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ALCOLIZZAZIONE PERCUTANEA ECOGUIDATA DEL NODULO TIROIDEO TOSSICO E PRETOSSICO
No full textAbstract non disponibil
Decompensated porto-pulmonary hypertension in a cirrhotic patient with thrombosis of portocaval shunt
No full textWe report a case of decompensated porto-pulmonary hypertension closely associated with the development of intra-portocaval shunt thrombosis. A woman with Laennec's cirrhosis was hospitalized because of severe dyspnea and edema. She underwent surgical portocaval anastomosis ten years ago. Imaging studies showed massive intra-shunt thrombosis, portal hypertension, ascites, pleuro-pericardial effusions and enlargement of right cardiac cavities. Cardiac catheterization allowed to rule out coronary and left-sided heart abnormalities and led to the diagnosis of pre-capillary pulmonary hypertension. Antithrombotic treatment with low molecular weight heparin was instituted. The management also included ACE inhibitors, spironolactone, low-salt diet and lactulose. The patient was discharged and three months later we observed the disappearance of edema, ascites and pleuro-pericardial effusions, a marked body weight reduction and improved dyspnea and liver function tests. A possible link between the development of intra-shunt thrombosis and clinical decompensation in our patient was hypothesized. In fact, it has been demonstrated that the increased portal pressure, caused by occlusion of portosystemic shunt, reduces renal plasma flow and increases systemic endothelin-1 concentration. In our patient the disappearance of edematous state and improved dyspnea observed after recanalization of the shunt strongly support this hypothesis
Combined factor VIII and IX inhibitors in a non-haemophilic patient: successful treatment with immunosuppressive drugs
No full textA rare case of a patient with Sjogren syndrome and spontaneously acquired inhibitors of both factor VIII and factor IX is reported. Complete remission was obtained by means of immunosuppressive drugs
Thrombin - antithrombin III complexes as an additional diagnostic aid in pulmonary embolism
No full textThromboprophylaxis with reviparin in a patient with acquired hemophilia
No full textReviparin sodium is a low–molecular weight heparin with an anti–factor Xa:anti–factor IIa ratio of ≥3.6 and negligible effects on global clotting tests. It has been shown to be as effective as unfractioned heparin in different prophylactic indications, causing fewer injection-site hematomas as well [1]. Here we report the case of a patient with acquired hemophilia successfully treated with standard therapy plus reviparin.
A 65-year-old man with a history of renal adenocarcinoma was hospitalized with extensive subcutaneous hematomas; he was under treatment with antipsychotic drugs. Hemoglobin was 80 g/L, bilirubin 60.2 μmol/L (indirect: 34.7 μmol/L), and lactate dehydrogenase (LDH) 14.7 μkat/L. Activated partial thromboplastin time (aPTT) was 97 seconds, prothrombin time was normal, fibrinogen level was 6.60 g/L and D-dimer 1751 ng/mL. The patient received fresh frozen plasma, packed red blood cells, and methylprednisolone (0.5 mg/kg per day) without any benefit, then he was transferred to our department. Positive direct antiglobulin test results and low haptoglobin indicated the diagnosis of autoimmune hemolytic anemia. The prolonged aPTT of a mixture of a 1:1 volume of patient’s plasma with normal plasma at 37°C for 2 hours suggested the presence of coagulation inhibitors [2]. Specificity for factor VIII was shown by incubating serial dilutions of the patient’s plasma with an equal volume of normal plasma and performing assays of factor VIII, IX, and XI at 0, 60, and 120 minutes on each mixed dilution [3]. Only factor VIII decreased over time, and the inhibitor titer was 2.6 Bethesda units. The discrepancy between severe bleeding and low titer of antibodies was not surprising; in fact, Bethesda assay underestimates the levels of acquired inhibitors, because of the complexity of reaction kinetics and variation in antibody affinities [4]. On day 3, the patient’s hemoglobin level was 47 g/L; computed tomography revealed a hemothorax and a sub capsular hepatic hematoma. The patient received fresh frozen plasma, packed red blood cells, human factor VIII (bolus of 150 IU/kg plus continuous infusion of 10 IU/kg per hour, to a maximum of 9000 IU), prednisone (1 mg/kg per day), and antifibrinolytic treatment with tranexamic acid (500 mg intravenously 3 times a day) [4,5]. Antipsychotic drugs were withdrawn, because acquired inhibitors may be associated with these drugs. Thromboprophylaxis with subcutaneous reviparin (4200 IU/d) was started, because of the evidence of ongoing intravascular fibrin formation (D-dimer elevation), risk factors for thrombosis (eg, immobilization), and the hemostatic imbalance induced by antifibrinolytic treatment. Although thrombotic events are unusual in acquired hemophilia, there has been a case report concerning pulmonary embolism associated with tranexamic acid therapy [6].
On day 9 aPTT was 85 seconds; there were no signs of active bleeding, but persisting hemolysis was demonstrated by laboratory tests. The patient was started on high-dose intravenous immunoglobulin G (400 mg/kg per day x 5 days, followed by periodic maintenance doses), which resulted in a sudden shortening of aPTT and reduction of the inhibitor titer [7]. On day 63, aPTT was 43 seconds, hemoglobin 108 g/ L, and inhibitors were undetectable. Any recurrence of renal malignancy was ruled out. One month after discharge the aPTT was 30 seconds, fibrinogen 4.46 g/L, D-dimer 342 ng/ mL, bilirubin 5.0 μmol/L, LDH 4.3 μkat/L, haptoglobin 1.83 g/L, and hemoglobin 127 g/L, showing a complete recovery.
In conclusion, antifibrinolytic therapy is of proven benefit in the treatment of bleeding episodes in patients with acquired hemophilia [5]. Nevertheless, tranexamic acid contributes to an increased thromboembolic risk in this setting. In our patient, prophylaxis with reviparin was safe and effective in the prevention of thrombotic events, without any evidence of bleeding complications
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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