Bibliography December 05

1. ABEDIN S, LEMSTER B, MICHEL JJ, HIRSCH RAPHAEL, VALLEJO AN: Indicators of immune exhaustion in juvenile idiopathic arthritis. Arthritis & Rheumatism 52:9, Suppl. S S443, 2005

2. ABREU P, BARDAL A, RUBIO-GARCIA J, RUIZ B, MORELL J, GAMIR M: Coxofemoral affectation on patients with juvenile idiopathic arthritis. Annals of the Rheumatic Diseases 64:Suppl. 3 507, 2005

3. ADIB N, SILMAN A, BAILDAM E, DAVIDSON JOYCE, FOSTER H, GARDNER-MEDWIN J, THOMSON W: Predictors of short term outcomes in a prospective inception cohort of 292 children with juvenile idiopathic arthritis (JIA). Arthritis & Rheumatism 52:9, Suppl. S S89, 2005

4. AEBI M: The adult scoliosis. Eur Spine J 14:10 925-948, 2005
   Organism: Institute for Evaluative Research in Orthopaedic Surgery, University of Bern, Bern, SwitzerlandFAU - Aebi, Max
   Abstract: Adult scoliosis is defined as a spinal deformity in a skeletally mature patient with a Cobb angle of more than 10 degrees in the coronal plain. Adult scoliosis can be separated into four major groups: Type 1: Primary degenerative scoliosis, mostly on the basis of a disc and/or facet joint arthritis, affecting those structures asymmetrically with predominantly back pain symptoms, often accompanied either by signs of spinal stenosis (central as well as lateral stenosis) or without. These curves are often classified as "de novo" scoliosis. Type 2: Idiopathic adolescent scoliosis of the thoracic and/or lumbar spine which progresses in adult life and is usually combined with secondary degeneration and/or imbalance. Some patients had either no surgical treatment or a surgical correction and fusion in adolescence in either the thoracic or thoracolumbar spine. Those patients may develop secondary degeneration and progression of the adjacent curve; in this case those curves belong to the type 3a.Type 3: Secondary adult curves: (a) In the context of an oblique pelvis, for instance, due to a leg length discrepancy or hip pathology or as a secondary curve in idiopathic, neuromuscular and congenital scoliosis, or asymmetrical anomalies at the lumbosacral junction; (b) In the context of a metabolic bone disease (mostly osteoporosis) combined with asymmetric arthritic disease and/or vertebral fractures. Sometimes it is difficult to decide, what exactly the primary cause of the curve was, once it has significantly progressed. However, once an asymmetric load or degeneration occurs, the pathomorphology and pathomechanism in adult scoliosis predominantly located in the lumbar or thoracolumbar spine is quite predictable. Asymmetric degeneration leads to increased asymmetric load and therefore to a progression of the degeneration and deformity, as either scoliosis and/or kyphosis. The progression of a curve is further supported by osteoporosis, particularly in post-menopausal female patients. The destruction of facet joints, joint capsules, discs and ligaments may create mono- or multisegmental instability and finally spinal stenosis. These patients present themselves predominantly with back pain, then leg pain and claudication symptoms, rarely with neurological deficit, and almost never with questions related to cosmetics. The diagnostic evaluation includes static and dynamic imaging, myelo-CT, as well as invasive diagnostic procedures like discograms, facet blocks, epidural and root blocks and immobilization tests. These tests may correlate with the clinical and the pathomorphological findings and may also offer the least invasive and most rational treatment for the patient. The treatment is then tailored to the specific symptomatology of the patient. Surgical management consists of either decompression, correction, stabilization and fusion procedures or a combination of all of these. Surgical procedure is usually complex and has to deal with a whole array of specific problems like the age and the general medical condition of the patient, the length of the fusion, the condition of the adjacent segments, the condition of the lumbosacral junction, osteoporosis and possibly previous scoliosis surgery, and last but not least, usually with a long history of chronified back pain and muscle imbalance which may be very difficult to be influenced. Although this surgery is demanding, the morbidity cannot be considered significantly higher than in other established orthopaedic procedures, like hip replacement, in the same age group of patients. Overall, a satisfactory outcome can be expected in well-differentiated indications and properly tailored surgical procedures, although until today prospective, controlled studies with outcome measures and pre- and post-operative patient's health status are lacking. As patients, who present themselves with significant clinical problems in the context of adult scoliosis, get older, minimal invasive procedures to address exactly the most relevant clinical problem may become more and more important, basically ignoring the overall deformity and degeneration of the spine

5. ASKANASE AD, KATHOLI M, BUYON JP: Frequency of neuropsychiatric disorders, autoimmune diseases and autoantibodies in anti-SSA/Ro-exposed children. Arthritis & Rheumatism 52:9, Suppl. S S528, 2005

6. AVCIN T, SILVERMAN ED, FORTE V, SCHNEIDER R: Nasal septal perforation: a novel clinical manifestation of systemic juvenile idiopathic arthritis/adult onset still's disease. J Rheumatol 32:12 2429-2431, 2005
   Organism: Division of Rheumatology, Department of Otolaryngology, The Hospital for Sick Children, University of Toronto, Ontario, CanadaFAU - Avcin, Tadej
   Abstract: Nasal septal perforation has been well recognized in patients with various rheumatic diseases. To our knowledge, this condition has not been reported in children with systemic juvenile idiopathic arthritis (SJIA) or patients with adult onset Still's disease (AOSD). We describe 3 patients with persistent SJIA/AOSD who developed nasal septal perforation during the course of their disease. As illustrated by these cases, nasal septal perforation may develop as a rare complication of SJIA/AOSD and can be considered as part of the clinical spectrum of the disease. In one case the nasal septal perforation was associated with vasculitis

7. BADOT V, DEBANDT M, DESLANDRE C, LE PHU Q, WOUTERS C, HATRON P, DUQUESNE AGNES, BLONDIN G, POIGNANT S, PRIEUR A: Efficacy and tolerance of thalidomide in refractory systemic onset juvenile idiopathic arthritis (So-JIA): A retrospective study in 19 patients. Arthritis & Rheumatism 52:9, Suppl. S S85, 2005

8. BELLINTANI C, CARLETTI V, FARRONATO G, MASTAGLIO C, GATTINARA M, GERLONI V: Classification criteria of juvenile idiopathic arthritis and temporomandibular involvement. Annals of the Rheumatic Diseases 64:Suppl. 3 196, 2005

9. BELT EA, IKAVALKO M, SKYTTA E: A novel method in re-operation of severely destroyed metacarpophalangeal joints using biodegradable implant and bone packing. Annals of the Rheumatic Diseases 64:Suppl. 3 101, 2005

10. BEUKELMAN T, ARABSHAHI B, CAHILL A, KAYE RD, CRON RQ: Benefit of intra-articular corticosteroid injection under fluoroscopic guidance for subtalar arthritis in juvenile idiopathic arthritis. Arthritis & Rheumatism 52:9, Suppl. S S85, 2005

11. BILLIAU AD, HU Y, VERDONCK A, CARELS CARINE, WOUTERS C: Temporomandibular joint arthritis in juvenile idiopathic arthritis: radiological aspects and their relation to dentofacial morphology and clinical disease characteristics. Arthritis & Rheumatism 52:9, Suppl. S S88, 2005

12. BOYKINOV N: Rehabilitation of children with JIA at the Bulgarien black-sea littoral. Annals of the Rheumatic Diseases 64:Suppl. 3 599, 2005

13. BRITISH SOC PAEDIAT ADOLESCENT_: The impact of a coordinated transitional care programme on adolescents with juvenile idiopathic arthritis: A controlled trial. Arthritis & Rheumatism 52:9, Suppl. S S695-S696, 2005

14. BROWN GT, WRIGHT FV, LANG BA, BIRDI N, OEN K, STEPHENS D, MCCOMAS J, FELDMAN BM: Clinical responsiveness of self-report functional assessment measures for children with juvenile idiopathic arthritis undergoing intraarticular corticosteroid injections. Arthritis Rheum 53:6 897-904, 2005
    Organism: Monash University, Frankston, Victoria, AustraliaFAU - Brown, G Ted
    Abstract: OBJECTIVE: The Childhood Health Assessment Questionnaire (CHAQ), Juvenile Arthritis Functional Assessment Report (JAFAR), and Juvenile Arthritis Functional Status Index (JASI) are widely used functional measures for juvenile idiopathic arthritis (JIA) that differ in content, format, and completion time. We compared the responsiveness and child-parent agreement of the JAFAR, CHAQ, and JASI in a prospective, multicenter study. METHODS: Children and adolescents from 5 rheumatology centers were enrolled. Subjects were about to undergo therapy (intraarticular corticosteroid injections [IAS] and methotrexate or hip surgery (MTX/hip]) expected to produce a functional improvement. All subjects were studied before the intervention and at 6 weeks and 6 months posttreatment. At each study visit, the 3 measures were administered in randomized, balanced order to both parents and children. RESULTS: A total of 92 subjects (mean age 12.8 years) were enrolled in the study, 74 of which were in the IAS group. The responsiveness of all 3 measures was moderate to strong. The standardized response mean at 6 weeks for the IAS group on the JAFAR, CHAQ, and JASI was 0.41 (95% confidence interval [95% CI] 0.18, 0.64), 0.70 (95% CI 0.47, 0.93), and 0.36 (95% CI 0.13, 0.59), respectively. The CHAQ was somewhat more responsive to change at 6 weeks (IAS group: relative efficiency 0.34 [JAFAR], 0.27 [JASI]), but less responsive at 6 months (MTX/hip group: relative efficiency 5.1 [JAFAR], 3.9 [JASI]). All 3 questionnaires showed acceptable parent-child agreement, and overall, there were few differences between the 3 questionnaires. CONCLUSION: The functional outcome measures currently used for JIA are all adequately responsive for use in trials or in the clinic setting. The choice of which measure to use should therefore be based on the time available for completion, the intended clinical/research use, and the depth of content required

