Clinical Pathology

Human clinical pathology has tought both medical doctors and patients a lot about immune complex diseases. One attributes the term lupus to Rogerius in the 13th century to describe erosive facial lesions reminiscent of wolf's bite. Around 1870 Kaposi distinguishes local discoid lupus from disseminated lupus featuring the following signs and symptoms: lymphadenopathy, arthritis, fever, weight loss, anemia and central nervous involvement. In the wake of Osler's (Baltimore) and Jadassohn's (Vienna) descriptions at the beginning of the 20th century one finds at the autopsy table the nonbacterial verrucous endocarditis (Libman-Sack) and wire-loop lesions in patients with glomerulonephritis leading to the construct of collagen disease proposed by Kemperer in 1941. The term collagen vascular disease encompasses mostly immune-complex diseases. We now realize the overlapping of immune-complex diseases with collagen vascular diseases and the term serum sickness (see there) becomes synonymous with immune-complex disease.

The discovery of the lupus erythematosus (LE) cell by Hargraves in 1948 heralds new diagnostic tools soon to be completed with immunofluorescence studies of histological tissue sections. Animal experiments, many of them with lupus prone mice NZB/W strain have helped to develop therapeutic regimens (www.lupus.org). After development of the C1q binding test to detect circulating immune complexes (Citation classic in CURRENT CONTENTS in 1987) colleagues challenged the significance of such findings in the absence of a known antigen in the complexes. Only years later, the Italo-American researcher Vincenzo Agnello found hepatitis C virus in cryoglobulins to underline the diagnostic importance of immune complex detection with subsequent endeavour to define the involved antigen. Today, thanks to commercial kits available, clinicians ask for immune complex detection in serum samples from their patients and they have learned to interpret the results to the benefit of their patients.