Neonatal and Maternal Hemostasis: Value of Molecular Markers in the Assessment of Hemostatic Status

Suárez, Carlos; Menendez, Cesar; Walenga, Jeanine M.; Fareed, Jawed

doi:10.1055/s-2007-1004433

Cited by 26 publications

(11 citation statements)

References 18 publications

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“…To date, ex vivo measurement of markers of throm bin regulation have not been measured in the unborn fetus. Cord blood samples obtained immediately after delivery have increased levels of fibrinopeptide A similar to 47 or higher than 48 those seen in maternal plasmas and AT III-thrombin complexes are increased in newborns immediately after birth. 76 This likely indicates activation of the hemostatic system in fetuses at the time of deliv ery.…”

Section: In Vivo Markers Of Thrombin Regulationmentioning

confidence: 89%

“…43 However, this finding may be interpreted as simply indicating differential production of Factor VIII and vWF. A discrepancy in the levels of Factor V measured using congenitally deficient plasma and plasma depleted of Factor V with Russell's viper venom has been found and interpreted as indicating the presence of thrombin-activated Factor V. 44 Subse quently, measurements of fibrinopeptide A during preg nancy have shown increased levels [45][46][47][48][49] over controls though there are a wide range of reported values. In addition, levels of thrombin-AT III complexes increase throughout gestation.…”

Section: In Vivo Markers Of Thrombin Generation and Inhibitionmentioning

confidence: 99%

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Thrombin Regulation in Mother and Fetus During Pregnancy

Delorme

Burrows²,

Ofosu³

et al. 1992

Semin Thromb Hemost

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Pregnancy is characterized by an increase in plasma concentration of several coagulants and with little or no change in plasma concentrations of inhibitors of thrombin or thrombin generation with the exception of a decrease in protein S. The net effect of these physiologic differences from nonpregnant adults is that, in vitro, thrombin generation is slightly increased in pregnancy plasma. Thrombin inhibition may be altered by the presence of circulating dermatan sulfate proteoglycan. Based on information on placental structure and function and ex vivo markers of thrombin generation, it is clear that there must be local generation of thrombin with fibrin deposition in the placenta. The roles of the alterations in the hemostatic system in regulating this increased thrombin activity remain to be elucidated. In addition, regulation of thrombin at the vessel wall of the placenta needs to be further explored, since it is likely important in preventing locally increased thrombin generation from producing systemic effects, that is, thrombosis. The fetal coagulation system is an immature, developing system, as is evident from low and gradually increasing plasma concentrations of both coagulants and inhibitors. Some of these low levels result from decreased gene expression in the immature liver. However, others (Factors II, VII and VIII) are related to other processes that remain to be determined. There is a progressive increase in the levels of these factors with increasing gestational age but most remain below adult values at term. As a result, thrombin generation and inhibition in vitro are decreased. Since bleeding and thrombotic complications are not a feature of normal fetal life, it is likely that the hemostatic system is balanced. In vivo data on thrombin generation and inhibition are lacking and the interaction of the physiologically different plasma of the fetus with the vessel wall is only now being explored.

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Section: In Vivo Markers Of Thrombin Regulationmentioning

confidence: 89%

Section: In Vivo Markers Of Thrombin Generation and Inhibitionmentioning

confidence: 99%

Thrombin Regulation in Mother and Fetus During Pregnancy

Delorme

Burrows²,

Ofosu³

et al. 1992

Semin Thromb Hemost

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“…Although most normal newborns do not have spontaneous bleeding and/or thrombosis, these relative deficiencies result in a tenuous balance that predisposes the newborn to hemorrhage as well as thrombosis when a pathologic insult such as birth asphyxia exists [1,2,4]. It has been previously reported [13,14] that newborn platelets are in a state of transient dysfunction secondary to platelet activation at the time of birth. The mechanisms of neonatal platelet activation during birth are multifaceted and may be related to thermal changes, stress with adrenergic stimulation, acidosis, hypoxia, and release of tissue factor [2].…”

Section: Discussionmentioning

confidence: 99%

Platelet Activation during the Early Neonatal Period

İrken

Mutafoglu²,

Olgun³

et al. 1998

Neonatology

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The first week of life is a time when hereditary or more frequently acquired factors lead to some important differences in the hemostatic mechanism of the newborn. It has been well known that ill neonates are prone to both hemorrhage and thrombosis. The aim of this study was to answer the question of whether there is a difference in platelet activation in healthy neonates during the first days of life that may contribute to both hemorrhage and thrombosis in the presence of additional pathologic insults. Platelet activation was determined with flow cytometry using monoclonal antibodies in 63 healthy children (29 neonates, 17 infants, and 17 older children). There was no significant difference in platelet activation among these three age groups (p > 0.05). In addition, platelet activation did not show any significant relationship to age, sex, mode of delivery, or blood bilirubin concentration (p > 0.05). It has been previously reported that platelet activation occurs at the time of birth. We could not find any evidence that healthy newborns during the first 3 days of life exhibit increased platelet activation. Further studies on platelet activation in ill neonates will help to clarify whether platelet activation plays a role in the pathogenesis of thrombotic and/or hemorrhagic disorders.

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“…The plasmatic haemostasis is a complex network with characteristic aspects of each age group re¯ecting a rather dynamic than static system evolving through several dierent phases [5,15,23,79]. The neonatal phase of the haemostatic system is profoundly dierent from the adult phase but also from the fetal phase [65] and is mainly characterized by a low reserve capacity [4].…”

Section: Neonatal Aspects Of Platelet Physiology and Haemostasismentioning

confidence: 99%

Neonatal platelet physiology and pathophysiology

Kühne

Imbach

1998

European Journal of Pediatrics

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Platelets contribute to primary haemostatic events and are closely linked to plasmatic coagulation. Their function is highly dependent not only on their number but also on their integral physiology. In comparison with adults or children, the haemostasis of newborn infants, although physiological, is characterized by a reduced functional reserve capacity leading to the rapid occurrence of bleeding disorders especially in the presence of additional risk factors such as prematurity, asphyxia, or infection. Morphological and biochemical differences reflect an immature cellular stage which results in platelet hyporeactivity and contributes to the reduced capacity of the neonatal haemostatic system. Additionally acquired and inherited platelet disorders markedly affect platelet function. Hence assessment of neonatal platelet physiology may supply important information, however, no adequate screening tests are currently available, and technical difficulties of blood sampling limit the value of laboratory testing. Evaluation of the neonatal platelet function is highly dependent on individual laboratory results and it is advisable to perform complex diagnostic procedures with the collaboration of specialists experienced in neonatal haematology. With the advent of new technology such as platelet flow cytometry more adequate tools are available, although still reserved for specialized laboratories, thus awaiting their clinical significance. The role of maternal influences on neonatal platelet function must be always considered. Thus, neonatal platelet physiology and pathophysiology is complex and require more studies and experience.

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Neonatal and Maternal Hemostasis: Value of Molecular Markers in the Assessment of Hemostatic Status

Cited by 26 publications

References 18 publications

Thrombin Regulation in Mother and Fetus During Pregnancy

Thrombin Regulation in Mother and Fetus During Pregnancy

Platelet Activation during the Early Neonatal Period

Neonatal platelet physiology and pathophysiology

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