15. BRUNNER HI, JOHNSON AL, BARRON AC, PASSO MH, GRIFFIN TA, GRAHAM TB, LOVELL DJ: Gastrointestinal symptoms and their association with health-related quality of life of children with juvenile rheumatoid arthritis: validation of a gastrointestinal symptom questionnaire. J Clin Rheumatol 11:4 194-204, 2005
    Organism: Division of Rheumatology E 4010, Cincinnati Children's Hospital Medical Center, University of Cincinnati, 3333 Burnet Avenue, Cincinnati, OH 45229-3039, USA herminebrunner@cchmcorgFAU - Brunner, Hermine I
    Abstract: OBJECTIVES: The objectives of this study were to perform an initial validation of the Gastrointestinal Symptom Scale for Kids (GISSK) in children with juvenile rheumatoid arthritis (JRA); and too evaluate the relationship between gastrointestinal (GI) symptoms and health-related quality of life (HRQOL) in JRA. METHODS: A convenience sample of 77 children (median age, 10 years; range, 2-18 years) with JRA requiring second-line agents and one of their parents were interviewed. GI symptoms during the preceding 1 week were measured using the GISSK, which consists of 2 components, a visual analog scale of GI symptom severity (GISSK-VAS) and an 8-item questionnaire (GISSK-Q; score 0-8; 0= no GI symptoms). Information on medications, joint involvement with arthritis, and a physician rating of disease activity were obtained. Patient-centered outcomes included the Childhood Health Assessment Questionnaire (CHAQ) to assess disability and discomfort. HRQOL was measured by the Pediatric Quality of Life Generic Core Scale (PedsQL-GC) and the Rheumatology Module (PedsQL-RM), as well as a visual analog scale (VAS-health). To determine test-retest reliability, the GISSK was completed by 40 parents twice within a 1- to 2-week period. To determine the quality of parent proxy-reporting, parent ratings were compared with those of their children aged 8 years or older. RESULTS: GI symptoms were present in the majority of the patients with JRA (58%). Compared with other patients with JRA, those with a GISSK-Q score of > or =2 had significantly lower HRQOL (PedsQL-GC: P < 0.04; PedsQL-RM: P < 0.05; VAS-health: P < 0.02) and more disability (CHAQ: P < 0.002), despite similar disease activity and joint findings. Similar relationships were observed for the GISSK-VAS with traditional outcomes and HRQOL. The test-retest reliability of the GISSK was good (ICCGISSK-Q = 0.60; ICCGISSK-VAS = 0.67). The quality of parent proxy-reporting was fair to good (ICCGISSK-Q = 0.47; ICCGISSK-VAS = 0.66). CONCLUSION: GI symptoms are frequent among children with JRA requiring advanced therapies and, if moderate or severe, are associated with significantly lower HRQOL. The GISSK is a reliable and valid measure of GI symptoms and their severity in JRA. This self-administered measure can be used to screen for GI symptoms in clinical practice and may be useful to assess the effects of medication changes on the perceived GI side effects in children with JRA

16. BRUNNER H, I, GRAHAM TB, RUTHERFORD CYNTHIA, JOHNSON AL, LOVELL DJ, PASSO MH, KOTAGAL UR: Change in the outcomes of polyarticular-course juvenile rheumatoid arthritis during the last decade. Arthritis & Rheumatism 52:9, Suppl. S S82, 2005

17. BRUNNER JKH, HERRMANN M, METZLER M, GAIPL U, HAAS P: The T-cell repertoire in peripheral blood and synovial fluid in patients with juvenile idiopathic arthritis shows a clonotypic archetype. Annals of the Rheumatic Diseases 64:Suppl. 3 127-128, 2005

18. BUCALA R, LOLIS E: Macrophage migration inhibitory factor: A critical component of autoimmune inflammatory diseases. Drug News Perspect 18:7 417-426, 2005
    Organism: Department of Medicine, Yale University School of Medicine, New Haven, USA eliaslolis@yaleeduFAU - Bucala, Richard
    Abstract: Autoimmune inflammatory diseases occur commonly in Western populations and include conditions such as juvenile-onset diabetes mellitus, rheumatoid arthritis, inflammatory bowel disease and systemic lupus erythematosus. The precise cause of these diseases remains enigmatic. However, current notions of pathogenesis support an important interplay between host genetics and acquired, or environmental, factors. From an immunologic perspective, autoimmune inflammatory diseases develop as a result of a loss of immune tolerance and the initiation of immune-mediated tissue injury. In the following review, we discuss recent studies pointing to an important role for the upstream mediator macrophage migration inhibitory factor in the effector responses producing autoimmune tissue damage. (c) 2005 Prous Science. All rights reserved

19. BUTBUL-AVIEL Y, KOREN A, HALEVY R, SAKRAN W: Procalcitonin as a diagnostic aid in osteomyelitis and septic arthritis. Pediatr Emerg Care 21:12 828-832, 2005
    Organism: Pediatric Department B, Ha'Emek Medical Center, Afula, IsraelFAU - Butbul-Aviel, Yonatan
    Abstract: OBJECTIVES: Plasma procalcitonin (PCT) increases rapidly during bacterial infections but remains low in viral infections and other inflammatory processes. High plasma PCT typically occurs in children with bacterial meningitis, severe bacterial infections, particularly in cases of septic shock or bacteremia, and in renal parenchymal damage. The aim of this study was to test the usefulness of plasma PCT analysis in the diagnosis of osteomyelitis, septic arthritis, and other skeletal inflammatory diseases in pediatric patients admitted because of fever and limping. METHODS: White blood cell count, erythrocyte sedimentation rate, C-reactive protein, and PCT levels were measured in children admitted to the pediatric department with fever, limping, and suspected osteomyelitis or septic arthritis. PCT levels were measured by an immunochromatography assay, based on monoclonal and polyclonal antibodies against katacalcin. RESULTS: Forty-four children were evaluated: 12 (27.3%) were diagnosed with osteomyelitis, 11 (25%) had septic arthritis, 5 children (11.4%) were diagnosed as a soft tissue infection, and transient synovitis or reactive arthritis was diagnosed in another 6 children (13.6%). Four children (9.1%) were diagnosed as having juvenile rheumatoid arthritis, and 6 (13.6%) with different diseases. PCT value was elevated in 7 patients (58.3%) with osteomyelitis, and only 3 children (27.2%) with the diagnosis of septic arthritis had a mildly elevated value. Among the children with other diagnosis, there were no positive PCT values (P < 0.001 between skeletal infection and all other diagnosis). CONCLUSIONS: In this study, PCT was found to be a useful marker in the diagnosis of osteomyelitis and not in septic arthritis. A larger group of patients needed to be studied to confirm our findings

20. CAKIR N, PAMUK ON, DERVIS E, IMERYUZ N, USLU H, BENIAN O, SENOCAK M: The prevalance of rheumatologic diseases in Havsa: The initial evaluation. Annals of the Rheumatic Diseases 64:Suppl. 3 551, 2005

21. CHAN AYK, LIU DTL, ARKELA-KAUTIAINEN M, HAAPASAARI J, LEIRISALO-REPO M, KOTANIEMI K: Uveitis in young adults with juvenile idiopathic arthritis (multiple letters). Annals of the Rheumatic Diseases (United Kingdom ) 64:12 1808, 2005

22. CHAN AT, KOLLNBERGER S, WEDDERBURN LUCY, BOWNESS P: Expansion and increased survival of natural killer and CD4 T cells expressing the Killer IG-like Receptor KIR3DL2 in spondyloarthritis. Arthritis & Rheumatism 52:9, Suppl. S S691, 2005

23. DE CIVITA M, EHRMANN F, MESHEFEDJIAN GA, DOBKIN PL, MALLESON P, CIARAN M: Caregiver recall of treatment recommendations in juvenile idiopathic arthritis (JIA). Arthritis & Rheumatism 52:9, Suppl. S S539, 2005

24. DE K, I, VERCOULEN Y, KLEIN M, ALBANI SALVATORE, KUIS W, PRAKKEN B: Human heat shock protein 60 as a natural antigen for CD4+ CD25+ regulatory T-cells and augments T-cell mediated immunoregulation at sites of tissue damage. Arthritis & Rheumatism 52:9, Suppl. S S446, 2005

25. DORE RK, MANDEL D, SCHECHTMAN J, ZHOU L, BEKKER P, PELOSO PM: Liquid etanercept results in clinically important improvements in rheumatoid arthritis patient reported outcomes. Annals of the Rheumatic Diseases 64:Suppl. 3 462, 2005

26. EBERHARD BA, SISON MC, BETH S, ILOWITE NT: Dose for intra-articular steroids: Is more really better? Arthritis & Rheumatism 52:9, Suppl. S S83, 2005

27. ESPADA G, MEIORIN SM, WEISSBROD PAULA, GAMIO S, TARTARA A, COUTO C: Etanercept therapy for JIA-associated refractory uveitis. Arthritis & Rheumatism 52:9, Suppl. S S87-S88, 2005

28. FALL N, BOVE KE, STRINGER K, DANIEL J, BRUNNER H, I, WEISS J, HIGGINS GC, SUSANNE L, GRAHAM TB, THORNTON S, GROM AA: High expression of angiostatic ELR-negative CXC-chemokines: Possible link to vasculopathy in juvenile dermatomyositis. Arthritis & Rheumatism 52:9, Suppl. S S305, 2005

29. FERLITO F, CORCIONE A, GREGORIO ANDREA, PISTOIA V, MARTINI A, GATTOMO M: B cells differentiation in the context of synovial tissue in patients with juvenile idiopathic arthritis. Arthritis & Rheumatism 52:9, Suppl. S S305, 2005

30. FERREIRA RA, FERRIANI VPL, SILVA CHM, MINEO J, SILVA DAO, SOPELETE MC, KISS MHB: Is measurement of IgM and IgA rheumatoid factor in juvenile rheumatoid arthritis clinically usefull? Annals of the Rheumatic Diseases 64:Suppl. 3 509, 2005

31. FILOCAMO G, SZTAJNBOK F, CESPEDES ADRIANA, RUPERTO N, VIOLA S, BUONCOMPAGNI A, LOY ANNA, MARTINI A, RAVELLI A: Development and initial validation of a new functional ability measure that is shorter and simpler than the C-HAQ. Arthritis & Rheumatism 52:9, Suppl. S S90-S91, 2005

32. FOELDVARI I, WIERRK A: Characteristics of patients with temporomandibular joint involvement associated to juvenile idiopathic arthritis. 33% the patients are asymptomatic despite sings of active arthritis on imaging studies. Annals of the Rheumatic Diseases 64:Suppl. 3 509, 2005

