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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systemic lupus erythematosus (SLE) is an autoimmune disease that affects primarily women of childbearing age. 20-30 years ago it was common belief that SLE is exacerbated during pregnancy. Recent studies, however, could not support this notion. The likelihood of an increase in clinical activity of SLE is similar during pregnancy and in nonpregnant patients. It correlates directly with the activity of disease at the time of conception. The pregnancy outcome in patients with SLE has improved considerably in recent years. The frequency of fetal loss, however, still remains higher in SLE patients than in healthy women. In most of the cases fetal loss is due to habitual abortions, intrauterine death and premature labors. The main reasons are anti-phospholipid antibodies and the activity of SLE at the onset of pregnancy, respectively during the pregnancy. For monitoring disease activity and especially for distinguishing between the development of eclampsia and exacerbation of SLE, periodic determinations of complement proteins CH50, C3, C4 and C3d are helpful. A prophylactic therapy e.g. with prednisone in pregnant SLE patients is not justified. However, when SLE is exacerbating immunosuppressive therapy with prednisone and, if needed in combination with azathioprine, should be administered. In cases with high antiphospholipid antibody titers and prior fetal loss a treatment with low-dose acetylsalicylic acid can be considered.
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PMID:[Systematic lupus erythematosus and pregnancy]. 139 29

A 28-year-old female patient with SLE was found to have complications from intrauterine fetal death, eclampsia, and brainstem vascular damage during pregnancy. These symptoms were associated with lupus anticoagulant (LAC). An LAC positive SLE case with accompanying cerebrovascular disease and fetal loss at the same time has rarely been reported. The first brain CT scan revealed the presence of multiple middle pons infarction. Ten days after onset, a brain MRI showed the change into hemorrhagic infarction in the same region, suggesting disseminated intravascular coagulation (DIC) caused by severe obstetric complications. Although the severity of the brain damage implied poor prognosis, her symptoms were alleviated by intensive care with a large amount of steroid therapy and active rehabilitation. LAC-positive SLE patients are apt to encounter obstetric complications in pregnancy. Therefore they must be treated by medical specialists in cooperation with gynecologists. When they also have accompanying with cerebrovascular diseases, active therapy for SLE is necessary for a good prognosis.
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PMID:[A case of pregnant woman with lupus anticoagulant positive systemic lupus erythematosus complicated with intrauterine fetal death, eclampsia, and brainstem vascular damage]. 192 97

A retrospective review of maternal mortality in the obstetric unit of Bangkok's Ramathibodi Hospital in 1969-82 was conducted. In this 14-year period, there were 72,872 live births and 26 maternal deaths, yielding a maternal mortality rate of 0.4/1000. Direct obstetric causes accounted for 77% of these deaths. The distribution of the 20 direct obstetric deaths was as follws: septic abortion (10 cases), puerperal infection (3 cases), pre-eclampsia (1 case), eclampsia (2 cases), amniotic fluid embolism (3 cases), and placenta percreta with uterine rupture (1 case). Among the 6 deaths attributable to indirect causes, viral hepatitis was responsible for 3, systemic lupus erythematosus was the cause in 2 cases, and cardiac failure occurred in the final case. The maternal mortality rate was 0.8/1000 amond women 19 years of age and below and 0.6/1000 among women 35 years of age and above compared with 0.2/1000 among those 20-34 years of age. Maternal mortality was 0.6/1000 for cesarean section delivery compared with 0.1 for normal delivery. Ongoing statistical analyses of maternal mortality are urged to serve as the basis for preventive measures.
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PMID:Maternal mortality in Ramathibodi Hospital: a 14-year review. 383 Dec 6

We present 84 pregnancies (3 twin pregnancies) of 80 women with Systemic Lupus Erythematosus. Although there was a multidisciplinary prenatal control, in 83% of the cases there were one or more complications during pregnancy, most of them being preterm labor, premature rupture of membranes and preeclampsia-eclampsia. There were flares up in 15 of 84 cases, (17.85%). Worsening of renal function was the most common finding. There were 9 abortions, 3 stillbirths, 1 neonatal death and two newborns with congenital heart block. No maternal deaths were present.
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PMID:[Systemic lupus erythematosus and pregnancy (analysis of 84 cases)]. 892 88

