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Financialbusinessnews.us: Todays Stocks to Watch: HSXI, OISI, AMGN, APGR

Lead Author: [none given]

M2 Presswire., 2008-02-28, pg. 1

MIB Abstract ID Number: 14704

Proquest Identifier: 1436479961

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Reliability and sensitivity to change of the Simple Erosion Narrowing Score compared with the Sharp-van der Heijde method for scoring radiographs in rheumatoid arthritis.

Lead Author: Dias EM

Additional Authors: Lukas C, Landewé R, Fatenejad S, van der Heijde D.

Ann Rheum Dis., 2008-03-01, 67(3):375-9. Epub 2007 Jul 20.

Department of Internal Medicine, Division of Rheumatology, University Hospital Maastricht, Maastricht, the Netherlands.

OBJECTIVE: To compare the performance of a simplified scoring method for structural damage on radiographs of patients with rheumatoid arthritis (the Simple Erosion Narrowing Score or SENS) with the Sharp-van der Heijde Score (SHS) as reference. METHOD: We used the radiographic data from the Trial of Etanercept and Methotrexate with Radiographic Patient Outcomes (TEMPO trial). The SENS was derived from the crude SHS data. Inter-observer reliability for status scores and change scores was determined by intraclass correlation coefficients and by the Smallest Detectable Change method. The ability to discriminate between treatment groups was assessed by the Mann-Whitney U test. Stratifying the sensitivity to change and discriminative ability for different levels of disease severity assessed a potential ceiling effect. RESULTS: Inter-observer reliability was similar for both methods. Intraclass correlation coefficients were higher for status scores than for change scores. The Smallest Detectable Change was 4.98 (1.1% of possible maximum score) for SHS and 2.28 (3.5%) for SENS. Sensitivity of SENS to detect progression above the Smallest Detectable Change, with reference SHS, ranged from 45.0 to 88.7%. Specificity ranged from 81.5 to 97.3%, and the kappa coefficient (between-method agreement) ranged from 0.58 to 0.66. Discriminative ability between treatment groups was good and similar for both methods. A ceiling effect could not be detected. CONCLUSIONS: With regard to most of the tested properties, the performance of SENS is as good as that of SHS. This confirms that SENS is a valuable method, which may be feasible in clinical practice.

MIB Abstract ID Number: 14708

PreMedline Identifier: 17644537

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The future of the IL-1 receptor antagonist anakinra: from rheumatoid arthritis to adult-onset Still's disease and systemic-onset juvenile idiopathic arthritis.

Lead Author: Kalliolias GD

Additional Authors: Liossis SN.

Expert Opin Investig Drugs., 2008-03-01, 17(3):349-59.

Hospital for Special Surgery, Arthritis and Tissue Degeneration Program, Department of Medicine, New York, NY 10021, USA.

MIB Abstract ID Number: 14705

PreMedline Identifier: 18321234

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Anakinra treatment for systemic juvenile idiopathic arthritis and adult onset Still disease.

Lead Author: Woo P.

Ann Rheum Dis., 2008-03-01, 67(3):281-2.

Comment on:

Ann Rheum Dis. 2008 Mar;67(3):302-8.

MIB Abstract ID Number: 14706

PreMedline Identifier: 18292104

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Interleukin-1 receptor antagonist (anakinra) treatment in patients with systemic-onset juvenile idiopathic arthritis or adult onset Still disease: preliminary experience in France.

Lead Author: Lequerré T

Additional Authors: Quartier P, Rosellini D, Alaoui F, De Bandt M, Mejjad O, Kone-Paut I, Michel M, Dernis E, Khellaf M, Limal N, Job-Deslandre C, Fautrel B, Le Loët X, Sibilia J; Société Francophone pour la Rhumatologie et les Maladies Inflammatoires en Pédiatrie (SOFREMIP); Club Rhumatismes et Inflammation (CRI).

Ann Rheum Dis., 2008-03-01, 67(3):302-8. Epub 2007 Oct 18.

Rheumatology Department, Rouen University Hospital & Inserm 905, 76031 Rouen, France. thierry.lequerre@univ-rouen.fr

MIB Abstract ID Number: 14707

PreMedline Identifier: 17947302

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POZEN To Present at the Cowen and Company 28th Annual Healthcare Conference

Lead Author: [none given]

Additional Authors:

Business Wire., 2008-03-04

POZEN Inc. (NASDAQ: POZN) announced today that John R. Plachetka Pharm.D., the company's chairman, president and chief executive officer, will present at the Cowen and Company 28th Annual Healthcare Conference on Tuesday, March 18, 2008 at 10:15 a.m. (ET) at the Marriott Copley Place Hotel in Boston. Dr. Plachetka's presentation will be webcast and archived on POZEN's home page at www.pozen.com.

POZEN is a pharmaceutical company committed to developing therapeutic advancements for diseases with unmet medical needs where it can improve efficacy, safety, and/or patient convenience. POZEN's efforts are focused primarily on the development of pharmaceutical products for the treatment of acute and chronic pain and other pain-related conditions. POZEN has development and commercialization alliances with GlaxoSmithKline for the proposed product candidate Treximet(TM) which is currently under review by the United States Food and Drug Administration for the acute treatment of migraine, and with AstraZeneca for the proposed product candidate PN 400 for conditions such as osteoarthritis and rheumatoid arthritis in patients who are at risk for developing NSAID-associated gastric ulcers. The company's common stock is traded on The Nasdaq Stock Market under the symbol "POZN". For detailed company information, including copies of this and other press releases, see POZEN's website: www.pozen.com.

POZEN Inc.

Bill Hodges

Chief Financial Officer

919-913-1030

or

Fran Barsky

Director, Investor Relations

919-913-1044

Logo: http://www.pozen.com

MIB Abstract ID Number: 14710

Proquest Identifier: 1439463381

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Emerging Markets Consulting, LLC.: Emerging Markets Consulting, LLC. : Emerging Equity Alerts

Lead Author: [none given]

Presswire., 2008-03-04, pg. 1

MIB Abstract ID Number: 14711

Proquest Identifier: 1438935141

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Biogen Idec Prices $1.0 Billion Senior Unsecured Notes Offering

Lead Author: [none given]

Additional Authors:

Business Wire. New York, 2008-02-29

Biogen Idec Inc. (NASDAQ: BIIB) announced today that it has priced a public offering of $1.0 billion principal amount of senior unsecured notes. The offering of senior unsecured notes includes $450 million in aggregate principal amount of 6.0% notes due 2013 and $550 million in aggregate principal amount of 6.875% notes due 2018. The sale of the notes is expected to close on March 4, 2008, subject to customary closing conditions.

Biogen Idec plans to use the net proceeds from this offering, together with cash on hand, to repay indebtedness under its $1.5 billion bridge facility, the proceeds of which were used to repurchase shares of Biogen Idec's common stock in a $3.0 billion "Dutch Auction" tender offer settled on July 2, 2007.

Goldman, Sachs & Co. and Merrill Lynch & Co. are the book-running managers for the offering. The offering of these securities is being made only by means of a prospectus and related prospectus supplement. Electronic copies of the prospectus and related prospectus supplement may be requested from Goldman, Sachs & Co. by mail at Goldman, Sachs & Co., Attention:

Prospectus Department, 85 Broad Street, New York, NY 10004, by fax at (212) 902-9316 or by email at prospectus-ny@ny.email.gs.com or by Merrill Lynch, Pierce, Fenner & Smith Incorporated at 4 World Financial Center, New York, New York 10080, Attention: Prospectus Department, 866-500-5408.

About Biogen Idec

Biogen Idec creates new standards of care in therapeutic areas with high unmet medical needs. Founded in 1978, Biogen Idec is a global leader in the discovery, development, manufacturing, and commercialization of innovative therapies. Patients in more than 90 countries benefit from Biogen Idec's significant products that address diseases such as lymphoma, multiple sclerosis, and rheumatoid arthritis. For product labeling, press releases and additional information about the company, please visit www.biogenidec.com.

MIB Abstract ID Number: 14712

Proquest Identifier: 1438345021

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Assessment of rituximab's immunomodulatory synovial effects (ARISE trial). 1: clinical and synovial biomarker results.

Lead Author: Kavanaugh A

Additional Authors: Rosengren S, Lee SJ, Hammaker D, Firestein GS, Kalunian K, Wei N, Boyle DL.

Ann Rheum Dis., 2008-03-01, 67(3):402-8. Epub 2007 Jul 20.

University of California, San Diego, Division of Rheumatology, Allergy, and Immunology, 9500 Gilman Drive, Mail Code 0943, La Jolla, CA 92093-0943, USA. akavanaugh@ucsd.edu

OBJECTIVE: Treatment with the anti-CD20 monoclonal antibody (mAb) rituximab is effective in rheumatoid arthritis (RA). Marked depletion of circulating B cells, seen in almost all patients, does not correlate with efficacy. The potential synovial immunomodulatory effects of rituximab have not been fully defined. METHODS: The ARISE trial is an open label, serial synovial biopsy (pre-treatment and 8 weeks) study of rituximab, given 1 g intravenously on days 0 and 14 without peri-infusional steroids, in active RA patients on concomitant methotrexate (MTX). Synovial tissue was analysed by immunohistochemistry with digital image analysis and gene expression by real-time PCR. RESULTS: The mean (SD) baseline DAS28 score was 6.5 (0.4), and mean MTX dose 17.3 mg/week. Of 13 patients, 11 had failed prior tumour necrosis factor (TNF) inhibitor therapy. With treatment, all patients experienced near complete depletion of circulating B cell numbers. During the 6 months after treatment, 7/13 patients achieved an American College of Rheumatology (ACR) 20% improvement (ACR20) response, 3/13 an ACR50 response and 2/13 an ACR70 response. There was a significant decrease in synovial B cells after treatment, but only a small trend towards greater reduction among clinical responders. Among the three patients with ACR50 responses there was a significant decrease in synovial immunoglobulin synthesis. CONCLUSIONS: These data suggest that unlike those in circulation, synovial B cells are decreased but are not eliminated by rituximab therapy. Patients with higher levels of response may have more consistent depletion of synovial B cells, and may also have an alteration in synovial B cell function, as indicated by decreases in synovial immunoglobulin synthesis. Thus, effects on synovial B cells may be necessary but not sufficient for inducing clinical efficacy. Other effects, such as on primary lymph organ B cell antigen presentation or cytokine production, may be operative.