33. FOELDVARI I, KUEMMERLE-DESCHNER J, NIELSON SUSAN, ESPADA G, HORNEFF G, BICA B, OLIVIERI AN, LEBLANC CLAIRE, FISCHBACH M, GARAY S, HENRICKSON M, KATSIKAS M, O'NEILL K, WHELAN PJ, WIERK A, SAUERENMANN T: Tumor necrosis factor alfa blocker are effective in the treatment of juvenile idiopathic arthritis associated uveitis refractory to second line agents: Results of the multinational survey. Arthritis & Rheumatism 52:9, Suppl. S S534-S535, 2005

34. FOELL D, WITTKOWSKI H, HAMMERSCHMIDT INGA, FROSCH M, VOGL T, ROTH J: Early detection of flare-ups by S100A12 serum levels in juvenile idiopathic arthritis. Arthritis & Rheumatism 52:9, Suppl. S S93, 2005

35. GAROFALO G, GRASSI W, LEHMAN T, ADLER R: Ultrasound is a reliable procedure in the assessment of the musculoskeletal system in pediatric population. Annals of the Rheumatic Diseases 64:Suppl. 3 512, 2005

36. GATTORNO M, RUPRECHT C, GREGORIO ANDREA, FERLITO F, MARTINI A, LANZAVECCHIA A, SALLUSTO FEDERICA: Coexpression of CD25 and CD27 identifies Foxp3(+) regulatory T cells in inflamed synovia in juvenile idiopathic arthritis. Arthritis & Rheumatism 52:9, Suppl. S S442-S443, 2005

37. GERLONI V, LURATI A, TERUZZI BARBARA, CRAPANZANO C, GATTINARA M, FANTINI F: Anti-cyclic citrullinated peptide antibodies in juvenile idiopathic arthritis (jia). A monocentric cross-sectional study. Arthritis & Rheumatism 52:9, Suppl. S S84, 2005

38. GERLONI V, PONTIKAKI I, DE M, GATTINARA M, VALCAMONICA E, LURATI ALFREDOMARIA, SALMASO A, TERUZZI B, FANTINI F: Long-term evaluation (efficacy and safety) of infliximab in the treatment of persistently active juvenile idiopathic arthritis (JIA), refractory to standard treatments. Arthritis & Rheumatism 52:9, Suppl. S S84, 2005

39. GIBSON DS, BLELOCK S, BROCKBANK S, CURRY JIM, HEALY A, ROONEY ME: Proteomic validation of a biomarker cluster associated with chronic joint inflammation in juvenile idiopathic arthritis. Arthritis & Rheumatism 52:9, Suppl. S S417-S418, 2005

40. GONG GRACE WK, YOUNG NL, DEMPSTER H, POREPA MICHELLE, FELDMAN BM: The Quality of my Life questionnaire: The minimal clinically important difference for pediatric rheumatology patients. Arthritis & Rheumatism 52:9, Suppl. S S661, 2005

41. GOTTLIEB B, SISON C, HIGGINS G, HUBER ADAM, KIMURA Y, LOVELL D, HASHKES P, SANDBORG CHRISTY, RABINOVICH CE, WALLACE C, WAGNER-WEINER L, LINDSLEY CAROL, SZER I, DIXON E, ROETTCHER P, BOWYER S, LONG T: Outcomes of juvenile rheumatoid arthritis (JRA): Changing treatment patterns and outcomes. Arthritis & Rheumatism 52:9, Suppl. S S81-S82, 2005

42. GRAVE C, POPELLA A: Education of children with juvenile idiopathic arthritis and theit parents. Annals of the Rheumatic Diseases 64:Suppl. 3 608, 2005

43. GUTIERREZ-SUAREZ R, CESPEDES A, RAVELLI ANGELO, PRIEUR A, MACHADO C, MURRAY K, SUSIC GORDANA, RUMBA I, NIELSEN S, TSAKALIDOU F, HARJACEK M, NIKISHINA I, MIHAYLOVA DIMITRINA, BURGOS-VARGAS R, RUPERTO N, MARTINI A: Does the perception of health related quality of life (hrql) in children with juvenile idiopathic arthritis (JIA) change among different cultures? Arthritis & Rheumatism 52:9, Suppl. S S696-S697, 2005

44. HAGEL S, ANDERSSON M, BRITT M, MOGARD E, LINDQVIST E: Multidisciplinary rehabilitation for patients with arthritis description of programme and evaluation of outcome. Arthritis & Rheumatism 52:9, Suppl. S S433, 2005

45. HARAOUI B, KEYSTONE E: Musculoskeletal manifestations and autoimmune diseases related to new biologic agents. Curr Opin Rheumatol 18:1 96-100, 2006
    Organism: aUniversite de Montreal, RDU CHUM, Hopital Notre-Dame, Montreal, Quebec, Canada bUniversity of Toronto, Rebecca MacDonald Centre for Arthritis and Autoimmunity, Mount Sinai Hospital, Toronto, Ontario, CanadaFAU - Haraoui, Boulos
    Abstract: PURPOSE OF REVIEW: The anti-tumor necrosis factor agents are now widely used in the management of patients with rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis and juvenile inflammatory arthritis. One of the most common observations made during their use is the development of autoantibodies. The purpose of this paper is to review this phenomenon and its clinical implications. RECENT FINDINGS: While the development of different autoantibodies is a common encounter, rare cases of lupus-like syndromes have been reported. On the other hand, a variety of immune-mediated clinical manifestations have been described, including vasculitis and demyelinating syndromes. Rare cases of cytopenia and non-specific lung injuries have also been reported. SUMMARY: While these clinical complications are rare and isolated events, clinicians must be aware of their occurrence. The experience with the anti-tumor necrosis factor agents is rather short and new, unusual immune-mediated complications may still appear. Clinicians should be prepared to recognize them

46. HAVEMOSE-POULSEN A, SORENSEN LK, STOLTZE K, BENDTZEN K, HOLMSTRUP P: Cytokine Profiles in Peripheral Blood and Whole Blood Cell Cultures Associated With Aggressive Periodontitis, Juvenile Idiopathic Arthritis, and Rheumatoid Arthritis. J Periodontol 76:12 2276-2285, 2005
    Organism: * Department of Periodontology, School of Dentistry, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark, dagger Institute for Inflammation Research, Rigshospitalet National University Hospital, Copenhagen, Copenhagen, Denmark
    Abstract: Background: Cytokines play a key role in the pathogenesis of inflammatory diseases. An obvious question is whether patients with aggressive periodontitis, juvenile idiopathic arthritis, or rheumatoid arthritis share blood cytokine profiles distinguishing them from individuals free of disease. Methods: The study population consisted of Danish white adults, <35 years of age, diagnosed with localized aggressive periodontitis (LAgP; N = 18), generalized aggressive periodontitis (GAgP; N = 27), juvenile idiopathic arthritis (JIA; N = 10), or rheumatoid arthritis (RA; N = 23) and healthy individuals with no systemic or oral diseases (control [CTRL]; N = 25). Enzyme-linked immunosorbent assays were used to determine the levels of interleukin (IL)-1alpha, IL-1beta, IL-1 receptor antagonist (IL-1Ra), IL-6, IL-10, tumor necrosis factor (TNF)-alpha, and lymphotoxin (LT)-alpha in peripheral blood (plasma) and unstimulated and stimulated whole blood cell cultures from the same blood collection. Autoantibodies (aAb) to IL-1alpha and IL-6 were quantitated by radioimmunoassay. Results: Similar patterns of slightly higher IL-10 levels in plasma were found for GAgP and RA patients and in unstimulated cultures for GAgP, RA, and JIA patients. Interestingly, unstimulated cultures also demonstrated similar patterns of higher TNF-alpha levels for these three groups of patients. Similar group patterns of periodontitis patients (LAgP and GAgP) included increased IL-1Ra levels in stimulated cultures, which also showed similar group patterns of arthritis patients (JIA and RA) with respect to higher IL-1alpha and lower LT-alpha levels. Low titers of aAb to IL-1alpha and IL-6 were found in almost all individuals. Conclusion: Patients with aggressive periodontitis and types of arthritis presented with similar components of blood cytokine profiles distinguishing them from individuals free of disease

47. HORNEFF G: [Biologics for treatment of juvenile idiopathic arthritis Consensus statement of the 7th Worlitzer Expertengesprache 2004 for the German Arbeitsgemeinschaft Kinder- und Jugendrheumatologie.]. Z Rheumatol .: 2005
    Organism: , Universitatsklinik und Poliklinik fur Kinder und Jugendmedizin, Halle
    Abstract: The group of biologics for the treatment of rheumatic diseases is continuously growing. They have become an important option not only for treatment of so far untreatable chronic inflammatory or rheumatic disease, but also for juvenile idiopathic arthritis. In addition, the velocity and the degree of improvement is better than with to conventional therapies. Furthermore, toxicity and risks seem to be lower with higher safety and compatibility. Although the data are scarce, they are widely used. Therefore, the German Arbeitsgemeinschaft Kinder- und Jugendrheumatologie is updating the current recommendation for the treatment of juvenile idiopathic arthritis using biologics [6]

48. HORNEFF G, KUESTER R, GIRSCHICK H, FOELDVARI I, MOEBIUS D: Safety of etanercept for treatment of juvenile idiopathic arthritis (JIA) - Data of the German etanercept JIA registry. Annals of the Rheumatic Diseases 64:Suppl. 3 72, 2005

49. HORNEFF G, GIRSCHICK H, FOELDVARI IVAN, MICHELS H, ROGALSKI B, SCHMELING H: Combination therapy with etanercept and methotrexate compared to etanercept monotherapy in patients with juvenile idiopathic arthritis. Arthritis & Rheumatism 52:9, Suppl. S S724-S725, 2005

50. HUBER A, TOMLINSON G, KOREN G, FELDMAN BM: An innovative method to assess pain relief by amitriptyline in juvenile rheumatoid arthritis (JRA). Arthritis & Rheumatism 52:9, Suppl. S S93, 2005

