Arthritis clinical presentation

Nesher G, Ruchlemer R. Alpha-interferon-induced arthritis clinical presentation treatment, and prevention. Semin Arthritis Rheum 1998 27(6) 360-5. 

Recognize the typical clinical presentation of rheumatoid arthritis. 

Viral arthritis is rather common and usually selflimited within a few weeks. The most common pathophysiological mechanism is not a direct virus invasion in the synovium but deposition of immune complexes. Viral infections frequently involve multiple joints and produce inflammation without suppuration. The typical clinical presentation is a peripheral and symmetrical polyarthritis, undistin-guishable from other inflammatory arthritis. Virtually all viruses can cause arthritis. There is no specific treatment and simple symptomatic measures are sufficient. 

Arthritis and arthralgia are well-known adverse effects of intravesical BCG instillation as part of therapy of bladder cancer (SED-13, 925). The etiology and the different clinical pictures of BCG immunotherapy have been discussed (51). Considering that mycobacteria are potent stimulators of the immune system and especially of T cells, it is not surprising to observe T cell-mediated aseptic arthritis after BCG therapy. The authors suggested that the site of immune stimulation is critical, since intradermal injection produces a clinical presentation similar to reactive arthritis, and intravesical therapy causes a clinical picture identical to Reiter s syndrome. 

Aseptic meningitis is a rare adverse effect of non-selective NSAIDs in patients with or without connective tissue disease or rheumatological disease. Rofecoxib has been implicated in five patients (four women and one man), in each case occurring within 12 days of the start of rofecoxib therapy (1). The clinical presentations and cerebrospinal fluid findings were typical of aseptic meningitis. One patient had rheumatoid arthritis. After drug withdrawal and recovery, two consecutive rechallenges in one patient led to relapses. 

Vasculitis usually is seen in patients with long-standing rheumatoid arthritis. Vasculitis may result in a wide variety of clinical presentations. Invasion of blood vessel walls by inflammatory cells results in an obliteration of the vessel, producing infarction of tissue distal to the area of involvement. Most commonly, small-vessel vasculitis produces infarcts near the ends of the fingers or toes, especially around the nail beds. These infarcts are usually of little consequence. 

Psoriasis is a chronic, inflammatory and hyperprolifera-tive disease of the skin, scalp, nails, and joints, affecting 1 to 2% of the U.S. population. It is found worldwide its frequency varies from 0 to 3% among different ethnic groups. Most of its variable clinical presentations eventuate into erythematous, scaly plaques with or without nail disease and arthritis. Susceptibility to psoriasis is umnistakably heritable, but the phenotype is controlled by multiple genes as well as enviromnental factors. Trauma, stress, and infections are important determinants of disease onset and severity. At the cellular level, psoriasis is characterized by markedly increased epidermal proliferation and incomplete differentiation elongation, dilatation, and leakiness of the superficial plexus of dermal capillaries and a mixed inflammatory and immune cell infiltrate of the epidermis and papillary dermis. A multitude of plausible pathomechanisms... 

A 40-year-old female was treated with leflxmomide for 10 years because of rheumatoid arthritis and presented with clinical symptoms suggestive of pulmonary tuberculosis, which was confirmed by sputum smear examination. She started on antitubercular treatment but there was no improvement of cough symptoms. The cough improved markedly after discontinuation of leflxmomide therapy [71 ]. 

Paradoxical inflammation such as psoriasis is a well-known phenomenon of anti-TNFa therapy approved for the treatment of autoimmxme diseases such as rheumatoid arthritis, Crohn s disease, ulcerative colitis and psoriasis. Likewise, infliximab is used to treat refractory sarcoidosis but recently a case of infliximab-induced cutaneous sarcoidosis was reported in a patient with ulcerative colitis [150 ]. The induction of psoriasis and other clinical presentations like psoriasiform exanthema and palmoplantar pustulosis as side effects of infliximab treatment is not xmderstood and the pathogenesis of such reactions has been further obscured by the finding of a patient with Crohn s disease who developed arthritis as well as the skin manifestations cf psoriasis after the administration of infliximab [151 ]. 

