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)

In patients at risk for pulmonary emboli, consideration is often given to placement of an inferior vena cava (IVC) filter to prevent propagation of a distal thrombus. However, long-term benefits remain controversial, and deep venous thrombosis and IVC thrombosis may result from the procedure itself. Whether a filter if beneficial or even detrimental in patients with the antiphospholipid syndrome (APS) is unclear. We reviewed clinical outcomes in 2 patients who had IVC filter placement years before the diagnosis of the APS and 1 who had a contraindication to anticoagulation. Recurrent pulmonary emboli were seen despite the presence of the filter. IVC pathology sometimes revealed thrombus both proximal and distal to the IVC filter. Pulmonary emboli in the APS may be secondary to deep venous thrombosis (DVT). They may also occur secondary to a cardiac source or in situ thrombosis in the pulmonary vessels. An IVC filter will not be of benefit if the heart or the lungs are the primary source for the emboli. It may also not protect against propagation of a more distal thrombus if collateral vessels develop around the filter or a thrombus is present on the proximal side of the filter. Recurrence of pulmonary emboli after a filter placement should alert the clinician to the possibility of a hypercoagulable state such as APS. Clinicians need to assess risks and benefits carefully before placing a permanent IVC filter in patients with APS. Whether a temporary or retrievable filter is safer in APS and more effective is unknown at the present time.
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PMID:Recurrent pulmonary embolism despite inferior vena cava filter placement in patients with the antiphospholipid syndrome. 1635 98

A case of a 34 year old woman with antiphospholipid syndrome, admitted to our hospital due to acute myocardial infarction, is presented. She had a history of deep vein thrombosis, two miscarriages and ischaemic stroke. The patient underwent successful primary coronary angioplasty and was discharged home. Factors predisposing to arterial thrombosis and treatment options are discussed.
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PMID:[Acute myocardial infarction in a young patient with a primary antiphospholipid syndrome -- a case report]. 1644 37

A 48-year-old woman presented to our hospital with epigastralgia and erythema on the left dorsalis pedis. Her medical history included deep venous thrombosis three months prior to admission to our hospital. Upon admission it was determined that she had severe anemia (hemoglobin level 4.6 g/dl). Bone marrow analysis indicated a markedly decreased number of erythroid progenitor cells. A skin biopsy specimen of the erythema revealed microthrombus. Anticardiolipin-beta2GPI antibody and lupus anticoagulant were positive. The patient was diagnosed with pure red cell aplasia (PRCA) and antiphospholipid syndrome (APS). After steroid pulse therapy and warfarinization, her anemia and purpura improved. Three months later she developed depression with positive anti-ribosomal P protein antibody that was indicative of central nervous system lupus. Although her psychometric condition did not respond to steroid pulse therapy, improvement was seen after she received three courses of cyclophosphamide pulse therapy. We report a rare case of CNS lupus that developed during corticosteroid therapy and warfarinization in a patient with PRCA and APS.
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PMID:[Appearance of central nervous system lupus during corticosteroid therapy and warfarinization in a patient with pure red cell aplasia and antiphospholipid syndrome]. 1650 2

Little is known regarding the association of primary antiphospholipid syndrome APLS and proliferative glomerulonephritis GN. We describe a biopsy-documented case with primary APLS and proliferative GN with no evidence of thrombotic microangiopathy TMA, and in the absence of other manifestations of systemic lupus erythematosus SLE. She presented initially with left popliteal deep venous thrombosis and nephrotic syndrome. Her first pregnancy at the age of 26 years resulted in intra-uterine fetal death at term. Two subsequent pregnancies ended up with miscarriages at 3 and 4 months of gestation. Urinalysis revealed glomerular red blood cells of 1.0000.000/ml and granular cast; proteinuria of 13.4 grams/24 hours, which was non-selective; hemoglobin 12 gm/dl, normal white blood cell and platelets; serum albumin 2.6 gm/dl; anti-nuclear antibody ANA and anti DNA were negative and complement levels normal. Lupus anticoagulant was positive leading to a diagnosis of primary APLS. The biopsy findings were consistent with membranoproliferative GN. She continued to have steroid-resistant proteinuria, but stable renal function after a 12-year follow up period. She had 2 pregnancies during this period and was delivered at term using caesarian section. She received heparin during the pregnancies. Later she developed hypertension easily controlled by atenolol. This case provides evidence that primary APLS can be associated with proliferative GN due to immune deposits and not only TMA as previously reported, and in the complete absence of SLE. Performing more renal biopsies in this group of patients may disclose a greater prevalence of proliferative GN and may help in devising a rationale for treatment.
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PMID:Proliferative glomerulonephritis and primary antiphospholipid syndrome. 1683 33

We describe a 32-year-old man with secondary antiphospholipid syndrome (APS) who received oral anticoagulation with phenprocoumon after deep vein thrombosis. Conventional monitoring of oral anticoagulation by INR measurement was impaired by coagulation factor inhibition in vitro due to a strong lupus anticoagulant. The case illustrates that monitoring of oral anticoagulation may require determination of single coagulation factor activities in selected patients with APS.
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PMID:Monitoring oral anticoagulation may require determination of single coagulation factor activities in patients with antiphospholipid syndrome. 1688 Oct 92