51. ISHIKAWA S, AOKI C, IMAGAWA T, MORI MASAAKI, TOMIITA M, IWATA N, MURATA T, MIYOSHI M, TAKEI SYUJI, AIHARA Y, MATSUBARA K, YOKOTA S, NISHIMOTO N: Distinction between systemic-onset type and polyarticular type juvenile idiopathic arthritis using gene expression profiles determined by oligonucleotide microarray. Arthritis & Rheumatism 52:9, Suppl. S S255, 2005

52. JAROSOVA K, SVIHALEK J, DUSEK L, VENCOVSKY J: Treatment with TNF alfa blocking agents in adult patients with juvenile idiopathic arthritis derived from the Czech national registry. Annals of the Rheumatic Diseases 64:Suppl. 3 511, 2005

53. JARVIS JN, PETTY HR, KINDZELSKI ANDREI, TESSIER P, JIANG K, TANG Y, MCGHEE JL, CENTOLA MICHAEL: Is polyarticular JRA a disease of neutrophils? Evidence for an intrinsic defect in neutrophil activation in polyarticular JRA. Arthritis & Rheumatism 52:9, Suppl. S S446-S447, 2005

54. JEPSEN K, V, PFEIFFER-JENSEN M, HERLIN T, STENBOEG E: Ultrasound measurement of joint cartilage in healthy children: Assessment of observer variability. A pilot study. Annals of the Rheumatic Diseases 64:Suppl. 3 516, 2005

55. JEUSIC M, BUKOVAC LT, MALCIC I, LUKIC I, DUBRAVCIC K, BATINIC D: Regulatory T cells in juvenile idiopathic arthritis. Annals of the Rheumatic Diseases 64:Suppl. 3 147, 2005

56. JEUSIC M, BUKOVAC LT, MALCIC I, LUKIC I, DUBRAVCIC K, BATINIC D: Interleukin-18 as a mediator of systemic juvenile idiopathic arthritis (JIA). Annals of the Rheumatic Diseases 64:Suppl. 3 142, 2005

57. KAMPHUIS S, VAN DER MA, KLEIN M, JAGER W, RIJKERS GT, MARTINI A, KUIS W, ALBANI SALVATORE, PRAKKEN BJ: Dynamics of T cell responses to HSP60 epitopes in JIA patients plead for an immunomodulatory role in disease pathogenesis. Arthritis & Rheumatism 52:9, Suppl. S S304, 2005

58. KAPITONOVA MY, OTHMAN M: Ultrastructural characteristics of synovial effusion cells in some arthropathies. Malays J Pathol 26:2 73-87, 2004
    Organism: Department of Anatomy, School of Medical Sciences, University Sains Malaysia, Kelantan, Malaysia marina@kbusmmyFAU - Kapitonova, M Yu
    Abstract: OBJECTIVE: To evaluate the range of activation changes of polymorphonuclear leukocytes (PMN) and the ratio of apoptosis and necrosis in synovial effusions of patients with various arthropathies, and to reveal possible correlations with clinical variants of joint inflammation. METHODS: Synovial effusions were aspirated from the knee joints of patients with rheumatoid arthritis (RA, 28 cases), and seronegative spondyloarthritides (SSA): Reiter's disease (RD, 9 cases), peripheral form of the ankylosing spondyloarthritis (6 cases) and psoriatic arthritis (6 cases); and primary osteoarthritis (OA, 9 cases). Cytospin preparations were processed for transmission electron microscopy and assessed for the incidence of apoptosis, necrosis, and cytophagocytic cells (CPC) in the synovial fluid (SF). The range of activation changes of the neutrophil granulocytes, the dominating cell population in the arthritic SF, was evaluated. RESULTS: In all arthropathies under investigation most of the synovial effusion cells had intact ultrastructure with a certain amount of apoptotic cells dominating over the cells with signs of necrosis, and a few CPC. The highest rate of apoptosis was discovered in the synovial effusions of patients with RA, the lowest in those with OA, while the rate of CPC among the inflammatory joint diseases was the lowest in RA. In RA the current disease activity correlated with the incidence of apoptotic cells and CPC, while the clinical stage was related only to the CPC rate. These data suggest that in RA, despite exposure to the anti-apoptotic signals, apoptosis of the synovial effusion PMN is maintained at a significantly higher level than in non-rheumatoid arthropathies, both inflammatory (SSA) and degenerative (OA), providing elimination of the neutrophils accumulating in the joint cavity and thus stimulating resolution of the joint inflammation

59. KEKOW J, KOCZAN D, KEKOW M, DRYNDA S, THIESEN H, GUTHKE R, OPPERMANN J: Application of gene expression profiling in patients with juvenile idiopathic arthritis (JIA) for the prediction of the outcome of anti-TNFalpha therapy. Annals of the Rheumatic Diseases 64:Suppl. 3 73, 2005

60. KISS G, KELEMEN J, BELY M, VERTES P: Clinically diagnosed fatal cerebral vasculitis in long-standing juvenile rheumatoid arthritis. Virchows Arch :1-3.: 1-3, 2005
    Organism: Intensive Care Unit, National Institute of Rheumatology and Physiotherapy, Frankel Leo u 17-19, 1023, Budapest, Hungary, bszende@korb1sotehu

61. KOKSVIK HS, MAGNUSSEN AS, SKOMSVOLL JF: One year follow-up of etanercept exposed pregnancies. Annals of the Rheumatic Diseases 64:Suppl. 3 449, 2005

62. KOSTIK MM, BARANOV DN, GLAZKOV PB, PACHOMOVA M, VORONTSOV IM, LARYONOVA V, I: Genetic markers and osteopenia in children with juvenile chronic arthritis in St.Petersburg. Annals of the Rheumatic Diseases 64:Suppl. 3 112, 2005

63. KOTTER I, DAIKELER T, AMBERGER C, TYNDALL A, KANZ L: Autologous stem cell transplantation of treatment-resistant systemic vasculitis--a single center experience and review of the literature. Clin Nephrol 64:6 485-489, 2005
    Organism: University Hospital, Department of Internal Medicine II (Oncology, Hematology, Immunology, Rheumatology, Pulmology), Tubingen, Germany inakoetter@meduni-tuebingendeFAU - Kotter, I
    Abstract: AIMS: Autologous peripheral blood stem cell transplantation (autoPBSCT) is increasingly and successfully applied to patients with treatment-resistant autoimmune diseases, mainly multiple sclerosis and systemic sclerosis, but also juvenile idiopathic arthritis and systemic lupus erythematosus. We intended to analyze the effects of autoPBSCT in patients with treatment-resistant systemic vasculitis by analyzing the outcome of 4 patients from our own hospital, and comparing them to cases reported in the literature. METHODS: 4 patients with treatment-resistant vasculitis (Wegener granulomatosis, Churg Strauss syndrome, Takayasu arteritis and relapsing polychondritis) received an autologous PBSCT. Stem cell mobilization was performed with cyclophosphamide (CY) and G-CSF, stem cells were purged by positively selecting CD34+ stem cells over a CliniMacs device, and the conditioning was performed with high dose CY and anti-thymocyte globulin (ATG). RESULTS: AutoPBSCT was well tolerated in all 4 patients. The patient with WG achieved complete remission although cANCA persisted, the other patients are in good partial remissions and respond to maintenance treatments which had been ineffective before PBSCT (CSA, azathioprin). Glucocorticosteroids (GC) could be reduced to a maximum of 10 mg in all patients. Shortly after the procedure, reactivation of viruses from the herpes family occurred in 3 of the patients and had to be treated. In the data base, 25 patients transplanted for severe systemic vasculitis are registered, in the literature, 6 additional vasculitis patients remitting after autoPBSCT are reported. CONCLUSIONS: Autologous PBSCT is feasible and effective in severe, treatment-resistant forms of systemic vasculitis. Data are sparse, further prospective studies are needed. These should also aim at evaluating more optimal regimens for conditioning and purging during PBSCT, as in most of the vasculitis patients reported until now, mostly good partial remissions, but less complete remissions were achieved

64. KRUITHOF E, VAN DB, V, DE R, VANDOOREN B, JOOS R, ELEWAUT D, DE KEYSER F, VEYS E, BAETEN D: Juvenile chronic arthritis displays synovial features distinct from both spondyloarthropathy and rheumatoid arthritis. Arthritis & Rheumatism 52:9, Suppl. S S89, 2005

65. KYNGAS HA: Predictors of good adherence shown by adolescnets with arthritis. Annals of the Rheumatic Diseases 64:Suppl. 3 583-584, 2005

66. LAI JH: Taiwan experience with etanercept in juvenile rheumatoid arthritis. J Microbiol Immunol Infect 38:6 451-454, 2005
    Organism: Division of Rheumatology, Immunology and Allergy, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan E-mail: haungben@tpts5seednettwFAU - Lai, Jenn Haung

67. LE GT, ABBENANTE G: Inhibitors of TACE and Caspase-1 as anti-inflammatory drugs. Curr Med Chem 12:25 2963-2977, 2005
    Organism: Centre for Drug Design and Development, Institute for Molecular Bioscience, University of Queensland, Brisbane, Qld 4072, AustraliaFAU - Le, Giang T
    Abstract: TNF-alpha neutralising agents such as Infliximab (Remicade), Etanercept (Enbrel) and the IL-1 receptor antagonist Anakinra (Kineret), are currently used clinically for the treatment of many inflammatory diseases such as Crohn's disease, rheumatoid arthritis, ankylosing spondylitis, juvenile rheumatoid arthritis, psoriatic arthritis and psoriasis. These protein preparations are expensive to manufacture and administer, need to be injected and can cause allergic reactions. An alternative approach to lowering the levels of TNF-alpha and IL-1beta in inflammatory disease, is to inhibit the enzymes that generate these cytokines using cheaper small molecules. This paper is a broad overview of the progress that has been achieved so far, with respect to small molecule inhibitor design and pharmacological studies (in animals and humans), for the metalloprotease Tumour Necrosis Factor-alpha Converting Enzyme (TACE) and the cysteine protease Caspase-1 (Interleukin-1beta Converting Enzyme, ICE). Inhibitors of these two enzymes are currently considered to be good therapeutic targets that have the potential to provide relatively inexpensive and orally bioavailable anti-inflammatory agents in the future

