Abstract:
Recently, the interest in research on the role of free radical-induced lipid peroxidation reactions in pathogenesis of rheumatic fever and hereditary
collagen dysplasias has considerably grown. The study tested blood plasma of 60 children: 18 carriers of hereditary collagen dysplasias and 42 children
with rheumatic fever. Twenty healthy individuals have constituted control group. All patients have undergone complex clinical and laboratory
examinations to evaluate process activity and disease stage, their familial and genealogical histories have been taken. Presence of rheumatoid factor was
determined by latex agglutination test. Other rheumatic fever markers were tested by common methods. Status of the lipid peroxidation process was
assessed by malondialdehyde content, using reaction with thiobarbituric acid and subsequent spectrophotometric measurement. Catalase activity was
measured spectrophotometrically. To diagnosticate hereditary collagen dysplasias, hydroxyproline levels in blood and urine were assayed. Content of
glycosaminoglycans was determined by electrophoresis, and levels of amino acids were measured chromatographically. In the majority of patients, the
tests detected an increased daily urinary excretion of hydroxyproline and glycosaminoglycans what reflects the process of collagen metabolism disorders.
The authors detected elevated levels of malondialdehyde, increased activity of superoxide dismutase and decreased activity of glutathione peroxidase and
catalase. These three markers are sufficiently sensitive to assess affection of immunocompetent cells in rheumatic fever and hereditary collagen dysplasias.
