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

The diagnosis of preeclampsia is made on the basis of hypertension, proteinuria and edema. Unfortunately, all three of these findings can be seen in the patient who is experiencing a flare of systemic lupus erythematosus. The management of these conditions is entirely different. Preeclampsia frequently results in the need for delivery and occasionally, especially when remote from term, can result in significant neonatal morbidity and mortality. Systemic lupus may be treatable with a variety of pharmacologic agents. It is not always possible to make the distinction between active lupus and preeclampsia, and occasionally the two occur concurrently. Nevertheless, the goal of the rheumatologist and perinatologist is to try to make that distinction. Physical findings and serologic markers can be useful in helping to distinguish between these two diagnoses. Under certain circumstances, delivery is indicated despite the presence of continued uncertainty as to the actual diagnosis.
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PMID:Hypertensive disorders of pregnancy. Differentiating preeclampsia from active systemic lupus erythematosus. 958 67

Anticardiolipin antibodies (ACAs) of IgA, IgG, and IgM isotypes were measured using an enzyme-linked immunosorbent assay (ELISA) in patients with SLE, and in other groups of subjects with a higher or lower risk of developing thrombosis. IgA ACAs were present in high titers in all groups and had little discriminant value in predicting thrombotic risk. In patients without the lupus anticoagulant (LAC) with conditions in which a thrombotic tendency was a feature (primigravidae with preeclampsia or intrauterine growth retardation, patients with angina or acute myocardial infarction, those on anticoagulant therapy for apparently spontaneous thrombosis, and patients with Behcet's syndrome in whom there was a history of thrombosis) ACAs of all isotypes were present in 44/191 (23%). In patients in whom a thrombotic tendency was not a feature (normal controls, primigravidae with normal deliveries, patients with rheumatoid arthritis, and with Behcet's syndrome in whom there was no thrombotic history) 22/241 (9%) had ACAs. Although ACAs were more likely to be present in a subset of patients without systemic lupus erythematosus (SLE) and/or the LAC, their presence was a poor discriminator of increased risk of thrombosis.
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PMID:Anticardiolipin antibodies in clinical conditions associated with a risk of thrombotic events. 962 37

Systemic lupus erythematosus and antiphospholipid antibody syndrome are associated with an increased risk of intrauterine growth restriction, miscarriage, stillbirth and premature delivery. Recent advances in therapy during pregnancy have improved the outcome but there is still significant fetal and maternal morbidity and mortality. Treatment of patients failing conventional therapy during the second half of pregnancy is difficult and may be complicated by the development of preeclampsia. The addition of intravenous immunoglobulin therapy offers a low risk strategy for reducing autoantibody mediated disease and improving placental function in severely compromised, growth restricted pregnancies.
Lupus 1998
PMID:Use of intravenous immunoglobulin therapy in pregnancy in systemic lupus erythematosus and antiphospholipid antibody syndrome. 979 43

Women with antiphospholipid antibodies (aPL = IgG anticardiolipin and/or lupus anticoagulants) and a history of either prior thrombotic events or pregnancy loss are at high risk during pregnancy for either another fetal death or thrombosis. The treatment of choice is anticoagulation with heparin. Both standard unfractionated heparin and low-molecular-weight heparin are used for prophylactic anticoagulation during pregnancy. The half-lives of either standard heparin, or low-molecular-weight heparin, and the peak values for each after subcutaneous injection, are lower than those in nonpregnant patients. Doses and injection intervals need to be adjusted when treating a pregnant woman. Clotting tests such as the activated partial thromboplastin time (aPTT) vary greatly during pregnancy, and the aPTT is often not even prolonged when antithrombotic levels of heparin are achieved. The aPTT is not a useful test when the patient has a lupus anticoagulant. Levels of plasma heparin are therefore needed to best care for pregnant women who need anticoagulation even for prophylaxis. Low-dose aspirin is often added empirically to heparin for treatment of aPL during pregnancy, but its efficacy has not been evaluated. Intravenous infusions of gamma globulins (IVGG) have been used as additional therapy when prior treatment with heparin during pregnancy failed to save the fetus, when severe and early onset preeclampsia has complicated a prior pregnancy (in such cases efficacy is unproven), or when there is an additional medical complication (such as immune thrombocytopenia) for which IVGG is an appropriate treatment. There are some situations in which treatment with corticosteroids is the best, or the only choice. However, corticosteroids should not be combined with heparin for long-term treatment during pregnancy because the risk for vertebral fracture is so high.
Lupus 1998
PMID:Treatment of antiphospholipid syndrome in pregnancy. 981 82