68. LIANG TC, YANG YH, LIN YT, CHIANG BL: Treatment with etanercept for patients with juvenile rheumatoid arthritis in Taiwan - a preliminary report. J Microbiol Immunol Infect 38:6 447-450, 2005
    Organism: Department of Pediatrics, National Taiwan University Hospital, Taipei, TaiwanFAU - Liang, Tien Chi
    Abstract: Tumor necrosis factor (TNF) is a major inflammatory cytokine involved in the pathogenesis of juvenile rheumatoid arthritis (JRA). Etanercept, approved in the United States and in Europe for use in patients with rheumatoid arthritis (RA) and JRA, is an effective inhibitor of TNF that has been shown to provide rapid and sustained improvement in both diseases. Here we report the preliminary results of etanercept use in 3 cases of JRA with poor response to traditional therapy including non-steroidal anti-inflammatory drugs and disease-modifying antirheumatic drugs. Two of the patients had polyarticular JRA and 1 had systemic JRA. Etanercept was administered at a dosage of 0.4 mg/kg (maximum 25 mg) subcutaneously twice a week. Clinical as well as inflammatory parameter improvement was noted after use of etanercept in all cases. The preliminary results of etanercept use in these 3 cases showed significant clinical benefit without obvious adverse effects

69. LIEBLING A, BACAL DA, THORNQUIST SC: Infliximab in refractory childhood uveitis. Annals of the Rheumatic Diseases 64:Suppl. 3 513, 2005

70. LIPHAUS BL, GOLDENSTEIN S, KISS MARIA HB: Increased expression of Fas and Bcl-2 proteins in juvenile systemic lupus erythematosus but not in juvenile rheumatoid arthritis and Juvenile dermatomyositis. Arthritis & Rheumatism 52:9, Suppl. S S532, 2005

71. LIU DT, CHAN AY: Assessment of inflammatory response in a study of uveitis associated with juvenile idiopathic arthritis: comment on the article by Smith et al. Arthritis Rheum 53:6 986-987, 2005

72. LOTITO ANA PN, SILVA CLOVIS AA, CAMPA A, SUZANA B: Interleukin-18 in juvenile idiopathic arthritis patients: A marker of disease activity and damage. Arthritis & Rheumatism 52:9, Suppl. S S254-S255, 2005

73. LOVELL DJ, RUPERTO N, CUTTICA RUBEN, WILKINSON N, ESPADA G, WOUTERS C, SILVERMAN E, BALOGH ZSOLT, HENRICKSON M, LAHDENNE P, PRIEUR A, GERLONI V, FASTH A, SAURENMANN RK, BAILDAM E, MARIA T, WOO P, MARTINI A, TRAVERS S, RAYCHAUDHURI APARNA, VISVANATHAN S, FASANMADE A, WAGNER C, GIANNINI EDWARD: Comparison of safety, efficacy and pharmacokinetics for 3 and 6 mg/kg infliximab plus methotrexate therapy in JRA patients. Arthritis & Rheumatism 52:9, Suppl. S S724, 2005

74. LOW JM, DOBBLER BE, OLIVER DA, TERRY L: Prognostic biomarkers of joint damage in juvenile idiopathic arthritis (JIA). Arthritis & Rheumatism 52:9, Suppl. S S254, 2005

75. LOW JM, CHAUHAN AK, PEPMUELLER PH, TERRY L: Relationship of immunoglobulin light (IgL) chain editing and complement activation in immune complexes (ICs) from the sera of patients with juvenile idiopathic arthritis (JIA). Arthritis & Rheumatism 52:9, Suppl. S S304-S305, 2005

76. LURATI A, TERUZZI B, SALMASO A, DE MARCO G, GATTINARA M, PONTIKAKI I, GERLONI V, FANTINI F: One case of macrophagic activation syndrome during anti IL1 receptor therapy in a patient affected by systemic juvenile arthritis. Annals of the Rheumatic Diseases 64:Suppl. 3 515-516, 2005

77. LURATI A, GERLONI V, GATTINARA M, SALMASO A, DE M, TERUZZI B, PONTIKAKI I, FANTINI F: Disease activity, delayed menarche and bone mineralisation in juvenile rheumatoid arthritis (JRA). Annals of the Rheumatic Diseases 64:Suppl. 3 514, 2005

78. LURATI A, PONTIKAKI I, TERUZZI BARBARA, DESIATI F, GERLONI V, GATTINARA M, CIMAZ ROLANDO, FANTINI F: A comparison of response criteria in patients with juvenile idiopathic arthritis treated with methotrexate and/or anti-TNF alpha agents. Arthritis & Rheumatism 52:9, Suppl. S S91, 2005

79. MACHADO SH, VON MUHLEN CA, BRENOL JC, BISOTTO L, XAVIER RM: [The prevalence of anti-cyclic citrullinated peptide antibodies in juvenile idiopathic arthritis]. J Pediatr (Rio J) 81:6 491-494, 2005
    Organism: Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, BrazilFAU - Machado, Sandra H
    Abstract: OBJECTIVES: To assess the presence of anti-cyclic citrullinated peptide antibodies in a cohort of patients with juvenile idiopathic arthritis. METHODS: Anti-cyclic citrullinated peptide antibodies was tested for with an enzyme linked immunoabsorbent assay (ELISA) in serum samples of patients from the Hospital de Clinicas de Porto Alegre, all less than 18 years old and with previous diagnosis for at least 6 months. IgMRF (rheumatoid factor) and antinuclear antibodies in Hep-2 cells were also assayed. RESULTS: Serum samples were analyzed from 45 patients. The presence of high levels of anti-cyclic citrullinated peptide antibodies was found in the serum of just one child (2%), who presented sero-positive polyarthritis. CONCLUSIONS: Anti-cyclic citrullinated peptide antibodies can be detected in children with juvenile idiopathic arthritis, but much less frequently than in adults with rheumatoid arthritis. It still remains to be determined whether anti-cyclic citrullinated peptide antibodies can identify a subset of juvenile idiopathic arthritis patients with the potential to progress to adult rheumatoid arthritis

80. MAGNI-MANZONI S, SOLARI N, PALMISANI ELENA, SALA E, PISTORIO A, RUPERTO N, CUGNO C, BOZZOLA ELENA, STROZZI C, FILOCAMO G, MARTINI A, RAVELLI ANGELO: Toward the development of a disease activity score for juvenile idiopathic arthritis. Arthritis & Rheumatism 52:9, Suppl. S S89-S90, 2005

81. MALIEVSKY VA, VALEEVA RN, SALIMOVA RM: The structure of juvenile idiopathic arthritis. Annals of the Rheumatic Diseases 64:Suppl. 3 508-509, 2005

82. MATES M, NAVON P, BREUER GS, NESHER GIDEON: Desesitization to hydroxychloroquine in four patients with hypersensitivity eruption. Arthritis & Rheumatism 52:9, Suppl. S S191-S192, 2005

83. MCDONAGH JE, HACKETT J, SOUTHWOOD T, SHAW KL: The pre-vocational and early-employment needs of adolescents with juvenile idiopathic arthritis: The adolescent perspective. Arthritis & Rheumatism 52:9, Suppl. S S666, 2005

84. MEIORIN SM, BARZOLA ML, COZZANI HUGO, HOWLIN L, VAZQUEZ H, ZAYAT A, GALLI B, AYUSO CLAUDIA, ESPADA G: Lipid abnormalities and dyslipoproteinaemia (DL) in juvenile rheumatoid arthritis (JRA). Prevalence and associated risk factors. Arthritis & Rheumatism 52:9, Suppl. S S92-S93, 2005

85. MELCHIORRE D, SIMONINI G, VIERUCCI SILVIA, GIANI T, FALCINI F: Ultrasonography of the temporomandibular joint is helpful in the early diagnosis of the oligoarticular and monoarticular-onset juvenile idiopathic arthritis. Arthritis & Rheumatism 52:9, Suppl. S S87, 2005

86. MELIHOVA N, I, KORESHKOV GG: Long-term follow up of endocrine glands functional state in patients with juvenile rheumatoid arthritis. Pediatriya (Moscow)4 42-46, 2005
    Abstract: Authors studied transformation of endocrine system functional state in 43 children with juvenile rheumatoid arthritis (JRA), including 24 children with articular variant and 19 patients with systemic variant of JRA. Endocrine functions were examined by radioimmine assay. Disorders of endocrine state in these patients presented in prevalence as systemic decreasing or increasing of hormones level in different parts of endocrine system, more significant in hypophysis - adrenal cortex system and in patients with systemic JRA variant and long duration of articular JRA variant. Initial difference of hormones level correlated significantly with activity and character of pat hologic process and testified to physiologic compensatory reaction of endocrine glands under the influence of intensive antigen stimulation (protective reaction). Fluctuations of hormones level during all the period of study were non-similar with deviation from control parameters but with persistence of self-control principle in majority of cases. Safe adaptation was formed slowly but continuously under the influence of adequate therapy; hormines level tended to normalization in majority of cases (96,8%). Adaptation without complete physiologic harmonization of endocrine system function occurred in 3,2% of cases in the end of study

87. MELSON PG, BRUNNER H, I, FORD KR, GREG D, DARNELL SC, RANZ J, V, HEWITT TE: The use of three dimensional motion analysis (MA) to improve objective measurement of lower extremity joint function and detect clinical changes in children with juvenile idiopathic arthritis (JIA). Arthritis & Rheumatism 52:9, Suppl. S S665-S666, 2005

88. MENDOZA D, SIANES FM, HERNANDEZ C, ARIZA-ARIZA R, SAENZ DE MIERA FT, SARABIA FN: Efficacy and toxicity of biologic treatments in a rheumatic outpatientscohort at the rheumatology department of a third level hospital. Annals of the Rheumatic Diseases 64:Suppl. 3 467, 2005

89. MIER R, BRUNNER H, ROSENBERG A, WALLACE CAROL: Diagnostic predictors of poor outcome of uveitis associated with juvenile idiopathic arthritis (JIA). Arthritis & Rheumatism 52:9, Suppl. S S88, 2005

