Search

SummaryWithout thromboprophylaxis, knee arthroscopy (KA) carries a low to moderate risk of venous thromboembolism. Over 5 million arthroscopies are performed worldwide yearly. It was our study objective to assess the efficacy and safety of rivaroxaban for thromboprophylaxis after therapeutic KA. Patients undergoing KA in nine Italian teaching or community hospitals were allocated to once-daily rivaroxaban (10 mg) or placebo for seven days in a phase II, multicentre, double-blind, placebo-controlled randomised trial. The primary efficacy outcome was a composite of all-cause death, symptomatic thromboembolism and asymptomatic proximal DVT at three months; major bleeding represented the primary safety outcome. All patients underwent whole-leg ultrasonography at day 7(+1), or earlier if symptomatic. A total of 241 patients were randomised (122 rivaroxaban, 119 placebo), and 234 completed the study. The primary efficacy outcome occurred in 1/120 of the rivaroxaban group and in 7/114 of the placebo group (0.8% vs 6.1%, respectively, p=0.03; absolute risk difference, −5.3%, 95% CI, −11.4 to −0.8; crude relative risk 0.14, 95% CI, 0.02 to 0.83; number-needed-to-treat=19). No major bleedings were observed. We found no association between different arthroscopic procedures and thrombotic events. Small sample size, high exclusion rate, and low number of anterior cruciate ligament reconstruction procedures are the main limitations of our study. In conclusion, a seven-day course of 10-mg rivaroxaban may be safely employed for thromboprophylaxis after KA. Whether prophylaxis after KA should be given to all patients, or to selected “high-risk” subjects, remains to be determined. A larger trial to verify our preliminary results is warranted.

We investigated the behavior of prothrombin fragment F1+2 and thrombin-antithrombin complexes in 70 patients treated with chronic anticoagulant therapy. Moreover, in a longitudinal study 37 patients were evaluated twice and 16 patients three times. Twenty-eight age-and sex-matched healthy subjects were also studied as a control group. Prothrombin fragment F1+2 and thrombinantithrombin complexes were significantly higher in controls than in patients on anticoagulants. There were no differences in prothrombin fragment F1+2 or thrombinantithrombin values among patients with different International Normalized Ratios, nor in the same patients studied two or three times. Our results confirm that oral anticoagulant treatment can effectively reduce thrombin activity. However, strong anticoagulation does not induce a further significant decrease in fragment F1+2 values. Therefore, we feel measurement of fragment F1+2 might be less useful than thought in optimizing oral anticoagulant therapy.

In 1959 a modified PT was introduced for monitorig oral anticoagulant therapy, the so-called Thrombotest (l). Thrombotest reagent is made of a brain thromboplastin together with bovine adsorbed plasma with constant amount of factor V and fibrinogen. The test can be performed using whole blood employing the manual tilt tube tecnique. Since only a thermostatic bath, rnicropipettes and a stop-watch are neede.d, “Thrombotest method” still represents a cheap and easy way for monitoring oral anticoagulant therapy. This means that the management of small groups of patients could be done even in country side out-patients Thrombosis Services without a more complex laboratory equipment such as centrifuge and coagulometer. We think that the matter is of interest since many patients encounter difficulties in coming periodically to city-centres. This problem is particularly relevant for the elderly. In fact they have oilen not prescribed oral anticoagulants since they live too far born the main centres, being of course impossible a correct monitoring of therapy. The aim of this study was to investigate whether the “old manual thrombotest tecnique” shows an agreement with the new adopted fast automated PT tecnique performed with a coagulometer in main hospital laboratories.

We have performed the BT test in 55 patients undergoing oral anticoagulant therapy monitored by means of Thrombotest (TT). Patients in steady state of anticoagulation showed longer BT than normal controls; patients in overdose phase had longer BT values than either controls or patients in steady state. After recovery the overdose phase patients showed BT values not different from those of the controls. Moreover we were able to find in our patients a significant linear correlation between BT and TT. Impairment in primary haemostasis could be due either to a scarce fibrin deposition in the haemostatic plug or to deficiency of a possible vitamin K dependent vascular "bleeding factor".

