Significantly decreased platelet serotonin contents were measured in rheumatoid arthritis, systemic lupus erythematosus (SLE), progressive systemic sclerosis, and mixed connective tissue disease. An inverse relationship between platelet serotonin levels and clinical disease activity was observed in both rheumatoid arthritis and systemic lupus erythematosus. SLE patients with multiple organ involvement showed the lowest platelet serotonin values. No correlation was observed between platelet serotonin contents and nonsteroidal antiinflammatory drug treatment, presence of circulating platelet reactive IgG, or the amount of circulating immune complexes. The results are interpreted as indicating platelet release occurring in vivo during inflammatory episodes of the rheumatic disorders investigated.In addition to their role in blood coagulation, platelets have been shown to play an important part as intravascular inflammatory cells (1). Substances such as thrombin, collagen, ADP, prostaglandin endoperox- Supported by the Deutsche Forschungsgemeinschaft, Sonderforschungsbereich 5 4 4 3 .
Using a C1q binding test, circulating immune complexes (IC) were detected in 33.3% of sera from 138 patients and in 19.4% of 124 spinal fluid samples from patients with multiple sclerosis. Most often they occur in sera alone. As a rule their detectable amount is small in sera as well as in spinal fluids. IC were observed with equal frequency during acute exacerbations and in stable phases of the disease. In patients with early MS of less than 3 months duration, IC were detected only rarely, whereas their frequency increased up to 50% in patients with longer standing disease. Immunosuppressive therapy has no influence on IC formation. Patients with immune complexes exhibited a more rapid clinical deterioration if compared as a group with IC-negativ ones. No correlations were found between immune complex formation and the CSF-IgG index or the rate of pleocytosis in spinal fluids. Neither the complement factors C3, C4, C3A nor total hemolytic complement activities (CH50) in serum were significantly decreased in patients with IC formation in serum as compared with the IC-negative group. The results demonstrate that IC formation probably is of no importance in the pathogenesis of multiple sclerosis.
Using a C1q binding test, immune complexes have been detected in one half of cerebrospinal fluid samples from patients with multiple sclerosis. These results provide additional evidence for the participation of an immune reaction in the disease process.
Sera from patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) were assessed for in vitro platelet activation as measured by serotonin release; 24% (30) of 124 tested RA sera and 51% (35) of 69 SLE sera induced a significant 3H serotonin release. Investigation of 17 synovial fluid samples from RA patients revealed significant release in 82%. Concomitant testing for lymphocytotoxic antibodies and immune complexes did not show any correlation to platelet activation. Upon gel filtration the release-inducing activity of positive sera was localized in the region of 160 000 Daltons. Further characterization by ion exchange chromatography, immune electrophoresis, chromatographic and SDS PAGE molecular weight determinations, as well as analytical ultracentrifugation all confirmed the IgG nature of the release-inducing protein. Negative blocking experiments performed by preincubation of platelets with Fc-IgG fragments prior to challenge with a release-inducing serum excluded the participation of Fc receptors in the reaction. It was concluded that the release was caused by a platelet reactive IgG antibody. This antibody may also cause release of platelet mediators in vivo and may thus contribute to the pathogenesis of the generalized vasculopathy in both diseases.
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