MIB Abstract ID Number: 14717

PreMedline Identifier: 17644541

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Common Polymorphisms in the Folate Pathway Predict Efficacy of Combination Regimens Containing Methotrexate and Sulfasalazine in Early Rheumatoid Arthritis.

Lead Author: James HM

Additional Authors: Gillis D, Hissaria P, Lester S, Somogyi AA, Cleland LG, Proudman SM.

J Rheumatol., 2008-03-01, [Epub ahead of print]

From the Division of Human Immunology, Institute of Medical and Veterinary Science; Arthritis Research Laboratory, Hanson Institute; Discipline of Pharmacology, School of Medical Sciences, University of Adelaide; and Rheumatology Unit, Royal Adelaide Hosp, Adelaide, Australia.

MIB Abstract ID Number: 14732

PreMedline Identifier: 18322994

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Clinical use and pharmacological properties of selective COX-2 inhibitors.

Lead Author: Shi S

Additional Authors: Klotz U.

Eur J Clin Pharmacol. , 2008-03-01, 64(3):233-252. Epub 2007 Nov 13.

Dr. Margarete Fischer-Bosch-Institut für Klinische Pharmakologie, Auerbachstraße 112, 70376, Stuttgart, Germany.

Selective COX-2 inhibitors (coxibs) are approved for the relief of acute pain and symptoms of chronic inflammatory conditions such as osteoarthritis (OA) and rheumatoid arthritis (RA). They have similar pharmacological properties but a slightly improved gastrointestinal (GI) safety profile if compared to traditional nonsteroidal anti-inflammatory drugs (tNSAIDs). However, long-term use of coxibs can be associated with an increased risk for cardiovascular (CV) adverse events (AEs). For this reason, two coxibs were withdrawn from the market. Currently celecoxib, etoricoxib, and lumiracoxib are used. These three coxibs differ in their chemical structure and selectivity for COX-2, which might explain some of their pharmacological features. Following oral administration, the less lipophilic celecoxib has a lower bioavailability (20-40%) than the other two coxibs (74-100%). All are eliminated by hepatic metabolism involving mainly CYP2C9 (celecoxib, lumiracoxib) and CYP3A4 (etoricoxib). Elimination half-life varies from 5 to 8 h (lumiracoxib), 11 to 16 h (celecoxib) and 19 to 32 h (etoricoxib). In patients with liver disease, plasma levels of celecoxib and etoricoxib are increased about two-fold. Clinical efficacies of the coxibs are comparable to tNSAIDs. There is an ongoing discussion about whether the slightly better GI tolerability (which is lost if acetylsalicylic acid is coadministered) of the coxibs is offset by their elevated risks for CV AEs (also seen with tNSAIDs other than naproxen), which apparently increase with dose and duration of exposure. In addition, the higher costs for coxibs (if compared to tNSAIDs, even when a "gastroprotective" proton pump inhibitor is coadministered) should be taken into consideration, if a coxib will be selected for certain patients with a high risk for GI complications. For such treatment, the lowest effective dose should be used for a limited time. Monitoring of kidney function and blood pressure appears advisable. It is hoped that further controlled studies can better define the therapeutic place of the coxibs.

MIB Abstract ID Number: 14731

PreMedline Identifier: 17999057

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NOVO NORDISK TO END 2 DRUG PARTNERSHIPS WITH SPINOFF; ZYMOGENETICS DOWNPLAYS MOVE

Lead Author: JOSEPH TARTAKOFF

Seattle Post - Intelligencer., 2008-03-05, pg. E.1

Novo Nordisk, the Danish health care company that spun off ZymoGenetics eight years ago, plans to pull out of two partnerships to develop drugs with the Seattle company - moves that ZymoGenetics downplayed but that one analyst said raised questions about the viability of the company's product pipeline.

Earlier this year, the Food and Drug Administration approved ZymoGenetics' first product, Recothrom, which is used to control bleeding during surgery. But the two drugs being developed with Novo Nordisk - Interleukin 21 and Interleukin 31 - are among five that ZymoGenetics considers to be candidates for future products.

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MIB Abstract ID Number: 14735

Proquest Identifier: 1441633301

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ARTHRITIS QUALITY OF CARE; Studies from University of British Columbia, Division of Rheumatology provide new data on arthritis quality of care

Lead Author: J. Reynolds

Pharma Law Weekly, 2008-03-05, EXPANDED REPORTING; Pg. 384

University of British Columbia, Division of Rheumatology, Faculty of Medicine, Vancouver, Canada.

Investigators publish new data in the report 'Abatacept: a novel treatment for moderate-to-severe rheumatoid arthritis.' According to recent research from Vancouver, Canada, "Rheumatoid arthritis is a chronic autoimmune disease that often leads to functional disability and reduced quality of life. The pathogenesis of synovial inflammation that is associated with this disease is thought to result from T-cell activation."

"To become fully activated, T cells require an antigen-specific signal through the T-cell receptor and a second signal through a costimulatory receptor. Abatacept is the first drug in a new class of disease-modifying antirheumatic drugs (DMARDs) known as selective costimulation modulators. Costimulation modulators block the second signal and decrease T-cell activation. Abatacept has been approved by the United States Food and Drug Administration for reducing signs and symptoms, inducing major clinical response, slowing the progression of structural damage, and improving physical function in adults with moderate-to-severe active rheumatoid arthritis who have had an inadequate response to at least one other DMARD, such as methotrexate or tumor necrosis factor (TNF)-alpha inhibitors. Randomized controlled trials have shown that abatacept improves both clinical outcomes and health-related quality of life in patients who have had an inadequate response to other DMARDs. Abatacept has been shown to be well tolerated. In clinical trials, however, abatacept treatment was associated with a higher rate of infections compared with placebo. This finding was compounded when abatacept was used with TNF-alpha inhibitors; thus, this combination should be avoided. Abatacept appears to be a useful treatment option for patients with rheumatoid arthritis who have previously failed other DMARDs," wrote J. Reynolds and colleagues, University of British Columbia, Division of Rheumatology.

The researchers concluded: "However, additional clinical trials evaluating its long-term effect on patient safety and disease outcomes are needed."

Reynolds and colleagues published their study in Pharmacotherapy (Abatacept: a novel treatment for moderate-to-severe rheumatoid arthritis. Pharmacotherapy, 2007;27(12):1693-701).

For additional information, contact J. Reynolds, University of British Columbia, Division of Rheumatology, Faculty of Medicine, Vancouver, Canada.

Publisher contact information for the journal Pharmacotherapy is: Pharmacotherapy Publications Inc., New England Medical Center, 806, 750 Washington St., Boston, MA 02111, USA.

MIB Abstract ID Number: 14740

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ARTHRITIS; Recent findings in arthritis described by researchers from Stanford University

Lead Author: V. Strand

Drug Law Weekly, 2008-03-04, EXPANDED REPORTING; Pg. 276

Stanford University, School Medical, Division Immunology Rheumatol, 306 Ramona Rd., Portola Valley, CA 94028, USA.

According to a study from the United States, "Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by inflammation of the articular synovium, resulting in bony erosions, deformity, and, ultimately, joint destruction. With associated comorbid conditions, especially cardiovascular, it can result in significant morbidity as well as early mortality."

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MIB Abstract ID Number: 14741

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Nocardia infection with adalimumab in rheumatoid arthritis.

Lead Author: Doraiswamy VA.

J Rheumatol., 2008-03-01, 35(3):542.

MIB Abstract ID Number: 14695

PreMedline Identifier: 18322980

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Does tumor necrosis factor alpha inhibition promote or prevent heart failure in patients with rheumatoid arthritis?

Lead Author: Listing J

Additional Authors: Strangfeld A, Kekow J, Schneider M, Kapelle A, Wassenberg S, Zink A.

Arthritis Rheum. , 2008-02-29, 58(3):667-677 [Epub ahead of print]

German Rheumatism Research Centre, Berlin, Germany.

OBJECTIVE: To determine the hazard risk of developing or worsening heart failure in rheumatoid arthritis (RA) patients treated with tumor necrosis factor alpha (TNFalpha) inhibitors. METHODS: RA patients ages 18-75 years who started treatment with infliximab, etanercept, or adalimumab (n = 2,757), or conventional disease-modifying antirheumatic drugs (controls; n = 1,491) at the time of enrollment in a German biologics register were studied. Cox proportional hazards models were applied to investigate the influence of disease-related and treatment-specific risk factors on the incidence or worsening of heart failure. RESULTS: The 3-year incidence rates of heart failure in patients with and patients without cardiovascular disease at the start of treatment were 2.2% and 0.4%, respectively. After adjustment for traditional cardiovascular risk factors, an increased risk of developing heart failure was found in patients who had a higher 28-joint Disease Activity Score at followup (hazard ratio [HR] 1.47 [95% confidence interval 1.07-2.02], P = 0.019). A residual nonsignificant risk related to treatment with TNFalpha inhibitors remained (adjusted HR 1.66 [95% confidence interval 0.67-4.1], P = 0.28). This residual risk was balanced by the efficacy of the anti-TNF treatment. When only baseline characteristics were taken into account, the HR related to TNFalpha inhibitor treatment decreased to 0.70 (95% confidence interval 0.27-1.84). CONCLUSION: The findings of this study indicate that TNFalpha inhibitor treatment that effectively reduces the inflammatory activity of RA is more likely to be beneficial than harmful with regard to the risk of heart failure, especially if there is no concomitant therapy with glucocorticoids or cyclooxygenase 2 inhibitors. Furthermore, the data suggest that TNFalpha inhibition does not increase the risk of worsening of prevalent heart failure.

