Abstract
Most rheumatic diseases are systemic autoimmune disorders in which not only the musculoskeletal system but other organ systems as well may be involved in the disease process. The primary cause of many of these diseases is still not clarified but many have a certain genetical susceptibility as appears from stronger associations with several HLA-types. Two well-known examples are Rheumatoid Arthritis (RA) and Systemic Lupus Erythematosus (SLE). In RA, the classical clinical picture is that of symmetric polyarthritis and erosive destruction of the joints by chronic inflammation. Extraarticular manifestations like e.g. scleritis, serositis or vasculitis, may accompany the joint symptoms. In SLE the joint involvement is often less symmetric and non-erosive and frequently there is arthralgia instead of arthritis. Symptoms of other organs e.g. skin, kidneys, neurologic system and gastrointestinal tract, diseased by inflammation, vasculitis or immune complex deposition, are more prominent in the clinical picture of SLE.(l)
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Stolk, J.N., Boerbooms, A.M.T., De Abreu, R.A., van de Putte, L.B.A. (1998). Azathioprine Treatment and Thiopurine Metabolism in Rheumatic Diseases. In: Griesmacher, A., Müller, M.M., Chiba, P. (eds) Purine and Pyrimidine Metabolism in Man IX. Advances in Experimental Medicine and Biology, vol 431. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5381-6_96
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DOI: https://doi.org/10.1007/978-1-4615-5381-6_96
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