Rheumatoid Arthritis: Boulman N

Slobodin G, Rozenbaum M, Boulman N, Rosner I. · Department of Internal Medicine A, Bnai Zion Medical Center and Ruth and Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel. · Semin Arthritis Rheum. · Pubmed #17350676 No free full text.

Abstract: BACKGROUND: The concept of "enthesis organ" allows a new look at the nature of enthesis involvement in some rheumatic and nonrheumatic systemic disorders. OBJECTIVES: To describe the various presentations of enthesopathy in the course of systemic medical disorders using the available literature data. METHODS: Review of relevant articles from 1996 to 2006 retrieved by a Medline search utilizing the index terms "enthesis," "enthesitis," and "tendonitis." The list of articles reviewed herein is not exhaustive, with preference given, where possible, to studies and surveys over case reports as well as the most recent literature reflecting new developments on the subject. RESULTS: Enthesis is defined as the site of insertion of a tendon, ligament, fascia, or articular capsule into bone. Pain originating in the free nerve endings enriched entheses (enthesalgia) may represent a potential cause of chronic musculoskeletal pain in some individuals. Enthesis involvement in the disease process is well appreciated in spondyloarthropathies and in rheumatoid arthritis, though overshadowed by synovitis in the latter. Calcium deposition diseases may constitute the most significant articular cause of enthesopathies in the general population. New data may shed light on the possible pathophysiologic role of enthesopathy in the development of osteoarthritis. Various metabolic and endocrine conditions may manifest with enthesopathy features. The pathogenic mechanisms of enthesis involvement are not uniform and differ in the diverse disorders. CONCLUSIONS: The concept of enthesopathy as a variety of syndromes in the course of many rheumatic, metabolic, and endocrine disorders should be appreciated. Exercise of a high level of suspicion toward enthesopathic involvement, and greater knowledge of enthesopathy's characteristic patterns and diagnostic possibilities, may allow better management of many patients in rheumatology practice.

Rozenbaum M, Boulman N, Slobodin G, Ayubkhanov E, Rosner I. · Department of Rheumatology, Bnai Zion Medical Center, Haifa, Israel. · J Clin Rheumatol. · Pubmed #17149054 No free full text.

Abstract: BACKGROUND: The treatment of rheumatoid arthritis (RA) has changed dramatically over the past decade with the introduction of antitumor necrosis factor (anti-TNF) agents. Although subsets of patients may have only partial or no response, there is no report yet on possible worsening of RA with this therapy. OBJECTIVE: The objective of this study was to determine whether infliximab may paradoxically exacerbate RA. METHODS: One hundred seven patients with RA refractory to 3 disease-modifying antirheumatic drugs were treated with 3 mg/kg infliximab and methotrexate for at least 6 months. RESULTS: In 3 patients, there was an exacerbation of RA associated with the use of infliximab. The flare occurred during the first 6 to 12 months of treatment with polyarthritis, fever, and elevated acute phase reactants. Increase of infliximab dose resulted in further deterioration. CONCLUSION: We describe a paradoxic reaction, an exacerbation of RA, with infliximab. The mechanism of this side effect is unclear but may be related to altered immunity induced by the inhibition of TNF activity in predisposed patients.

Toubi E, Kessel A, Slobodin G, Boulman N, Pavlotzky E, Zisman D, Rozenbaum M, Rosner I. · Division of Clinical Immunology and Allergy, Bnai Zion Medical Center, P O Box 4940, Haifa 31048, Israel. · Ann Rheum Dis. · Pubmed #17148544 No free full text.

Abstract: OBJECTIVE: To assess changes in macrophage phenotype and function after rituximab-induced B cell depletion in patients with rheumatoid arthritis (RA). METHODS: 10 patients with RA were treated with rituximab, achieving significant B cell depletion 4 months later. Clinical improvement, rheumatoid factor (RF), anti-cyclic citrullinated peptide (anti-CCP) antibodies, mRNA of B cell activating factor (BAFF), interleukin (IL) 10 and CD86 in human monocyte-derived macrophages (HMDMs) and tumour necrosis factor alpha (TNFalpha) secretion from cultured HMDMs were assessed at baseline and after the depletion. RESULTS: A clinical response of American College of Rheumatology (ACR) 50% improvement was noted in six patients, and another two patients responded with moderate improvement, equivalent to ACR 20-50% improvements. RF and anti-CCP antibodies were positive at baseline in seven of ten patients. RF disappeared or declined in six patients 4 months after treatment, correlating with clinical improvement. By contrast, anti-CCP remained unchanged in six patients. After rituximab treatment, and in association with clinical improvement, BAFF, IL10 and CD86 mRNA expression in HMDM were significantly upregulated compared with values at baseline. A significant decrease in TNFalpha in the supernatant of cultured HMDM was also noted. CONCLUSIONS: In addition to B cell depletion and attenuation in some of the specific autoantibodies, clinical improvement in rituximab-treated patients with RA occurred in association with changes in macrophage function.

Suleiman M, Wolfovitz E, Boulman N, Levy Y. · Department of Internal Medicine D, Rambam Medical Center, P.O. Box 9602, Haifa 31096, Israel. · Scand J Rheumatol. · Pubmed #12195635 No free full text.

Abstract: We report a case of a young woman with pyrexia and progressive lung disease who developed acute respiratory distress syndrome (ARDS) and required prolonged mechanical ventilator support. The patient had a markedly elevated serum ferritin concentration of 7880 micrograms/L, a specific finding for the adult onset Still's disease (AOSD). Treatment of the patient with supportive and immunosuppressive therapy, resulted in patient survival and cure. The early consideration of the diagnosis of AOSD in patients with fever of unknown origin and a compatible clinical course may modify its severe complications.

Rosner I, Haddad A, Boulman N, Feld J, Avshovich N, Slobodin G, Rozenbaum M. · No affiliation provided · Rheumatology (Oxford). · Pubmed #17684027 No free full text.

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Boulman N, Rozenbaum M, Slobodin G, Rosner I. · No affiliation provided · Clin Exp Rheumatol. · Pubmed #17207395 No free full text.

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Rimar D, Rozenbaum M, Zisman D, Boulman N, Slobodin G, Eder L, Feld J, Rosner I. · No affiliation provided · J Rheumatol. · Pubmed #16862661 No free full text.

This publication has no abstract.