MIB Abstract ID Number: 14696

PreMedline Identifier: 18311816

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ANCA-associated renal vasculitis following anti-tumor necrosis factor alpha therapy.

Lead Author: Simms R

Additional Authors: Kipgen D, Dahill S, Marshall D, Rodger RS.

Am J Kidney Dis., 2008-03-01, 51(3):e11-4.

Renal Unit, Western Infirmary, Glasgow, Scotland, UK. rozsimms@doctors.net.uk

We report the case of a 62-year-old woman with rheumatoid arthritis treated with adalimumab, an anti-tumor necrosis factor alpha drug, who presented with 4 weeks of lethargy, upper respiratory tract symptoms, a vasculitic skin rash, and rapidly deteriorating renal function. She had cytoplasmic antineutrophil cytoplasmic antibodies and skin and renal biopsy specimens diagnostic of small vessel vasculitis and necrotizing crescentic glomerulonephritis, respectively. After immunosuppressive therapy and discontinuation of adalimumab therapy, vasculitis resolved and renal function recovered. This is the first report of antineutrophil cytoplasmic antibody associated necrotizing glomerulonephritis with adalimumab.

MIB Abstract ID Number: 14699

PreMedline Identifier: 18295046

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Treatment choices, preferences and decision-making by patients with rheumatoid arthritis.

Lead Author: Chilton F

Additional Authors: Collett RA.

Musculoskeletal Care., 2008-03-01, 6(1):1-14.

Rheumatology Department, South Warwickshire NHS Trust Hospital, Warwick, UK.

Objectives: To explore rheumatoid arthritis (RA) patient treatment preferences, their decision-making and the treatment choices they would make when faced with three anti-tumour necrosis factor-alpha (TNF-alpha) therapy options.Methods: Two methods of enquiry were used: postal questionnaire and one-to-one interviews. RA patients not taking anti-TNF-alpha medications were asked to complete a questionnaire after reading a written scenario, which involved choosing and identifying factors that influenced their treatment choice from three anti-TNF-alpha therapies: etanercept (Enbrel), adalimumab (Humira) and infliximab (Remicade). Patients who had tried more than one anti-TNF-alpha medication were asked at one-to-one interviews for their treatment preferences and how their current treatment had been decided.Results: Both interviewees and questionnaire respondents chose adalimumab as their preferred treatment. Interviewees identified lack of control, convenience and technical issues as influencing treatment choice. Questionnaire respondents were less likely than interviewees to want to participate in making decisions about the selection of anti-TNF-alpha therapy. There were few gender differences. Patients younger than 61 years old were more confident about self-administering treatment, and preferred subcutaneous (sc) over intravenous (iv) medication, as this reduced regular hospital attendance. Older patients preferred health care staff to administer treatment and more readily identified 'contact with other patients/meeting others' and 'staff availability if problems arise' as factors influencing choice.Conclusions: RA patients demonstrate a clear treatment preference. Different factors influence patients who choose sc compared with iv medications. Many RA patients either wished to share in treatment decisions or relinquish responsibility to the health professional when choosing anti-TNF-alpha therapy. Patients require reassurance and continuing dialogue with clinicians to manage their condition optimally. Copyright (c) 2007 John Wiley & Sons, Ltd.

MIB Abstract ID Number: 14702

PreMedline Identifier: 17726671

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MONOCLONAL ANTIBODIES; New monoclonal antibodies research from T. Mittendorf and colleagues discussed

Lead Author: T. Mittendorf

Pharma Law Weekly, 2008-03-05, EXPANDED REPORTING; Pg. 2187

Leibniz University Hannover, Center Health Economics, Koenigsworther Pl 1, D-30167 Hannover, Germany.

"In patients with longstanding severe rheumatoid arthritis (RA) receiving chronic treatment with adalimumab, health related quality of life (HRQOL) was assessed using new instruments [Functional Assessment of Chronic Illness Therapy-Fatigue scale (FACIT-Fatigue) and Health Utilities Index Mark 3 (HUI3)] and a more conventional instrument [Medical Outcomes Study Short Form-36 Health Survey (SF-36)]. Different measures for collecting patient-reported outcomes were applied simultaneously during the 3-year study period," scientists in Hannover, Germany report.

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MIB Abstract ID Number: 14749

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Spondylarthritis in the absence of B lymphocytes.

Lead Author: Baeten D

Additional Authors: Kruithof E, Breban M, Tak PP.

Arthritis Rheum., 2008-02-29, 58(3):730-733 [Epub ahead of print]

University of Amsterdam, Amsterdam, The Netherlands.

The highly effective treatment of rheumatoid arthritis by B cell depletion and the presence of B cells in the peripheral and axial lesions of patients with spondylarthritis (SpA) raise the question as to whether B lymphocytes could also be an appropriate therapeutic target in the latter disease. We describe 2 male HLA-B27-positive patients who had active SpA despite absence of B cells. One patient developed SpA with sacroiliitis and asymmetric oligoarthritis after having been diagnosed as having severe Bruton agammaglobulinemia. Since extensive investigations excluded an infectious origin of the SpA, this case illustrates that functional B cells and/or gamma globulins are not strictly required for SpA pathogenesis. The second patient had severe axial and peripheral SpA that was treated successfully with etanercept. After discontinuation of etanercept treatment because of non-Hodgkin's B cell lymphoma, both axial and peripheral SpA symptoms relapsed rapidly, and this exacerbation of articular disease activity was not modulated by successful B cell depletion therapy for the lymphoma. Although case reports have obvious limitations, our clinical observations provide evidence that active SpA can occur in the absence of functional mature B cells and thus emphasize the need for systematic studies of the exact role and function of B lymphocytes in this disease.

MIB Abstract ID Number: 14755

PreMedline Identifier: 18311807

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Etanercept reduces synovitis as measured by magnetic resonance imaging in patients with active rheumatoid arthritis after only 6 weeks.

Lead Author: Lisbona MP

Additional Authors: Maymo J, Perich J, Almirall M, Pérez-García C, Carbonell J.

J Rheumatol. , 2008-03-01, 35(3):394-7. Epub 2008 Jan 15.

From the Department of Rheumatology, IMAS, and Department of Radiology, IDIMAS-CRC, Hospital del Mar, Barcelona, Spain.

MIB Abstract ID Number: 14758

PreMedline Identifier: 18203329

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Short-Term Course of Chronic Hepatitis B and C Under Treatment with Etanercept Associated with Different Disease Modifying Antirheumatic Drugs without Antiviral Prophylaxis.

Lead Author: Cansu DU

Additional Authors: Kalifoglu T, Korkmaz C.

J Rheumatol., 2008-03-01, 35(3):421-4. Epub 2008 Jan 15.

From the Division of Rheumatology, Department of Internal Medicine, Eskisehir Osmangazi University, Eskisehir, Turkey.

MIB Abstract ID Number: 14759

PreMedline Identifier: 18203328

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Spontaneous regression of EBV-associated diffuse lymphoproliferative disease in a patient with rheumatoid arthritis after discontinuation of etanercept treatment.

Lead Author: Park SH

Additional Authors: Kim CG, Kim JY, Choe JY.

Rheumatol Int., 2008-03-01, 28(5):475-7. Epub 2007 Oct 18.

Department of Internal Medicine, Catholic University of Daegu School of Medicine, 3056-6 Namgu Daemyung 4-Dong, 705-718, Daegu, South Korea.

MIB Abstract ID Number: 14760

PreMedline Identifier: 17943259

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The magnitude of early response to methotrexate therapy predicts long-term outcome of patients with juvenile idiopathic arthritis.

Lead Author: Bartoli M

Additional Authors: Tarò M, Magni-Manzoni S, Pistorio A, Traverso F, Viola S, Magnani A, Gasparini C, Martini A, Ravelli A.

Ann Rheum Dis., 2008-03-01, 67(3):370-4. Epub 2007 Jul 27.

The magnitude of early response to methotrexate therapy predicts long-term outcome of patients with juvenile idiopathic arthritis.

OBJECTIVE: To investigate the relationship between the magnitude of clinical response in the first 6 months of methotrexate (MTX) therapy and long-term outcome in children with juvenile idiopathic arthritis (JIA). METHODS: The clinical charts of 125 JIA patients who were started with MTX and then followed for at least 5 years were reviewed. Based on the level of American College of Rheumatology (ACR) Pediatric response at 6 months, patients were divided in four mutually exclusive groups: (1) non-responders, (2) responders at 30%, (3) responders at 50%, and (4) responders at 70%. The long-term outcome in each response group was evaluated by calculating the percentage change in active and restricted joint counts from baseline to 1, 2 and 5 years and the frequency of inactive disease at 5 years. RESULTS: At 6 months, 42 patients were classified as non-responders, 24 as 30% responders, 26 as 50% responders, and 33 as 70% responders. Patients who had achieved a 70% response showed a significantly greater percentage improvement in active joint count between baseline to 5 years compared with non-responders and 30% responders, and a significantly greater percentage improvement in restricted joint count between baseline to 5 years compared with 30% responders. The 70% responders also had a greater frequency of inactive disease at 5 years compared with 30% responders, CONCLUSIONS: Our results show that the achievement of an ACR Pediatric 70 response at 6 months after start of MTX therapy predicts a more favorable long-term outcome of patients with JIA. 

MIB Abstract ID Number: 14770

PreMedline Identifier: 17660217

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Overcoming drug resistance induced by P-glycoprotein on lymphocytes in patients with refractory rheumatoid arthritis.

Lead Author: Tsujimura S

Additional Authors: Saito K, Nawata M, Nakayamada S, Tanaka Y.

Ann Rheum Dis., 2008-03-01, 67(3):380-8. Epub 2007 Jul 27.

The First Department of Internal Medicine, University of Occupational & Environmental Health, School of Medicine, 1-1 Iseigaoka, Yahata-nishi, Kitakyushu 807-8555 Japan.

