Immunologic rheumatic disorders

Abstract

We provide the basics for clinicians who might be called on to consider the diagnosis of diseases such as systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA) in their practice. We will emphasize clinical recognition and first-line laboratory testing. Only characteristics of the classic rheumatic inflammatory diseases (ie, RA, seronegative spondyloarthropathy, SLE, antiphospholipid syndrome, Sjögren syndrome, scleroderma, and polymyositis/dermatomyositis) will be covered. In the past decade, treatment for RA and seronegative spondyloarthropathy has substantially improved. Their treatment has been revolutionized by the use of methotrexate and, more recently, TNF inhibitors, T-cell costimulation modulators, and B-cell depletion. The goal of RA treatment today is to induce a complete remission as early as possible in the disease process, with the mantra being "elimination of synovitis equals elimination of joint destruction." The hope is that if the major mediators of Sjögren syndrome, SLE, or scleroderma can be identified and then blocked, as in the example of TNF inhibitors in patients with RA, more specific treatments will become available. Thus RA has become an excellent model of this evolving paradigm. Through the identification of major mediators in its pathogenesis, novel and highly efficacious therapeutic agents have been developed.

Prognostic contributions of the underlying inflammatory disease and acute organ dysfunction in critically ill patients with systemic rheumatic diseases

“…As shown in Table 3, life-sustaining interventions included mechanical ventilation in 59 (40%) patients (length, 7 days [3][4][5][6][7][8][9][10][11][12][13][14][15]), vasoactive drugs in 46 (31%; length, 4 days [2][3][4][5][6][7]), and renal replacement therapy in 29 (19%; length, 5.5 days [2][3][4][5][6][7][8][9][10][11][12][13][14][15]). In the subset of patients with polymyositis/dermatomyositis (n=9), four patients received mechanical ventilation for respiratory muscle weakness (44%).…”

“…Various forms of SRD (e.g. systemic lupus erythematous [SLE], rheumatoid arthritis [RA], antineutrophil cytoplasmic antibody-associated vasculitis [AAV], and cryoglobulinemia) share many immunological mechanisms, clinical manifestations, and treatment options [2]. Over the last decade, the introduction of new immunosuppressive drugs (e.g., TNFα-antagonists, anti-CD20 antibodies, and mycophenolate mofetil) has changed the outcome of severe forms of SRD [3][4][5][6].…”

Therapeutic Targeting of B Cells for Rheumatic Autoimmune Diseases

“…Testing specific patterns of autoantibody reactivity in the sera of patients is essential for establishing the correct diagnosis and, in some cases, the prognosis of most autoimmune diseases, despite the lack of any direct proof that their primary pathogenic characteristics have an affect on such diseases (Joseph et al, 2010). For example, the presence of ANAs serves as a very sensitive diagnostic test for SLE.…”

Evaluation of the Reactivity of Sera from Patients with Systemic Lupus Erythematosus Against the Human MCP1

“…However, ANA has a limited specificity, being relatively common in healthy populations [18,19], and anti-dsDNA has a reduced sensitivity, never appearing in some SLE patients [20]. In this context, we analyzed the reactivity of sera from SLE or from other autoimmune diseases with MCP1 in order to evaluate this autoantigen as a clinical disease marker and compared its reactivity with that of ANA and of dsDNA.…”