Gene/Protein Disease Symptom Drug Enzyme Compound
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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 prevalence and activity of human herpesvirus-6 in patients with collagen vascular diseases (CVD) was determined. One hundred and fifty patients with CVD (56 with systemic lupus erythematosus-SLE, 92 with rheumatoid arthritis-RA, 1 with Sharp's syndrome and 1 with atypical polyclonal lymphoproliferation-APL and rheumatoid features) were screened serologically (IFA and ELISA) for antibodies against human herpesvirus-6 (HHV-6), Epstein-Barr virus (EBV) and cytomegalovirus (CMV). Virus isolation was attempted from peripheral blood lymphocytes (PBL) of 25 persons with various disorders. PBL were grown in tissue culture and tested with standard HHV-6-positive antisera for viral antigen expression. Supernatants of the patient's lymphocyte cultures were used to infect HSB2 cells, and virus infection in these cells was proven by IFA, in situ hybridization and by electron microscopy. Fifty-five percent of the SLE patients, 6.5% of the RA patients and both patients with Sharp's syndrome or with APL had antibody titers indicative of active HHV-6 infection. Virus cultures were positive in 9 of the 25 attempts with establishment of stable virus lines. These patients were 5 with SLE or UCVD, and one each with RA, CFS, APL as well as one healthy control. Reactivated and chronic active HHV-6 infections are frequent in SLE like EBV in RA. The role of these viruses in the pathogenesis of the diseases or in their reactivation still needs further investigation.
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PMID:Isolation of human herpesvirus-6 (HHV-6) from patients with collagen vascular diseases. 165 47

This prospective study is an attempt to address the issues of whether or not antiphospholipid antibodies (aPL) constitute a significant risk factor for pregnancy in individuals with systemic lupus erythematosus (SLE) and whether or not combination therapy of high-dose prednisolone (PSL) and low-dose acetylsalicylic acid (ASA) offers efficient control. Antibodies against six phospholipids were measured in sera of patients with stable SLE who had no severe complications before pregnancy, and were followed up during subsequent pregnancies. Four of 12 patients with SLE demonstrated aPL-positivity. Six of 8 patients without aPL had appropriate-for-date (AFD) live babies, the remaining two suffering intrauterine fetal death (IUFD) in the first trimester, one having a chromosome abnormality. Two aPL-positive patients treated only with 5-15 mg/day PSL during pregnancy ended in IUFD in the second trimester. In contrast, the other two patients treated with high-dose PSL and low-dose ASA each had AFD live babies at 38 weeks gestation. The results suggest that APL is a crucial risk factor in pregnancy with stable SLE. Combination therapy of high-dose PSL and low-dose ASA may enable aPL-positive patients with SLE to have AFD live babies.
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PMID:A prospective study on pregnancy risk of antiphospholipid antibodies in association with systemic lupus erythematosus. 776 81

We have presented a working hypothesis showing the possible interrelations between proliferative, aproliferative and autoimmune disorders that may follow infection with lymphotropic herpesviruses. Aproliferative disorders in this context may also indicate immune or hematopoietic deficiency. Although this hypothesis can currently be best documented with the lymphotropic viruses (herpesviruses as well as similarly HTLV and HIV), the model may apply as well--with certain variations--to other viral infections such as with hepatitis virus B or C with acute or chronic infectious diseases, post-infectious arthritis, aplastic anemia, and other autoimmune liver diseases, as well as neoplastic diseases (hepatocellular carcinoma, chronic lymphocytic leukemia). The working hypothesis as depicted in Figure 2 permits a preview of which combinations of symptoms may occur in an individual disease independent of its initial classification and what clinical testing should be done respectively, and it also permits certain prognostic considerations. The above-mentioned transitions or combinations of various disease patterns have been repeatedly described in the medical literature (to refer to only a few examples: APL and MPD, HD and MDS, SLE and aplastic anemia, SLE and Kikuchi's disease; 23, 80-83). Finally the hypothesis can ideally serve as the basis for future planning of clinical research.
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PMID:A unifying concept of viral immunopathogenesis of proliferative and aproliferative diseases (working hypothesis). 789 76

Antiphospholipid antibodies (aPL) present in systemic lupus erythematosus and the primary antiphospholipid syndrome are a well-known risk factor for thrombosis. Most of them require the presence of a cofactor, beta 2-glycoprotein I for anticardiolipin antibodies, prothrombin for lupus anticoagulant. These aPL are of the "immune" type. APL are also found in various non-immunological conditions, in which repeated endothelial or membranous damages appear to be frequent, but thromboses are rare. Most of these aPL are cofactor-independent, except those induced by chlorpromazine, and might belong to "natural" antibodies.
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PMID:[Antiphospholipid antibodies: cause of thrombosis or an epiphenomenon?]. 853 23

Anticardiolipin antibodies and the lupus anticoagulant are strongly associated with thrombosis and appear to be the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanism(s) whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, several theories have been advanced. Because the aPTT is unreliable in patients with lupus anticoagulant and is not usually prolonged in patients with anticardiolipin antibodies, definitive tests, such as ELISA for IgG, IgA, and IgM anticardiolipin antibodies and the dRVVT (followed by cephalin correction for confirmation) for lupus anticoagulant, should be immediately ordered when suspecting antiphospholipid syndrome in persons with otherwise unexplained thrombotic or thromboembolic events or fetal wastage syndrome. The laboratory diagnosis of APL-T syndrome is summarized in Figure 1.
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PMID:The antiphospholipid-thrombosis syndromes. Fact, fiction, confusion, and controversy. 804 99