OBJECTIVE: P-glycoprotein (P-gp), a member of the ATP-binding cassette transporter family, causes drug resistance by exclusion of intracellular drugs. Here, we elucidate the clinical relevance of P-gp expression on lymphocytes to drug resistance in patients with rheumatoid arthritis (RA). METHODS: P-gp expression on lymphocytes from 20 normal volunteers and 100 RA patients was analysed by flow cytometry. Drug exclusion analysis of lymphocytes was conducted by radioisotope-labelled dexamethasone. RESULTS: P-gp was overexpressed on RA lymphocytes compared with normal lymphocytes. P-gp expression levels were higher in partial responders with a Disease Activity Score (DAS) 28-3 of >5.1 despite taking at least two disease-modifying antirheumatic drugs (DMARDs) or one DMARD and corticosteroids for at least 2 years. P-gp expression levels correlated with DAS28-3. Intracellular dexamethasone levels (IDLs) in RA lymphocytes decreased according to P-gp expression. Tacrolimus, a P-gp inhibitor, restored IDLs in RA lymphocytes. P-gp overexpression in patients with highly active RA was suppressed by methotrexate but enhanced by corticosteroids. Furthermore, infliximab (3 mg/kg) resulted in improvement of RA disease activity, reduction of P-gp and recovery of IDLs. CONCLUSIONS: P-gp overexpression on lymphocytes might cause efflux of corticosteroids and DMARDs, P-gp substrates, from lymphocytes, resulting in drug resistance in patients with highly active RA. P-gp inhibition/reduction could overcome such drug resistance. Measurement of P-gp expression on lymphocytes could be a potentially useful marker for assessing drug resistance in RA, and may be suitable for selecting infliximab or DMARDs including tacrolimus for RA treatment. 

MIB Abstract ID Number: 14771

PreMedline Identifier: 17660216

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Tumour immunity: effector response to tumour and role of the microenvironment

Lead Author: Alberto Mantovani a Prof MD

Additional Authors: Pedro Romero b Prof MD; A Karolina Palucka c Prof MD; Francesco M Marincola d, * Dr MD

The Lancet, 2008-03-01, Pg. 771 Vol. 371 No. 9614 ISSN: 0140-6736

FMarincola@cc.nih.gov

Substantial evidence shows that inflammation promotes oncogenesis and, occasionally, participates in cancer rejection. This paradox can be accounted for by a dynamic switch from chronic smouldering inflammation promoting cancer-cell survival to florid, tissue-disruptive inflammatory reactions that trigger cancer-cell destruction. Clinical and experimental observations suggest that the mechanism of this switch recapitulates the events associated with pathogen infection, which stimulate immune cells to recognise danger signals and activate immune effector functions. Generally, cancers do not have danger signals and, therefore, they cannot elicit strong immune reactions. Synthetic molecules have been developed that mimic pathogen invasion at the tumour site. These compounds activate dendritic cells to produce proinflammatory cytokines, which in turn trigger cytotoxic mechanisms leading to cancer death. Simultaneously, dendritic cells capture antigen shed by dying cancer cells, undergo activation, and stimulate antigen-specific T and B cells. This process results in massive amplification of the antineoplastic inflammatory process. Thus, although anti-inflammatory drugs can prevent onset of some malignant diseases, induction of T cells specific for tumour antigen by active immunisation, combined with powerful activation signals within the cancer microenvironment, might yield the best strategy for treatment of established cancers.

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MIB Abstract ID Number: 14772

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The Risk of Hospitalized Infection in Patients with Rheumatoid Arthritis.

Lead Author: Smitten AL

Additional Authors: Choi HK, Hochberg MC, Suissa S, Simon TA, Testa MA, Chan KA.

J Rheumatol., 2008-03-01, 35(3):387-393. Epub 2008 Feb 1.

From the Departments of Epidemiology and Biostatistics, Harvard School of Public Health; Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston; i3DrugSafety, Auburndale, Massachusetts; Division of Rheuma

OBJECTIVE: To determine whether patients with rheumatoid arthritis (RA) are at increased risk of hospitalized infection and whether the risk varies by RA treatment. METHODS: A retrospective cohort study was conducted using data from a medical and pharmacy claims managed-care database from 1999 to 2006. A total of 24,530 patients were included in the RA cohort; a random sample of non-RA patients served as a comparison cohort (n = 500,000). Rates of hospitalized infection were compared between the cohorts. A nested case-control analysis was performed within the RA cohort to assess the effect of current RA medication use on hospitalized infection risk. RESULTS: A total of 1,993 patients with RA and 11,977 non-RA patients experienced a hospitalized infection. The rate of first hospitalized infection was higher in the RA cohort [adjusted hazard ratio = 2.03; 95% confidence interval (CI) 1.93-2.13]. In the case-control analysis, the current use of biological disease modifying antirheumatic drugs (DMARD) was associated with slightly increased risk of hospitalized infection [rate ratio (RR) = 1.21; 95% CI 1.02-1.43]. Methotrexate and hydroxychloroquine were associated with decreased risk. Oral corticosteroid use increased risk (RR = 1.92; 95% CI 1.67-2.21), and there was a dose-related effect [</= 5 mg/day: RR = 1.32 (95% CI 1.06-1.63), 6-10 mg/day: RR = 1.94 (95% CI 1.53-2.46), > 10 mg/day: RR = 2.98 (95% CI 2.41-3.69)]. CONCLUSION: These data confirm that individuals with RA are at increased risk of hospitalized infection compared to those without RA. Oral corticosteroid use was associated with a dose-related increase. Biological DMARD use was associated with slightly elevated risk; however, this may reflect confounding and channeling bias.

MIB Abstract ID Number: 14721

PreMedline Identifier: 18260176

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Clinical Outcome and Imaging Changes After Intraarticular (IA) Application of Etanercept or Methylprednisolone in Rheumatoid Arthritis: Magnetic Resonance Imaging and Ultrasound-Doppler Show No Effect of IA Injections in the Wrist After 4 Weeks.

Lead Author: Boesen M

Additional Authors: Boesen L, Jensen KE, Cimmino MA, Torp-Pedersen S, Terslev L, Koenig M, Danneskiold-Samsøe B, Røgind H, Bliddal H.

J Rheumatol., 2008-03-01, [Epub ahead of print]

From The Parker Institute Frederiksberg Hospital; Rigshospitalet, Department of Radiology, MRI Section, Copenhagen, Denmark; and Rheumatologic Clinic, Department of Internal Medicine, University of Genoa, Genoa, Italy.

MIB Abstract ID Number: 14743

PreMedline Identifier: 18322991

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Comparison of an in vitro Tuberculosis Interferon-gamma Assay with Delayed-type Hypersensitivity Testing for Detection of Latent Mycobacterium tuberculosis: A Pilot Study in Rheumatoid Arthritis.

Lead Author: Greenberg JD

Additional Authors: Reddy SM, Schloss SG, Kurucz OS, Bartlett SJ, Abramson SB, Bingham CO 3rd.

J Rheumatol., 2008-03-01, [Epub ahead of print]

From the Department of Rheumatology, NYU-Hospital for Joint Diseases, New York, New York; and Division of Rheumatology and Division of Allergy and Clinical Immunology, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA.

OBJECTIVE: Recommendations for screening for latent Mycobacterium tuberculosis (MTB) infection have been proposed but are not well studied in patients with rheumatoid arthritis (RA). We estimated the prevalence of anergy in RA and evaluated different methods to detect MTB exposure. METHODS: This was a prospective pilot study of 61 patients with RA and 42 healthy controls. Tuberculin skin test (TST) antigen, Candida, and tetanus toxoid were injected intradermally using the Mantoux method. Subjects negative for TST returned for a second-step test. Whole-blood interferon-gamma (IFN-gamma) release to mycobacterial antigens was evaluated with the first-generation QuantiFeron(R) test (QIFN). RESULTS: Cutaneous anergy in patients with RA was not significantly different than healthy controls (p = 0.154), and was not affected by disease modifying antirheumatic drugs (p = 0.270). In patients with RA, 16.4% had positive TST with 10 mm cutoff vs 11.9% of controls. Using a 5 mm cutoff, 21.3% of patients with RA were positive, and this increased to 29.5% with a second-step TST. QIFN detected MTB exposure in 18% of patients with RA and 19% of controls (p = 0.897). However, indeterminate QIFN tests were higher in RA patients (11.5%) compared to controls (2.4%), demonstrating a lower sensitivity to detect latent MTB. CONCLUSION: Cutaneous anergy may be less common than previously reported in patients with RA. patients. However, the single-step TST and 10 mm cutoff may fail to detect all cases of latent exposure in RA patients. High rates of indeterminate results in QIFN testing suggest that QIFN should not be employed as an alternative, single-screening test in patients with RA. These pilot results require confirmation in larger studies to determine the optimal screening strategy in RA.

MIB Abstract ID Number: 14744

PreMedline Identifier: 18322990

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[Whipple's disease with segmental lesions in the proximal small intestine]

Lead Author: Prassler R

Additional Authors: Kempmann T, Vierling P.

Dtsch Med Wochenschr., 2008-03-01, 133(10):460-3.

Innere Abteilung, Städtisches Krankenhaus Oberndorf. Dr.Prassler@Krankenhaus-Oberndorf.de

[Article in German]

HISTORY AND ADMISSION FINDINGS: A 67-year-old man with anemia was referred to our hospital. He had suffered from rheumatoid arthritis for ten years. Two months before admission he had been an inpatient at another hospital because of heart failure. He presented with edema, slightly elevated temperature and effusion in the right knee. INVESTIGATIONS: Laboratory findings revealed a chronic inflammation and an anemia of iron malabsorption. Duodenal histology showed PAS-positive macrophages typical for Whipple's disease. Tropheryma whippelii-DNA was found by polymerase chain reaction (PCR) in synovial and cerebrospinal fluid and broncho-alveolar lavage. TREATMENT AND COURSE: Antibiotic therapy was initiated, the antirheumatic medication terminated and iron was administered intravenously. The outcome was satisfactory. CONCLUSIONS: Rare systemic diseases should be considered in patients presenting with symptoms involving several organs. Whipple's disease can be cured only by adequate antibiotic therapy. The use of PCR facilitates the correct diagnosis.

