Background Cationic proteins (CP) of neutrophils are characteristically detected in patients with rheumatoid arthritis (RA), and growing evidence suggest that they are involved in disease pathogenesis.
Objectives We investigated the concentration of the cationic proteins (CP) in lysosomes of neutrophils in systemic lupus erythematosus (SLE), RA, systemic scleroderma (SSd), activity of the blood complement system (CH50) and concentration of immune complexes (CIC) in the blood serum.
Methods The study group included 105 patients with RA, SLE 158, 45 patients with SSd, and 78 healthy controls. CP content of neutrophils were assayed by fluorescent cytochemical method (lysosomal cationic test)/Neutrophils were stained with fast blue and asur II. Hemolytic complement activity was determined by the standard method using sheep red blood cells in units of 50% hemolysis (CH50). Circulating immune complexes were measured using polyethylene glycol 6000.
Results CP in SLE, RA and SS significantly fall in all diseases. Decrease in CP followed by increased levels of the CIC in SLE and RA. Correlation of reduced complement activity with the CEC was marked in SLE and RA but not in SSc. At the same time, CH, increased levels of CIC complexes significantly correlated with the activity of SLE and, to a lesser extent RA. In systemic sclerosis increase levels of circulating immune complexes found only in severe Raynaud's syndrome and progressive lung disease
Conclusions These findings suggest that peripheral blood neutrophils are involved in the pathogenesis of RA, SLE and SSc. In SLE and RA with great confidence we can assume the relationship of these changes with CIC. Significant decrease in complement activity in patients with SLE and RA confirms this hypothesis. Lower levels of complement in SLE may also indicate in favor of the rapid depletion of the complement system, genetically inherent in this disease. Data obtained in patients with scleroderma show significant differences from SLE and RA, and therefore evidence in favor of special pathogenesis of this disease.
Disclosure of Interest None declared
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