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Protein C and Protein S
Published in Hau C. Kwaan, Meyer M. Samama, Clinical Thrombosis, 2019
Protein S is a 69,000-Da vitamin K-dependent factor45 which differs from protein C in several important respects:46 it is synthesized by endothelial cells as well as liver cells, it is not a protease but rather serves as a cofactor for protein C., and two thirds of the circulating protein S is bound to the fourth component of complement (C4b) binding protein and does not have anticoagulant activity. The plasma concentration of protein S is 25 µg/ml, of which 10 µg/ml is unbound.46 Protein S may be measured by functional48 and immunological methods.49 However, the latter measures total protein S, which includes the inactive bound molecule. To assay free protein S, the bound protein S must first be precipitated with polyethylene glycol.50 These assays have been used to study patients with congenital and acquired protein S 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
The available tests for the diagnosis of protein S deficiency are free antigen level, total antigen level, and functional (APC cofactor activity) level. Routine testing of antigenic total protein S is not usually necessary. The functional test is influenced by factors other than protein S activity, and should be interpreted with caution. Fluctuations in protein S levels have been noted over time. Thus, the diagnosis should be confirmed with a second test.37,59
Cerebral venous sinus thrombosis associated with protein S deficiency during pregnancy: a case report
Published in Journal of Obstetrics and Gynaecology, 2020
Miyu Usui, Tadashi Ozawa, Younhee Kim, Takafumi Mashiko, Kosuke Matsuzono, Keiko Maruyama, Koichi Kokame, Rie Usui, Reiji Koide, Shigeru Fujimoto
Protein S deficiency is a coagulation disorder associated with an increased risk of venous thrombosis. This condition is often hereditary, but may be acquired. The hereditary form is usually inherited in an autosomal dominant manner and is caused by a mutation in PROS1. The deficiency is acquired in the presence of liver disease, HIV infection, Vitamin K deficiency and pregnancy. During pregnancy, protein S activity decreases from the first to the third trimester (38± 17.8%) and becomes minimum in the third trimester. Because our patient showed a much lower protein S activity than those described in previous reports, we performed genetic testing of PROS1 to investigate the possibility of hereditary protein S deficiency. The result showed no causative mutation in PROS1. Furthermore, the fact that her protein S activity returned to normal levels after delivery suggests that her protein S deficiency was not hereditary. Castaman et al. reported that the polymorphism (c.A2001G and p.Pro667Pro) observed in our patient does not affect plasma protein S activity, but it cannot be excluded that the polymorphism could be associated with other genetic or environmental factors (Castaman et al. 2007). It remains unclear whether this polymorphism is related to a predisposing factor for protein S activity decline during pregnancy.
Bariatric venous thromboembolism prophylaxis: an update on the literature
Published in Expert Review of Hematology, 2019
Rachelle Hamadi, Christina F. Marlow, Samah Nassereddine, Ali Taher, Antoine Finianos
The outcome measured was VTE rates within 30 days post-operatively confirmed by imaging and requiring treatment. The strongest risk factors included congestive heart failur2 (CHF) (OR 6.58), paraplegia (OR 5.71), return to operating room (OR 5.11), dyspnea at rest (OR 3.95), non-gastric band surgery (OR 2.44), age > 60 years (OR 1.96), Male (OR 1.92), BMI >/50 kg/m2 (OR 1.67), length of stay (LOS) >/3 days (OR 1.58), and operation time >/3 hours (OR 1.57). The team was able to generate a risk model that was calibrated using Hosmer-Lemeshow. The test is available at http://www.riskcalc.org which has better predictive value than BMI alone. However, the history of previous VTE and hypercoagulable disorders were not included in the database [3]. In fact, thrombophilia has been shown in some reports to be prevalent in obese patients and thus could be an important risk factor for development of VTE in these patients [21]. For example, Hollander et al reported protein S deficiency to be significantly more prevalent in obese patients versus controls (2.97% versus 0.21%) [1] .
Association of PC and AT levels in the early phase of STEMI treated with pPCI with LV systolic function and 6-month MACE
Published in Acta Clinica Belgica, 2021
Slobodan Obradovic, Edin Begic, Slobodan Jankovic, Radoslav Romanovic, Nemanja Djenic, Boris Dzudovic, Zoran Jovic, Dragana Malovic, Vesna Subota, Milena Stavric, Farid Ljuca, Zumreta Kusljugic
Antithrombin III (AT III) inhibits serine proteases. Its anticoagulant activity is mainly due to the inhibition of thrombin, activated factor X (FXa) and, to a lesser degree, other activated clotting factors (FIXa, FXIa, and FXIIa) [4]. It has been established that heparin potentiates AT III effect [5]. The most common manifestations caused by the deficiency of PC, protein S, AT III and aPC are deep vein thrombosis of the lower extremities, accounting for approximately 90% of all venous thrombotic episodes and pulmonary embolism [6]. Furthermore, deficiency of PC, protein S and AT III significantly increase the risk of venous thromboembolism (VTE) only in the presence of other risk factors (immobilization, surgery, trauma, pregnancy). AT III values are decreased after administration of heparin due to degradation of the ternary complex [4]. Only few studies and case reports have discussed the implications of thrombophilic defects in arterial thrombosis. The results are controversial. In one study, arterial events were diagnosed in 8% of 144 subjects with PC or protein S deficiency, and 1% of 94 subjects with AT III deficiency [7]. Many researchers examined whether deficiencies in PC, protein S, and AT III are related to the incidence of acute myocardial infarction [8–10], but this relationship has never been clearly established. In another study, PC has been shown to play a protective role against ischemic stroke, but not against myocardial infarction [11]. Early formation of aPC and PC inhibitors can be detected in patients diagnosed with non-ST-elevation myocardial infarction (NSTEMI) who have troponin I values within a normal range [12]. Therefore, measurements of aPC and PC might provide opportunities for additional risk assessment of the acute coronary syndrome [12]. In one case report, for example, the PC deficiency was shown to be a significant risk factor in young patients with myocardial infarction [13].