MIB Abstract ID Number: 14745

PreMedline Identifier: 18302096

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Anakinra treatment for systemic juvenile idiopathic arthritis and adult onset Still disease.

Lead Author: Woo P.

Ann Rheum Dis., 2008-03-01, 67(3):281-2.

Comment on:

Ann Rheum Dis. 2008 Mar;67(3):302-8.

<<No Abstract Available>>

MIB Abstract ID Number: 14747

PreMedline Identifier: 18292104

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Limits and perspectives of ultrasound in the diagnosis and management of rheumatic diseases.

Lead Author: Delle Sedie A

Additional Authors: Riente L, Bombardieri S.

Mod Rheumatol., 2008-02-28, [Epub ahead of print]

Rheumatology Unit, Department of Internal Medicine, University of Pisa, Via Roma 67, Pisa, 56126, Italy, adellese@lycos.com.

Musculoskeletal sonography (MSUS) has played a growing role in the diagnosis and management of rheumatic diseases, enabling the imaging of synovitis, bone erosion, and cartilage damage in the early phase of arthritis. "Dynamic" evaluation of tendons and help in guiding needle positioning in interventional manoeuvres are some of the other reasons for its success. MSUS, particularly when coupled with power Doppler (PD) examination, has recently been shown to be an efficient tool for monitoring disease activity and progression in rheumatoid arthritis, spondyloarthritis, crystal-related arthropathy, and osteoarthritis, with general consensus on its interesting results. More specifically, the PD signal has proved to be a simple and promising tool for short-term monitoring of synovial vascularity changes induced by steroids or biological agents in RA patients. MSUS has some limits, because of the physical properties of US and the quality of the equipment; it is, moreover, an operator-related imaging technique, with few standardized protocols. Future goals should be standardization of the examining approach in grey scale and Doppler ultrasound (US), including use of new equipment (3D US), extensive use in other fields (i.e. connective tissue diseases and vasculitis), and possible new applications (e.g. thoracic US). 

MIB Abstract ID Number: 14816

PreMedline Identifier: 18306005

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Lack of association between PADI4 and functional severity in Japanese rheumatoid arthritis patients.

Lead Author: Nishimoto K

Additional Authors: Ikari K, Mochizuki T, Tomatsu T, Toyama Y, Hara M, Yamanaka H, Kamatani N, Momohara S.

Ann Rheum Dis., 2008-03-01, 67(3):431-2.

<<No Abstract Available>>

MIB Abstract ID Number: 14817

PreMedline Identifier: 18292109

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CTLA-4 CT60 polymorphism is not an independent genetic risk marker of rheumatoid arthritis in a Japanese population.

Lead Author: Tsukahara S

Additional Authors: Iwamoto T, Ikari K, Inoue E, Tomatsu T, Hara M, Yamanaka H, Kamatani N, Momohara S.

Ann Rheum Dis., 2008-03-01, 67(3):428-9.

<<No Abstract Available>>

MIB Abstract ID Number: 14818

PreMedline Identifier: 18292106

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Anakinra treatment for systemic juvenile idiopathic arthritis and adult onset Still disease.

Lead Author: Woo P.

Ann Rheum Dis. , 2008-03-01, 67(3):281-2.

Comment on:

Ann Rheum Dis. 2008 Mar;67(3):302-8.  

<<No Abstract Available>>

MIB Abstract ID Number: 14820

PreMedline Identifier: 18292104

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Methotrexate-Induced and Epstein-Barr Virus-Associated B-Cell Lymphoma of the Spine: MR and PET/CT Imaging.

Lead Author: Nguyen BD

Additional Authors: Roarke MC, McCullough AE.

Clin Nucl Med., 2008-03-01, 33(3):208-210.

From the Departments of *Radiology, and †Department of Laboratory Medicine and Pathology, Mayo Clinic, Scottsdale, Arizona.

MIB Abstract ID Number: 14822

PreMedline Identifier: 18292104

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Abnormal collagen deposition in synovia after collagen type V immunization in rabbits.

Lead Author: Ogido LT

Additional Authors: Teodoro WR, Velosa AP, de Oliveira CC, Parra ER, Capelozzi VL, Yoshinari NH.

Histol Histopathol., 2008-03-01, 23(3):263-9.

Discipline of Rheumatology, Faculty of Medicine, University of São Paulo, Brazil.

Sinovitis in Scleroderma (SSc) is rare, usually aggressive and fully resembles rheumatoid arthritis. Experimental models of SSc have been used in an attempt to understand its pathogenesis. Previous studies done in our laboratory had already revealed the presence of a synovial remodeling process in rabbits immunized with collagen V. To validate the importance of collagen type V and to explore the quantitative relationship between this factor and synovia remodeling as well as the relationship between collagen type V and other collagens, we studied the synovial tissue in immunized rabbits. Rabbits (N=10) were immunized with collagen V plus Freund's adjuvant and compared with animals inoculated with adjuvant only (N=10). Synovial tissues were submitted to histological analysis, immunolocalization to collagen I, III and V and biochemical analysis by eletrophoresis, immunoblot and densitometric method. The synovial tissue presented an intense remodeling process with deposits of collagen types I, III and V after 75 and 120 days of immunization, mainly distributed around the vessels and interstitium of synovial extracellular matrix. Densitometric analysis confirmed the increased synthesis of collagen I, III and V chains (407.69+/-80.31; 24.46+/-2.58; 70.51+/-7.66, respectively) in immunized rabbits when compared with animals from control group (164.91+/-15.67; 12.89+/-1.05; 32+/-3.57) (p<0.0001). We conclude that synovial remodeling observed in the experimental model can reflect the articular compromise present in patients with scleroderma. Certainly, this experimental model induced by collagen V immunization will bring new insights in to pathogenic mechanisms and allow the testing of new therapeutic strategies to ameliorate the prognosis for scleroderma patients. 

MIB Abstract ID Number: 14825

PreMedline Identifier: 18072083

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Serum IgG antibodies to peptidylarginine deiminase 4 in rheumatoid arthritis and associations with disease severity.

Lead Author: Halvorsen EH

Additional Authors: Pollmann S, Gilboe IM, van der Heijde D, Landewé R, Ødegård S, Kvien TK, Molberg Ø.

Ann Rheum Dis., 2008-03-01, 67(3):414-7. Epub 2007 Nov 15.

Institute of Immunology, University of Oslo, Rikshospitalet University Hospital, 0027 Oslo, Norway. eirikhha@medisin.uio.no

MIB Abstract ID Number: 14828

PreMedline Identifier: 18006540

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Gastrointestinal tolerability of etoricoxib in rheumatoid arthritis patients: results of the etoricoxib vs diclofenac sodium gastrointestinal tolerability and effectiveness trial (EDGE-II).

Lead Author: Krueger K

Additional Authors: Lino L, Dore R, Radominski S, Zhang Y, Kaur A, Simpson R, Curtis S.

Ann Rheum Dis., 2008-03-01, 67(3):315-22. Epub 2007 Oct 27.

Praxiszentrum St. Bonifatius, Munchen, Germany.

OBJECTIVE: A randomised, double-blind study to compare the gastrointestinal (GI) tolerability, safety and efficacy of etoricoxib and diclofenac in patients with rheumatoid arthritis (RA). PATIENTS AND METHODS: A total of 4086 patients (mean age 60.8 years) diagnosed with RA were enrolled and received etoricoxib 90 mg daily (n = 2032) or diclofenac 75 mg twice daily (n = 2054). Use of gastroprotective agents and low-dose aspirin was allowed. The prespecified primary end point consisted of the cumulative rate of patient discontinuations due to clinical and laboratory GI adverse experiences (AEs). General safety was also assessed, including adjudicated thrombotic cardiovascular event data. Efficacy was evaluated using the Patient Global Assessment of Disease Status (PGADS; 0-4 point scale). RESULTS: Mean (SD; maximum) duration of treatment was 19.3 (10.3; 32.9) and 19.1 (10.4; 33.1) months in the etoricoxib and diclofenac groups, respectively. The cumulative discontinuation rate due to GI AEs was significantly lower with etoricoxib than diclofenac (5.2 vs 8.5 events per 100 patient-years, respectively; hazard ratio 0.62 (95% CI: 0.47, 0.81; p<or=0.001)). The incidence of discontinuations for hypertension-related and oedema-related AEs were significantly higher with etoricoxib (2.5% and 1.1% respectively) compared with diclofenac (1.5% and 0.4% respectively; p<0.001 for hypertension and p<0.01 for oedema). Etoricoxib and diclofenac treatment resulted in similar efficacy (PGADS mean changes from baseline -0.62 vs -0.58, respectively). CONCLUSIONS: Etoricoxib 90 mg demonstrated a significantly lower risk for discontinuing treatment due to GI AEs compared with diclofenac 150 mg. Discontinuations from renovascular AEs, although less common than discontinuations from GI AEs, were significantly higher with etoricoxib.

MIB Abstract ID Number: 14831

PreMedline Identifier: 17965424

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B cell depletion therapy for patients with systemic lupus erythematosus results in a significant drop in anticardiolipin antibody titres.

Lead Author: Ioannou Y

Additional Authors: Lambrianides A, Cambridge G, Leandro MJ, Edwards JC, Isenberg DA.

Ann Rheum Dis., 2008-03-01, 67(3):425-6. Epub 2007 Sep 28.

Centre for Rheumatology, Department of Medicine, University College London, 250 Euston Road, London NW1 2PG, UK. j.ioannou@ich.ucl.ac.uk

MIB Abstract ID Number: 14837

PreMedline Identifier: 17905784

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Serum levels of sex steroid hormones and matrix metalloproteinases after intra-articular glucocorticoid treatment in female patients with rheumatoid arthritis.

Lead Author: Weitoft T

Additional Authors: Larsson A, Rönnblom L.

Ann Rheum Dis., 2008-03-01, 67(3):422-4. Epub 2007 Sep 18.

