Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three women and five men with chronic biological false-positive seroreactions for syphilis and circulating anticoagulants exhibited a vascular syndrome consisting of recurrent deep venous thrombosis of the extremities and necrotizing purpura with painful superfacial starlike ulcers around the ankles. The skin biopsies revealed a unique picture of massive proliferation of hemorrhagic dermal capillaries without a significant inflammatory reaction. Some virus infection may function as a trigger of this peripheral vascular syndrome, because 6 of the 8 patients had a preceding pneumonia with pleural vascular effusion. Considering that the three women had clinical and laboratory evidence of systemic lupus erythematosus (SLE) this syndrome may be related to SLE.
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PMID:A peripheral vascular syndrome overlapping with systemic lupus erythematosus. Recurrent venous thrombosis and hemorrhagic capillary proliferation with circulating anticoagulants and false-positive seroreactions for syphilis. 90 39

Thirty-four-year-old George Talbot was admitted to your medical/surgical unit with deep vein thrombosis of his left leg, probably related to intravenous drug abuse. So it's no surprise that Mr. Talbot is receiving heparin IV. Today, however, you notice that his physician has prescribed one dose (2.4 million units) of benzathine penicillin IM. You're not sure why until you check the patient's lab work. Mr. Talbot's rapid plasma reagin (RPR) test was reactive. The physician is treating Mr. Talbot for syphilis.
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PMID:Syphilis. A new look at an old killer. 232 82

We describe deep vein thrombosis associated with lupus anticoagulant and anticardiolipin antibodies in three children aged 10 to 14 years. One of them also had arterial thromboses. None of the patients had systemic lupus erythematosus when the thrombosis first occurred, but one fulfilled the criteria for systemic lupus erythematosus 3 years later. At presentation all had symptoms suggestive of pulmonary embolism and evidence of an autoimmune disease: Addison's disease in one, anti-DNA or antinuclear antibodies in all three, and a positive Coombs' test in two. Two of the three gave a false-positive test for syphilis. In the patient with systemic lupus erythematosus recurrent thrombocytopenia and severe haemolytic anaemia necessitated splenectomy. A child should be tested for lupus anticoagulant or anticardiolipin antibody if venous or arterial occlusion occurs without a known predisposing cause, or if there is pulmonary embolism or symptoms or laboratory findings suggestive of a connective tissue disease.
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PMID:Venous thrombosis associated with lupus anticoagulant and anticardiolipin antibodies. 314 18

Myocardial infarction in association with pregnancy in patients with the antiphospholipid syndrome has been reported once previously. Our patient, a 22-year-old multiparous woman, experienced a myocardial infarction in the postpartum period. She fulfilled the criteria for the diagnosis of the antiphospholipid syndrome (elevated anticardiolipin antibody levels, false-positive syphilis serology, history of deep vein thrombosis). Cardiac catheterization demonstrated appropriate central filling pressures, cardiac output of 7.14 L/min, and normal-appearing coronary arteries. She was treated with corticosteroids and indomethacin and recovered. Our article is relevant to clinical practice for the following reasons. First, it is the second time myocardial necrosis has been reported in a recently pregnant woman with the antiphospholipid syndrome. Second, the finding of normal-appearing coronary arteries at the time of catheterization lends credence to the hypothesis that either vasospasm or thrombosis are the inciting events. We speculate on the utility of various treatment regimens.
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PMID:Postpartum myocardial infarction in a patient with antiphospholipid syndrome. 815

Lupus anticoagulants (LAs) are immunoglobulins which prolong 1 or more of the in vitro phospholipid-dependent tests of coagulation (e.g., activated partial thromboplastin time [APTT], dilute Russell viper venom time [dRVVT], kaolin clotting time [KCT], and textarin time [TT]). Paradoxically, patients with LAs rarely experience hemorrhagic problems. Approximately 1/3 of individuals with LAs experience thromboembolic complications such as stroke, deep vein thrombosis, and pulmonary emboli. LAs are members of the antiphospholipid antibody (APA) family. The APA family includes: LAs, anticardiolipin antibodies (ACAs), and reagin (the antibody responsible for the positive serologic test for syphilis). In approximately 60% of the patients, a LA and an ACA will both be present. The diagnosis of LAs requires an organized approach. Careful preparation of platelet poor plasma (PPP) is essential to assure maximum detection of LA. In order to rule out LAs, it is necessary to perform at least 2 screening tests (e.g., APTT, dRVVT). Additional steps in the diagnosis of LAs include mixing studies to identify the presence of an inhibitor and confirmatory procedures to demonstrate phospholipid-dependence of the inhibitor. It is also important to rule out any other potential coagulopathies which may account for the prolonged screening studies.
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PMID:Lupus anticoagulants: diagnostic dilemma and clinical challenge. 1016 22

Since the association between antiphospholipid antibodies and syphilis was first described, many other viral, bacterial and parasitic infections have been shown to induce antiphospholipid antibodies, notably anticardiolipin antibodies. These aPL are usually associated neither with anti-beta2 glycoprotein I antibodies (anti-beta2-GPI) nor with thrombotic events, even if cases of arterial and deep venous thrombosis have been reported in such circumstances. A literature review shows that anticardiolipin antibodies occur frequently in viral infections, particularly in HIV (49.8%), HBV (24%) and HCV (20%). The prevalence of anti-beta2 glycoprotein I antibodies (anti-beta2GPI) is lower (HCV: 1.7%, HIV: 5.6%, HBV: 3.3%) and there is no demonstrated association with a risk of thrombotic events or hematological manifestations defining antiphospholipid syndrome (APS). Regarding other viral infections, including viral hepatitis A, herpes virus (CMV, EBV, VZV), parvovirus B19 and HTLV-1 infections, only a few studies are available but data confirm the high prevalence of antiphospholipid antibodies at the acute phase. Finally, antiphospholipid antibodies, mainly anticardiolipin, are frequently associated with viral infections. Their presence may probably reflect an intense or chronic antigenic stimulation of the immune system. However, their evolution under antiviral therapy and correlation with the quality of the virological control and/or the immune restoration remain to be determined.
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PMID:[Antiphospholipid antibodies, antiphospholipid syndrome and viral infections]. 1892 4

A pro-thrombotic condition was described in 1983 which was characterised by the presence of circulating antiphospholipid antibodies, as well as peripheral thrombosis (e.g. DVT), a tendency to internal organ involvement, repeated miscarriage, and, occasionally, thrombocytopenia (aPL) (Hughes, Br Med J 287:1088-1089, 1983). Previously, there had been a number of observations, mainly in patients with lupus having "false positive" tests for syphilis, miscarriage and circulating lupus anticoagulants. The description in 1983 had three notable features (a) a detailed comprehensive clinical picture of the syndrome; (b) this description differed from other coagulopathies in showing a propensity for arterial thrombosis (e.g. stroke and heart attack); and (c) this was a syndrome quite independent from lupus. There are indications that the primary antiphospholipid syndrome will turn out to be more common than lupus, though this could still be a reflection of referral practice.
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PMID:Hughes syndrome (the antiphospholipid syndrome): a disease of our time. 2113 65