Plasma Bβ 15–42 and fibrinopeptide A (FPA) concentrations, which are respectively indicators of plasmin and thrombinin vivo activity, were measured in 46 patients with ischemic arterial disease without signs of acute thrombosis. In the group as a whole, an increase in both Bβ 15–42 and FPA was found. When the patients were divided in two groups on the basis of their reversible (transitory ischemic attacks and unstable angina) or irreversible (stroke and myocardial infarction) ischemic episodes, the levels of Bβ 15–42 were significantly elevated only in the former group when compared to controls (p

SummaryThe aim of this study was to compare recombinant thromboplastin (rTF, ISI = 0.82) with rabbit thromboplastin (RT, ISI = 1.46) in order to evaluate which performed better in our thrombosis centre. To this purpose we randomized 67 patients to be double-blind monitored in two groups for three months either with PT performed with RT or with PT performed with rTF. After this period each patient was shifted to the other group. We considered the following as end points of the study: percentages of PT results within the therapeutic range, number of visits and therapeutic dose adjustments per patient. The “last check in file” method was used to evaluate the laboratory quality of oral anticoagulation for both thromboplastins. The results show that there was no difference in the number of visits per patient between the two groups: 6.9 ± 1.7 in the rTF group versus 7.3 ± 1.9 in the RT group (p = 0.19). The variations of therapeutic dose per patient were not different in the two groups: the dose was changed once (range 0-8) in the rTF group and once (range 0-11) in the RT group (p = 0.15). The percentages of PT results within the therapeutic range were not different between the two groups. The “last check in file” method showed similar percentages in both groups: PT results in the therapeutic range were 67.2% in the RT group and 68.8% in the rTF group. We conclude that the two thromboplastins had a similar effect on the end points of the study in spite of the relatively high ISI of the RT.

The aim of our study was to investigate the effect of a diet with a known vitamin K content on the monitor test for oral anticoagulant therapy. We studied 10 poorly controlled patients (7 women and 3 men, mean age 48+15 years) in therapy with acenocoumarol for at least 1 year. Another group of 10 poorly controlled patients was considered as a control group. After a baseline period, during which a free diet was allowed, patients were administered a diet with a controlled vitamin K content; in the same period, control subjects were not subjected to any dietary restriction. Thrombotest (Nyegaard, Oslo) was employed for monitoring oral anticoagulant therapy, with a therapeutic range between 2.3 and 4.8 INR. We found a significant difference by thrombotest between the percentages within the therapeutic range obtained before and during dietary treatment (p = 0.0001). The difference in percentages was -0.31 and the 95% CI, of the difference ranged from -0.45 to -0.17. No significant difference was shown in the control group in the same periods. Our data suggest that a diet with a controlled vitamin K content is effective in increasing the percentage of tests within the therapeutic range in patients with poorly controlled anticoagulation.

SPARC (secreted protein acid and rich in cysteine), also known as osteonectin or BM-40, is a glycoprotein associated with the extracellular matrix of bone as well as with many soft tissues that produce extracellular matrix, including matrix-producing tumours. Northern and slot-blot analyses were used to study SPARC expression in tumours induced in vivo by methylcholanthrene (MCA) and in transformed cells induced in vitro by Kirsten-MSV and SV-40 infection. MCA-induced tumours expressed SPARC mRNA at quantitatively different levels. Fibroblasts transformed in vitro by Kirsten-MSV, and, to a lesser extent, by SV-40, showed reduced levels of SPARC mRNA expression compared with normal fibroblasts. Run-on assay indicated that transcription of SPARC was lower in the Kirsten-MSV transformed cells than in the normal parental fibroblast culture. However, SPARC mRNA in the transformed culture was as stable as that in normal culture. The difference, therefore, between levels of SPARC mRNA in transformed and normal culture was mainly due to different rates of transcription. Cloned cell lines derived from the Kirsten-MSV transformed culture also showed heterogeneous expression of SPARC: two lines had high and two had low expression of the gene. The level of mRNA correlated with that of the protein secreted. The SPARC expression might contribute to the malignant phenotype.