Department of Research and Development, County Council of Gävleborg/Uppsala University, Section of Rheumatology, Gävle Hospital, Sweden. tomas.weitoft@lg.se

OBJECTIVES: To study metalloproteinase activity and sex steroid hormone production in serum after intra-articular glucocorticoid treatment for knee synovitis. METHODS: 18 female patients with rheumatoid arthritis and synovitis of the knee with need for intra-articular glucocorticoid treatment were included in this study. Serum samples of matrix metalloproteinases (MMP-1/TIMP complex and MMP-3), dehydroepiandrosterone sulphate, testosterone, oestradiol, steroid hormone binding globulin, follicle stimulating hormone and luteinising hormone were collected before injection with 20 mg triamcinolone hexacetonide, and 24 h, 48 h, 1 week and 2 weeks after injection, respectively. RESULTS: Serum levels of MMP-3 were significantly decreased, but MMP-1/TIMP complex was unaffected. Dehydroepiandrosterone sulphate, testosterone and oestradiol levels all decreased and tended to return to baseline levels during the observation period. Steroid hormone binding globulin, follicle stimulating hormone and luteinising hormone levels were unchanged. CONCLUSIONS: Intra-articular glucocorticoid treatment causes a temporary, but considerable suppression of sex steroid hormone secretion. The reduction of MMP-3 indicates an inhibition of the inflammatory, but probably also the cartilage destructive processes within the treated joint. 

MIB Abstract ID Number: 14838

PreMedline Identifier: 17878211

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Associations between human leukocyte antigen, PTPN22, CTLA4 genotypes and rheumatoid arthritis phenotypes of autoantibody status, age at diagnosis and erosions in a large cohort study.

Lead Author: Karlson EW

Additional Authors: Chibnik LB, Cui J, Plenge RM, Glass RJ, Maher NE, Parker A, Roubenoff R, Izmailova E, Coblyn JS, Weinblatt ME, Shadick NA.

Ann Rheum Dis., 2008-03-01, 67(3):358-63. Epub 2007 Jul 31.

Division of Rheumatology, Allergy, and Immunology, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA. ekarlson@partners.org

BACKGROUND: HLA-DRB1 shared epitope (HLA-SE), PTPN22 and CTLA4 alleles are associated with cyclic citrullinated peptide (CCP) and rheumatoid arthritis (RA). OBJECTIVE: We examined associations between HLA-SE, PTPN22, CTLA4 genotypes and RA phenotypes in a large cohort to (a) replicate prior associations with CCP status, and (b) determine associations with radiographic erosions and age of diagnosis. METHODS: A total of 689 RA patients from the Brigham RA Sequential Study (BRASS) were genotyped for HLA-SE, PTPN22 (rs2476601) and CTLA4 (rs3087243). Association between genotypes and CCP, rheumatoid factor (RF) erosive phenotypes and age at diagnosis were assessed with multivariable models adjusting for age, sex and disease duration. Novel causal pathway analysis was used to test the hypothesis that genetic risk factors and CCP are in the causal pathway for predicting erosions. RESULTS: In multivariable analysis, presence of any HLA-SE was strongly associated with CCP+ (odds ratio (OR) 3.05, 95% CI 2.18-4.25), and RF+ (OR 2.53, 95% CI 1.83-3.5) phenotypes; presence of any PTPN22 T allele was associated with CCP+ (OR 1.81, 95% CI 1.24-2.66) and RF+ phenotypes (OR 1.84, 95% CI 1.27-2.66). CTLA4 was not associated with CCP or RF phenotypes. While HLA-SE was associated with erosive RA phenotype (OR 1.52, 95% CI 1.01-2.17), this was no longer significant after conditioning on CCP. PTPN22 and CTLA4 were not associated with erosive phenotype. Presence of any HLA-SE was associated with an average 3.6 years earlier diagnosis compared with absence of HLA-SE (41.3 vs 44.9 years, p = 0.002) and PTPN22 was associated with a 4.2 years earlier age of diagnosis (39.5 vs 43.6 years, p = 0.002). CTLA4 genotypes were not associated with age at diagnosis of RA. CONCLUSIONS: In this large clinical cohort, we replicated the association between HLA-SE and PTPN22, but not CTLA4 with CCP+ and RF+ phenotypes. We also found evidence for associations between HLA-SE, and PTPN22 and earlier age at diagnosis. Since HLA-SE is associated with erosive phenotype in unconditional analysis, but is not significant after conditioning on CCP, this suggests that CCP is in the causal pathway for predicting erosive phenotype.

MIB Abstract ID Number: 14839

PreMedline Identifier: 17666451

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Effects of a novel tyrosine kinase inhibitor in rheumatoid arthritis synovial fibroblasts.

Lead Author: Huber LC

Additional Authors: Künzler P, Boyce SH, Michel BA, Gay RE, Ink BS, Gay S.

Ann Rheum Dis., 2008-03-01, 67(3):389-94. Epub 2007 Jul 27.

Center of Experimental Rheumatology, University Hospital Zurich, Gloriastrasse 25, CH-8091 Zurich, Switzerland. Lars.Huber@usz.ch

MIB Abstract ID Number: 14840

PreMedline Identifier: 17660218

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Long-term effects of infliximab on bone and cartilage turnover markers in patients with rheumatoid arthritis.

Lead Author: Chopin F

Additional Authors: Garnero P, le Henanff A, Debiais F, Daragon A, Roux C, Sany J, Wendling D, Zarnitsky C, Ravaud P, Thomas T.

Ann Rheum Dis., 2008-03-01, 67(3):353-7. Epub 2007 Jul 20.

INSERM U890, Rheumatology Department, University Hospital of St-Etienne, France.

BACKGROUND: Rheumatoid arthritis (RA) is associated with systemic bone loss, subchondral bone erosion and cartilage degradation under the control of pro-inflammatory cytokines, including tumour necrosis factor alpha (TNFalpha). Therefore, we tested the hypothesis that administration of infliximab, an anti-TNFalpha drug in the treatment of RA, would modulate systemic and local bone resorption and reduce cartilage degradation. METHODS: We performed a prospective study of a multicentric cohort of 48 women, mean (SD) age 54.2 (12.1) years old, with severe RA for 11.4 (7.8) years, who started infliximab after failure of other disease-modifying antirheumatic drugs. At baseline and 6, 22 and 54 weeks after initiating Infliximab therapy we measured the following biochemical markers: pro-collagen serum type I N-terminal propeptide (PINP), a marker of bone formation; serum C-terminal cross-linked telopeptide of type I collagen (CTX-I), a marker of cathepsin K-mediated bone collagen degradation believed to reflect systemic bone resorption; serum C-terminal cross-linked telopeptide of type I collagen (ICTP), an index of matrix metalloprotease (MMP) mediated type I collagen degradation reflecting preferential joint metabolism; and urinary CTX-II a biochemical markers of cartilage degradation. Total hip and lumbar spine bone mineral density (BMD) was assessed at baseline, and after 6 and 12 months by dual-energy x-ray absorptiometry (DXA). No patient received bisphosphonates while 77% were under oral glucocorticoids. RESULTS: BMD remained stable over 1 year. Serum CTX-I levels rapidly decreased by 19% and 28% at week 6 and week 22, respectively (analysis of variance (ANOVA) p = 0.032) values returning to pre-treatment level at week 54. By contrast, ICTP levels progressively declined with a maximal 25% decrease at week 54 (ANOVA p = 0.028). By contrast, PINP levels remained stable over time, which led to a 30 to 40% improvement in bone remodelling balance, as assessed by the ratios PINP/CTX and PINP/ICTP (p<0.05). There was no significant change of urinary CTX-II in the whole population, but a slight decrease (ANOVA p = 0.041) in those with pre-treatment levels above the upper limit of normal range. CONCLUSIONS: In summary, the improvement in the formation/resorption marker ratio suggests beneficial systemic and local bone effects of infliximab in patients with RA.

MIB Abstract ID Number: 14841

PreMedline Identifier: 17644538

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Evidence for an influence of chemokine ligand 3-like 1 (CCL3L1) gene copy number on susceptibility to rheumatoid arthritis.

Lead Author: McKinney C

Additional Authors: Merriman ME, Chapman PT, Gow PJ, Harrison AA, Highton J, Jones PB, McLean L, O'Donnell JL, Pokorny V, Spellerberg M, Stamp LK, Willis J, Steer S, Merriman TR.

Ann Rheum Dis. , 2008-03-01, 67(3):409-13. Epub 2007 Jun 29.

Department of Biochemistry, University of Otago, PO Box 56, Dunedin, New Zealand.

MIB Abstract ID Number: 14842

PreMedline Identifier: 17604289

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LIFE SCIENCES; Study data from Sahmyook University, Department of Pharmacy provide new insights into life sciences

Lead Author: S. Han

Biotech Business Week, 2008-03-03, EXPANDED REPORTING; Pg. 1674

Sahmyook University, Dept. of Pharmacy, Nowon-gu, Seoul 139-743, Korea.

A report, 'Auranofin inhibits overproduction of pro-inflammatory cytokines, cyclooxygenase expression and PGE2 production in macrophages,' is newly published data in Archives of Pharmacal Research. According to recent research published in the journal Archives of Pharmacal Research, "Auranofin (AF), a gold compound, is an orally active therapeutic agent used to treat rheumatoid arthritis (RA), a self-perpetuating inflammatory disease. RA is characterized by autoimmune-mediated proliferation of synovial cells that leads to inflammation, pain, and swelling in most major joints: However, the mechanism as to how AF relieves RA symptoms has not been fully elucidated."

"The object of this study was to examine the ability of AF to immunomodulate macrophages as antigen presenting cells (APCs). Macrophages are recognized as playing an important role in the pathogenesis of RA, in that there is a relative abundance of macrophage-derived cytokines, such as tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) in rheumatoid synovium. In this work, we tested whether AF (2.5-20 mM) could inhibit inflammatory activity in the macrophage cell line RAW 264.7. AF decreased production of nitric oxide (NO) and the pro-inflammatory cytokines, TNF-alpha, IL-1beta and IL-6 in macrophages. Furthermore, AF inhibited cyclooxygenase-2 (COX-2)-dependent prostaglandin E2 (PGE2) production in a concentration-dependent manner," wrote S. Han and colleagues, Sahmyook University, Department of Pharmacy.

