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PubMed · 7437607

The bleeding patient.

S J Machin
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Abstract

The author has commented on the more frequently encountered acquired haemostatic defects and briefly outlined the relevant routine laboratory investigations that should be performed and their clinical significance. It is important that any replacement therapy with plasma, coagulation factor preparations and concentrates, and platelet infusions should be given promptly and their effectiveness assessed at regular intervals (Urbaniak and Cash, 1977). One's approach to the bleeding patient should be a combination of clinical assessment and interpretation of laboratory data, thus allowing an effective flexible policy to be followed.

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Blood CoagulationBlood Coagulation DisordersBlood Platelet DisordersDisseminated Intravascular CoagulationHemorrhagic DisordersHumansLiver DiseasesVascular DiseasesJournal Article

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S J Machin. 1980. The bleeding patient.. https://pubmed.ncbi.nlm.nih.gov/7437607/

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Herpesviruses have been previously correlated to vascular disease and shown to cause thrombogenic and atherogenic changes to host cells. Herein we show that even in the absence of cells, purified cytomegalovirus (CMV) and herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) can initiate thrombin production. Functional assays demonstrated that purified HSV-1 and HSV-2 provide the necessary phospholipid (proPL) for assembling the coagulation factors Xa and Va into prothrombinase, which is responsible for generating thrombin. These observations are consistent with our earlier studies involving CMV. The presence of proPL on all three herpesviruses was confirmed directly by flow cytometry and electron microscopy by using annexin V and factor Va, respectively, as proPL-specific probes. Of equal importance, we found that CMV, HSV-1, and HSV-2 were also able to facilitate factor Xa generation from the inactive precursor factor X, but only when factor VII/VIIa and Ca2+ were present. Monoclonal antibodies specific for tissue factor (TF), the coagulation initiator, inhibited this factor X activation and, furthermore, enabled identification of TF antigen on each virus type by flow cytometry and electron microscopy. Collectively, these data show that CMV, HSV-1, and HSV-2 can initiate the generation of thrombin by having essential proPL and TF activities on their surface. Unlike the normal cellular source, the viral activity is constitutive and, therefore, not restricted to sites of vascular injury. Thus cell-independent thrombin production may be the earliest event in vascular pathology mediated by herpesviruses.

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