Inflammatory Arthritis

Inflammatory Arthritis

Inflammatory arthritis includes a large number of arthritic conditions in which the predominant feature is synovial inflammation. This disparate group includes postviral arthritis, rheumatoid arthritis, seronegative arthritis, crystal arthritis and Lyme arthritis. The diagnosis of these conditions is helped by the pattern of joint involvement, along with any nonarticular disease; a past and family history may be helpful. The distribution of the affected joints (symmetrical or asymmetrical; large or small) as well as the periodicity of the arthritis (relapsing, chronic and progressive; single acute) may also help in the diagnosis.

Certain nonarticular disease – for example, psoriasis, iritis, inflammatory bowel disease, non-specific urethritis or recent dysentery – may suggest a seronegative spondarthritis. There may be evidence of recent viral illness (rubella, hepatitis B or parvovirus), of rheumatic fever, or of a tick bite and skin rash (Lyme disease). In early arthritis it may not be possible to make a specific diagnosis until the disease has evolved.

There is a distinct genetic separation of rheumatoid-pattern synovitis and the seronegative group; RA is associated with a genetic marker in the class II major histocompatibility genes, whilst seronegative spondarthritis shares certain alleles in the B locus of class I MHC genes, usually B27.

In general the pain and stiffness of inflammatory arthritis are worse in the morning and after rest. This early-morning exacerbation may last several hours, in contrast to the much shorter post-rest gelling of OA. Inflammatory markers (ESR and CRP) are often raised in inflammatory arthritis, and there is often a normochromic normocytic anaemia.

 

Reference for content:
Kumar, P and Clark, M: Clinical Medicine. (4th Edition). London, W.B. Saunders, Harcourt Publishers Ltd, (1998).

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