Hemostasis in children with dysbacteriosis in chronic constipation

Citation
Iv. Kirgizov et al., Hemostasis in children with dysbacteriosis in chronic constipation, CL APPL T-H, 7(4), 2001, pp. 335-338
Citations number
12
Categorie Soggetti
Hematology
Journal title
CLINICAL AND APPLIED THROMBOSIS-HEMOSTASIS
ISSN journal
10760296 → ACNP
Volume
7
Issue
4
Year of publication
2001
Pages
335 - 338
Database
ISI
SICI code
1076-0296(200110)7:4<335:HICWDI>2.0.ZU;2-G
Abstract
The purpose of the study was to investigate hemostasis in children with dys bacteriosis disturbance in chronic constipation. The disturbance of factors in the inner mechanism of blood coagulation (VII, IX, XL XII) in compensat ed chronic constipation was defined based on the reduction in colon bacillu s levels. We observed hypocoagulation caused by the reduced activity of the prothrombin complex factors, disaggregate thrombocytopathy, and endothelio sis with fibrinolysis inhibition in subcompensated chronic colostasis with continuous reduction of colon bacillus levels and pathogenic microflora app earance. In decompensated colostasis there was an increase in pathogenic mi croorganisms and a continuous reduction of colon bacillus levels. In hemost asis there was a factor deficiency in inner (XII, XI, IX, VIII) and outer ( II, V, VII, X) blood coagulation mechanisms. Fibrinolysis inhibition, endot heliosis development with thrombocyte aggregation, and microthrombosis form ation were determined. Thus, in children with chronic constipation, there w as a marked reduction in the amount of colon bacillus. which led to the rep roduction of pathogenic bacteria. We also observed chronometric hypocoagula tion with the inner (XII, XI, IX, VIII) and outer (II, V VII, X) mechanisms of blood coagulation, at the base of which there is the deficiency of vita min K-dependent factors (II, VII IX. X) and a slightly marked disturbance i n the final stage of coagulation. In thrombocyte vascular hemostasis, throm bocytopathy was observed with increased adenosine-5-diphosphate aggregation and the inhibition of the inner mechanism with fibrinolysis and endothelio sis.