Cutaneous vasculitis

Cutaneous vasculitis (CV), a complication seen in approximately 5-15% of patients with RA, is associated with positive, often high-titer, RF, anti-endothelial antibodies of IgA class, anti-Ro and anti-cardiolipin antibodies, advanced erosive disease, and increased patient morbidity and mortality (Quismorio et al., 1983; Ziff, 1990; Coremans et al., 1992). CV should be suspected in advanced disease associated with fever, weight loss, and fatigue (Fig. 4). CV can be present without active joint disease. Frequently, other extra-articular features are present like episcleritis, pleural, and peri-cardial effusions, a raised ESR, a low serum albumin, and sometimes liver enzymes disturbances (Harris Jr., 1994). The most frequently observed features are chronic deep-skin ulcers and nailfold lesions. The latter occur in about 5% of patients and are not associated with a worse prognosis. The clinical implication is that the primary joint inflammatory process is poorly controlled. Manifestations are often precipitated by abrupt discontinuation of systemic therapy with rebound circulating immune complex disease. CV can be classified by the size of the largest vessel involved and by the presence or absence of systemic involvement. The severity of the vasculitis cannot be defined by the cutaneous examination alone; a

Figure 3. Rheumatoid nodule. There is a central area of fibrinoid necrosis surrounded by palisading epithelioid macrophages and other mononuclear cells.

thorough evaluation searching for systemic involvement is essential. Jorizzo and Daniels (1983) divided the RV spectrum of disease in cutaneous vessels, ranging from severe with multisystem larger-vessel vasculitis, to moderate with cutaneous small vessel and possibly systemic small-vessel vasculitis, and mild with Bywaters lesions only.

As described in many studies, immune complexes are assumed to be responsible for patho-genesis of RV. IgM and C3 were identified in many patients. The presence of circulating immune complexes and hypocomplementaemia during the development of the vasculitis strongly suggest a

Bywaters Lesions
Figure 4. Severe rheumatoid cutaneous vasculitis (Dieppe, 1984).

pathogenesis of immune complex-mediated vascu-litis occurring in patients with RA (Scott et al., 1981). To establish the diagnosis, a full thickness skin and muscle biopsy must be performed (Harris Jr., 1994). Serological tests are of limited value for the diagnosis of RV. In the past several autoan-tibodies have been suggested to be present, more frequently in patients with RV compared to patients without. However, none of them is path-ognomonic. Some reports are contradictory. ANA are present in a large proportion of CV patients (Scott, 1981; Quismorio et al., 1983; Jorizzo, 1983).

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