We determined prospectively the prevalence of avascular osteonecrosis (AON) by magnetic resonance imaging (MRI) of both lower limbs in a group of 40 systemic lupus erythematosus (SLE) patients, and correlated the results with their serum antiphospholipid antibody (APL Ab) status and their glucocorticoid (GC) intake. APL Ab were detected by anticardiolipin ELISA and by lupus anticoagulant assays. Cumulated prednisolone doses were computed by chart review. The prevalence of AON was 37.5%, with most patients being asymptomatic despite involvement of multiple sites. The number of epiphyseal, metaphyseal and diaphyseal AON sites per patient did not differ between APL Ab-positive and APL Ab-negative patients nor between patients with high and low APL Ab titres. By contrast, a striking correlation was found between the prevalence and severity of AON and GC therapy. In conclusion, this prospective MRI study indicates that the prevalence of AON in SLE patients correlates strongly with GC therapy, but not with APL Ab status.
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PMID:Magnetic resonance imaging-detected avascular osteonecrosis in systemic lupus erythematosus: lack of correlation with antiphospholipid antibodies. 961 98

In this paper we tried to define the capillaroscopic pattern of anti phospholipid syndrome able to differentiate between the primary (PAPS) and the systemic lupus erythematosus-associated form (SLE-APS) and to be a predictive marker of thrombotic manifestations. Eight PAPS and five SLE-APS patients were studied. In each patient the evaluation was based on anti cardiolipin antibody levels, nailfold capillaroscopy, retinal fluorangiography and transcranial doppler sonography. Statistical analysis has been performed using chi 2 analysis. Morphological alterations of capillary loops, venular visibility and sludging of blood were often observed in both groups. While we found in higher prevalence a variability of capillary loop length in PAPS patients, the SLE-APL group significantly differed for the presence of microhaemorrhages (p < 0.001). When we evaluated the clinical history, a marked microcirculatory damage was related with the occurrence of thrombotic manifestations in the PAPS patients. Anti cardiolipin antibody levels, retinal fluorangiography and transcranial doppler sonography did not correlate with clinical history in either group. In conclusion, nailfold capillaroscopy can be usefully employed in the differentiation between primary and SLE-associated anti phospholipid syndrome, and it can help to identify the patients at higher risk of thrombotic disease.
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PMID:[Nailfold capillary microscopy in patients with antiphospholipid syndrome]. 979 74

Antiphospholipid antibodies (aPL) are associated with an increased incidence of fetal loss, but the pathophysiology remains unclear. One mechanism may involve the binding of aPL directly to the placenta where they may initiate placental thrombosis and infarction. We have developed an immunofluorescent technique to detect human aPL binding to human placenta. Endogenous immunoglobulins were eluted by extensive washing and residual staining was prevented by incorporating multiple blocking steps. APL were affinity purified on both cardiolipin and phosphatidylserine liposomes from the sera of six patients with aPL (five antiphospholipid syndrome (APS) patients and one post bone marrow transplant patient). Heterogeneous binding to normal term placenta, involving either the trophoblast microvillous surface, stromal and peri-vascular regions was demonstrated by affinity purified aPL from five of six patients. Preliminary sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) and western blotting studies have demonstrated that aPL bind a number of placental proteins. beta2GPI was not the predominant protein bound by aPL using this technique. This study provides further evidence for the involvement of aPL in mediating placental damage.
Lupus 1999
PMID:Affinity purified human antiphospholipid antibodies bind normal term placenta. 1048 30

Arterial and venous thrombosis are the most common and clinically relevant events of the so-called antiphospholipid syndrome; they are reported in approximately one third of patients with the antiphospholipid (aPL) antibodies. APL antibodies are part of a wide family of immunoglobulins directed against proteins complexed with negatively charged phospholipids. They include lupus anticoagulants (LA), anticardiolipin (aCL) antibodies, and the most recently recognized anti-beta-2-glycoprotein I (beta 2-GPI) and antiprothrombin (aPT) antibodies. Previous thrombotic events and the presence of LA, particularly if identified by the dilute Russell viper venom test, appear to be the strongest risk factors for vascular complications. High-titer aCL antibodies have been reported to be associated with an increased thrombotic tendency, but this was not confirmed in all studies. The data only partially support the concept that anti-beta 2-GPI and aPT antibodies may be considered as independent risk factors for thrombosis. Further prospective studies are required.
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PMID:The epidemiology of the antiphospholipid syndrome: who is at risk? 1147 44

Antiphospholipid syndrome (APS) is an autoimmune disorder in which antiphospholipid antibodies (aPL) are thought to be involved in the development of venous and/or arterial thrombosis. APL found in this syndrome are antibodies directed against a variety of phospholipid (PL) binding-proteins of which beta3-glycoprotein I (beta2GPI) and prothrombin are considered to be the major antigens. Some of these antibodies prolong PL-dependent clotting reactions and are termed lupus anticoagulants (LA). Autoimmune aPL which bind through beta2GPI to cardiolipin are called anticardiolipin antibodies (aCL). Clinical studies indicate that LA is a stronger risk factor for thrombosis than aCL. The production of monoclonal antibodies against beta2GPI and prothrombin has enabled us to understand the mechanism by which LA prolong coagulation in vitro. LA form bivalent antigen-antibody complexes with increased affinity for PL which compete with coagulation factors for the same catalytic surface. These LA positive monoclonal antibodies may be helpful in further improving the laboratory diagnosis of LA.
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PMID:Antiphospholipid syndrome: diagnostic aspects of lupus anticoagulants. 1148 46


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