Traitements spécifiques au milieu psychiatrique et thrombogenèse

Abstract

The causes of venous thrombosis (DVT) are multifactorial. Psychiatric patients present several etiologic features. Our objective was to determine the role of specific treatments of the psychiatric community on thrombogenesis. retrospective, descriptive and analytical study of 20 cases of DVT in psychiatric patients. We searched MEDLINE (PubMed) between 1959 and 2009. We reviewed article titles and abstracts and full text of selected studies of psychiatric patients with venous thromboembolism (VTE) disease. We identified 31 studies that investigated the association between psychiatric disease and venous thromboembolic events. Our population was young, with an average age of 44.8 years. Lower limb VT is predominant (16 cases). The most common psychiatric disorders are: anxiety-depression (12 cases), unclassifiable psychotic disorders (seven cases) and major depressive disorder (five cases). Their average duration was of 6.4 years. Seventy percent of our patients were taking first generation neuroleptics (NLP), of short half-life (13/14 cases) and at high doses (11/14 patients). Our sample is characterized by the frequency of thrombophilia (45%) and detention in a psychiatric community (35%). Our results are relatively consistent with aggregate data from the literature, underlining a facilitating and pejorative role of the psychiatric community with regard to venous thromboembolic disease. In the psychiatric community, venous thromboembolic disease is conditioned by a combination of several thromboembolism risk factors: linked in part to the psychiatric illness itself; but above all to the specific therapeutic methods in the psychiatric community (antipsychotics, restraint…) which are easily preventable. The relationship between antipsychotic medication and VTE was first suggested about four decades ago, only a few years after the introduction of phenothiazines and reserpine. An association between atypical antipsychotic agents and VTE has been previously suggested for clozapine among young adults with psychiatric disorders. More recently, an increased risk of VTE was suspected for olanzapine or risperidone. The risk for VTE seems to be highest during the initial months of treatment with antipsychotics. Several biological mechanisms of action have been proposed to explain this relationship. One plausible mechanism derives from research suggesting that conventional antipsychotic drugs are associated with enhanced platelet aggregation. A second possible explanation stems from the presence of anticardiolipin antibodies, which increase the risk of venous or arterial thrombosis, as well as in some patients prescribed chloropromazine. A third hypothesis is that venous stasis exacerbated by sedation, commonly found in patients treated with low-potency antipsychotic drugs, may contribute to processes that increase the risk of thrombosis. Other than the medical aspect, the psychiatric community itself is characterized by a large number of variables, providing a particularly encouraging and derogatory hypothesis on the advent and development of VTE.