90. MOALIC V, FEREC C: [HLA typing, analysis methods, and clinical applications]. Presse Med 34:15 1101-1108, 2005
    Organism: Laboratoire de genetique moleculaire et d'histocompatibilite, CHU Augustin Morvan, Brest (29) virginiemoalic@chu-brestfrFAU - Moalic, V
    Abstract: The polygenic HLA system is a well known region of the human genome. Its main function is to present antigenic peptides to the immune system and thereby regulate induction of immune responses. Extensive genetic polymorphisms characterize some HLA genes. Initially, genetic variations were analyzed by a serological typing technique (microlymphocytotoxicity). The introduction of polymerase chain reaction (PCR) in the mid-1980s led the development of a variety of methods that use molecular biology. An international nomenclature, regularly updated, governs the names of HLA antigens defined by serology as well as of HLA alleles. Knowledge of the specific polymorphisms of individuals is essential in organ and stem cell transplantation and highly useful in disease association studies

91. MODER KG, VONWALD L, HOMBURGER H: Antichromatin antibodies help differentiate mixed connective tissue disease from other connective tissue diseases. Arthritis & Rheumatism 52:9, Suppl. S S427, 2005

92. MOR-VAKNIN N, PUNTURIERI A, SITWALA KAJAL, FAULKNER N, LEGENDRE M, CLEARY J, KHODADOUST M, BURRELL B, RUTH JH, KOCH AE, GLASS DN, PETRUZZELLI LILLI, ADAMS BS, MARKOVITZ DM: The nuclear protein DEK, a putative autoantigen in JRA, is secreted by activated human macrophages and exhibits chemokine activity. Arthritis & Rheumatism 52:9, Suppl. S S442, 2005

93. MORI M, IMAGAWA T, FUJIKAWA SATOSHI, TAKEI S, TOMIITA M, MURATA T, YOKOTA S: Analysis of clinical characteristics of juvenile idiopathic arthritis in Japan - A multicenter cohort study. Arthritis & Rheumatism 52:9, Suppl. S S91, 2005

94. NIELSEN S, RUPERTO N, SIMONINI GABRIELE, ALPIGIANI MG, BARCELLONA R, GERLONI VALERIA, ZULIAN F, CORTIS E, CORONA F, ROSSI FEDERICA, LOMBARDINI G, MAGNI-MANZONI S, MARTINI ALBERTO, RAVELLI A: Preliminary evidence that etanercept is more effective than methotrexate in suppressing inflammation and in reducing radiographic progression in juvenile idiopathic arthritis. Arthritis & Rheumatism 52:9, Suppl. S S82-S83, 2005

95. NIEWERTH M, MINDEN K, LISTING J, SCHOENTUBE M, ZINK A: Health-related quality of life in children with juvenile idiopathic arthritis. Annals of the Rheumatic Diseases 64:Suppl. 3 510-511, 2005

96. OWLIA MB, SOLEIMANI H, MORTAZAVIZADEH MR: Macrophage Activation Syndrome (MAS) and thrombotic thrombocytopenic purpura (TTP) - Are they from a single spectrum? Journal Indian Academy of Clinical Medicine (India ), 6:4 337-340, 2005
    Abstract: Macrophage Activation Syndrome is a life-threatening condition of special rheumatologic disorders secondary to activation of massive number of lymphocytes and macrophages. It is a severe complication of childhood systemic inflammatory disorders primarily systemic type juvenile rheumatoid arthritis and occasionally systemic lupus erythematosus. Clinical manifestations, laboratory parameters and outcome are very similar to thrombotic thrombocytopenic purpura so that we suggest the terminology of autoimmune-based TTP as an equivalent for macrophage activation syndrome (MAS). Herein we describe a 21 year-old-girl patient with adult onset Still's disease (AOSD) complicated with 'TTP-MAS syndrome' and successfully treated with plasmapheresis, steroid and cyclosporine A

97. PALMISANI E, SOLARI N, MAGNI M, RUPERTO N, PANIGADA S, LABO E, CORTINOVIS SHEILA, SALA I, MARTINI A, RAVELLI A: Correlation between juvenile idiopathic arthritis severity measures in early versus late disease. Arthritis & Rheumatism 52:9, Suppl. S S90, 2005

98. PAY S, TURKCAPAR N, KALYONCU M, SIMSEK I, BEYAN E, ERTENLI I, OZTURK MA, DUZGUN N, ERDEM H, OZBALKAN Z, KIRAZ S, KINIKLI G, BESBAS N, DINC A, ATES A, OLMEZ U, CALGUNERI M, TIRYAKI AO, BAKKALOGLU A, TURAN M, TURGAY M, KARAASLAN Y, TOPALOGLU R, DUMAN M, OZEN S: A multicenter study of patients with adult-onset Still's disease compared with systemic juvenile idiopathic arthritis. Clin Rheumatol :1-6.: 1-6, 2005
    Abstract: Adult-onset Still's disease (AOSD) has often been regarded as the adult spectrum of systemic juvenile idiopathic arthritis (sJIA). The present study aims to compare the clinical and laboratory features, the disease course and the response to treatment in patients having AOSD with those having sJIA. Retrospective review of all available data that were filled out by adult and paediatric rheumatologists from six centers using a standard data extraction form was performed. A total of 95 patients with AOSD and 25 patients with sJIA were recruited for the study. The frequency of fever, rash, myalgia, weight loss and sore throat was higher in patients with AOSD. The pattern of joint involvement differed slightly. Laboratory findings were similar in both groups, except that liver dysfunction and neutrophilia were more common among adults. A multiphasic pattern dominated the childhood cases, whereas the most frequent course was a chronic one in adults. Corticosteroids and methotrexate were the most commonly employed therapy; however, chloroquine was another popular therapy in the adult group. We showed a difference in the rate of clinical and laboratory features between patients with AOSD and those with sJIA. AOSD and sJIA may still be the same disease, and children may simply be reacting differently as the result of the first encounter of the putative antigens with the immune system

99. PERERA SA, HULL RG, LEAK A, BARKER DP, EVANS AR: Uveitis screening in juvenile idiopathic arthritis: When to screen? Annals of the Rheumatic Diseases 64:Suppl. 3 505-506, 2005

100. PHILLIPS WJ, SMITH DJ, BONA CA, BOT A, ZAGHOUANI H: Recombinant immunoglobulin-based epitope delivery: a novel class of autoimmune regulators. Int Rev Immunol 24:5 501-517, 2005
     Organism: MultiCell Immunotherapeutics, San Diego, California, USAFAU - Phillips, William J
     Abstract: Over the past decades, there has been significant progress in understanding the mechanisms of autoimmune diseases at a molecular level. Diseases such as juvenile diabetes, multiple sclerosis, celiac disease, rheumatoid arthritis, and others appear to be mediated by pathogenic T cells that recognize self-epitopes and escape natural tolerance. Seminal observations correlating autoimmunity with HLA and disease-associated epitopes, in conjunction with recent characterization of T regulatory (Treg) cells, promoted a renewed interest in antigen or epitope-based methods of interfering with pathogenic autoimmune reactions. Recombinant immunoglobulin-peptides encompassing disease-associated self-epitopes (IgPP) integrate effective targeting of antigen-presenting cells (APCs) with a potential to generate Treg cells and thus are being developed for treatment of selected autoimmune disorders. In the current review, we outline the main features of this new class of active immunotherapeutics and directions of future development

101. PONTIKAKI I, GERLONI V, LURATI ALFREDOMARIA, GATTINARA M, SALMASO A, VALCAMONICA ELISABETTA, DE MARCO G, TERUZZI B, FANTINI F: Side effects of anti-Tnf alpha therapy in Jia, in an open monocentric prospective study of 151 patients. Arthritis & Rheumatism 52:9, Suppl. S S83, 2005

102. PRAHALAD S, HONEGGAR M, THOMPSON SUSAN, GLASS D, BOHNSACK J, BAMSHAD M: Lack of association of CTLA4 polymorphisms with juvenile rheumatoid arthritis. Arthritis & Rheumatism 52:9, Suppl. S S302, 2005

103. PRAKKEN BJ, ALBANI SSA, DE KI, I, KAMPHUIS S, KUIS W, ZONNEVELD EE: Regulatory T cells and their potential use in cell based therapy. Annals of the Rheumatic Diseases 64:Suppl. 3 27-28, 2005

104. PUNARO L, ALLANTAZ F, STICHWEH DOROTHEE, PASCUAL V: Clinical and microarray follow-up of systemic onset juvenile idiopathic arthritis patients treated with anakinra. Arthritis & Rheumatism 52:9, Suppl. S S254, 2005

105. QIU JJ, WEI M: [Macrophage activation syndrome in a patient with systemic type juvenile idiopathic arthritis.]. Zhonghua Er Ke Za Zhi 43:11 874-875, 2005

106. RAMOS FO, RESENDE C, COSTA M, NETO A, COSTA J, QUEIROZ M, V: Evaluation of uveitis in Portuguese children with juvenile idiopathic arthritis. Annals of the Rheumatic Diseases 64:Suppl. 3 513, 2005

107. RAPOFF MA, BELMONT JM, LINDSLEY CB, OLSON NY: Electronically monitored adherence to medications by newly diagnosed patients with juvenile rheumatoid arthritis. Arthritis Rheum 53:6 905-910, 2005
     Organism: University of Kansas Medical Center, Kansas City, KS 66160-7330, USA mrapoff@kumceduFAU - Rapoff, Michael A
     Abstract: OBJECTIVE: To describe patterns of adherence to nonsteroidal antiinflammatory drugs (NSAIDs) in newly diagnosed patients with juvenile rheumatoid arthritis (JRA), and to examine demographic and disease-related variables as potential predictors of adherence. METHODS: Adherence to NSAIDs was monitored in 48 children with JRA (mean age 8.6 years) over 28 consecutive days using an electronic monitoring device. Measures of disease activity (active joint counts, morning stiffness) and demographics (age, sex, ethnicity, socioeconomic status) were also obtained. RESULTS: Using an 80% adherence cut point, 25 (52%) patients were classified as adherent and 23 (48%) as nonadherent. There was considerable variability across patients, with full adherence (taking all doses on time) ranging from 0 to 100% of the monitored days. Logistic regression showed that active joint count and socioeconomic status were the only significant predictors. Both were positively related to adherence. The model correctly classified 70.5% of patients as either adherent or nonadherent (Cox and Snell R(2) = 0.295, P = 0.0005). CONCLUSION: Children newly diagnosed with JRA are more likely to adhere to an NSAID regimen if they have a greater number of active joints or their families have higher socioeconomic status. The former finding suggests that children's adherence is symptom-driven, while the latter suggests that families of lower socioeconomic status deserve special attention to address adherence issues

