General Approach to Laboratory Testing

When a dermatologist, family practitioner, internist, or rheumatologist first sees a patient with CLE, their principal concern should be to rule out evidence of systemic disease. After all, 15% of patients with CLE progress to SLE in 10-15 years of observation (Rowell 1984). In addition to a complete medical history and physical examination, clinical laboratory findings can be very helpful in this regard. Specifically, a blood chemistry panel allows screening for renal or hepatic involvement. Creatine phosphokinase testing assists in ruling out muscle inflammation. Evidence for autoimmune hemolytic anemia or thrombocytopenia is looked for in the complete blood cell count as well as in the lactic dehydrogenase, reticulocyte count, Coombs' direct antibody testing, serum haptoglobin, and antiplatelet antibodies. A routine urinalysis free of cellular casts or protein makes it highly unlikely that the kidney is involved. Specific autoantibodies, almost never observed in CLE, if found, can suggest central nervous system disease (antiribosomal P, antineuronal), mixed connective tissue disease (anti-RNP), or other disease subsets. In our practice, all patients have annual chest radiographs and electrocardiograms, since there are no blood tests to screen for cardiac or pulmonary involvement. Finally, additional imaging or electrical tests (electromyography, nerve conduction studies, 2-D echocardiography with Doppler) are occasionally ordered, and the results should be normal in CLE. If not, muscle, nerve, cardiac, or pulmonary disease representing visceral involvement should be ruled out.

This chapter assumes that the presence of systemic disease is not under consideration. The question remains, are there any laboratory tests worth ordering to monitor or better characterize CLE?

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