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R Hervé

Publications and source records attributed to R Hervé.

12 recordsLinked to original sources

[Thromboembolic disease and cancer].

Many anomalies in primary haemostasis, coagulation and fibrinolysis have been described which favour thrombosis in cancer patients. Cancer is often associated with other risk factors for thromboembolism which explain much of the increased frequency of thrombosis in these patients. Thromboembolism may precede cancer and sometimes is the inaugural manifestation leading to the diagnosis of cancer. Cancer occurs more frequently in patients with idiopathic recurrent venous thrombosis than in those with thrombosis due to other risk factors for thromboembolism. The results of antivitamin K therapy are disappointing: in retrospective series, recurrent thromboembolism occurred in 9% of the treated patients and severe haemorrhage in 27%. New therapies should be assessed in cancer patients with thromboembolism.

Anticoagulants

Simultaneous progressive multifocal leukoencephalopathy, Epstein-Barr virus (EBV) latent infection and cerebral parenchymal infiltration during chronic lymphocytic leukemia.

We report a non-HIV patient who had B chronic lymphocytic leukemia (CLL) with progressive multifocal leukoencephalopathy (PML) and diffuse cerebral leukemic parenchymal infiltration in the presence of JC virus and Epstein-Barr virus (EBV) cerebral co-infection. Multiple subcortical hypodensities lining the cortico-subcortical junction were present within the white matter on computerized tomography (CT) scan, with large areas of high signal intensity on T2-weighted sequences on magnetic resonance imaging (MRI). JCV DNA was identified in peripheral blood nuclear cells and cerebrospinal fluid polymerase chain reaction (PCR) DNA/DNA hybridization plus Southern blot analysis. Frontal stereotactic biopsy confirmed the diagnosis of PML by immunocytochemistry, in situ hybridization (ISH) with JC Enzo probe and electron microscopy. Leukemic B cells with the same phenotype as leukemic blood cells were disseminated in the demyelinated areas. They were labeled by anti-latent membrane protein and by BamHl W EBV probe after ISH. Adhesion and activation molecules were positive for CD23. Autopsy showed diffuse visceral leukemic infiltration without acutization. EBV-transformed B lymphocytes would favour JCV penetration and/or intracerebral reactivation of previously latent JCV infection with further development of simultaneous PML and cerebral CLL infiltration in an immunosuppressed patient.

B-Lymphocytes

[Cervical mucus].

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Antigens