The researchers concluded: "These findings may provide an explanation for the clinical effects of AF in patients with RA."

Han and colleagues published their study in Archives of Pharmacal Research (Auranofin inhibits overproduction of pro-inflammatory cytokines, cyclooxygenase expression and PGE2 production in macrophages. Archives of Pharmacal Research, 2008;31(1):67-74).

For additional information, contact S. Han, Sahmyook University, Dept. of Pharmacy, Nowon-gu, Seoul 139-743, Korea.

The publisher's contact information for the journal Archives of Pharmacal Research is: Pharmaceutical Society Korea, 1489-3 Suhcho-Dong, Suhcho-Ku, Seoul 137-071, South Korea.

MIB Abstract ID Number: 14843

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Arthritis; FDA Agrees to Review Cimzia(R) File for the Treatment of Rheumatoid Arthritis

Lead Author: [none given]

Medical Letter on the CDC & FDA, 2008-02-28, pg. 48

UCB announced that the U.S. Food and Drug Administration (FDA) agreed to accept, for filing and review, a biologics license application (BLA) for Cimzia(R) (certolizumab pegol) for the treatment of adult patients with active rheumatoid arthritis (RA). Cimzia(R) is an investigational agent. If approved, Cimzia(R) will be the first and only PEGylated anti-TNF (Tumor Necrosis Factor) biologic therapy available for the treatment of rheumatoid arthritis.

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MIB Abstract ID Number: 14845

Proquest Identifier: 1428978531

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Recent insights in the pharmacological actions of methotrexate in the treatment of rheumatoid arthritis

Lead Author: J. A. M. Wessels

Additional Authors: T. W. J. Huizinga, H.-J. Guchelaar.

Rheumatology, 2008-03-01, Vol. 47, Iss. 3; pg. 249, 7 pgs

MIB Abstract ID Number: 14850

Proquest Identifier: 1432863121

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The evaluation of latent tuberculosis in rheumatologic diseases for anti-TNF therapy: experience with 192 patients.

Lead Author: Hanta I

Additional Authors: Ozbek S, Kuleci S, Kocabas A.

Clin Rheumatol., 2008-03-05, [Epub ahead of print]

School of Medicine, Department of Chest Diseases, Çukurova University, 01330, Balcali, Adana, Turkey, ihanta@cu.edu.tr.

It is recommended to evaluate the presence of latent tuberculosis infection (LTBI) before initiating antitumor necrosis factor alpha (anti-TNF) therapy for rheumatologic diseases. We aimed to present the follow-up results of 192 patients with rheumatologic diseases before anti-TNF therapy for LTBI. We enrolled 192 patients who were given anti-TNF therapy for their rheumatologic diseases between April 2005 and January 2008. The demographic characteristics of the patients were recorded. Chest X-ray was obtained and tuberculin skin test (TST) was performed in all patients before anti-TNF therapy. LTBI was assessed by detailed history of close contact with infectious cases within the last year, abnormal chest radiography, and positive TST (>/=5 mm) before initiating anti-TNF therapy. Patients with anti-TNF therapy were followed with 2-month intervals for active tuberculosis by pulmonary and extrapulmonary symptoms, physical examination, and chest X-ray. Of 192 patients, 104 (54.2%) patients were women, age (mean +/- SD) 43.1 +/- 12.7 years and 88 (45.8%) patients were men, age (mean +/- SD) 39.3 +/- 11.2 years. Ninety-one (47.4%) of them had rheumatoid arthritis (RA); 92 (47.9%) had ankylosing spondylitis (AS), and nine (4.7%) had psoriatic arthritis. Isoniazid treatment was started in 129 (67.2%) patients in whom LTBI was detected. No significant difference was observed for TST positivity (TST >/= 5 mm) between the patients with RA and AS (p = 0.101). Similarly, no significant difference was also observed for TST positivity between the patients who received immunosuppressive therapy and those who did not (p = 0.154). Only three (1.6%) patients developed active tuberculosis at the study period. We suggested that in despite of the presence of rheumatologic disease and/or immunosuppressive therapy, TST is an acceptable and available diagnostic test for detecting LTBI before anti-TNF therapy.

MIB Abstract ID Number: 14851

PreMedline Identifier: 18320137

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Recent insights in the pharmacological actions of methotrexate in the treatment of rheumatoid arthritis.

Lead Author: Wessels JA

Additional Authors: Huizinga TW, Guchelaar HJ.

Rheumatology (Oxford)., 2008-03-01, 47(3):249-55. Epub 2007 Nov 28.

Department of Clinical Pharmacy and Toxicology, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands.

This review presents recent data supporting the methotrexate (MTX) mechanisms of action, which are likely to account for its anti-proliferative and immunosuppressive effects in rheumatoid arthritis (RA). The effects of MTX in vivo may be mediated by reducing cell proliferation, increasing the rate of apoptosis of T cells, increasing endogenous adenosine release, altering the expression of cellular adhesion molecules, influencing production of cytokines, humoral responses and bone formation. Several reports indicate that the effects of MTX are influenced by genetic variants, specific dynamic processes and micro-environmental elements such as nucleotide deprivation or glutathione levels. The challenge for the future will be linking biological and genetic markers relevant to the response to MTX in RA.

MIB Abstract ID Number: 14853

PreMedline Identifier: 18045808

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ARTHRITIS; Scientists at University of Duisburg-Essen discuss research in arthritis

Lead Author: A. Heiligenhaus

Pharma Law Weekly, 2008-03-04, EXPANDED REPORTING; Pg. 373

University of Duisburg Essen, St. Franziskus Hospital, Dept. of Ophthalmology, Hohenzollernring 74, D-48145 Munster, Germany.

In this recently published article, scientists in Munster, Germany conducted a study "To study the value of methotrexate (MTX) and the requirement for additional anti-inflammatory drugs for the treatment of severe chronic iridocyclitis associated with juvenile idiopathic arthritis (JIA). Institutional study of 35 consecutive patients with JIA started on MTX as the single systemic immunosuppressive drug for the treatment of associated iridocyclitis."

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MIB Abstract ID Number: 14856

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Lupus nephritis and Raynaud's phenomenon are significant risk factors for vascular thrombosis in SLE patients with positive antiphospholipid antibodies.

Lead Author: Choojitarom K

Additional Authors: Verasertniyom O, Totemchokchyakarn K, Nantiruj K, Sumethkul V, Janwityanujit S.

Clin Rheumatol., 2008-03-01, 27(3):345-51. Epub 2007 Sep 2.

Division of Allergy-Immunology-Rheumatology, Department of Medicine, Ramathibodi Hospital, 270 Rama6 Road, Bangkok, 10400, Thailand.

This study is aimed to determine the predictors of nongravid vascular thrombosis in systemic lupus erythematosus (SLE) patients with positive antiphospholipid antibodies (SLE-aPL). A cohort of 67 SLE-aPL patients who had at least one positive test for lupus anticoagulant (LA), anticardiolipin (aCL), or anti-beta2glycoprotein-1(B2) was examined. Main outcome was the presence of vascular thrombosis. Association between thrombosis and risk factors was examined by contingency table. The odds ratio (OR) of significant predictors was determined by logistic regression. Three percent of patients were LA(+), 6% were aCL(+), 31% were B2(+), 3% were aCL(+)LA(+), 35.8% were aCL(+)B2(+), 7.5% were LA(+)B2(+), and 13.4% were positive for all tests. As for clinical manifestations, 79% had lymphopenia, 76% had lupus nephritis (LN), 41.8% had autoimmune hemolytic anemia, 34.3% had thrombocytopenia, 20.9% had abortion, and 19.4% had Raynaud's phenomenon (RP). Thrombosis occurred in 26 patients. The prevalence of thrombosis for SLE-aPL was 38.8%. Thrombosis was observed more frequently in patients with LA(+) (12 of 18) than the others (14 of 49; p = 0.01). Two-by-two table showed that oral contraceptive and LN were significantly associated with increased risk of thrombosis, while lymphopenia and antimalarials were significantly associated with decreased risk of thrombosis. Multivariate analysis confirmed that LN and RP were associated with increased risk of thrombosis (OR = 6.2 and 3.2; p = 0.005 and 0.008), while lymphopenia and antimalarials were associated with decreased risk of thrombosis (OR = 0.86 and 0.18; p = 0.02 and 0.034). LA is the strongest test to determine the risk of thrombosis in SLE-aPL. The presence of LN and RP strongly predicts thrombosis, while lymphopenia and antimalarials are protective. These findings help to identify patients who may benefit from prophylactic therapy.

MIB Abstract ID Number: 14906

PreMedline Identifier: 17805483

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Leflunomide as adjuvant treatment of dermatomyositis.

Lead Author: Boswell JS

Additional Authors: Costner MI.

J Am Acad Dermatol., 2008-03-01, 58(3):403-6. Epub 2008 Jan 14.

Department of Dermatology, University of Texas Southwestern Medical Center at Dallas, Dallas, USA.

We report 3 cases of recalcitrant dermatomyositis that responded to the addition of daily leflunomide, a novel immunomodulatory drug that is currently used to treat rheumatoid arthritis. In our patients, leflunomide proved both safe and effective as adjuvant therapy in treating dermatomyositis.

MIB Abstract ID Number: 14858

PreMedline Identifier: 18194823

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Serum uric acid is independently associated with hypertension in patients with rheumatoid arthritis.

Lead Author: Panoulas VF

Additional Authors: Douglas KM, Milionis HJ, Nightingale P, Kita MD, Klocke R, Metsios GS, Stavropoulos-Kalinoglou A, Elisaf MS, Kitas GD.

J Hum Hypertens., 2008-03-01, 22(3):177-82. Epub 2007 Oct 25.

