Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A previous retrospective study has found an increased risk of uterine cervical atypia in women with systemic lupus erythematosus (SLE) who have been treated with cytotoxic drugs. Our objective was to prospectively reveal any increased incidence of cervical atypia in SLE patients and to evaluate the relationship to previous chemotherapy. A total of 39 SLE women were prospectively referred for cytologic PAP smears of the uterine cervix. A significantly higher incidence of cervical atypia was found in SLE women (35.9%) compared with non-SLE control groups (< or = 5%; P < 0.01). No significant difference was found between the incidence of atypia in patients previously treated by cytotoxic medications such as cyclophosphamide pulses or methotrexate (4 of 9) compared with SLE women not receiving cytotoxic drugs (10 of 30). Colposcopically directed biopsies revealed three cases of cervical intraepithelial neoplasia (CIN) I-III (23%) among the cases with atypia. We conclude that women with SLE should have regular cytologic cervical smears because of a significantly increased incidence of atypia, regardless of previous cytotoxic therapy.
Lupus 1994 Feb
PMID:Systemic lupus erythematosus: predisposition for uterine cervical dysplasia. 802 89

The 'lupus anticoagulant' phenomenon is the best documented functional effect of antiphospholipid (aPL) antibodies, occurring either by inhibition of the prothrombinase and/or Factor X activation reactions. Understanding the mechanism by which aPL antibodies inhibit phospholipid dependent coagulation reactions may yield important clues about their 'thrombogenic effects' in vivo. We conducted a series of studies to determine the specificity, diversity, and mechanism by which aPL antibodies inhibit phospholipid dependent reactions. Results showed that purified immunoglobulins with lupus anticoagulant and anti-cardiolipin activities were absorbed by negatively charged phospholipids and both activities were recovered from the phospholipid-antibody precipitate. Purified aPL antibodies inhibited the prothrombinase reaction in a plasma free system in which beta 2-glycoprotein 1 (beta 2-GP1) was absent. Affinity purified aPL antibodies had 25-50 times the inhibitory activity of immunoglobulin preparations. The phospholipid binding proteins, beta 2-GPI and placental anticoagulant protein I (PAP I), independently inhibited the prothrombinase reaction, and when these proteins were combined with aPL, inhibition of the prothrombinase reaction was additive. Antibodies of syphilis had no inhibitory effect, partially accounted for by lack of specificity for phosphotidylserine (PS). Although aPL antibodies inhibited the protein C activation reaction, there was no correlation of these activities with inhibition of the prothrombinase reaction. Together, these results show that aPL exert their effects by interaction with negatively charged phospholipids, in particular phosphotidylserine, but lack of correlation between inhibition of the prothrombinase and protein C activation reactions, suggests that the nature of the coagulation protein is also important.
Lupus 1996 Oct
PMID:Functional effects of anticardiolipin antibodies. 890 63

A 48-years old man complained of dyspnea and was admitted to the hospital. Chest enhanced CT confirmed the presence of the thrombus in the pulmonary artery. Cardiac catheterization showed severe pulmonary hypertension (mean PAP 75 mmHg). ATIII level, protein C and S antigen were within normal range. Anticardiolipin antibody and lupus anti-coagulant determination were negative. He was diagnosed as chronic pulmonary thromboembolism, and underwent pulmonary thromboendarterectomy via median sternotomy under deep hypothermic intermittent circulatory arrest. At the same time IVC filter was inserted. The origin of the thrombus was not detected before operation, but after surgery, MR angiography of total body showed a cavernous hemangioma at left lower limb. We speculated this lesion was the origin of pulmonary embolism.
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PMID:[Surgical treatment of chronic pulmonary thromboembolism caused by a cavernous hemangioma at the lower limb]. 1159 38