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Protein C and Protein S
Published in Hau C. Kwaan, Meyer M. Samama, Clinical Thrombosis, 2019
Several years ago, Epstein et al.35 demonstrated that protein C antigen declines rapidly after a single 40-mg dose of warfarin. The estimated half-life was only 6 h, comparable to that of Factor VII. Subsequently, other workers showed that protein C anticoagulant activity declines even more rapidly than protein C antigen, that levels of functional protein C activity are lower than protein C antigen,13 and that they take longer to recover after warfarin therapy is discontinued.36 Since many patients suspected of having heterozyous protein C deficiency will be referred for testing while receiving oral anticoagulants, measurement of protein C under these circumstances may provide results that are difficult to interpret. Two strategies may be employed to circumvent this problem. First, another vitamin K-dependent factor, such as Factor X, can be measured concomitantly. If the patient has been receiving warfarin for 3 or more weeks (steady-state anticoagulation), the ratio of protein C antigen to Factor X antigen should be 0.5 or greater.37 A lower ratio would imply preexisting protein C deficiency. Second, both functional and immunologic measurements of protein C may be made in the same patient (Figure 1). Functional protein C is approximately 50% lower than protein C antigen in warfarin-treated subjects.38 Disproportionately low functional activity, or ratio of functional-to-immunologic activity approaching unity, suggests reasons other than warfarin for protein C deficiency.
Evaluation of hypercoagulable states and molecular markers of acute venous thrombosis
Published in Peter Gloviczki, Michael C. Dalsing, Bo Eklöf, Fedor Lurie, Thomas W. Wakefield, Monika L. Gloviczki, Handbook of Venous and Lymphatic Disorders, 2017
Diane M. Nitzki-George, Joseph A. Caprini
Protein C deficiency should be diagnosed with a functional protein C level.37,43 This level is not elevated during an acute VTE episode, which enables testing to be done at any time.58 A finding of a normal protein C level during an acute event would rule out deficiency.50 Warfarin and other vitamin K antagonists are the most common reasons for low protein C functional or antigenic levels; thus, waiting to test until 2–4 weeks after warfarin is discontinued is prudent.37,50
Thrombophilia testing in patients with portal vein thrombosis
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2020
Malene Helligsø Kirkeby, Julie Brogaard Larsen, Henning Grønbaek, Anne-Mette Hvas
Janssen et al. reported an increased risk of factor V Leiden mutation and protein C deficiency in PVT patients compared to healthy individuals [6], which is not in line with our findings. The discrepancy concerning protein C deficiency might be explained by both the rarity of the condition and the difficulty of evaluating the nature of the deficiency (inherited versus acquired). The present study overcomes this challenge by additional genetic testing verifying an inherited deficiency. Two meta-analyses of the Western European population showed significantly increased prevalence of factor V Leiden and prothrombin G20210A mutations in PVT patients [7,9]. However, due to heterogeneity concerning characteristics of control groups and inconsistency in inclusion of cirrhotic patients in the included studies by Dentali et al. [7] and separate analysis in cirrhotic and non-cirrhotic patients by Qi et al. [9], the present study adds information beyond the results of the meta-analyses.
Aetiology of recurrent miscarriage and the role of adjuvant treatment in its management: a retrospective cohort review
Published in Journal of Obstetrics and Gynaecology, 2018
Samuel James Alexander Dobson, Kanna Mannadiar Jayaprakasan
As per the RCOG (Regan et al. 2011), screening investigations were performed as follows. Inherited thrombophilia was excluded by screening for Factor V Leiden mutation, antithrombin 3 deficiency and protein S deficiency. In this study, the clinicians involved also screened for protein C deficiency and hyperhomocysteinaemia. While these are not recommended tests by the RCOG, they are recognised as causes of systemic thrombosis and as such have been included. Antiphospholipid syndrome was confirmed with two positive tests for lupus anticoagulant, Beta-2 Glycoprotein antibodies or anticardiolipin antibodies (IgM and/or IgG titres above the 99th percentile or of >40 g/L or >40 ml/L) 12 weeks apart (Regan et al. 2011). Where available, karyotyping was obtained both from products of conception of the third or subsequent miscarriage and from peripheral blood karyotyping in the parents if miscarriage tissue was found to have an abnormal karyotype. Pelvic ultrasound was used to screen for uterine abnormalities. 3 D ultrasound or MRI was done to classify uterine anomalies correctly, if conventional 2 D scan was suggestive of an anomaly. Our units also offered screening for thyroid disorders and thyroid peroxidase antibodies only as part of the TABLET trial.
Ghrelin, growth hormone and insulin-like growth Factor-I levels in people with protein C deficiency
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2022
Anna Dons-Jensen, Sascha Siig Horup, Anne-Mette Hvas, Esben Thyssen Vestergaard, Rakel Fuglsang Johansen
Protein C is an important natural anticoagulant. Mild protein C deficiency does, most likely, not result in abnormal clot formation [4], but there is a risk of deep vein thrombosis in combination with pregnancy [5] and liver disease [4,6] among others conditions. The prevalence of milder forms of protein C deficiency is about 1 in 200–500 people in the general population [7], but it is considered a rare genetic disorder because of underdiagnosis and underreporting. A study investigating bovine and murine plasma showed, that activated protein C furthermore acts as a ghrelin endopeptidase and splits ghrelin in shorter fragments [8]. People with protein C deficiency could, hypothetically, due to the loss of protein C endopeptidase function, have higher levels of AG.