Hemorrhagic vasculitis (HV) or Henoch-Scholein purpura (IgA vasculitis) holds a leading position among systemic vasculitides. Data analysis in literary studies on HV in children, both in Ukraine and abroad, has shown the increasing incidence of the disease in the modern times. The recent findings indicate that the extent of HV in Ukraine is 4.9 per 10,000 population by children under 14. The clinical picture of HV is characterized by the lesions of skin, joints, gastrointestinal tract and kidneys. The long-term prognosis depends on direct kidney involvement . Along with the frequency of occurrence and the “rejuvenation” of HV for the recent years, there is a tendency towards the increase of the proportion of its severe forms (such as lightning, abdominal) and the progression of complications involving the formation of chronic pathology of both organs and systems. Renal syndrome, observed in 20-50% of patients with HV, leads to complications . The transition to chronic renal failure is observed in 25-30% of patients, who acquired HV - associated nephritis, which leads to disabilities and possible dialysis treatment of patients . In this regard, over the last decade the search for prognostic markers of HV progression has being made. In particular, serum Gd-IgA1 and urinary IgA, IgG, IgM, IL-8, IL-10, IgA-IgG complexes, p-cresol sulfate, and 3-carboxy-4-methyl-5-pentyl-2-furanopropanoic acid , IL-6, serum amyloid A have been extensively examined, and the role of nitric oxide (NO), cytokines, tumor necrosis factor α (TNFα) has been identified.
For the time being the immune-complex origin of the disease has already been proven, which involves the development of “aseptic inflammation” in microvessels, leading to walls’ destruction, thrombosis and the manifestation of purpura of various localization as a result of the damaging effect of low-molecular weight circulating immune complexes (IC) and the activated components of the complement system. The significance of the immune mechanisms and cytokine cascade, responsible for the triggering of the mechanisms of development and progression of hemorrhagic vasculitis, has been outlined.
The purpose of the research is enhancing the efficiency of diagnosing and prognosis of hemorrhagic vasculitis on the basis of exploration of the direct link between the components of the complement system (C3 and C4, MAC) and the markers of inflammatory response (TNF, IL-8) and their interrelationship with the homeostasis changes in blood serum.
The obtained data contribute to the clarification of the notion of the role of the complement system in the mechanisms of formation and complications of HV, and the development of renal syndrome in children. It has been proved that the indicators of the complement system and proinflammatory cytokines varied regardless of the sex and the age of the child, however, they changed significantly in the different forms and phases of HV. The investigation has resulted in obtaining a better understanding of the indicators of adverse course and the development of renal complications in children with HV, which can serve as a basis for the development of more effective methods of pathogenetic corrective therapy in this disease and timely prevention of its complications.
Through the monitoring of proinflammatory cytokines and the complement system components’ indication there has been proven the expediency of the timely diagnosis of renal syndrome formation in children with hemorrhagic vasculitis. The detection of the levels of C3, C4, MAC and IL-8, TNF in blood plasma allows the doctor to improve the quality and the accuracy of the prognosis of HV course and to prevent the possibilities of complications.
The methods of early forecasting of the development of renal syndrome in children with hemorrhagic vasculitis have been justified and suggested. When established in the blood serum at the very start of clinical manifestations the indicators C3 <1.17 g / l and C4 <0.38 g / l, MAC> 980.7 mIU / ml, IL - 8> 17.8 pg / ml and TNF> 7 , 67 pg / ml identify the possibility of renal syndrome development in children with HV.
