Evolution of Blood Clotting Factor Levels in Premature Infants during the First 10 Days of Life: A Study of 96 Cases with Comparison Between Clinical Status and Blood Clotting Factor Levels

Jensen, A Hurlet-Birk; Josso, F; Zamet, P; Monset-Couchard, M; A, Minkowski

doi:10.1203/00006450-197307000-00007

Cited by 40 publications

(7 citation statements)

References 10 publications

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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%

“…prothrombin are lower in the presence of moderate to severe Inhibition of thrombin and detection of thrombin-inhibition RDS (8,26). The overall effect of the alterations in the hemostatic complexes.…”

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.…”

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confidence: 99%

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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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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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confidence: 99%

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Thrombin Inhibition Is Impaired in Plasma of Sick Neonates

et al. 1992

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“…Blood coagulation factor activity measurements in premature infants are available by study of these infants after delivery or by study of fetuses of women undergoing abortion. The values obtained in these studies emphasize the wide variation in factor activities (2,9, 10, 13,15,23). The variability may be normal or may also be variability in association with the stresses of hysterotomy, labor, and delivery.…”

Section: Speculationmentioning

confidence: 99%

Development of Blood Coagulation—A Fetal Lamb Model

1981

Pediatr Res

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SummaryTo study the normal development of blood coagulation factor activities in a growing fetus while avoiding the effects of labor and delivery, a chronic fetal lamb model was developed in which serial blood samples from 10 fetuses were studied during the third trimester of pregnancy and 24 hr after birth. Under operating room conditions with sterile technique, a polyethylene catheter to which heparin had been bound to both internal and external surfaces was inserted into the femoral artery of the fetus. The catheter was brought out through a skin pouch to the side of the ewe and enclosed in a zip lock bag. Blood samples were withdrawn from the catheter three times each week for measurement of coagulation factor activities. Levels of coagulation factor activities at birth in noncatheterized animals were not different from those found in catheterized animals except for factor IX activity which was 12% higher in the catheterized animals (0.02 t P < 0.05). The patterns of development for each of the coagulation factors were similar in all 10 animals studied. Fibrinogen, prothrombin, and factor VII show a decrease in activity early in the last trimester of pregnancy whereas other factors V, VIII, IX, X, XI, XII, and XI11 show a gradual increase in activity throughout the last trimester of pregnancy. Both factors VIII and IX show a significant increase in activity (23% factor VIII and 12% factor IX) associated with the process of delivery. The levels of coagulation factor activities at birth in the lamb relative to adult sheep normals are similar to those found in humans with the exception of factor XIII. Factor XIII is at normal levels in the newborn lamb and is reported to be at levels approximately 50% of the adult level in human infants. SpeculationThe development of a chronic fetal lamb preparation has allowed the construction of developmental patterns for coagulation factor activities throughout the last trimester of pregnancy. Further studies into the biology of the changes in coagulation factor activities observed and the influences of such stresses as hypoxemia and premature delivery should enhance our understanding of the bleeding neonate.

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“…Factors of the coagulation system in the fetal circulation have to be synthesized by the fetus and do not cross the placenta. The absolute and relative concentrations of some compo nents of the coagulation system differ from the adults, and they are dependent on both the gestational age and postnatal age [2,6,[19][20][21][22][23]. Additionally, functional abnormalities of several coagulation proteins, especially fibrin ogen [24][25][26][27] and prothrombin [28], have been described in full-term newborns.…”

Section: Discussionmentioning

confidence: 99%

The Role of α<sub>2</sub>-Antiplasmin in the Inhibition of Clot Lysis in Newborns and Adults

Ries

Klinge²,

Rauch³

et al. 1996

Neonatology

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The fibrinolytic system is involved in a wide variety of biological phenomena and differs physiologically in newborns compared to older children or adults. Newborn’s plasminogen differs from adult plasminogen in carbohydrate composition, cell binding and activation kinetics. The fetal plasminogen has an increased concentration of sialic acid similar to fetal fibrinogen. In a previously reported study on plasminogen activation kinetics, we demonstrated differences in the reaction kinetics between fetal plasmin and plasmin inhibitors as compared to the reaction between adult plasmin and inhibitors. Hitherto, there are no investigations on the role of α₂-antiplasmin in the inhibition of clot lysis in newborns. We studied the contributions of purified α₂-antiplasmin to the regulation of fibrin clot lysis by use of a microtiter clot lysis assay. The lysis time of clots without adding purified α₂-antiplasmin correlated to the activator dose. When purified α₂-antiplasmin was incorporated at final concentrations ranging from 10 to 40 μg/ml, strong dose-dependent inhibition resulting in a prolongation of 50% lysis time was observed. The inhibition in newborns at all α₂-antiplasmin concentrations was less pronounced than that of the adults if 50% lysis time was < 55 min. If 50% lysis time was > 55 min, the prolongation of 50% lysis time was more pronounced in newborn than in adult plasma. The fact that we have less effects of α₂-antiplasmin in newborn infants at short reaction times despite the lower plasminogen levels, is consistent with slower reaction kinetics between plasmin and α₂-antiplasmin in newborns. These differences raise an explanation for the findings of Idell et al. [Am J Respir Crit Care Med 1994;149:767–775] in premature baboons with neonatal respiratory distress syndrome (RDS). The knowledge of different reaction kinetics between plasmin and α₂-antiplasmin and the role of α₂-antiplasmin in the inhibition of clot lysis in newborns can be helpful to elucidate the significance of the fetal fibrinolytic system in neonatal RDS and to establish treatment strategies for fîbrinolytic therapy of progressive RDS.

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Evolution of Blood Clotting Factor Levels in Premature Infants during the First 10 Days of Life: A Study of 96 Cases with Comparison Between Clinical Status and Blood Clotting Factor Levels

Cited by 40 publications

References 10 publications

Thrombin Inhibition Is Impaired in Plasma of Sick Neonates

Thrombin Inhibition Is Impaired in Plasma of Sick Neonates

Development of Blood Coagulation—A Fetal Lamb Model

The Role of α<sub>2</sub>-Antiplasmin in the Inhibition of Clot Lysis in Newborns and Adults

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