scholarly journals Plasma levels of protein C and vitamin K-dependent coagulation factors in patients on long-term oral anticoagulant therapy.

1986 ◽  
Vol 149 (4) ◽  
pp. 351-357 ◽  
Author(s):  
HOYU TAKAHASHI ◽  
MASAHARU HANANO ◽  
SENJI HAYASHI ◽  
YUTAKA ARAI ◽  
NORIKO YOSHINO ◽  
...  
Keyword(s):  
Anticoagulant Therapy ◽  
Vitamin K ◽  
Plasma Levels ◽  
Oral Anticoagulant ◽  
Protein C ◽  
Oral Anticoagulant Therapy ◽  
Coagulation Factors

Suspension of Vitamin K Antagonists Is Not Required for Cataract Surgery: A Prospective Study in a Cohort of 135 Consecutive Patients on Long-Term Anticoagulant Therapy.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 882-882
Author(s):  
Berardino Pollio ◽  
Giuseppe A. Demarie ◽  
Patrizia Ocello ◽  
Grazia Delios ◽  
Marco Tucciarone ◽  
...  
Keyword(s):  
Cataract Surgery ◽  
Anticoagulant Therapy ◽  
Vitamin K ◽  
Oral Anticoagulant ◽  
Oral Anticoagulant Therapy ◽  
Vitamin K Antagonists ◽  
Management Service ◽  
Corneal Incision ◽  
Standardized Protocol

Abstract The perioperative management of oral anticoagulant therapy (OAT) often arouses controversy between surgeons and internists. In geriatric patients, cataract surgery for those who are taking vitamin K antagonists is a common clinical procedure. Phacoemulsification requires a 3 mm incision involving a tissue devoid of blood vessels. This study reports the experience of an Italian Anticoagulation Management Service (AMS) with 135 anticoagulated patients on long-term anticoagulant therapy who underwent phacoemulsification performed by the same ophthalmologist team from January 2001 to December 2005. The patients received either topical (30%) or peribulbar (70%) anaesthesia. Data were collected by physicians with specialized software, but the dosage of oral anticoagulant was manual. Two oral vitamin K antagonisists are available in Italy: acenocumarol and warfarin. We prepared all patients in accordance with the following standardized protocol : the scheduled dose was always omitted the day before surgery an INR measurement was provided 3–5 days before the invasive procedure; if the patient’s INR was below 3, we simply omitted the scheduled dose of the day before cataract surgery if the patient’s INR was above 3, we withheld two or more scheduled doses to allow the INR to fall to 2.5 or less 1 hour before cataract surgery, INR was measured if the patient’s INR was below 2.5, phacoemulsification was performed Results: This standardized procedural protocol allowed the surgeon to carry out phacoemulsification with INR always below 2.5. We observed only one peribulbar bleeding (0.7%) during peribulbar anaesthesia before the corneal incision was made. No thromboembolic complications were registered during three months of follow up. We compared our results with the data of an earlier cohort of 7014 conventional patients who underwent this eye surgery in the same ophthalmologic institute. We did not observe statistical differences between the two groups with regard to hemorragic complications. Conclusions: The risk of thromboembolism when antithrombotic therapy is interrupted is a well-grounded concern, particularly for patients with mechanical heart valves. Low molecular weight heparin bridging is a valid but more complicated alternative. Our study demonstrates the feasibility and safety of this simple standardized protocol which avoids OAT interruption. Therefore, we conclude that in patients receiving OAT, it is not necessary for the anticoagulant effect to wear off before cataract surgery is performed.

ACUTE INTERRUPTION OF ORAL ANTICOAGULANT THERAPY: A THROMBOTIC RISK?

1987 ◽  
Author(s):  
J Rouvier ◽  
H Vidal ◽  
J Gallino ◽  
M Boccia ◽  
A Scazziota ◽  
...  
Keyword(s):  
Anticoagulant Therapy ◽  
Vitamin K ◽  
Oral Anticoagulant ◽  
Protein C ◽  
Oral Anticoagulant Therapy ◽  
Factor Vii ◽  
Factor X ◽  
Functional Protein ◽  
Thrombotic Risk ◽  
Factor Ii

