Diagnosis

As in many other chronic diseases, diagnosis is in general readily performed once the illness has fully developed. Due to the often smoldering disease onset and the uncharacteristic changes ocurring early on in SSc, including Raynaud's phenomenon, joint pain or swelling clinical diagnosis of SSc and the differentiation from other diffuse inflammatory connective tissue diseases (rheumatoid arthritis, systemic lupus erythemtosus, polymyositis) or disorders characterised by abnormal extracellular deposition (e.g. amyloidosis) may be difficult if not impossible. Although each of the diffuse inflammatory connective tissue diseases are clinically distinct entities, they share some general analogies and often display a high level of clinical variability resulting not uncommonly in overlap syndromes which pose a particular diagnostic and therapeutic challenge.

Investigations related to the autoimmune phenomena and the vascular changes (e.g. capillaroscopy) are therefore necessary to perform. In some cases, follow up of the patient over time will indicate whether the patient finally develops inflammatory connective tissue disease, overlap syndrome etc. or may experience remission of an early flare up of autoimmune phenomena reflecting undifferentiated connective tissue disease (Williams et al. 1999).

The identification of autoantibodies is helpful in establishing the correct diagnosis, indicating the prognosis and providing a guide to treatment and follow up (Fritzler 1993). In several studies, more than 95% of patients show

Autoantibody Profile limited SSc limited SSc

diffuse SSc overlap syndromes diffuse SSc overlap syndromes

Fig. 2. Antibody profile and clinical classification of progressive systemic sclerosis and overlap syndromes

Table 1. Clinical Characteristics of Autoantibodies Associated with Progressive Systemic Sclerosis

Antibody

Antigen

Comments

Frequency

Scl-70

DNA-topoisomerase I

increased risk for tumors

up to 70% of dSSc; 10 to 20% of SSc

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