The main risk factors for deep vein thrombosis in pregnancy and after delivery are preeclampsia, operative delivery, adiposity, prolonged bed rest, and haemostatic defects (antithrombin, protein C and protein S deficiencies), activated protein C resistance, lupus anticoagulant/antiphospholipid antibodies. Hyperhomocystinaemia is a general risk factor for deep vein thrombosis. The clinical diagnosis of deep vein thrombosis is difficult and must be confirmed by imaging techniques. Positive D-dimer has high sensitivity, but low specificity to detect acute thrombosis. Standard treatment is unfractionated heparin intravenously for 7-10 days, followed by subcutaneous injections. Anticoagulant treatment is prolonged for 6-12 weeks after delivery, usually with warfarin. During pregnancies associated with high risk of thrombosis, low molecular heparin prophylaxis is given during pregnancy and 6-12 weeks after delivery. Thrombosis in pregnancy must be followed by adequate investigation for an underlying thrombotic predisposition.
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PMID:[Deep venous thrombosis in pregnant women]. 984 15

The effect of pregnancy on disease activity in systemic lupus erythematosus remains controversial. Studies on lupus flares in pregnancy are discussed, including prospective data on severity of flares and organ involvement from the Hopkins Lupus Pregnancy Center. The major fetal concerns of miscarriage (due to the antiphospholipid antibody syndrome), pre-term birth (largely due to pre-eclampsia or premature rupture of membranes) and neonatal lupus, are reviewed.
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PMID:Pregnancy in SLE. 989 Jan 7

There are two distinct histological manifestations of impaired placental implantation in humans--incomplete trophoblastic vascular invasion and atherosis. Both have been described to occur in pregnancies affected by a variety of disorders such as preeclampsia, fetal growth restriction, systemic lupus erythematosus, and diabetes. Our purpose was to integrate recent developments in the understanding of implantation site disorders into a pathophysiological scenario that interrelates these placentation disorders and associated pregnancy complications. Sources were identified from a MEDLINE search of English-language articles published from 1966 to 1997. Additional sources were identified from references cited in relevant reports. We selected articles relating to the following topics: atherosis, implantation site disorders, trophoblastic invasion, preeclampsia, fetal growth restriction, implantation site development, atherosclerosis, and endothelial activation-damage. A contemporary version of normal placentation, including vascular adaptation, was reviewed with comments on normal trophoblastic differentiation and vascular invasion. Specific abnormalities of the implantation site, including atherosis and incomplete trophoblastic invasion, were discussed in the context of placental site hypoperfusion and the association with pregnancy complications. It was concluded that atherosis and incomplete trophoblastic invasion may be both a consequence and a cause of placental site hypoperfusion resulting in the development of preeclampsia and a variety of other pregnancy disorders.
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PMID:Atherosis revisited: current concepts on the pathophysiology of implantation site disorders. 1007 38

The object of this study was to evaluate the changes in fibrinolysis and clotting inhibitors in patients with preeclampsia and to describe the connection between preeclampsia and blood pressure values. Two groups of pregnant women were prospectively studied at delivery: group 1 women without preeclampsia and group 2 patients with preeclampsia. The variables that were registered are: diastolic blood pressure (DBP), systolic blood pressure (SBP), mean blood pressure (MBP), hemoglobin (Hb), platelet count (Plt), lupus like inhibitor, anticardiolipin antibodies (ACA), antinuclear antibodies (ANA), fibronectina, D dimer, protein S (PS), protein C (PC) and vo Willebrand factor (vWF). 62 pregnant women were included. The patients of group 2 presented high values of Hb (p 0.01), fibronectin (p 0.0001), D-dimer (p 0.01) and lower PC (p 0.04). We found an association between fibronectin and higher values of SBP, DBP, MBP and Hb (p 0.0007) versus lower values of VFW and PC (p 0.002). The low values of total PS were associated with high D-dimer and SBP results (p 0.04 and 0.002 respectively). All patients were ACA/ANA negative. In preclampsia there is a increased hemoconcentration and drop in clotting inhibitors (PC), without fibrinolytic compensatory response (lower D-dimer) and remarked vasopressive effect (hig fibronectin). This changes depend on the stratification of blood pressure. Th SBP and MBP values depend on the haemodynamic changes (Hb, fibronectin), while the increase in DBP expresses a non compensated thrombophilic state.
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PMID:[Changes in the thrombophilic status in patients with pre-eclampsia]. 1036 18

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

Sera from one thousand pregnant primiparous women from the antenatal clinic of the University Hospital of the West Indies (UHWI) were screened for lupus anticoagulant. Twenty-three women (2.3%) were seropositive. A review was performed after delivery and eight hundred and sixty-eight (87%) of the case notes were found: 20/23 (87%) of those with positive tests and 848/977 (87%) of those with negative tests. The outcome variables examined were pre-eclampsia, postpartum haemorrhage, type of delivery, birth weight of the baby, foetal outcome, foetal distress, still birth, neonatal death, Apgar score at birth and need for admission to the special care nursery. No differences were found between the two groups for any of these variables.
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PMID:Lupus anticoagulant in Jamaican primiparae and the clinical significance in asymptomatic patients. 1055 57


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