It is still on discussion how oral anticoagulant therapy must be interrupted. A progressive diminution of drug intake have been proposed in order to avoid a MreboundM of vitamin K-dependent procoagulant factors. At the present, it is well known that coumarin drugs affect not only the biologic activity of factors II, VII, IX and X but also Protein C (PC), an inhibitor of coagulation kinetics, and their cofactor Protein S. With the aim to determine the recovery level of PC in relation with the others vitamin K-dependent factors, the effect of suppression of anticoagulant therapy in patients under chronic treatment with acenocoumarin was studied.Quick time, functional factors II, VII, X (one stage methods), functional PC (Francis method) and immunological Factor II and Protein C (Laurell) were determined before and 36 hours after suspension of acenocoumarin administration.Results showed that: 1) Recovery levels of functional Protein C (increased from 28.55% ±2.57 to 72.64% ±5.9) were significantly higer than functional Factor II (22.09% ±2.34 to 30.73% ±8.64), Factor VII (22.55% ±2.01 to 40.73% ±4.85) and Factor X (23.27% ±2.66 to 39.18% ±3.19). Statistical analysis (Newmann-Keuls test) showed at least a p<0.01 between PC increase and factors II, VII or X increment.2) No significant differences were seen between immunological levels of Factor II before and after suspension of acenocoumarin.3) Levels of immunological PC in patients under anticoagulant therapy were higer than functional PC. After acenocoumarin suppression, not correlation was seen between immunological and functional Protein C recovery.It is concluded that acute suppression of acenocoumarin does not induce a thrombotic tendency because the recuperation of functional Protein C is more important than factors II, VII and X recovery.

RESPONSE OF PROTEIN C AND PROTEIN S INHIBITORS IN LONG-TERM ORAL ANTICOAGULANT THERAPY

1987 ◽  
Author(s):  
M Mukhlova Montiel ◽  
H Bussey
Keyword(s):  
Anticoagulant Therapy ◽  
Oral Anticoagulant ◽  
Protein C ◽  
Oral Anticoagulant Therapy ◽  
Anticoagulation Therapy ◽  
Protein S ◽  
Factor Vii ◽  
Control Group ◽  
Statistical Regression

Protein C (PC) and its coenzyme Protein S (PS) are physiologic inhibitors of activated factors Va and Villa. Deficiency of either one of these inhibitors has been associated with venous thrombosis. Their activity is dependent on vitamin K for hepatic gamma carboxylation and it is depressed during oral anticoagulant therapy. Because rebound thrombosis complicates cessation of anticoagulant therapy, we investigated the response of PC and PS during long term oral anti coagulation. The study encompassed 30 patients ranging between 26 and 76 years of age, who have received therapeutic doses of coumadin from 15 days to more than 8 years. The conditions for which treatment was initiated were deep vein thrombosis, cerebral vascular accidents and cardiac valve replacements.Factor VII and X activity was assayed by one step routine clotting assays. PC antigen (ag), total PSag and free PSag were assayed by Laurel 1 Rocket electroimmunodiffusion method. The measurement of the free PS was carried out after precipitation of C4b-binding protein with polyethylene glycol. PC activity was measured by clotting assay using PC deficient plasma to which was added patient plasma as a source of PC. Control group of 30 individuals in similar age group were assayed parallel with the patient samples. Compared with the control group the coumadin-treated patients showed substantial decrease of all factors studied. Statistical regression analysis of the coumadin group showed a significant increase in PS free (p = 0.014)during long term anti coagulation, while all of the other variables did not change significantly.PCag and total PSag were decreased and their activities, as expected, were more severely affected. The ratio of PC activity to PCag averages 0.39 (normal >0.80) and free PS represented only 27% of the total PSag (normal about 40%). The inhibitors' persistent activity parallels that of the depression of Factors VII and X and there appears to be a balanced coagulation-inhibi-tion system. If PC and PS play a role in rebound thrombosis after a prolonged anticoagulation therapy, the changes may occur after discontinuation of medication.

Oral anticoagulation reduces activated protein C less than protein C and other vitamin K–dependent clotting factors

Blood ◽  
2002 ◽  
Vol 100 (12) ◽  
pp. 4232-4233 ◽  
Author(s):  
Marleen J. A. Simmelink ◽  
Philip G. de Groot ◽  
Ronald H. W. M. Derksen ◽  
José A. Fernández ◽  
John H. Griffin
Keyword(s):  
Anticoagulant Therapy ◽  
Vitamin K ◽  
Oral Anticoagulant ◽  
Protein C ◽  
Anticoagulant Activity ◽  
Oral Anticoagulant Therapy ◽  
Activated Protein C ◽  
Clotting Factor ◽  
Factor X ◽  
Clotting Factors

