Heparin Cofactor II, Antithrombin and Protein C in Plasma from Term and Preterm Infants

Andersson, Terje R.; Bangstad, Hans‐Jacob; Kobæk-Larsen, Morten

doi:10.1111/j.1651-2227.1988.tb10688.x

Cited by 9 publications

(4 citation statements)

References 16 publications

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“…As the functional activity of PS is related directly to the concentration of free PS not bound to C4bBP, our findings provide some indirect evidence that capillary PS functional activity is probably higher than that in venous samples. Contrary to ATIII and PS antigen, PC antigen levels in capillary and venous plasma were almost identical and were similar to those reported in most previous studies (15)(16)(17)(18). The functional activity of PC was, on the other hand, significantly lower in capillary plasma.…”

Section: Discussionsupporting

confidence: 88%

Comparison of antithrombin III, protein C and protein S levels in capillary and venous blood of newborn infants

Fok¹,

Yin²,

Yuen³

1992

Acta Paediatrica

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The plasma concentrations of antithrombin III, protein C and protein S in capillary and venous blood samples obtained simultaneously from 30 neonates were compared in order to determine the suitability of using capillary blood for estimation of these proteins with anticoagulant action. Our findings showed that while capillary and venous blood did not differ significantly in antithrombin III functional activity and protein C antigen levels, the capillary samples had significantly lower protein C functional activity and higher antithrombin III antigen level. Protein S antigen level was also significantly higher in the capillary samples although the difference was relatively small. The capillary and venous concentrations of the binding protein of protein S, C4b binding protein, were almost identical.

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Section: Discussionsupporting

confidence: 88%

Comparison of antithrombin III, protein C and protein S levels in capillary and venous blood of newborn infants

Fok¹,

Yin²,

Yuen³

1992

Acta Paediatrica

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“…By 75 s, mean prothrombin levels were <0.05 U/mL. lating plasma concentrations of coagulation factors are decreased The time point of maximum thrombin generation coincided compared with healthy neonates (7)(8)(9)(10)(11)(12)(13)(14)(15). One of the most conwith the time of maximum prothrombin consumption (data not sistently reported alterations in RDS is low plasma levels of the shown).…”

Section: Resultsmentioning

confidence: 99%

“…In contrast, sick neonates with problems such as respiratory distress are prone to develop both hemorrhagic and thrombotic complications. The plasma concentrations of many procoagulants and inhibitors are decreased in sick premature neonates compared with healthy agematched counterparts (7)(8)(9)(10)(11)(12)(13)(14)(15). The net effect of the altered concentrations of coagulants and inhibitors on thrombin regulation in sick neonates has not been studied previously with sensitive techniques that quantitate both the generation and inhibition of thrombin.…”

