Effects of cyclosporin on joint damage in rheumatoid arthritis. The Italian Rheumatologists Study Group on Rheumatoid Arthritis.

According to the most recent literature, few antirheumatic drugs can claim disease-controlling properties over the anatomical joint damage in rheumatoid arthritis (RA). A small number of studies have favored one or another of the available agents, in particular parenteral gold salts, sulphasalazine and methotrexate, but the evidence regarding their efficacy is not convincing when analysed using methodological criteria known to be important in evaluating radiologic evidence of joint damage. The radiologic results in long-standing RA patients have shown that CsA may be of benefit in reducing disease progression.

Plasminogen activator and receptor in osteoarthritis.

Evidence indicates that breakdown of articular cartilage resulting in the loss of normal joint function is the distinctive feature of osteoarthritis. Degradation of cartilage extracellular matrix components involves the action of at least 2 classes of proteinases: serine proteinases and metalloproteinases. Receptors have been described on a wide range of cell lines for many such proteinases [urokinase-type plasminogen activator (u-PA), plasminogen/plasmin, collagenase], which subsequently activate each other on the solid phase of the cell surface, leading to cartilage destruction.

[Hypersensitivity vasculitis after thrombolytic therapy with APSAC (anisoylated plasminogen streptokinase activator complex). Presentation of a clinical case and review of the literature].

We describe a rare case of hypersensitivity vasculitis associated with APSAC administration in a 54-year-old man. Fifteen days after receiving thrombolytic therapy (APSAC 30 U) for acute myocardial infarction, the patient was admitted to our department for myalgia, livedo reticularis and erythema of the legs with an ulcerative necrotic lesion of the fifth toe of the right foot. The presence of circulating immune complexes at high titer supported the diagnosis of hypersensitivity vasculitis.