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[Alpha 2-antiplasmin in childhood]
Insights
Alpha 2-antiplasmin levels increase in newborns with sepsis, acting as an acute phase reactant. Lower levels indicate poor prognosis, suggesting diagnostic value in pediatric sepsis and related conditions.
Area of Science:
- Biochemistry
- Pediatric Medicine
- Hematology
Background:
- Alpha 2-antiplasmin is a key inhibitor in the fibrinolytic system.
- Its role in neonatal sepsis and related conditions requires further elucidation.
Purpose of the Study:
- To investigate alpha 2-antiplasmin levels in pediatric patients, particularly newborns with sepsis.
- To assess the diagnostic utility of alpha 2-antiplasmin as an acute phase reactant.
Main Methods:
- Chromogenic substrate S-2251 was used to determine alpha 2-antiplasmin levels in 119 children.
- Measurements were compared between healthy newborns, septic infants, and those with other conditions like respiratory distress.
Main Results:
- Healthy newborns had 65% of adult alpha 2-antiplasmin levels.
- Septic infants showed elevated alpha 2-antiplasmin, increasing during the sepsis course.
- Alpha 2-antiplasmin correlated with fibrin binding and acted as an acute phase reactant.
- Lower levels were observed in patients with shock or declining health.
- Reduced levels were noted in respiratory distress and non-septic disseminated intravascular coagulation.
Conclusions:
- Alpha 2-antiplasmin is a valuable acute phase reactant in pediatric sepsis.
- Its levels provide diagnostic insights into sepsis, disseminated intravascular coagulation, and other critical conditions.
- Monitoring alpha 2-antiplasmin may aid in assessing disease severity and prognosis in neonates and infants.
Abstract:
In 119 children, predominantly newborns and babies with sepsis, alpha 2-Antiplasmin was determined by the use of the chromogenic substrate S-2251. In healthy newborns, the inhibitor level averaged 65 per cent of the adult level. Already in the initial phase of sepsis, enhanced alpha 2-antiplasmin values were observed. During the further course, they increased markedly. Thus, alpha 2-antiplasmin proved to be an acute phase reactant together with fibrinogen, factors II and X, and alpha 1-antitrypsin measured as trypsin inhibitor capacity. The correlation analysis in all subgroups showed moderately tight binding to fibrin. In patients with shock or in those who decreased, lower levels were measured. The overproduction is assumed to be caused by disseminated intravascular coagulation processes. In other diseases such as respiratory distress, alpha 2-antiplasmin was reduced. In case of disseminated intravascular coagulation that was not caused by sepsis consumption of components dominated. In the probability paper, distribution of the values of the subgroups was found to differ markedly. Thus, the inhibitor proved to be of diagnostic value.