Annales de medecine interne最新文献

Placental vascular diseases consist of obstetrical pathologies assumed to be linked to placental ischemia. Preeclampsia, defined as the association of hypertension, proteinuria and edema, occur in 3% of deliveries, in a non-selected population. Eclampsia, defined as the occurrence of convulsions in preeclamptic women, occur in 5 per 10,000 deliveries. Risk factors for preeclampsia are: preeclampsia in the previous pregnancy, maternal age <20 years, multiple pregnancies, and nulliparity. Placenta abruption, defined as premature separation of the placenta before delivery, occur in 5 to 15 per 1,000 deliveries. Risk factors are smoking, infertility, and preeclampsia or placental abruption in the previous pregnancy. Stillbirth, defined as fetal death between 24 weeks of gestation and delivery, occur in 1.5 per 1,000 deliveries, with a higher frequency in case of placental abruption, intrauterine growth restriction or preeclampsia.

We analyzed the statistical relationship described between the principal laboratory anomalies related to thrombophilia and obstetrical pathology and risk of maternal thromboembolism.

Objective: We designed a controlled study comparing referred women with an eating disorder (ED) to a matched normal control group to answer the following questions: what are the frequencies of anxiety disorders (AD) in anorexia nervosa (AN) and bulimia nervosa (BN), according to DSM-IV criteria? Are AD significantly more frequent among women with an ED than among women from the community?

Method: We assessed frequencies of six specific AD among 271 women with a current diagnosis of AN or BN and 271 controls, using the Mini International Neuropsychiatric Interview (MINI), French DSM-IV version.

Results: Seventy-one percent of both the AN and the BN subjects had a lifetime comorbidity with at least one AD, significantly more (p<0.001) than the percentage of controls with an AD. Prevalence was significantly higher in the ED groups than in controls for most types of AD, and between 41.8% and 53.3% of comorbid cases had an AD preceding the onset of the ED.

Conclusion: Evidence that AD are significantly more frequent in subjects with ED than in the community has important etiological and therapeutic implications.

Pregnancy and puerperium are well-known risk factors for venous thromboembolism, but the actual incidence of the disease is low (about 1/1,500 pregnancies). Pregnancy-associated venous thromboembolism is rare, though it is still the second cause of maternal death in France. Several types of prophylaxis are available, mainly clinical vigilance and aggressive investigation of women with symptoms of venous thromboembolism, or antithrombotic prophylaxis. Given the low incidence of the pathology, it seems desirable to select high-risk groups of women for such strategies. The most studied and identified risk factors are prior episodes of venous thromboembolism and biological thrombophilias. Prophylaxis through low molecular weight heparin during pregnancy and the puerperium should be considered mainly in these two groups. Noteworthy, no prospective and randomized study is available, and treatment recommendations are grade C.

Risk factors for venous thromboembolic disease, during pregnancy and post-partum, can be identified in as much as 75% of pregnant women, who present such an accident. Different risk factors are usually associated in the same women. Risk factors can be attribuated to the pregnant women (age over 35 years, overweight, varicose veins, smoking, previous deep venous thrombosis and/or pulmonary embolism) or to the conditions of the pregnancy (multiparity, immobilisation, hypertension and pre-eclampsia, cesarean delivery). Inherited or acquired biological thrombophilia enhance the risk of thrombosis but the magnitude of this effect in ante-partum, puerperium or post-partum depends on the nature of the abnormality. The analysis of all these risk factors and their cumulative effect enable classifying pregnant women into groups with very high risk, high risk or moderate risk for venous thromboembolism and to propose an adapted strategy to prevent the occurrence of such accidents.

Thromboembolism in pregnancy and the puerperium and inherited or acquired thrombophilia are associated. Thrombophilia can be revealed by pregnancy. Thrombotic risk during pregnancy and the puerperium is higher in asymptomatic women with than without thrombophilia. Antithrombin deficiency, combined deficiencies and homozygous or double-heterozygotes factor V Leiden and factor II G 20210 A mutations are associated with a higher thrombotic risk than heterozygote mutations or protein S and C deficiencies, whereas hyperhomocysteinemia does not appear as a risk factor for maternal thromboembolic disease. Antiphospholipid syndrome with lupus anticoagulant is strongly associated with thrombotic risk in pregnancy and the puerperium. Further studies are required to assess the thrombotic risk in women with preeclampsia as well as early or late recurrent pregnancy loss.

The vascular placental pathology (VPP) is associated with many etiologies. Some are the consequence of a maternal genetic or acquired predisposition. Others are associated with a chronic maternal disease (hypertension, lupus, obesity, diabetes, ...). Finally, some others are associated with placental implantation leading to fetal ischemia (multiple pregnancy, chorioangioma, primiparity, feto-placental hydrops) or to environmental (altitude) or nutritional factors (famine and specific alimentary depressions). We classify these factors into three categories according to the risk level (moderate, significant and elevated). While any of these factors can increase the risk of VPP, no one is sufficiently sensitive or specific in predict inevitable onset of VPP. In most cases VPP results from a combination of two (or more) risk factors. The risk factors of VPP classified as moderate include age (> or = 35 years), increased blood pressure during the second trimester of pregnancy, a new paternity, dietetic factors or environmental factors, smoking and controlled diabetes (class B, C), or inactive systemic diseases. Risk is significantly elevated among obese (BMI > or = 25), primiparous women, women with a past familial history (first degree) of preeclampsia or eclampsia, cocaine use or association of tobacco and caffeine use, increased placental mass (associated with twin pregnancy, fetal hydrops or molar pregnancy), uncontrolled diabetes, lupus, active scleroderma. Risk is considered to be high among patients with chronic hypertension, women with a past history of preeclampsia, diabetes (class D, F, R), patients with active systemic disease or with antiphospholipid antibodies or women with lupus or renal lesions and/or proteinuria as well as chronic kidney disease resulting in proteinuria, hypertension and renal insufficiency. Finally, the risk of VPP is considered to be increased in the presence of acquired thrombophilia. It remains moderate in the presence of isolated genetic thrombophilia, except in forms presenting with multiple genetic mutations or associated with an hyperhomocysteinemia. A "high-risk group" is defined among women with past history of deep venous thromboembolic events outside pregnancy, or with a past history of placental vascular pathology (intra-uterine death, placental abruptio, severe and precocious placental, intra-uterine growth retardation, early and repetitive fetal loss) and who, in addition, present with acquired thrombophilia (antiphospholipid antibodies, thrombocytemia), unique homozygous genetic thrombophilia, amultiple genetic thrombophilia or unique heterozygous genetic thrombophilia associated with hyperhomocysteinemia. Prophylactic treatment of acquired thrombophilia and of the multiple genetic forms or associated with hypercysteinemia is a logical rationale, particularly among women with a past history of placental vascular pathology, or with a past history of venous thromboembolic events. On the contrary, pr

Thrombophilia is characterized by clinical tendency to thrombosis or molecular abnomalities of hemostasis that predisposes to thromboembolic disease. Hereditary thrombophilia may be due to antithrombin deficiency, or protein C or protein S deficiency. More recently, other molecular abnormalities have been described: activated protein C resistance due to factor V Leiden, G 20210 A polymorphism on the prothrombin gene, increased factor VIII plasma levels or hyperhomocysteinemia. Acquired thrombophilia is frequently associated with the antiphospholipid syndrome characterized by thrombosis and presence of lupus anticoagulant or phospholipid-binding antibodies. In some cases, no molecular abnormality is found despite recurrent thrombosis observed in patient and his/her family. This situation can be considered as clinical thrombophilia.