Oral anticoagulant therapy, which is used for prophylaxis and management of thrombotic disorders, causes similar reductions in plasma levels of vitamin K–dependent procoagulant and anticoagulant clotting factor zymogens. When we measured levels of circulating activated protein C, a physiologically important anticoagulant and anti-inflammatory agent, in patients on oral anticoagulant therapy, the results unexpectedly showed that such therapy decreases levels of activated protein C substantially less than levels of protein C, prothrombin, and factor X, especially at lower levels of prothrombin and factor X. Thus, we suggest that oral anticoagulant therapy results in a relatively increased expression of the protein C pathway compared with procoagulant pathways not only because there is less prothrombin to inhibit activated protein C anticoagulant activity, but also because there is a disproportionately higher level of circulating activated protein C.

Long-Term Outcomes in Patients Undergoing Coronary Stenting on Dual Oral Antiplatelet Treatment Requiring Oral Anticoagulant Therapy

2008 ◽  
Vol 102 (12) ◽  
pp. 1618-1623 ◽  
Author(s):  
Roberta Rossini ◽  
Giuseppe Musumeci ◽  
Corrado Lettieri ◽  
Maria Molfese ◽  
Laurian Mihalcsik ◽  
...  
Keyword(s):  
Anticoagulant Therapy ◽  
Oral Anticoagulant ◽  
Oral Anticoagulant Therapy ◽  
Coronary Stenting ◽  
Long Term Outcomes ◽  
Antiplatelet Treatment

scholarly journals Compliance with and awareness about long-term oral anticoagulant therapy among Saudi patients in a University Hospital, Riyadh, Saudi Arabia

2016 ◽  
Vol 7 (1) ◽  
pp. 10 ◽  
Author(s):  
NervanaM. K Bayoumy ◽  
ShehanahFahad Al-Omair ◽  
NorahAhmed Musallam ◽  
NoraYazid Al-Deghaither ◽  
NoufAbdulwahab Al-Sadoun
Keyword(s):  
Saudi Arabia ◽  
Anticoagulant Therapy ◽  
Oral Anticoagulant ◽  
Oral Anticoagulant Therapy ◽  
University Hospital ◽  
Saudi Patients

Bleeding complications to long-term oral anticoagulant therapy

1994 ◽  
Vol 1 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Annette Lemche Gull�v ◽  
Birgitte Gade Koefoed ◽  
Palle Petersen
Keyword(s):  
Anticoagulant Therapy ◽  
Oral Anticoagulant ◽  
Oral Anticoagulant Therapy ◽  
Bleeding Complications

Inhibition of Activated Protein C Anticoagulant Activity by Prothrombin

Blood ◽  
1999 ◽  
Vol 94 (11) ◽  
pp. 3839-3846 ◽  
Author(s):  
Mikhail D. Smirnov ◽  
Omid Safa ◽  
Naomi L. Esmon ◽  
Charles T. Esmon
Keyword(s):  
Anticoagulant Therapy ◽  
Oral Anticoagulant ◽  
Protein C ◽  
Anticoagulant Activity ◽  
Oral Anticoagulant Therapy ◽  
Membrane Surface ◽  
Activated Protein C ◽  
Significant Risk ◽  
Thrombotic Risk ◽  
Factor Va

Abstract In this study, we test the hypothesis that prothrombin levels may modulate activated protein C (APC) anticoagulant activity. Prothrombin in purified systems or plasma dramatically inhibited the ability of APC to inactivate factor Va and to anticoagulate plasma. This was not due solely to competition for binding to the membrane surface, as prothrombin also inhibited factor Va inactivation by APC in the absence of a membrane surface. Compared with normal factor Va, inactivation of factor Va Leiden by APC was much less sensitive to prothrombin inhibition. This may account for the observation that the Leiden mutation has less of an effect on plasma-based clotting assays than would be predicted from the purified system. Reduction of protein C levels to 20% of normal constitutes a significant risk of thrombosis, yet these levels are observed in neonates and patients on oral anticoagulant therapy. In both situations, the correspondingly low prothrombin levels would result in an increased effectiveness of the remaining functional APC of ≈5-fold. Thus, while the protein C activation system is impaired by the reduction in protein C levels, the APC that is formed is a more effective anticoagulant, allowing protein C levels to be reduced without significant thrombotic risk. In situations where prothrombin is high and protein C levels are low, as in early stages of oral anticoagulant therapy, the reduction in protein C would result only in impaired function of the anticoagulant system, possibly explaining the tendency for warfarin-induced skin necrosis.

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