P e r f o r m a n c e o f P r o t h r o m b i n -P r o c o n v e r t i n T i m e a s a M o n i t o r i n g T e s t o f O r a l A n t i c o a g u l a t i o nT h e r a p y Oral anticoagulation therapy (OAT) with vitamin K antagonists (VKA) is most commonly monitored with the prothrombin clotting time (PT), which is sensitive to decreases in activity of any of the v i t a m i n K-dependent coagulation factors (F), II, VII, or X, as well as to decreases in fibrinogen or coagulation factor V (FV). 1 In the past, the PT was usually reported as a ratio of patient to control plasma clotting times (PT-ratio), but a system of international standardization was developed because of variability in clotting times obtained with different thromboplastins and variability in the methods of reporting the results. Accordingly, for the purpose of OAT control, PT results are now generally reported as international normalized ratios (INRs), 2 ' 3 ie, PT ratios are transformed to the ratio that would have been obtained if a standard reference thromboplastin preparation with an assigned international sensitivity index (ISI) of 1.0 had been used.
2,3When the PT is not done on fresh samples, a prolongation of the clotting time may occur from ex vivo factor V degradation (if plasma is stored at room temperature for more than 6 hours), whereas artifactual shortening may occur because of cold activation of FVII if plasma is stored at 4°C. 4 One way to circumvent these problems is to apply the prothrombin-proconvertin time (PP or P&P) on plasma kept at room temperature. The PP is a modified PT that is only sensitive to changes in FTJ, FVII, and FX because addition of adsorbed bovine plasma to the thromboplastin supplies the test mixture with optimal amounts of fibrinogen and FV for clot formation.5 When the PP is done on dilute patient plasma, it is also insensitive to direct anticoagulants, such as the lupus anticoagulant or heparin.6 ' 7 The PP results traditionally have been reported as the percentage of total coagulant activity of HI, FVII, and FX based on a dilution curve of normal plasma and not as clotting time ratios (or INR). This complicates the interpretation of anticoagulation intensity in relation to PT-based results and may be one reason for the decreasing use of the PP as a monitoring device. Also, although the PP is derived from the PT, clinical studies using the INR calculated directly from the PP are lacking. In clinical studies using the PP, conversions to INR have 672 Downloaded from https://academic.oup.
A 36-year-old male was evaluated for treatment-resistant hypertension. A high platelet count 828 x 10(9).l-1, led to the diagnosis of essential thrombocythemia (ET). Aorto-renal angiography revealed critical bilateral renal artery stenosis and coronary angiography showed three-vessel disease. Percutaneous transluminal renal angioplasty was only partially successful. The patient received a 12-week course of busulphan and subsequently the thrombocyte count decreased to 200 x 10(9).l-1. Renal angiography 12 months later showed bilateral regression of the renal artery stenosis with lowering of the blood pressure to normal levels.
In a randomized, cross‐over study 27 patients had diastolic blood pressure of ≥ 96 mmHg during four visits without treatment. Following captopril 25 mg b.i.d. nine patients' blood pressure was ≤ 90 mmHg. The remaining 18 were randomized into two treatment modalities, captopril and moderate dietary salt reduction, and captopril and hydrochlorothiazide 25 mg daily. Following a wash‐out period the groups crossed over to the alternative treatment. At the end of the control period the average blood pressure was 151/100 ± 12/6 mmHg recumbent and 140/91 ± 11/7 standing, following captopril 144/94 ± 13/5 and 132/92 ± 12/6, respectively, with low salt diet addded to captopril 140/91 ± 12/6 and 128/89 ± 11/6 and with hydrochlorothiazide and captopril 133/86 ± 12/7 and 120/84 ± 11/7 mmHg supine and erect, respectively. It is concluded that moderate dietary salt reduction, which is easily advised, will significantly potentiate the blood pressure fall following captopril treatment in moderate arterial hypertension.
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