Non-specific skin changes may be observed in patients with RA. The skin can become atrophic and lead to fragility and easy bruisability (Sayah and English, 2005) (Table 3). Skin overlying the digits
Skin manifestations in Rheumatoid arthritis
1. Nailfold lesions
2. Digital infarcts
7. Purpura may become pale or even translucent. Nail changes may occur in RA patients. Michel et al. (1997) evaluated the frequency and the specificity of nail changes associated with RA in a case-controlled study including 50 patients suffering from RA and 50 controls. The only nail abnormalities significantly associated with RA were longitudinal ridging (on-ychorrhexis) and clubbing of the fingers. Nails of the RA patients also manifest periungual erythema with teleangectasia, onycholysis, red lunula, or pterygium inversum (Jorizzo et al., 1983; Daniel et al., 1985).
Specific cutaneous manifestations of RA are varied and encompass a number of entities, some of which define the dominant clinical features, such as the rheumatoid papule or subcutaneous cords, while others allude to the histopathology, i.e. rheumatoid neutrophilic dermatosis (RND) (Chen et al., 2002). Magro and Crowson (2003) proposed a more simplified classification scheme using the adjectival modifiers of 'rheumatoid-associated' and then further categorizing the lesions according to the dominant reaction pattern. Three principal reaction patterns are recognized, namely (i) extravascular palisading granulomatous inflammation; (ii) interstitial and/or subcuticular neutrophilia; and (iii) active vasculopathy encompassing lymphocyte-dominant, neutrophil-rich, and granulomatous vasculitis. In most cases, an overlap of the three reaction patterns is seen.
Rheumatoid nodules are the classic cutaneous manifestation of RA (Fig. 2). They are not diagnostic for this disease and can be seen in other processes, especially other connective tissue diseases. Rheumatoid nodules occur in about 25% of patients with RA, and reflect high levels of disease activity and severity (Ziff, 1990). Clinically, rheumatoid nodules are extremely relevant as they correlate with more severe arthritis, higher levels of RF, and with an increased incidence of rheumatoid vasculitis (RV). The presence of RF within rheumatoid nodules suggests the possibility of immune complex-mediated vasculitis as the initiating event in rheumatoid nodule development (Chu et al., 1994). Clinically, they are firm, dome-shaped, skin-coloured papules within the subcutaneous tissue. They are mobile and non-tender. Typically, they are present at pressure areas throughout the skin, like extensor areas of the forearm, finger joints, ischial and sacral prominences, occipital scalp, and Achilles tendon (Jorizzo et al., 1983; Chu et al., 1994; Harris Jr. et al., 1994). Rheumatoid nodules are firm and frequently adherent to the underlining periosteum. Rarely, they are the first presenting symptom of the disease and occasionally are present in internal organs, i.e. lungs, gallbladder, and heart (Abbas and Byrd, 2000; Kitamura et al., 2004). Histopathologically, the rheumatoid nodules manifest three characteristic zones (i) an inner central necrotic zone; (ii) a surrounding zone of palisading granulomas (predominantly macrophages); and (iii) an outer zone with peri-vascular infiltration of chronic inflammatory cells (Ziff, 1990). The granulomas are surrounded by third zone of fibrotic tissue reaction containing fibroblasts, plasma cells, and lymphocytes. The lesion is assumed to be the result of small-vessel vasculitis with fibrinoid necrosis (Fig. 3). Local collagenase and proteinase production may explain the central necrosis (Palmer et al., 1987). Nodules may regress during effective treatment with DMARDs as disease activity reduces (Harris Jr., 1994). However, MTX has been reported to induce or aggravate nodulosis, especially over finger tendons, despite reduction of disease activity (Duong et al., 1999; Agarwal et al., 2004). Braun et al. (2004) recently reported three cases of nodulosis during LEF therapy. Progression and acceleration of nodulosis during MTX therapy in RA patients is caused by adenosine A1 receptor promotion of multinucleated giant cell formation by human monocytes. LEF has no known influence on adenosine metabolism, so different pathogenetic mechanisms must be assumed for the induction of nodulosis by LEF.
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