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Dysfunctional antithrombin III in sick premature infants

M Andrew, P Massicotte-Nolan, L Mitchell

    Pediatric Research
    |February 1, 1985
    PubMed

    Insights

    Sick premature infants may have dysfunctional antithrombin III (ATIII). This protein, crucial for blood coagulation, shows reduced biological activity in sick premature infants after the first week of life and in those with disseminated intravascular coagulation.

    Area of Science:

    • Biochemistry
    • Neonatal Medicine
    • Hematology

    Background:

    • Antithrombin III (ATIII) is a key inhibitor of coagulation factors.
    • Human infants, particularly premature ones, exhibit lower immunological levels of ATIII.
    • The functional capacity of ATIII in sick premature infants remains incompletely understood.

    Purpose of the Study:

    • To assess the functional status of the antithrombin III molecule in sick premature infants.
    • To compare ATIII functionality across different infant groups and adult controls.
    • To investigate potential molecular dysfunction in ATIII in specific neonatal conditions.

    Main Methods:

    • Collected plasma samples from adult controls, healthy full-term infants, sick premature infants (day 1 and >7 days), and infants with disseminated intravascular coagulation (DIC).
    • Measured plasma antithrombin III levels using both biological (chromogenic substrate S2238) and immunological (radial immunodiffusion) assays.
    • Analyzed ATIII functionality via biologic/immunologic ratios and performed crossed immunoelectrophoresis to assess molecular integrity.

    Main Results:

    • Antithrombin III biologic/immunologic ratios were near unity in adults, healthy full-term infants, and sick premature infants on day 1.
    • Sick premature infants beyond the first week of life and those with DIC showed significantly lower biologic activity relative to immunological levels (B/I ratios < 1).
    • Crossed immunoelectrophoresis indicated a normal ATIII molecular structure in most infants, with one exception in the DIC group.

    Conclusions:

    • Sick premature infants may develop a dysfunctional antithrombin III molecule during the postnatal period.
    • Impaired ATIII function is evident in sick premature infants after the first week and in those with DIC.
    • Further investigation into the clinical implications of dysfunctional ATIII in neonates is warranted.

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