We describe, the case of a 34-year-old mestizo Mexican woman with previous history of fetal loss, deep vein thrombosis that developed avascular necrosis (AVN) of the right knee with strong positive levels of anticardiolipin antibodies (aCL) IgG and IgM. AVN of bone in association with aCL has been seen principally in systemic lupus erythematosus patients. However, few cases have been reported of AVN as a clinical manifestation of primary antiphospholipid syndrome. A review of the association of aCL and AVN in patients with systemic lupus erythematosus, primary antiphospholipid syndrome, and idiopathic osteonecrosis is presented.
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PMID:Avascular necrosis of bone associated with primary antiphospholipid syndrome: case report and literature review. 1704 12

Antiphospholipid syndrome (APS) is characterized by recurrent arterial or venous thromboembolism or pregnancy loss in association with antibodies directed against anionic phospholipids or plasma proteins bound to anionic phospholipids. A common cause of the huge variety of clinical manifestations is vaso-occlusive disease and not vasculitis in venous or arterial blood vessels of different sizes and sites (i.e. deep vein thrombosis, pulmonary embolism, cerebrovascular disease). In accordance with this, fetal abortion, typically beyond the tenth week of gestation, is also caused by infarctions of blood vessels in the placenta. Establishing the correct diagnosis of APS is not easy. To estimate the risk of thrombotic complications is challenging, as well as the questions of, which, how long and in what strength anticoagulation is recommended. This paper should enable the reader to apply international consensus classification criteria correctly, to interpret the different laboratory tests for anti-phospholipid antibodies and to gain an awareness of the different forms of anticoagulation in order to stratify therapeutic decisions.
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PMID:[Antiphospholipid syndrome]. 1716 9

Making decisions about any modality of secondary prophylaxis in patients with venous thromobembolism (VTE) has to balance the risk of bleeding induced by anticoagulants against the benefit of reducing the risk of recurrent disease. It has to be kept in mind that the magnitude of risk is not only defined by the number of events per time period but also by the impact of the event on the fate of the patient. With standard intensity vitamin K antagonists (VKA), the risk of bleeding is more closely related to comorbidities than to other factors, eg age. The risk of VTE recurrence differs largely between patient groups. The criterion of presence or absence of a permanent or transient clinical trigger factor for the actual VTE episode has a greater impact than an abnormal result in thrombophilia testing. The standard period of secondary prophylaxis for proximal DVT and for PE is three to six months. The concept of prolonging this period for several months according to the risk of recurrence is seriously challanged by the observation that the prolongation period seems to delay recurrencies rather than truly avoiding them. For this reason, patients who clearly are threatened by recurrent episodes should receive indefinitive secondary prophylaxis. This is the case for cancer patients, patients with the antiphospholipid syndrome, and those who belong to families with severe and symptomatic protein C, protein S, or antithrombin deficiencies. Patients with recurrent VTE, with idiopathic VTE, or with combined thrombophilic conditions may only benefit from indefinitive secondary prophylaxis if the bleeding risk of the anticoagulant regimen under consideration is very low.
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PMID:[Secondary prophylaxis of venous thromboembolism]. 1727 74

We describe a 58-year old female patient with rapid development of arterial and venous thromboembolisms, including deep vein thrombosis (DVT) in the lower limbs, recurrent cerebral infarctions and bilateral pulmonary emboli. Her laboratory data on admission showed positive anticardiolipin antibody of IgG isotype (IgG aCL) and positive anti-beta2 glycoprotein-I antibody of IgG isotype (IgG abeta2-GPI), and decreased protein C activity and protein S antigen. Systemic examinations revealed the presence of an ovarian cancer. Surgical resection was attempted, but her cancer infiltrated the pelvic wall and could not be resected. Despite treatment with unfractionated heparin followed by warfarin, she died due to recurrent episodes of cerebral infarction. This case was considered as probable catastrophic antiphospholipid syndrome (CAPS), which might be associated with ovarian cancer. Known as Trousseau's syndrome, arterial and, more commonly, venous thrombosis is a frequent complication of cancer and sometimes a harbinger of occult cancer. Our case indicates that there is an overlap between antiphospholipid syndrome (APS) and Trousseau's syndrome. It is important to bear in mind that a thrombotic event associated with cancer can be the first manifestation of CAPS.
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PMID:Catastrophic antiphospholipid syndrome associated with malignancies (case report and review of the literature). 1728 88

In 1983, a detailed clinical description of a new syndrome was published. This prothrombotic syndrome was initially called the anticardiolipin syndrome and subsequently the antiphospholipid syndrome (APS), or Hughes Syndrome. Almost uniquely, it results in arterial as well as venous thrombosis and is marked by the presence of circulating antiphospholipid antibodies. Clinical features are protean, ranging from peripheral deep vein thrombosis (DVT) to involvement of internal organs such as the liver, kidneys, and adrenals. Likewise, arterial thrombosis can result in life-threatening infarction of organs such as the heart. The nervous system is frequently affected, with migraine, memory loss, balance disorders, stroke, and atypical multiple sclerosis being prominent. Other features include recurrent miscarriage, thrombocytopenia, and livedo reticularis. More recent observations have included ischemic bone fractures, renal and celiac artery stenosis, and a possible tendency toward accelerated atherosclerosis. The condition is seen in patients with lupus, but, significantly, occurs without associated lupus ("primary" APS)-indeed, increasing clinical recognition of Hughes Syndrome suggests that this condition will overtake lupus in prevalence. Treatment at present is by anticoagulation. The mechanisms for thrombosis are being worked out; it has been suggested that in some situations (e.g., pregnancy loss), an inflammatory component as well as thrombosis may play a part.
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PMID:Hughes Syndrome: the antiphospholipid syndrome--a clinical overview. 1742 56


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