Rheumatoid arthritis clinical presentation

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 ]. 

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. 

Recognize the typical clinical presentation of rheumatoid 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. 

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. 

Despite a good overall safety profile, anti-TNF antibodies can induce a number of adverse effects, including autoimmunity and infections. A trial in the treatment of Crohn s disease noted infusion reactions, transient increased of anti-dsDNA antibodies, and serum sickness-like delayed hypersensitivity with retreatment. Induction of human-antichimeric-antibodies was suggested as the cause of some of the infusion reactions [90]. A prospective study in 35 patients with Crohn s disease showed induction of ANA and anti-dsDNA autoantibodies in 53% and 35% of infliximab-treated patients [91]. A single patient showed clinical features consistent with drug-induced lupus, including the presence of ANA and anti-dsDNA autoantibodies, which quickly resolved after discontinuation of infliximab. Reports on renal adverse effects of anti-TNF antibodies are very rare. Saint Marcoux described the occurrence of crescentic GN in as few as 2 patients out of a cohort of 39 patients, treated with an anti-TNF antibody for rheumatoid arthritis [92]. A case report by Chin et al. [93] described the case of a 29-year-old Australia-born Vietnamese who presented with nephrotic syndrome. A renal biopsy showed membranous nephropathy. Symptoms attenuated after discontinuation of infliximab therapy. 

Recognized in 1961 (KIO), these are now well described (B18) and mimic the syndrome of mixed cryoglobulinemia (see 6.13). Skin lesions in this condition are raised, painful, and edematous with or without necrosis. Biopsy always reveals arteritis with a mononuclear and neutro-phile infiltrate. There is in most cases a preceding history of rheumatoid arthritis, Sjogren s syndrome, syphilis, sarcoidosis or other hyperimmune states, and this will dominate the clinical findings. Rarely the protein interactions build up to a level presenting as a viscosity syndrome so that this group can overlap with 7.7.1 unless the serum is carefully examined. 

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. 

At the present time, the efficacy and the clinical benefit of cyclosporin therapy has been conclusively demonstrated for severely affected patients in four diseases autoimmune uveitis, psoriasis, idiopathic nephrotic syndrome and rheumatoid arthritis, as well as in transplant patients. 

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