In 107 asymptomatic and untreated patients with inherited syndromes associated with thrombophilia (antithrombin III, protein C and protein S deficiencies), we compared in parallel two plasma peptides which reflect activation of the common coagulation pathway: the prothrombin fragment 1 + 2 (F1+2) and fibrinopeptide A (FPA). Both F1+2 and FPA were measured with simple, commercially available ELISA methods. High levels of F1+2 or FPA were found in about one fourth of the patients as a whole. When patients were divided according to the type of inherited thrombophilic syndrome, it appeared that F1+2 was more frequently elevated in protein C and protein S deficiencies than in antithrombin deficiency; and that, in general, it was no more frequently elevated than FPA. Although our data confirm the existence of a procoagulant imbalance in inherited thrombophilic syndromes due to defects of natural anticoagulant proteins, they do not confirm that such imbalance can be more frequently diagnosed by measuring F1+2 levels, particularly in patients with antithrombin deficiency.
Markers of procoagulant imbalance in patients with inherited thrombophilic syndromes / P.M. Mannucci, A. Tripodi, B. Bottasso, F. Baudo, G. Finazzi, V. De Stefano, G. Palareti, C. Manotti, M.G. Mazzucconi, G. Castaman. - In: THROMBOSIS AND HAEMOSTASIS. - ISSN 0340-6245. - 67:2(1992), pp. 200-202.
Markers of procoagulant imbalance in patients with inherited thrombophilic syndromes
A. TripodiSecondo
;
1992
Abstract
In 107 asymptomatic and untreated patients with inherited syndromes associated with thrombophilia (antithrombin III, protein C and protein S deficiencies), we compared in parallel two plasma peptides which reflect activation of the common coagulation pathway: the prothrombin fragment 1 + 2 (F1+2) and fibrinopeptide A (FPA). Both F1+2 and FPA were measured with simple, commercially available ELISA methods. High levels of F1+2 or FPA were found in about one fourth of the patients as a whole. When patients were divided according to the type of inherited thrombophilic syndrome, it appeared that F1+2 was more frequently elevated in protein C and protein S deficiencies than in antithrombin deficiency; and that, in general, it was no more frequently elevated than FPA. Although our data confirm the existence of a procoagulant imbalance in inherited thrombophilic syndromes due to defects of natural anticoagulant proteins, they do not confirm that such imbalance can be more frequently diagnosed by measuring F1+2 levels, particularly in patients with antithrombin deficiency.Pubblicazioni consigliate
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