The classic example of an antiinflammatory dmg is aspirin [50-78-2], acetosahcyflc acid, an effective analgesic for many years. It is well tolerated by the dog and the horse, but is relatively toxic to cats. Under the proper clinical circumstances, it can be used for prolonged therapy in chronic inflammatory diseases such as arthritis. Rimadyl is presently used. 

It is an autoantibody whose autoantigen is the Fc portion of IgG. Rheumatoid factors may be of any immunoglobulin isotype but it is IgM rheumatoid factor that is commonly measured in rheumatoid arthritis. Classification criteria for rheumatoid arthritis include only one serological test, namely rheumatoid factor. However, it is not diagnostic test rather it may be confirmatory when a number of other clinical features are present. 

Psoriasis is a common inflammatory skin disorder which is estimated to affect 1.5% to 3% of the Caucasian population.1,2 It may present at any age.3,4 Ethnic factors influence disease prevalence. In the United States, prevalence among blacks (0.45% to 0.7%) is lower than in the remainder of the United States population (1.4% to 4.6%).1 Between 10% and 30% of patients with psoriasis will also have psoriatic arthritis.5 In 10% to 15% of psoriatic patients with arthritis, joint symptoms actually appear prior to skin involvement.3 Clinical depression is another frequent comorbid illness in these patients. A recent United States survey showed that 8% to 10% of psoriatic patients aged 18 to 54 years old actively contemplated suicide because of their psoriasis.6... 

LP is a 58-year-old man with newly diagnosed stage IIIA non-small cell lung cancer who presents to the clinic complaining of loss of appetite, excess thirst, nausea and vomiting, and confusion x 2 days. The medication history lists NKDA, hydrochlorothiazide 50 mg by mouth daily for hypertension, and naproxen 500 mg by mouth twice daily for arthritis. 

It has been estimated that 1-2 per cent of the US population suffer from autoimmune conditions, including rheumatoid arthritis, MS and some forms of diabetes. In many instances, an autoimmune response results from the inappropriate activation of a specific subset of B- and/or T-lymphocytes. The most common immunotherapeutic approach to potentially treat such diseases is to induce depletion of the individual s T- and B-cell populations. This could be achieved by administration of an antibody raised against a surface antigen present on such cells. Initial trials, for example, have shown that injection of an (unconjugated) anti-CD4 antibody (cell surface glycoprotein present on many T-lymphocytes) over 7 days significantly reduced the clinical symptoms of rheumatoid arthritis for several months. 

For classification purposes, a patient is said to have rheumatoid arthritis if he or she has satisfied at least four of these seven criteria. Criteria 1 through 4 must be present for at least 6 weeks. Patients with two clinical diagnoses are not excluded Designation as classic definite, or probable rheumatoid arthritis is not to be made. 

This point of view overlooks the fact that every well and normal individual is potentially an ill individual, and the roots of disease may be present in his make-up years before there is any overt disease. A dozen young men used as normal controls may each have metabolic peculiarities that point toward a different metabolic derangement gout, multiple sclerosis, diabetes, anemia, atherosclerosis, hypertension, nephrosis, hypothyroidism, rheumatoid arthritis, rheumatic heart disease, liver cirrhosis, and myasthenia gravis, for example, and yet at the time of their use as controls these young men may show no symptoms of the disease which is to appear later in life. It seems far from safe to assume that because an individual on clinical examination seems well, all of his blood values, for example, are normal and meaningless so far as disease susceptibilities are concerned. 

The advent of recombinant DNA technology led to the development of antibodies and fragments that are tailored for optimal behaviour in vivo [7,8]. Humanized and chimeric antibodies can be constructed to circumvent the human anti-mouse antibody response elicited by mouse antibody treatment of patients, which severely hampers the application of these powerful molecules. The treatment of rheumatoid arthritis patients with doses of as high as 10 mg kg cA2 chimeric antibody specific for TNFa [9], emphasizes that at present the production and purification methods for these proteins have been optimized to such extent that clinical studies can be considerably intensified. 

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