108. RICCI L, MASI L, SIMONINI G, DEL M, DE MARTINO M, FALCINI F: Osteopontin (OPN) serum profile and the response pattern to etarnecept treatment in juvenile idiopathic arthritis. Arthritis & Rheumatism 52:9, Suppl. S S87, 2005

109. ROSENKRANZ ME, WILSON D, MIYAMAE TAKAKO, LEMSTER B, WELSH M, MALEHORN DE, BIGBEE W, YOKOTA S, HIRSCH R: Serum proteomic profiles distinguish Kawasaki disease from systemic JIA. Arthritis & Rheumatism 52:9, Suppl. S S443, 2005

110. ROSENKRANZ ME, WILSON D, THOMPSON S, LUYRINK LK, PREUSS A, LIEBMAN M, HIRSCH R: Synovial fluids from JIA subtypes reveal distinct protein profiles. Arthritis & Rheumatism 52:9, Suppl. S S253-S254, 2005

111. ROTH J, SCHEER I, KRAFT S, KEITZER R, RIEBEL T: Uncommon synovial cysts in children. Eur J Pediatr :1-4.: 1-4, 2005
     Organism: Pediatric Rheumatology, Charite-Universitaetsmedizin, Berlin, Germany
     Abstract: Popliteal synovial cysts (Baker's cysts) are a common occurrence in children and adults. Synovial cysts in other locations and/or with atypical extension are less common and may be confounded with tumors or other medical conditions. In this article we describe the underlying disease, clinical presentation and clinical course in six children with a sudden onset of paraarticular soft tissue masses or non-specific chronic pain. Ultrasound was the initial imaging method used in all cases; this was supplemented by MRI in three patients. Four children were diagnosed to be suffering from juvenile idiopathic arthritis (JIA), one child from Lyme Arthritis, whereas in one child no underlying disease was identified. Well-demarcated hypoechogenic lesions without signs of perfusion extending from the shoulder (two patients), elbow (one patient), hip (one patient), knee (1) or ankle (one patient) far into the adjacent musculature were detected on ultrasonography. A direct connection to the joint was demonstrated in all cases. All synovial cysts in the five arthritic patients resolved rapidly with medical treatment for arthritis, whereas the cyst persisted in the non-JIA patient. Conclusion: Uncommon synovial cysts occur in particular as a complication of arthritis. Ultrasonography is the initial and follow-up imaging method of choice, which can be supplemented by MRI in unusual cases. Apart from treatment for arthritis, no specific therapeutic interventions were required in the present cases

112. ROTH J, TZARIBACHEV N, LINGE M, SCHWEIZER R, KUEMMERIE-DESCHNER J: Abnormal bone geometry and sarcopenia persist in juvenile idiopathic arthritis - pathophysiological and therapeutical conclusions from a 4 year follow up study. Annals of the Rheumatic Diseases 64:Suppl. 3 351-352, 2005

113. ROTH J, TZARIBACHEV N, LINGE MELANIE, KUEMMERLE-DESCHNER J: The musculoskeletal system in juvenile arthritis - A 4-year follow-up. Arthritis & Rheumatism 52:9, Suppl. S S92, 2005

114. ROVENSKA E, STVRTINA S, MICHALKA P, ROVENSKY J: Perivascular infiltrates around synovial lymphatic capillaries in rheumatoid arthritis and juvenile idiopathic arthritis. Annals of the Rheumatic Diseases 64:Suppl. 3 166-167, 2005

115. SALAZAR CD, GUZMAN S, SOTO H, CHAIDEZ R, ILIZALITURRI-SANCHEZ V, NIEVES-SILVA J, VALERO G, AGUILERA-ZEPEDA J, HERNANDEZ GL: Assessment of quality of life (QOL) between adults with juvenile idiopatic arthritis diagnosis and non health services demands. The diferences. Annals of the Rheumatic Diseases 64:Suppl. 3 510, 2005

116. SALMASO A, LURATI A, DE MARCO G, GATTINARA M, TERUZZI B, PONTIKAKI I, GERLONI V, FANTINI F: Atlo-epistropheal involvement in oligoarthritis subset of juvenile idiopathic arthritis: Observation of five cases. Annals of the Rheumatic Diseases 64:Suppl. 3 514, 2005

117. SCHEIBEL IM, XAVIER RM, VEIT TIAGO, BISOTTO L, PREZZI SH, KOHEM C, BRENOL JC, CHIES JOSE AB: Association of CCR5 chemokine receptor Delta 32 polymorphism with Juvenile Idiopathic Arthritis. Arthritis & Rheumatism 52:9, Suppl. S S306-S307, 2005

118. SCHLENK J, LORENZ HM, HAAS JP, HERRMANN M, HOHENBERGER G, KALDEN JR, ROLLINGHOFF M, BEUSCHER HU: Extravasation into synovial tissue induces CCL20 mRNA expression in polymorphonuclear neutrophils of patients with rheumatoid arthritis. J Rheumatol 32:12 2291-2298, 2005
     Organism: Institute for Clinical Microbiology, Immunology and Hygiene, University of Erlangen-Nuremberg, Erlangen, GermanyFAU - Schlenk, Judith
     Abstract: OBJECTIVE: Examination of expression of the chemokine macrophage inflammatory protein-3a (CCL20/Mip-3alpha) in blood polymorphonuclear neutrophils (PMN) and synovial fluid (SF) PMN of patients with rheumatoid arthritis (RA). METHODS: Paired samples of blood PMN and SF PMN were obtained from 11 patients with RA. In addition, SF was prepared from 9 patients with osteoarthritis (OA) and 10 patients with juvenile idiopathic arthritis (JIA). PMN were isolated via density centrifugation to a purity of 98%. Total RNA was isolated and the expression of CCL20 was determined by reverse transcription-polymerase chain reaction (RT-PCR) and quantitative real-time PCR. In some experiments blood PMN obtained from healthy donors were stimulated with individual SF of patients with RA. For quantitative considerations, CXCL8, CCL20, interleukin 1, and tumor necrosis factor-alpha (TNF-alpha) levels were determined in SF by ELISA. RESULTS: In SF of RA patients CCL20 and CXCL8 levels were elevated, up to 7.5 ng/ml and 23.6 ng/ml, respectively. No significant level of either chemokine was found in SF of patients with JIA and OA. CCL20 mRNA was undetectable in blood PMN of all patients with RA. In SF PMN, CCL20 mRNA was found in 6/11 RA patients. Expression of CCL20 mRNA in 5/6 SF PMN samples was observed in the absence of detectable TNF-alpha levels in SF. Cell culture experiments, however, confirmed the ability of TNF-alpha in SF to induce CCL20 mRNA expression in blood PMN. Notably, expression of CCL20 was also found in PMN after stimulation with SF lacking TNF-alpha. CONCLUSION: Recruitment of PMN to the synovial microenvironment induces expression of CCL20 mRNA independent of the concentrations of TNF-alpha accumulating in SF of patients with RA

119. SOHN DI, LABORDE HA, BELLOTTI M, SEIJO L: Juvenile rheumatoid arthritis and bronchiolitis obliterans organized pneumonia. Clin Rheumatol :1-4.: 1-4, 2005
     Organism: Division Reumatologia, Hospital de Clinicas Jose de San Martin, 8 degrees Piso, Cordoba 2351 (1120), Buenos Aires, Argentina, debysohn@yahoocomar
     Abstract: Diverse pleuropulmonary manifestations, including pleural effusion, rheumatoid nodulosis, fibrosis, obliterans brochiolitis, bronchiectasias, vasculitis, drug-induced lung disease, and obliterans bronchiolitis with organized pneumonia, have been described in patients with rheumatoid arthritis (RA). Bronchiolitis obliterans organized pneumonia (BOOP) is an uncommon condition described in patients with RA but not in juvenile RA (JRA). We described a patient with JRA who developed a BOOP

120. SOUTHWOOD TR, CUMMINS CL, FOSTER H, RAHMAN JK, COTTER KB: Adverse events in juvenile idiopathic arthritis patients treated with etanercept or the combination of etanercept and methotrexate. Arthritis & Rheumatism 52:9, Suppl. S S85-S86, 2005

121. STENBOEG E, PFEIFFER-JENSEN M, KASPER V, HERLIN T: Ultrasound measurement of joint cartilage in large and small joints in healthy children. A pilot study assessing observer variability. Arthritis & Rheumatism 52:9, Suppl. S S88-S89, 2005

122. SUKAL SA, NADIMINTI L, GRANSTEIN RD: Etanercept and demyelinating disease in a patient with psoriasis. J Am Acad Dermatol 54:1 160-164, 2006
     Organism: Department of Dermatology, Weill Medical College of Cornell University, New York-Presbyterian Hospital, New York, New York, USAFAU - Sukal, Sean A
     Abstract: The tumor necrosis factor-alpha antagonist (TNF-alpha) etanercept has been approved for the treatment of rheumatoid arthritis, juvenile rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and psoriasis. Earlier reports on the use of etanercept or infliximab in patients with rheumatoid arthritis, psoriatic arthritis, or juvenile rheumatoid arthritis suggested an increased risk of demyelinating disease. It is imperative that dermatologists have a keen awareness of this possible adverse event given the increased use of this class of drugs. We report a case of demyelinating disease occurring in a patient treated for psoriasis. The relation of TNF-alpha antagonist therapy to demyelinating disease/multiple sclerosis is explored. It is recommended that patients be diligently screened before starting TNF-alpha antagonist therapy and that vigilance for symptoms of demyelinating disease/multiple sclerosis be included in follow-up examinations during treatment with these drugs

123. SUPPIAH V, HEGGARTY S, ALLOZA IRAIDE, PATTERSON C, ROONEY M, VANDENBROECK K: Polymorphisms in the interleukin-4 and interleukin-4 receptor genes are associated with chronic inflammatory arthropathies. Arthritis & Rheumatism 52:9, Suppl. S S147, 2005