Vascular damage is a well known cause of hypopituitarism since Sheehan's report of postpartum pituitary necrosis; it has subsequently been reported that also sickle-cell anemia, eclampsia, pituitary apoplexy and other pathologies may induce failure of the anterior hypophysis through this mechanism. The antiphospholipid syndrome (APS) is characterized by widespread arterial and venous thrombosis with resulting different clinical features; Addison's disease due to adrenal thrombosis is the only endocrine involvement reported so far in this syndrome. We report here a case of global anterior pituitary insufficiency which developed soon after cerebral ischaemic stroke in a 62 year aged woman with Lupus aicoagulant activity (LAC) and large atrial thrombosis; underlying pathologies were excluded by appropriate investigations. Therefore in our opinion this is the first case in which anterior hypopituitarism is reported in the clinical constellation of APS and the second type of endocline involvement.
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PMID:Hypopituitarism and antiphospholipid syndrome. 958 17

Maternal death during pregnancy, although uncommon, may result from a broad range of conditions. In this paper, a case of thrombotic thrombocytopenic purpura diagnosed by postmortem examination is presented. Thrombotic thrombocytopenic purpura is one of a subset of diseases that result in the formation of microthrombi within the vasculature, either as a primary or secondary manifestation. Other conditions included in the differential diagnosis during pregnancy are hemolytic uremic syndrome, systemic lupus erythematosus, preeclampsia-eclampsia and the HELLP syndrome, acute fatty liver of pregnancy, antiphospholipid antibody syndrome, and disseminated intravascular coagulation. The histologic manifestations of these diseases can be similar and in most cases do not provide adequate information to accurately differentiate these diseases in the postmortem period. This paper addresses the need for clinical history (i.e., symptomatology, trimester of onset) and antemortem laboratory testing in addition to a thorough autopsy to accurately differentiate among the conditions named previously. In the absence of an adequate clinical history and antemortem laboratory testing, the more general diagnosis of "thrombotic microangiopathy of pregnancy" is acceptable.
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PMID:Death due to thrombotic thrombocytopenic purpura in pregnancy: case report with review of thrombotic microangiopathies of pregnancy. 1041 63

A 33 year-old woman developed eclampsia with HELLP syndrome. Laboratory results revealed lupus anticoagulant and anticardiolipin antibodies. Imaging tests showed liver and spleen infarctions. The patients was given enoxaparin and supportive care and there was a good evolution. We discuss some aspects about liver infarction and its association with toxemia of pregnancy and the antiphospholipid syndrome.
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PMID:[Hepatic hemorrhagic infarction in eclampsia and HELLP Syndrome associated with the antiphospholipid syndrome]. 1053 8

We examined the relationship between placental histology and thrombophilia status in women who were admitted with severe pre-eclampsia/eclampsia, placental abruption, intrauterine growth restriction or unexplained stillbirth. All women had thrombophilia screen at least 10 weeks after delivery (antithrombin III, protein C, protein S, activated protein C resistance, anticardiolipin antibodies, lupus anticoagulant, fasting plasma homocysteine and specific mutations to methylenetetrahydrofolate reductase C677T, G20210A prothrombin gene and factor V Leiden. Placental histology reports were examined to identify the frequency of thrombotic lesions in the placenta including fetal stem vessel thrombosis, fetal thrombotic vasculopathy, placental infarction, perivillous fibrin deposition, intervillous thrombosis and placental floor infarction. During a 17 month period, a cohort of 79 women met the study criteria. Thirty (70%) out of 43 women with abnormal thrombophilia screen had abnormal placental histology. Twenty-eight (78%) out of 36 women with negative thrombophilia screen had abnormal placentae. No specific histological pattern could be identified when thrombophilia positive and thrombophilia negative groups were compared. We propose that there is a poor correlation between thrombophilia status and pathological changes of the placenta in women with severe pregnancy complications.
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PMID:Do placental lesions reflect thrombophilia state in women with adverse pregnancy outcome? 1115 44

Antiphospholipids including lupus anticoagulants (LA) and anticardiolipins (ACL) are known to be able to lead to many obstetricals complications like gravidic chorea, eclampsia and repeated spontaneous abortion. Our objective was to determine place of antiphospholipids among women presenting repeated spontaneous abortion in Senegal. We tested prospectively 96 women in a breeding age with a past history of at least 2 spontaneous abortion. 14.6% and 21.1% of tese women present present respectively LA and ACL. The prevalence of antiphospholipids in among women presenting repeated abortion is higher in Senegal and similar to those previously reported confirming its place in this pathology important. A strategy of diagnosis should be defined between obstetricians and biologists in order to improve the obstetrical prognosis.
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PMID:[Antiphospholipid antibodies and recurrent spontaneous abortions at the Aristide Le Dantec University Hospital Center]. 1467 79

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, prophylaxis using low-molecular-weight heparin in the event of asymptomatic genetic thrombophilic mutations and for women without a past history of deep venous thromboembolism or vascular placental pathology remains controversial.
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PMID:[Vascular placental pathology in high-risk groups: definition and synopsis]. 1502 87


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