofAGTRL1gene
VTE are more frequent than ATE. Among the underlying mechanisms of (rs9943582,G/A)andthenonsynonymousSNP(rs223050,G/A,Val372Ile)
VTEinAPS,ithasbeensuggestedthatacquiredactivatedproteinC(APC) inPRKCHareassociatedwithAPSandthromboticeventsinpatientswith
resistance may be a candidate mechanism. However this is difficult to APS.Ourresultssuggestthatthese2SNPsareadditionalgeneticriskfactors
demonstrate with tests based on aPTT because of the effects of lupus forAPS,especiallythromboticeventsinAPSinJapanesepopulation.
anticoagulantsonthisparameter.InordertoinvestigateAPCresistancein
APSwehaveconductedastudywithathrombingenerationtest(calibrated Disclosure:H.Nakagawa:None;T.Horita:None;T.Odani:None;Y.Fujieda:
None;M.Kato:None;K.Otomo:None;Y.Nakagawa:None;S.Yasuda:None;T.
automatedthrombography).APCresistancewasdeterminedwithmeasure-
Atumi:None;T.Koike:None.
mentofendogenousthrombinpotential(ETP)atbaselineandafteraddition
ofAPC.TheAPCsensitivityratio(sr)wasdefinedasETPwithAPC/baseline
ETP.
Weincluded92patients(37withprimaryantiphospholipidsyndrome,15 3
withSLEwithoutantiphospholipidantibodiesPAPS,11withbothAPSand
Anti-(cid:1)2GlycoproteinIAntibodiesfromLeprosyPatientsDoNotShow
SLEand29withantiphospholipidantibodies(APA)butwithoutAPS)and39
ThrombogenicEffectsinanInVivoAnimalModel. RicardoForastiero2,
controls. APCsr was higher in all patient groups compared to controls
indicatingresistancetoactivatedproteinC:APCsrwas0.45(cid:1)0.20,p(cid:2)0.005 Marta Martinuzzo2, Mariano Vega-Ostertag2, Gabriela de Larranaga2 and
inPAPS,0.55(cid:1)0.16,p(cid:3)0.001ininSLE,0.65(cid:1)0.16,p(cid:3)0.0001inpatients SilviaS.Pierangeli1.1UnivofTXMedicalBranch,Galveston,TX,2Univer-
withbothPAPSandSLEand0.53(cid:1)0.22,p(cid:3)0.0001inpatientswithAPA sidadFavaloro,BuenosAires,Argentina
withoutAPSwhereascontrols0.30(cid:1)0.11.OfnoteAPCsrwasalsohigher
inpatientswithbothSLEandAPSthaninpatientswithPAPS(p(cid:2)0.009). Background: The APS-associated aPL are autoantibodies directed
against(cid:1)2GPIandprothrombin.Patientswithleprosypresenthighfrequency
Moreover APCsr in patients with venous thrombosis was higher than in
controls:0.47(cid:1)0.22vs0.30(cid:1)0.11,p(cid:3)0.001. of IgM aPL that bind (cid:1)2GPI, but they do not develop thrombosis. Anti-
(cid:1)2GPIfromAPSmainlybindtodomainIof(cid:1)2GPIwhileinleprosyare
OveralltheseresultssuggestthatacquiredAPCresistanceisapotential
directedagainstdomainV.ThereisconvincingevidencethataPL/anti-(cid:1)2GPI
riskfactorforthrombosisinSLEandPAPSandismoremarkedwhenboth
fromAPSarepathogenicinvivoandinvitro.
conditions are present. Furthermore APC resistance seems to be more
Objective:toinvestigatethethrombogenicandpro-inflammatoryeffects
specificallyassociatedwithvenousthromboembolism.
ofaPLfromleprosyandtocomparewithaPLfromAPS.
Methods:Serafrom6patientswithAPSand6withleprosywereusedas
Disclosure:D.Wahl:None;S.Zuily:None;A.Brunette:None;M.Prestat-Tilly:
None;V.Regnault:None;J.Devignes:None;T.Lecompte:None. thesourceofIgM.AllAPSand5leprosypatientshadstrongLAactivity,and
hightitersofIgMaCL/anti-(cid:1)2GPI.TheremainingleprosypatientwasaPL
negative(control).WetreatedCD1mice,ingroupsof5,at0hoursand48
2 hours later with IgM aPL/anti-(cid:1)2GPI isolated from patients with leprosy
(IgM-leprosy) or APS (IgM-APS) or with IgM from 2 healthy controls
AGTRL1andPRKCHAreGeneticRiskFactorsforAntiphospholipid (IgM-NHS)or1leprosyaPLnegativecontrol.Seventy-twohoursafterthe
Syndrome. HisakoNakagawa1,TetsuyaHorita2,ToshioOdani2,Yuichiro firstinjection,theadhesionofleukocytes(#WBC)toendothelialcells(EC)in
Fujieda2, Masaru Kato2, Kotaro Otomo2, Yasuko Nakagawa2, Shinsuke cremastermuscle(asanindicationofECactivationinvivo),aswellasthe
Yasuda2,TatsuyaAtumi2andTakaoKoike2. 1DepartmentofMedicineII, sizeofaninducedthrombusinthefemoralveinofthemicewereexamined.
Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido, Results:IgM-APSsignificantlyincreasedthethrombussize(inmum2)
Japan,2DepartmentofMedicineII,HokkaidoUniversityGraduateSchoolof whencomparedtoIgM-NHSorIgM-leprosytreatedmice(p(cid:3)0.001).There
Medicine. was no difference in mice injected with IgM-leprosy, IgM-NHS or IgM-
leprosy control. IgM-APS increased the #WBC adhering to EC, when
Background:Singlenucleotidepolymorphisms(SNPs)ofAngiotensin comparedtoIgM-NHSorIgM-leprosy(p(cid:3)0.001).
receptor-like1(AGTRL1)andProteinkinaseCeta(PRKCH)werereported
to be associated with cerebral infarction in recent genomewide association IgM-leprosy
IgM-APS IgM-leprosy IgM-NHS control
studyinJapanesepopulation.AGTRL1,alsonamedAPJ,isamemberofthe
G protein-coupled receptor gene family and has important roles for the Meanthrombus 4446 1378 748 851
size
modulationofangiogenesisandalsoactasahumanimmunodeficiencyvirus
#WBC 5.1(cid:1)2.2 2.0(cid:1)1.0 3.5(cid:1)1.6 1.3(cid:1)0.5
coreceptor.PRKCHregulatesvariousimportantcellularfunctionsincluding
proliferation,differentiationandapoptosisisismainlyexpressedinvascular Conclusions:OurdatashownthataPL/anti-(cid:1)2GPIfromleprosypatients
endothelialcellsandfoamymacrophagesinhumanatheroscleroticlesions.In havenotthrombogenicandpro-inflammatoryeffectsinvivowhencompared
thisstudy,weinvestigatedthepossibleassociationofthefunctionalSNPin withaPLderivedfromAPS.
anSp1-bindingsiteofAGTRL1gene(rs9943582,G/A)andthenonsynony-
mousSNP(rs223050,G/A,Val372Ile)inPRKCHgenewithantiphospho- Disclosure:R.Forastiero:None;M.Martinuzzo:None;M.Vega-Ostertag:None;
lipidsyndrome(APS)inJapanesepopulation. G.deLarranaga:None;S.S.Pierangeli:None.
S1
4 itsefficacyforthediagnosisofantiphospholipidsyndrome(APS)aswellas
itspredictivevalueforthedevelopmentofthromboticeventsinpatientswith
8 AntiphospholipidAntibodiesinChildrenwithSystemicLupusErythem- autoimmune diseases (Presentation Number 1216 in ACR 2009). In the
r atosus–18YearsofClinicalExperiencefromNorthIndia. SurjitSingh2, presentstudy,wefurtheranalyzedtheassociated-riskofthrombosisforeach
be Jasmina Ahluwalia1, Shano Naseem3, Deepti Suri2 and Amit Rawat2. aPLassayinautoimmunediseases.Further,weinvestigatedtherelationship
em 1DepartmentofHematology,PostGraduateInstituteofMedicalEducation betweentheaPL-SandeachsingleaPLtest.