Department of Rheumatology, Dudley Group of Hospitals NHS Trust, Russells Hall Hospital, Dudley, West Midlands, UK.

Hypertension (HT) is highly prevalent in rheumatoid arthritis (RA). Serum uric acid (SUA) has been associated with HT in the general population. The mutual exclusion of gout and RA, and the systemic inflammatory component of RA may alter this association in this patient population. We explored a potential association between SUA levels and HT in RA and evaluated whether this association is independent of HT risk factors, RA characteristics and relevant drugs. A total of 400 consecutive RA patients were assessed. SUA and complete biochemical profile were measured. Demographic, HT-related factors, RA characteristics and drugs were assessed as potential covariates. Results were analysed using binary logistic models to test the independence of the association between SUA and HT. SUA levels were higher in hypertensive compared to normotensive RA patients (5.44+/-1.6 mg dl(-1) (323.57+/-95.17 micromol l(-1)) vs 4.56+/-1.1 mg dl(-1) (271.23+/-65.43 micromol l(-1)), P<0.001). When adjusted for HT risk factors, renal function, RA characteristics, non-steroidal anti-inflammatory drugs, oral prednisolone, cyclosporine, leflunomide and low-dose aspirin, the odds of being a hypertensive RA patient per 1 mg dl(-1)(59.48 micromol l(-1)) SUA increase were significantly increased: OR=1.59 (95% CI: 1.21-2.1, P=0.001). This was also significant for the subgroup of patients who were not on diuretics (OR=1.5, 95% CI: 1.1-2.05; P=0.011). This cross-sectional study suggests that SUA levels are independently associated with HT in RA patients. Prospective longitudinal studies are needed to confirm and further explore the causes and implications of this association.

MIB Abstract ID Number: 14859

PreMedline Identifier: 17960169

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Sensitivity to change of the Rheumatoid Arthritis Self-Efficacy scale (RASE) and predictors of change in self-efficacy.

Lead Author: Hewlett S

Additional Authors: Cockshott Z, Almeida C, Richards P, Lowe R, Greenwood R, Kirwan J; the RASE Study Group.

Musculoskeletal Care., 2008-03-01, 6(1):49-67

School of Nursing, University of the West of England, Bristol UK.

Objectives: Patient education in rheumatoid arthritis (RA) aims to improve health outcomes by prompting people to adopt self-management behaviours. One precursor for initiating behaviour change is self-efficacy (SE), a belief that you can do a task. This study tested the sensitivity to change of a new scale to measure SE for self-management in people with RA, the Rheumatoid Arthritis Self-Efficacy scale (RASE). Exploratory analysis examined potential predictors of change in SE.Methods: People with RA at 11 rheumatology centres, who had accepted an education programme as part of clinical care, completed questionnaires at baseline, and two and eight weeks after their programme end. Programmes were not standardized, as this was a pragmatic study in clinical practice.Results: A total of 128 patients participated. After controlling for baseline scores, the RASE showed small but significant improvements in SE from baseline (RASE 107.57, CI 105.42-109.72) to two weeks after programme end (RASE 110.80, CI 108.60-112.99), and eight weeks (RASE 110.62, CI 108.40-112.85, p < 0.001). Standardized response means, calculated both by absolute and percentage change, were 0.339 and 0.371 at two weeks after programme end, and 0.321 and 0.352 at eight weeks. Changes in the RASE were associated with behaviour initiation at two and eight weeks (r = 0.419, r = 0.342, p < 0.001). No substantial predictors of change in SE could be identified.Conclusions: The RASE is sensitive to change in a cohort of people with RA in the UK receiving education programmes as routine clinical care. Exploratory analysis did not identify clinical or psychological factors that predict change in SE, suggesting that programmes should not be restricted to particular patients. Copyright (c) 2008 John Wiley & Sons, Ltd.

MIB Abstract ID Number: 14722

PreMedline Identifier: 18228530

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Acute myoclonus following spinal anaesthesia.

Lead Author: Alfa JA

Additional Authors: Bamgbade OA.

Eur J Anaesthesiol., 2008-03-01, 25(3):256-7.

<<No Abstract Available>>

MIB Abstract ID Number: 14861

PreMedline Identifier: 18226283

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Immunoregulatory properties of vasoactive intestinal peptide in human T cell subsets: implications for rheumatoid arthritis.

Lead Author: Gutiérrez-Cañas I

Additional Authors: Juarranz Y, Santiago B, Martínez C, Gomariz RP, Pablos JL, Leceta J.

Brain Behav Immun., 2008-03-01, 22(3):312-7. Epub 2007 Oct 24.

Departamento de Biología Celular, Facultad de Biología, Universidad Complutense de Madrid, 28040 Madrid, Spain.

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease whose pathogenesis is not completely understood. Unbalanced Th1/Th2 T-cell polarization has been suggested to play a pathogenetic role and therefore, modulation of T-cell polarization is a potential therapeutic target. Vasoactive intestinal peptide (VIP) is a broadly distributed peptide that exerts anti-inflammatory and immunomodulatory effects, in the collagen-induced arthritis (CIA) murine model of RA, and ex vivo, in synovial cells from RA patients. In the present study, we have found that polyclonal stimulation of peripheral blood lymphocytes (PBL) from RA patients produces higher levels of inflammatory mediators and lower levels of Th1 cytokines than PBL from healthy controls; moreover, VIP has negligible effects on inflammatory mediators and Th1 cytokines produced by PBL from healthy controls but favours Th2 profile and enhanced IL-10 production after stimulation. VIP increases the levels of IL-10 and IL-4 in the supernatant of human CD4(+)CD45RA(+) cells cultured in a non-conditioned or a Th2-conditioned situation. In contrast, VIP does not modify the production of these cytokines in a Th1-conditioned medium. In summary, VIP can differentially modify the functional capacity of human lymphocytes by inducing Th2/Treg differentiation depending on their previous phenotype.

MIB Abstract ID Number: 14862

PreMedline Identifier: 17951026

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Life expectancies of Japanese patients with rheumatoid arthritis: a review of deaths over a 20-year period.

Lead Author: Shinomiya F

Additional Authors: Mima N, Nanba K, Tani K, Nakano S, Egawa H, Sakai T, Miyoshi H, Hamada D.

Mod Rheumatol., 2008-03-04, [Epub ahead of print]

Centre for Rheumatic Disease, Mima Hospital in Yoshinogawa City, 494 Kamojima Jougejima, Yoshinogawa, 776-0013, Japan, ayutarou@mima-gr.jp.

We investigated trends in life expectancy in rheumatoid arthritis (RA) patients, reviewing records for 286 patients (204 female, 82 male) who had died over the past 20 years. The average age at death was 68.8 years before 1990, increasing to 72.1 years after 2001. Trends in disease modifying anti-rheumatic drugs (DMARDs) saw gold preparations (45.2%) predominate before 1990, sulphydryl donor agents (53.6%) from 1991 to 2000, then methotrexate (43.0%) after 2001. The most common causes of death were infectious diseases up to 1995, rheumatic disease 1996-2000, and cardiovascular events and malignancies after 2001. Major advances in surgical interventions, such as joint replacement surgery, occurred after 1990. Surgical intervention followed by a period of rehabilitation maintained a favourable level of activities of daily living (ADLs), The requirements for favourable life expectancy are control of RA inflammation and maintenance of a favourable level of ADLs. Although recently developed DMARDs and biological agents show promise, caution is required to avoid serious adverse reactions. Optimum care of patients with RA will require preventive measures and early intervention for infections and rheumatic diseases, as well as for lifestyle diseases, osteoporosis and malignancies.

MIB Abstract ID Number: 14871

PreMedline Identifier: 18317879

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[The pathologists: Aschoff, Klinge and Gräff.]

Lead Author: Keitel W.

Z Rheumatol., 2008-03-01, [Epub ahead of print]

Am Kiefernhang 3, 39245, Gommern, Deutschland.

[Article in German]

The article presents three pathologists who have made important contributions to the understanding of rheumatic diseases.Ludwig Aschoff's (1866-1942) work formed the foundation and was for a long time at the centre of the discussion on pathology of rheumatic diseases. Impetus was added from a rheumatological perspective by the discovery of the Aschoff nodule as an indicator of rheumatic myocarditis. Thus, newly manifested rheumatic carditis is only diagnosed when rheumatic nodules are found.Fritz Klinge (1892-1974), following in Aschoff's footsteps, broke new ground in rheumatology in Germany. From extensive animal tests at a Leipzig institute he induced inflammatory reactions, necrosis and cell proliferation which, due to repeated sensitization, lead to arthritis and periarthritis. He identified therein a relationship to human rheumatism, which he considered to be caused by an allergic (hyperergic) reaction of the mesenchyme. In his opinion, the varying manifestations of rheumatic fever and rheumatoid arthritis presented one and the same pathological event. His main achievements were to close the gap between method-related deficits in morphology and the myriad clinical observations in the field of"rheumatic" diseases and to create a pathoanatomic platform for"rheumatism".Siegfried Gräff (1899-1947) was a strong critic of Klinge. He only ever relied on individual post mortem observations and was skeptical of animal testing in a rheumatological context. He considered"rheumatism" as a symptom, refuting its status as a disease. He distinguished rheumatic fever, as characterized by the Aschoff granuloma, from a second"rheuma-symptom" disease group, namely non-specific chronic polyarthritis (rheumatoid arthritis).

MIB Abstract ID Number: 14873

PreMedline Identifier: 18309501

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Macrophage activation syndrome: A frequent but under-diagnosed complication associated with rheumatic diseases.

Lead Author: Tristano AG.

Additional Authors:

Med Sci Monit., 2008-03-01, 14(3):RA27-36.

Department of Internal Medicine, Dr. Domingo Luciani Hospital, Caracas, Venezuela and Department pf Pharmaceutical and Administrative Sciences, College of Pharmacy, Nova Southeastern University, Fort Lauderdale, FL, U.S.A.

MIB Abstract ID Number: 14877

PreMedline Identifier: 18301366

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