Biomedical subjects
Publications and source records attributed to C Boinot.
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INTRODUCTION: We conducted a prospective study to determine the prevalence and the prognosis of antiphospholipid syndrome (APS) in patients with retinal venous occlusion (RVO). PATIENTS: Consecutive patients presenting with retinal vein occlusion were screened for vascular risk factors (diabetes mellitus, hypertension, hyperlipidemia) and for antiphospholipid antibodies (aPL): anticardiolipin (aCL), anti-beta2-glycoprotein I, and lupus anticoagulant. Patients with a serum sample positive for aPL returned at least 6 weeks later for a new screening to determine the prevalence of antiphospholipid syndrome. All patients were followed to determine the outcome. RESULTS: Sixty-eight patients presented with RVO, 16 had vascular risk factors for RVO. After two screenings for aPL, nine cases of antiphospholipid syndrome associated with RVO were diagnosed (13.2%). Eight patients were over age 50 years and none had a previous thrombotic event before RVO. All patients were treated with aspirin (160 mg/day). With a mean follow-up of 26.1+/-8.2 months (range, 16-36 months), there were no recurrences. CONCLUSION: Retinal venous occlusion is multifactorial in origin. In patients aged 50 years and older, without previous thrombotic event, aPL might not be predictive of recurrences and treatment with aspirin might be sufficient. In such patients, the routine screening for aPL does not appear warranted, but a randomized study should be conducted to really ascertain the pathogenic role of aPL and the most appropriate treatment in RVO.
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This prospective multicentric register was initiated by the European Forum of Antiphospholipid Antibodies (APL) in 2003 after approval by local ethic committees. This register allows the investigation of infants after written informed parental consent. It collects mothers' clinical pattern of antiphospholipid syndrome (APS), course and outcome of pregnancy, treatment and immunological status. For the babies, clinical and immunological examinations are performed at birth; neurodevelopmental conditions followed up to five years. A re-evaluation of lupus anticoagulant (LA), anticardiolipin (ACL) or other antibodies will be done if they are positive at birth to follow their kinetics. A descriptive and a case control study of babies with versus without APL at birth will be possible after the inclusion of 300 cases.
Lepirudin is an alternative anticoagulant therapy in heparin-induced thrombocytopenia (HIT) during cardiopulmonary bypass (CPB). We report a case of a female patient with HIT referred for aortocoronary bypass graft despite persistence of antibodies to platelet factor 4-heparin complexes. Anticoagulation management is described. Whole blood hirudin concentration attempted during CPB was above 4 microg ml(-1). To obtain this concentration, lepirudin administration was managed as follows: 0.1 mg kg(-1) h(-1) lepirudin during preoperative course, 0.2 mg kg(-1) bolus just before CPB and 0.2 mg kg(-1) in the priming solution, complementary boluses of 5 and 10 mg during procedure (according to whole blood ecarin clotting time). Aprotinin was administered simultaneously according to Royston protocol. Anticoagulation was monitored with whole blood ecarin time performed in the operation room (patient's whole blood was diluted one half and one third with normal whole blood; in vitro calibration curve was constructed using normal whole blood spiked with lepirudin). CPB duration was 73 min. When measured, whole blood hirudin concentration was 3.8-5.8 microg ml(-1). Total lepirudin administration was 44 mg. No haemorrhagic or thrombotic events were observed during surgical procedure and postoperative course. Despite lepirudin administration is not yet clearly precise for CPB procedure, its use seems adapted and safe in subjects without renal insufficiency but requiring precise coordination for anaesthesiological, surgical and biological teams.
Population-based case-control studies and cases previously published suggest that the prothrombin G20210A mutation is a weak risk factor for thrombosis, leading to clinical expression mainly in the presence of other risk factors. We report the results of plasma and genetic analyses performed in a 13-year-old symptomatic boy homozygous for the 20210A allele and in his family, which are in accordance with this suggestion. These analyses demonstrated the presence of several PROC (R-5W, R87H) and PROS (R60C, T103N) gene mutations in this family. These additional mutations have modulating effects on clinical expression of the G20210A mutation. The present family study illustrates the concept of 'mild' mutation and the hypothesis that familial thrombophilia is a multifactorial disease.
There is no consensus concerning thromboembolic prophylaxis in high-risk pregnant women with a previous history of heparin-induced thrombocytopenia. An alternative anticoagulant therapy is danaparoïd, whereas unfractioned and low-molecular-weight heparin therapy is contraindicated. We report a case of successful thrombosis prophylaxis using danaparoïd in a high-thrombosis-risk pregnant woman with a history of heparin-induced thrombocytopenia during a previous pregnancy and Widal's disease.
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Plasma chlorophacinone determinations were performed in three cases of intoxication. The data collected in this study confirm the particularly prolonged anticoagulant effect of this compound and show that the knowledge of plasma concentrations may be very useful for clinicians since it allows to confirm the diagnosis and to evaluate the duration of the treatment. The determination of half-lives was investigated and the results indicate that the greater the quantity absorbed, the longer the half-life. The effect of phenobarbital on the elimination of cholorophacinone could be studied in one case. An increased elimination was noted when phenobarbital was administered.
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Platelets from a patient with the Hermansky-Pudlak syndrome were studied. These platelets had decreased amounts of serotonin and adenine nucleotides, and a decreased number of mepacrine-labeled dense bodies. beta-Thromboglobulin and acid hydrolases contained in alpha-granules and lysosomes respectively were present in normal amount. Platelets in platelet-rich plasma did not respond to collagen, but arachidonic acid and ionophore A 23187 induced normal aggregation and normal thromboxane (TX) synthesis. Alpha-granule release was found impaired and remained subnormal even with high doses of inducers. In response to thrombin aggregation, release and TX synthesis of isolated metrizamide gradient platelets were found at lower than normal levels. Phosphorylation of P20 and P43 proteins was normal. Only a combination of ADP plus thrombin could restore a normal aggregation, with normal alpha-granule and lysosome release and normal TX synthesis. These results indicated that in the absence of dense bodies: the release of other granules is impaired; the TX synthesis is delayed except when induced by arachidonic acid and A 23187 ionophore; the absence of dense bodies could be compensated for by the addition of ADP which restores the impaired release reaction and TX formation; and P20 and P43 polypeptides were phosphorylated as rapidly as those in normal platelets.
Two case-reports of thrombopenias induced by pentosane polysulfate (PSP) are reported. PSP may play a direct role in the genesis of the thrombopenia appearing between the 5th and 15th day of treatment, or a sensitizing role where the thrombopenia occurs quite rapidly following heparin treatment. The clinical complications are haematomas, arterial or venous thromboses and haemorrhages. The platelet aggregation test is always positive in the presence of PSP. The immunological origin is probable. Monitoring of the platelet count is recommanded with this treatment.
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BACKGROUND: Cerebral thrombosis associated with protein S deficiency is very rare and is mainly related to hereditary form of protein S deficiency. CASE REPORT: A 19-year-old girl with acute lymphoblastic leukemia presented hemianopsy within a few days after the first administration of L-asparaginase. Magnetic resonance of the brain showed a cortical infarct. A marked decrease of the level of protein S was documented. Few days later, the patient was free of symptoms and protein S level was restored to the normal suggesting that the cerebral thrombosis was caused by transient protein S deficiency induced by L-asparaginase administration. DISCUSSION: Patients with neurological complication caused by L-asparaginase should be tested for protein S and other anticoagulant deficiencies.