ov andResearch,Chandigarh,India,2DivisionofPediatricAllergyandImmu- Patients and Methods: This study comprised 411 patients with auto-
N nology, Advanced Pediatrics Centre, Post Graduate Institute of Medical immunediseaseswhovisitedourRheumaticandConnectiveTissueDisease
ay, EducationandResearch,Chandigarh,India,3DivisionofPediatricHematol- Department. Between 2002 and 2003, five Lupus Anticoagulant (LAC)
nd ogy,AdvancedPediatricsCentre,PostGraduateInstituteofMedicalEduca- assays (the mixing studies: activated partial thromboplastin time (APTT),
Mo tionandResearch,Chandigarh,India kaolinclottingtime,thediluteRussel’svipervenomtest(dRVVT),andthe
confirmatorytests:APTTanddRVVT)and6ELISAs(IgG/Manticardiolipin
Background:Pediatricsystemiclupuserythematosus(p-SLE)isusually (aCL)antibodies,IgG/Manti-beta2-glycoproteinI(a(cid:1)2GPI)antibodiesand
moreseverethanitsadultcounterpartandfrequentlyinvolvesvitalorgans IgG/M phosphatidylserine dependent antiprothrombin (aPS/PT) antibodies)
(e.g.kidneys).Anti-phospholipidantibodies(APLA)havebeenreportedin were performed in all subjects. Among all the patients, 296 (72.0%) were
38–87%patientswithp-SLEinandreportssuggestthatpresenceofAPLA followed-upwithameandurationof67(cid:1)15months.Thediseaseprofileof
canmodifydiseaseexpression.Higherincidenceofneuropsychiatric,renal thesepatientswasasfollows;17(6%)primaryAPS,26(9%)APSassociated
andhematologicalmanifestationshasbeenreportedinAPLApositivep-SLE, with other autoimmune disease, 89(29%) SLE (without APS), 50(17%)
butinfluenceofAPLAondiseasecourseremainsunclear.WhileAPLAhave rheumatoidarthritisand114patientswithseveralotherautoimmunediseases.
beenextensivelystudiedinadultswithSLE,thereispaucityofdataonAPLA ToevaluatethepredictivevalueofthrombosisforeachaPL-analyzedtest,
inp-SLE. positive results in each assay were contrasted with the presence of new
MaterialsandMethods:Wereportasinglecentrestudyon64patients thromboticeventsduringthefollow-upperiod.
withp-SLEseenduringtheperiodJune1992-May2010inwhomAPLA Results: Thirty-two patients newly developed thromboses during the
testingwasperformed.DiagnosisofSLEwasbasedonACRcriteria.Mean observationperiod;22arterialthrombosesand14venousthromboses.
ageatdiagnosiswas10.3years(range3–17)withafemale:maleratioof3:1. PatientswitheitherpositiveLACorIgGaPS/PThadastrongerriskof
Of these 24 (37.5%) had renal, 17 (26.6%) hematological (7-hemolytic thrombosisthanthosewithout.Theoddsratio(OR[95%CI])associatedto
anemia,6-thrombocytopeniaand4-leucopenia),14(21.9%)neurological,8 eachtestwas3.26[1.55–6.90,p(cid:2)0.001]and4.80[2.03–11.04,p(cid:2)0.0001],
(12.5%) pulmonary, 29 (45.3%) musculo-skeletal and 42 (65.6%) had respectively.TheORvaluesinpatientswithaPL-Smorethan10,30and50
mucocutaneousinvolvement.APLAtestedincluded:i)lupusanticoagulant were 2.86 [1.33–6.16, p(cid:2)0.006], 5.27 [2.32–11.95, p(cid:3)0.0001] and 5.31
[bykaolinclottingtime,dilutedRussellvipervenomtime(LAScreenandLA [1.81–15.53,p(cid:2)0.0008],respectively.Thus,thepositivepredictivevaluesof
Confirm,DadeBehring)andSTACLOT-LAkit]ii)anticardiolipinantibodies aPL-Smorethan30and50werehigherthananyothervalueofeachsingle
(ACLA)–IgG,IgMandiii)anti-(cid:1)2glycoproteinI((cid:1)2GPI)antibodies–IgG, aPLtest(seefigure.).ThenegativepredictivevaluesofaPL-S,LACandIgG
IgM (Orgentec GmBH by ELISA). Our laboratory is registered in World aPS/PTwerewithinthesimilarlevels(90.7–92.9%).
HealthOrganization’sUnitedKingdomNationalExternalQualityAssurance Conclusion: The aPL-S may be a useful comprehensive quantitative
Schemeforthesetests. markerforpredictingthrombosisinautoimmunediseases.
SummaryofResults:PatientswastestedforAPLAon155occasions-
minimumbeingonceandmaximumbeing10duringameanfollow-upperiod Disclosure:K.Otomo:None;T.Atsumi:None;Y.Fujieda:None;M.Kato:None;
of 59.3 months (range 1–211 months). Thirty eight (59.4%) patients were O.Amengual:None;T.Horita:None;S.Yasuda:None;T.Koike:None.
positiveforoneorotherAPLAatsomepointoftimeoftheirdisease.Overall
LAwaspositivein39.1%,IgGACAin23.4%andIgMACAin18.6%.At 6
diagnosis, 37.8% children were positive for LA, 16.3% for IgG ACA and
20.9%forIgMACA.Duringfollow-upLAwaspositivein26.2%patients, Antiphospholipid Syndrome (APS) Clinical Research Task Force
IgGACAin31%,IgMACAin19%patients.Anti-(cid:1)2GPI(IgGandIgM) (CRTF)Report. DorukErkan2,RonaldDerksen6,RogerA.Levy3,Samuel
could be tested in 10 patients only and was found to be positive for Machin5, Thomas Ortel1, Silvia S. Pierangeli4, Robert A. S. Roubey7,
anti-(cid:1)2GPIIgGin1patient. MichaelD.Lockshin2andonBehalfofAPSClinicalResearchTaskForce.
