الفهرس 
Rheumatoid ArthritisOnly 14 pages are availabe for public view
 |  | from | 285 |  |  |
| | | from | 285 | | |
Abstract
Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease of unknown cause. The hallmark feature of this condition is persistent symmetric polyarthritis (synovitis) that affects the hands and feet, though any joint lined by a synovial membrane may be involved. Extra-articular involvement of organs such as the skin, heart, lungs, and eyes can be significant (Komano Y et al., 2013).
No laboratory test results are pathognomonic for RA, but the presence of anti−cyclic citrullinated protein antibody (ACPA) and rheumatoid factor (RF) is highly specific for this condition (Daha NA and Toes RE, 2011).
The prognosis is guarded. However, advances in understanding the pathogenesis of the disease have fostered the development of new therapeutics, with improved outcomes (Aletaha D et al, 2010).
Disease-modifying antirheumatic drugs (DMARDS) represent the most important measure in the successful treatment of RA. Early DMARDs therapy has become the standard of care as DMARDs not only can retard or prevent disease progression, thus, joint destruction and subsequent loss of function, but also may induce more remissions. Until the full action of DMARDs takes effect, anti-inflammatory or analgesic medications may be required as bridging therapy to reduce pain and swelling (Saag KG et al, 2008).
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that can affect almost any organ system; thus, its presentation and course are highly variable, ranging from indolent to fulminant (Livingston B & Bonner A, 2011).
The diagnosis of SLE is based on a combination of clinical findings and laboratory evidence. Familiarity with the diagnostic criteria helps clinicians to recognize SLE and to subclassify this complex disease based on the pattern of target-organ manifestations (Petri M et al, 2012).
Management of systemic lupus erythematosus (SLE) often depends on disease severity and disease manifestations (Broder A et al, 2011).
The specific agent selection of DMARDS is generally indicated by the patient’s organ involvement and disease severity (Furie RA et al, 2009).
Scleroderma is a group of rare, progressive diseases that involve the hardening and tightening of the skin and connective tissues, the fibers that provide the framework and support for your body. Localized scleroderma affects only the skin. Systemic scleroderma also harms internal organs, such as the heart, lungs, kidneys and digestive tract (Hummers LK, et al, 2010).
The many complications of scleroderma can have a major impact on a person’s sense of well-being. Patients are greatly concerned about changes in their appearance (William C. Shiel Jr& charles Patrick Davis, 2012).
There are no specific tests for scleroderma. Tests may be done to detect specific types of antinuclear antibodies (ANAs). It does not necessarily prove that a patient has scleroderma but could help diagnose, treat, and monitor people with scleroderma (Nash RA et al, 2007).
There is still no cure for scleroderma; however, patients should receive treatments for specific complications as early as possible in the course of the disease to reduce progression before irreversible hardening of tissues occurs (Henness S, Wigley FM, 2007).
Antiphospholipid syndrome (APS) is an autoimmune disorder of unknown cause that manifests clinically as recurrent venous or arterial thrombosis and/or fetal loss. characteristic laboratory abnormalities in APS include persistently elevated levels anticardiolipin [aCL] antibody, antiphosphatidylserine or beta-2 glycoprotein I (apolipoprotein H); or evidence of a circulating anticoagulant (Ruiz-Irastorza G et al, 2010).
Complement activation has been increasingly recognized as a possible significant role in the pathogenesis of APS and may be a primary event in pregnancy loss (Ruiz-Irastorza G et al, 2010).
Treatment regimens for APS must be individualized according to the patient’s current clinical status and history of thrombotic events. Asymptomatic individuals in whom blood test findings are positive do not require specific treatment (Keeling D et al, 2012). Therapeutic agents are based on anticoagulant properties, and benefits are weighed carefully against their significant risks (Ernest JM et al, 2011).
Sjögren’s syndrome is an autoimmune inflammatory disease that can affect many different parts of the body, but most often affects the tear and saliva glands (Christopher Wise, MD, 2012).
Sjögren syndrome is estimated to be the second most common rheumatologic disorder, behind SLE. The cause of Sjogren syndrome is unknown (Kruszka P& O’Brian RJ , 2009). The pathogenesis of salivary gland damage is multi-factorial, thought to involve immunological, genetic, hormonal, and viral components (Scheinfeld N, 2006).
No curative agents for Sjögren syndrome exist. The treatment of the disorder is essentially symptomatic. However, the inhibition of protease activity in EBV-mediated apoptotic cells may be a potential therapeutic approach in the treatment of Sjögren syndrome (Katayama I et al, 2010).
Mixed connective tissue disease (MCTD) is a rare autoimmune disorder which has features of three other connective tissue diseases: SLE, Scleroderma and Polymyositis (Aringer M, Smolen JS, 2007). The cause is not known yet. In some cases, it gets worse and develops into scleroderma or lupus. Several factors, however, suggest that mixed connective tissue disease is a distinct disorder in its own right (Bodolay E & Szegedi G, 2009).
The overall goal of therapy is to control symptoms and to maintain function. Target medical therapy to specific organ involvement and extent of disease activity. Monitoring for development of complications, such as pulmonary hypertension or infection, is important (Zandman-Goddard G et al, 2011).