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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, Magn