124. SUPPIAH V, HEGGARTY S, O'DOHERTY CATHERINE, ROONEY M, VANDENBROECK K: CTLA-4 gene polymorphisms in chronic inflammatory arthropathies. Arthritis & Rheumatism 52:9, Suppl. S S147, 2005

125. SZTAJNBOK F, DIAZ M, CORONEL-MARTINEZ DL, NOVARINI C, RUPERTO NICOLINO, FELICI E, TRAIL L, MAGNANI A, MARTINI ALBERTO, RAVELLI A: Discordance between physician and parent global assessments in juvenile idiopathic arthritis. Arthritis & Rheumatism 52:9, Suppl. S S90, 2005

126. TAYLOR J, LOVELL D, THEILE D, GULLA PAM, MIRUS J, SMITH C, BRITTO M, PASSO M: Development of patient portals to improve quality of care for children with juvenile rheumatoid arthritis. Arthritis & Rheumatism 52:9, Suppl. S S666, 2005

127. THASTUM M, HERLIN T, KRISTENSEN ODA, ZACHARIAE R: Health beliefs as a predictor of pain in children with JIA - A longitudinal study. Arthritis & Rheumatism 52:9, Suppl. S S697, 2005

128. TREHANE A, RAHMEH F, THOMPSON P, CORNELL P: Are parents and children with juvenile idiopathic arthritis happy to be managed in the district general hospital? Annals of the Rheumatic Diseases 64:Suppl. 3 590, 2005

129. TUSZKIEWICZ-MISZTAL E, TABARKIEWICZ J, OLESINSKA E, OPOKA-WINIARSKA V: "Circulating immature dendritic cells in blood of children with JIA in during exacerbation and remission. Annals of the Rheumatic Diseases 64:Suppl. 3 73, 2005

130. TWILT M, TEN CATE R, MOBERS SMLM, SUIJLEKOM-SMIT LWA: The course of temporomandibular joint involvement in juvenile idiopathic arthritis. Annals of the Rheumatic Diseases 64:Suppl. 3 512-513, 2005

131. UEECK BA, MAHMUD NA, MYALL RWT: Dealing with the effects of juvenile rheumatoid arthritis in growing children. Oral and Maxillofacial Surgery Clinics of North America (United States ) 17:4 SPEC. ISS. 467-473, 2005
     Abstract: Juvenile rheumatoid arthritis is a chronic childhood disease that has a multiplicity of effects on the growth and development of the facial skeleton. An understanding of the disease in general and its therapy is necessary for successful surgical-orthodontic care. (c) 2005 Elsevier Inc. All rights reserved

132. VAN ROSSUM MA, VAN SOESBERGEN R, ZWINDERMAN AH, BOERS M, DIJKMANS BA, DUTCH J: Long-term outcome of juvenile idiopathic arthritis following a placebo-controlled trial: Sustained benefits of early sulfasalazine treatment. Arthritis & Rheumatism 52:9, Suppl. S S86, 2005

133. VASTERT SJ, DE K, I, KLEIN M, KUIS W, ALBANI S, PRAKKEN BJ: Effects of anti-TNF-alpha therapy on (regulatory) T cell function in juvenile idiopathic arthritis. Arthritis & Rheumatism 52:9, Suppl. S S490, 2005

134. VISVANATHAN S, MARINI JC, LOVELL DANIEL, GIANNINI E, RUPERTO N, MARTINI A, PETTY ROSS, PRIEUR A, WOO P, TRAVERS S, GATHANY TIMOTHY, WAGNER C: The effect of infliximab plus methotrexate therapy on the modulation of inflammatory disease markers in patients with juvenile rheumatoid arthritis. Arthritis & Rheumatism 52:9, Suppl. S S86, 2005

135. VOJINOVIC J, ZIVANOVIC D, STANKOVIC A: Five years follow up on MTX efficacy in JIA. Annals of the Rheumatic Diseases 64:Suppl. 3 510, 2005

136. WEDDERBURN LR, PHAROAH D, PATEL A, WILLIAMS B, KLEER I, DE JAGER W, PRAKKEN B: Juvenile arthritis: Perpetuation of inflammation. Annals of the Rheumatic Diseases 64:Suppl. 3 35, 2005

137. WEISS J, HENRICKSON M, WALCO GARY, FEINSTEIN A, KIMURA Y: Combination therapy with Anakinra and anti-TNF agents in refractory systemic JIA (SJIA). Arthritis & Rheumatism 52:9, Suppl. S S84-S85, 2005

138. WENKERT D, MUMM S, WIEGAND S, MCALISTER WH, WHYTE MP: Absence of MMP2 mutations in idiopathic multicentric osteolysis with nephropathy in 2 American boys. Arthritis & Rheumatism 52:9, Suppl. S S304, 2005

139. WITTKOWSKI H, AHLMANN M, FROSCH MICHAEL, DASSMANN S, WULFFRAAT N, VOGL T, ROTH J, FOELL DIRK: Pro-inflammatory proteins S100A8/S100A9 and S100 A12 as diagnostic markers for systemic onset juvenile idiopathic arthritis (SOJIA). Arthritis & Rheumatism 52:9, Suppl. S S253, 2005

140. WOJTECKA-LUKASIK E, MUSIEJ-NOWAKOWSKA E, MASLINSKI S: The activity of serum n-acetyl-beta-d-hexosaminidase (NAHase) and 127 KD ectonucleotide pyrophosphohydrolase (NTPphase) in juvenile idiopathic arthritis (JIA). Annals of the Rheumatic Diseases 64:Suppl. 3 512, 2005

141. WOO P, WILKINSON N, PRIEUR A, SOUTHWOOD T, LEONE V, LIVERMORE P, WYTHE H, THOMSON D, KISHIMOTO T: Proof of principle of the efficacy of IL-6 receptor blockade in severe systemic juvenile idiopathic arthritis (SJIA). Annals of the Rheumatic Diseases 64:Suppl. 3 84, 2005

142. WU JD, LAW L, CUSH JJ: Tuberculin skin testing in patients receiving TNF inhibitors. Arthritis & Rheumatism 52:9, Suppl. S S411, 2005

143. YAN Z, LAMBERT NC, GUTHRIE K, NELSON JL: Prospective study of cell-free fetal DNA and disease activity in women with inflammatory arthritis during pregnancy. Arthritis & Rheumatism 52:9, Suppl. S S149, 2005

144. YAO TC, HUANG JL: Comparison of RANTES and monocyte chemoattractant protein-1 in juvenile idiopathic arthritis between the active and remission stages. Arthritis & Rheumatism 52:9, Suppl. S S306, 2005

145. YAYLI SEVGI BS, ALPAY K, CIMSIT G, COBANOGLU U, TOSUN M: Pyoderma gangrenosum in association with juvenile rheumatoid arthritis. J Dermatol 32:10 827-830, 2005
     Organism: Department of Dermatology, Karadeniz Technical University, Medicine Faculty, Trabzon, TurkeyFAU - Yayli Sevgi Bahadir, Savas
     Abstract: A 17-year-old girl presented with multiple, painful, erythematous blisters and ulcerated lesions on the shins and buttocks. She also had arthralgia. She had suffered from juvenile rheumatoid arthritis (JRA) and received anti-inflammatory agents and oral glucocorticoids for eight years. A biopsy of a lesion showed epidermal ulceration with marked neutrophilic infiltrates in the dermis. The patient was diagnosed with pyoderma gangrenosum (PG). PG is an uncommon cutaneous ulceration within the spectrum of the neutrophilic dermatoses that is reported in association with a number of systemic disorders, including inflammatory bowel disease, hematologic disease, internal malignancies, arthritis, immune abnormalities, and solid tumors. To our knowledge, this is the first reported case of PG associated with JRA

146. YOKOTA S, MIYAMAE T, KUROSAWA R, OZAWA REMI, IMAGAWA T, MORI M, NISHIMOTO N: Long-term treatment of systemic onset juvenile idiopathic arthritis (SO-JIA) with humanized anti-IL-6 receptor monoclonal antibody, tocilizumab (Actemra (R)). Arthritis & Rheumatism 52:9, Suppl. S S725, 2005

147. YU EN, MENICONI ME, TUFAIL F, BALTATZIS S, FOSTER CS, CHRISTEN WG: Outcomes of treatment with immunomodulatory therapy in patients with corticosteroid-resistant juvenile idiopathic arthritis-associated chronic iridocyclitis. Ocular Immunology and Inflammation (United Kingdom ) 13:5 353-360, 2005
     Abstract: Purpose: To describe the clinical outcome of patients with juvenile idiopathic arthritis (JIA)-associated chronic iridocyclitis unresponsive to conventional therapy, in whom inflammation was eventually controlled using immunomodulatory therapy (IMT), and to determine if patients treated early with IMT have better visual acuity outcomes than those treated with corticosteroid alone. Methods: Patients with JIA-associated chronic iridocyclitis receiving immunomodulatory therapy at the Ocular Immunology and Uveitis Service of the Massachusetts Eye and Ear Infirmary between 1981 and 2001 were studied. Inclusion criteria: JIA with chronic corticosteroid-dependent uveitis; IMT for a minimum of one year; minimum follow-up of three years; inflammation eventually controlled for a minimum of six consecutive months by IMT Results: At last visit, 51% of eyes (23 eyes) had acuity of 20/20 to 20/40, 16% (7 eyes) had 20/50 to 20/100, and 33% (15 eyes) had 20/200 or less. In patients whose chronic inflammation was eventually controlled within three years from onset of the uveitis, final bilateral vision was maintained within 20/20 to 20/30, except for a patient whose one eye had poor vision at initial consultation. When acuities at the end of the follow-up period of patients treated early with IMT were compared with acuities at the initial consultation of patients treated late with IMT, with duration of uveitis matched for each patient, visual acuities of those treated early were statistically significantly better than those treated late with IMT (p < 0.005 right and left eyes pooled; p = 0.0075 best eyes; p = 0.0375 worst eyes). Conclusions: We noted improvement or maintenance of visual acuity (86%) during the course of follow-up of patients with treatment-resistant JIA-associated uveitis treated with effective IMT However, only IMT given early in the disease course was noted to be associated with bilateral visual acuity of 20/30 or better. Copyright (c) Taylor & Francis Inc