Thrombosiswasseenin5patients-ofthese,4(80%)werepositivefor 1Duke University Health System, Durham, NC, 2Hospital for Special Sur-
APLA.Ofthe24patientswithnephritis,classIInephritiswasseenin4—of gery,NewYork,NewYork,NY,3UnivEstadoDoRiodeJaneiro,Riode
thesenonewaspositiveforanyoftheAPLA;classIIInephritiswasseenin Janeiro, Brazil, 4Univ of TX Medical Branch, Galveston, TX, 5University
1–patienttestedpositiveforAPLA;classIVnephritiswasseenin15—of College London Hospitals, London, UK, 6University Medical Centre,
these9(60%)werepositivefor1oftheAPLA;classVnephritiswasseenin Utrecht,Netherlands,7UniversityofNorthCarolina,ChapelHill,NC
3–of these 2 (66.6%) were positive for APLA. Of the 17 patients with
hematological involvement, 11 (64.7%) had positive APLA; of 14 with Background:The13thInternationalCongressonAntiphospholipidAn-
neurological involvement, 12 (85.7%) had positive APLA. Six (9.4%) tibodies(aPL)washeldinGalveston,TXinApril2010.TheAPSCRTFwas
childrenhadafatalcourse—5(83.3%)ofthesehadpositiveAPLA. oneofsixtaskforcesdevelopedbythemeetingorganizationcommitteewith
Conclusion: 59.4% p-SLE patients had APLA positivity during the the purpose of: a) evaluating the limitations of APS clinical research and
diseasecourse.ThecommonestAPLAwasLA(39.1%),followedbyIgG developing guidelines for researchers to help improve the quality of APS
ACA(23.4%)andIgMACA(18.6%).APLApositivityismorecommonin research;andb)prioritizingtheideasforawell-designedmulticenterclinical
p-SLEpatientswithadvancednephritis,neurologicalinvolvement,thrombo- trialanddiscussingthepragmaticsofgettingsuchatrialdone(organization,
sisandafatalcourse.Presenceorpersistenceoftheseantibodies,however, idealprotocols,practicalprotocols,andfinancing).
maynotalwayspredictthrombosisinchildrenwithp-SLE. Objective:Thepurposeofthisabstractistosummarizethediscussions
andprogressofAPSCRTF.
Disclosure:S.Singh:None;J.Ahluwalia:None;S.Naseem:None;D.Suri:None; Methods: The original eight members of CRTF were chosen among
A.Rawat:None. experienced APS researchers. The task force working algorithm was: a) a
questionnairethatwassenttothemembersbeforethecongress;b)asummary
5 report that was prepared based on the responses to facilitate discussions
duringthepre-meetingworkshop;c)apre-meetingworkshop;d)twoplenary
AntiphospholipidScore(aPL-S):AComprehensivePredictiveMarkerof sessionsbasedontheconclusionsofthetaskforcediscussionswhereinput
DevelopingThrombosisinAutoimmuneDiseases. KotaroOtomo1,Tat- fromallthemeetingattendeeswasreceived;ande)afinalreportthatwas
suyaAtsumi2,YuichiroFujieda3,MasaruKato3,OlgaAmengual3,Tetsuya circulatedamongallthetaskforcechairsforfinalremarks.
Horita3,ShinsukeYasuda3andTakaoKoike3.1HokkaidoGraduateSchool Results: The task force identified five major issues that impede APS
ofMedicine,DepartmentofMedicineII,Sapporo,Hokkaido,Japan,2Hok- clinicalresearchandtheabilitytodevelopevidence-basedrecommendations
kaido Graduate School of Medicine, Department of Medicine II, Sapporo, forthemanagementofaPLpositivepatients:1)aPLdetectionhasbeenbased
Japan,3HokkaidoGraduateSchoolofMedicine,DepartmentofMedicineII onpartiallyornon-standardizedtests,andclinical(andbasic)APSresearch
studieshaveincludedpatientswithheterogeneousaPLprofileswithdifferent
Objective: We have previously defined the Antiphospholipid Score clinicaleventrisks;2)clinical(andbasic)APSresearchstudieshaveincluded
(aPL-S)bytestingmultipleantiphospholipidantibodies(aPL),andevaluated aheterogeneousgroupofpatientswithdifferentaPL-relatedmanifestations
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