Abstract

Background: The aim of study was to clarify the biochemical mechanisms of severe hemorrhagic forms of erysipelas and find the possible early predictors of its development. Methods & Materials: 90 patients with erysipelas of the lower extremities (ELE) were examined. 44 patients had erythematous (1th group), 24 - bullous (2th group) and 32 - hemorrhagic (3th group) forms of ELE. The level of macrophage inflammatory protein-1A (MIP-1a) was investigated in the dynamics of ELE. Also we studied the phagocytic activity of neutrophils and monocytes. Results: In the acute phase of disease the level of MIP-1a in 1th and 2th groups was lower than in healthy individuals: 9.10pg/ml (95%CL 7.84-10.36pg/ml), 10.8pg/ml (95%CI 9.43±12.17pg/ml) and 13.6pg/ml (95%CI 11.88±15.32pg/ml) accordingly, p-value 1-n=0.03, p-value 2-n=0.04. In 3th group it was significantly higher in comparison with all other groups 290.7pg/ml (95%CI 284.49-296.91pg/ml). Phagocytic activity was considerably higher in patients of 3th group than in patients of 1th group: 92,5% (95%CI 91.88-93.12%) and 83,5% (95%CI 82.49- 84.51%) for neutrophils (p-value 1-3=0.001) and 88,5% (95%CI 87.94-89.06%) and 80,0% (95%CI 77.77-82.23%) for monocytes (p-value 1-3=0.002). In the convalescent period the level of MIP-1a increased to 11.7 pg/ml (95%CI 8.14-15.26pg/ml) at erythematous form and 13.5% (95%CI 10.26-16.74 pg/ml) at bullous form without difference between them and normal level. In 3th group it was down to the level of a norm 13.7 pg/ml (95%CI 10.46-16.94 pg/ml). Within 12 months of follow-up period we observed only 1 relapse in 3th group, 3 - in 2th group and 6 in 1th group. Conclusion: Identified changes in the level MIP-1a reflect its role in the implementation of the phagocytic activity. Mostly it refers to the monocytes, as evidenced by an increase in its level in patients with hemorrhagic form of erysipelas, where their activity was maximal. Significant reduction of relapses in patients with hemorrhagic erysipelas probably connected with increased PA, which can stimulate nonspecific resistance via activation of phagocytosis.

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