mentioning

confidence: 99%

Thrombin Inhibition Is Impaired in Plasma of Sick Neonates

et al. 1992

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ABSTRACT. The sick neonate may develop spontaneous or catheter-related thromboses, which must in part reflect poor regulation of the formation and activities of the coagulation enzyme, thrombin. We hypothesized that the balance between the generation and inhibition of thrombin may differ in sick neonates compared with healthy neonates. Fifty neonates with respiratory failure requiring mechanical ventilation and 40 healthy neonates were studied on d 1 of life. All neonates had normal coagulation screenine tests and a ~latelet count greater than 150 X 109/L. plasma pools from neonates with similar gestational age (GA), birth weight, and health status were prepared. Eight plasma pools from 40 healthy neonates of GA 30-38 wk were compared with six plasma pools from 30 sick neonates of GA 30-38 wk. An additional four plasma pools prepared from 20 sick neonates of GA <30 wk were studied. Thrombin generation was measured by amidolysis of a chromogenic substrate, S2238, after defibrination, contact activation, and recalcification of the test plasmas. The contributions of antithrombin 111, heparin cofactor 11, and a2-macroglobulin as inhibitors of '251-thrombin were quantitated by SDS-PAGE followed by autoradiography and densitometry. Thrombin generation was similar for both healthy and sick neonates of GA 30-38 wk. However, the inhibition of thrombin was impaired in plasma from sick neonates of GA 30-38 wk compared with plasma from healthy neonates of GA 30-38 wk (4.37 2 0.22 versus 5.21 2 0.21 nmol; p < 0.05). Plasma levels of antithrombin 111 and a2-macroglobulin were significantly lower in sick neonates of GA 30-38 wk compared with healthy neonates of GA 30-38 wk (0.30 f 0.03 versus 0.41 f 0.03 U/mL; p < 0.05 and 0.93 f 0.07 versus 1.29 f 0.10 U/mL; p < 0.05, respectively). The sick neonates of GA <30 wk had values similar to sick neonates of GA 30-38 wk for the generation and inhibition of thrombin and for plasma levels of inhibitors antithrombin I11 and a2-macroglobulin. Thus, sick neonates are able to generate thrombin as well as healthy age-matched neonates, but their ability to inhibit thrombin is significantly decreased. This acquired imbalance between the generation and inhibition of thrombin may place the sick neonate at risk for thrombotic complications in the immediate postnatal period. (Pediatr Res 31: 391-395, 1992) Received The coagulation system in healthy preterm and full-term neonates is immature at birth and gradually evolves postnatally toward the mature adult system. The plasma concentrations of both procoagulants and inhibitors differ in healthy neonates compared with adults (1-3). The differences in the concentration of the procoagulants results in diminished ability to generate thrombin in neonates compared with adults (4,5). Similarly, the concentrations of thrombin inhibitors are also altered, resulting in an impaired ability to inhibit thrombin in neonates compared with adults (6).However, in healthy neonates, thrombin expression is controlled such that neither hemorrhagic nor thrombotic ...

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“…Differences exist between the mechanism of action of heparin in neonates and adults. Levels of antithrombin (AT) are low in newborns and alpha‐2‐macroglobulin, an alternative heparin co‐factor, may be of greater importance . The optimal regimes for heparin treatment are controversial and have largely followed from practice in adults; however, this may not always be appropriate .…”

Section: Monitoring Of Coagulation and Anticoagulationmentioning

confidence: 99%

Coagulation and the surgical neonate

Arnold

2013

Pediatric Anesthesia

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Both coagulopathy and abnormal thrombosis can complicate the anesthetic and surgical management of neonatal patients; however, the patterns of bleeding and thrombosis in neonates differ from those in adults or older children. Severe coagulopathic bleeding most commonly occurs during heart surgery and almost certainly contributes to morbidity and mortality in this population. Such severe bleeding is rare during other surgery; the exception is babies presenting to the operating room with established coagulopathy secondary to severe sepsis. Alternatively, pathological thrombosis will mainly occur in association with indwelling vascular access devices or surgically created vascular shunts. There are important differences between the coagulation system in neonates and older patients. The implication of this is that therapies established in other patient groups will not be optimal for neonates without adaptation. While evidence from high-quality clinical trials is rarely available, an understanding of how coagulation in neonates differs can help to guide practice. This review will discuss important differences between the coagulation system of neonates and older patients and how these relate to newer models of coagulation. The emphasis will be on issues likely to impact on perioperative care. In particular, the management of severe bleeding, the manipulation of coagulation during heart surgery, and the management of coagulopathy in septic neonates will be discussed in detail.

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Heparin Cofactor II, Antithrombin and Protein C in Plasma from Term and Preterm Infants

Cited by 9 publications

References 16 publications

Comparison of antithrombin III, protein C and protein S levels in capillary and venous blood of newborn infants

Comparison of antithrombin III, protein C and protein S levels in capillary and venous blood of newborn infants

Thrombin Inhibition Is Impaired in Plasma of Sick Neonates

Coagulation and the surgical neonate

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