Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cancer patients show an increased susceptibility to develop thromboembolic diseases, suggesting that disorders of coagulation are very common in this pathology. Tumor cells possess the capacity to interact with the hemostatic system, activating the coagulation cascade and stimulating the prothrombotic properties of other blood cell components; the same events while inducing a hypercoagulable state, also contribute to the processes of tumor growth, neoangiogenesis and metastatic formation. Multiple risk factors associated with malignant disease contribute to the hypercoagulability state: stasis induced by prolonged bed rest, vascular invasion by the tumor and iatrogenic complications including the use of central vein catheters and chemotherapy. Several tests have been developed to assess the hypercoagulable state, however their clinical significance still needs to be defined, especially in terms of their predictive value for thrombosis. Clinical manifestations vary from localized deep venous thrombosis (DVT) or pulmonary embolism, more generally associated with solid tumors, to disseminated intravascular coagulation, frequent in hematologic malignancies and metastatic cancer. Diagnosis of idiopathic DVT, in the absence of other risk factors, could indicate the presence of occult cancer, but the usefulness of an extensive work-up to detect malignancy in terms of cost to benefit ratio still has to be demonstrated. Patients with cancer and thromboembolism must be treated with anticoagulant therapy; a large number of studies have shown that either low molecular weight heparins or standard unfractionated heparin for the treatment of acute deep vein thrombosis in hospitalized patients are equally safe and effective; however, the first treatment has been reported to be associated with a lower mortality. After an episode of thrombosis the patients should be protected by a long term course of oral anticoagulation, remaining high the risk of recurrence for as long as the cancer is active.
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PMID:[Blood coagulation changes and neoplastic pathology]. 1107 43

A 22-year-old woman with a newly detected chondroid liposarcoma located in the iliac muscle was diagnosed as having bilateral pulmonary embolism. Gadolinium-enhanced MRI further revealed a long distance thrombus reaching from the iliac vein to the right atrium. The thrombus was attributed to a hypercoagulability state which has been described for chondroid liposarcoma. High-dose chemotherapy with autologous stem cell support reduced the tumor burden and led to a symptom-free interval of 6 months. Despite therapeutic anticoagulation, repeated imaging showed no reduction or remodeling of the thrombus. However, when the thrombus progressed again, the patient underwent cardiac surgery and histology revealed the intravascular growth of the known chondroid liposarcoma. We conclude that in sarcoma patients intravascular tumor growth must be kept in mind when imaging is suggestive for thrombosis.
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PMID:Thrombectomy discloses intravascular growth of chondroid liposarcoma mimicking a long distance vena cava thrombosis. 1536 85

Primary pulmonary artery sarcomas (PASs) are rare and lethal tumors. They are easily misdiagnosed as chronic pulmonary embolism, mediastinal mass or tumor emboli, which delay a proper treatment. Although the advanced technologies are now increasingly being used, their diagnosis is usually hard to establish preoperatively at the present time. We report here a case of a 68-year-old female with PAS with lung metastases, who firstly presented with symptoms of common cold and anemia. Although a PAS had been suspected, the final diagnosis of pulmonary intimal sarcoma was made only postoperatively by histological and immunohistochemical examination. The patient died 8 months after the operation because of tumor growth progression, despite adjuvant chemotherapy and radiation therapy. Although pulmonary intimal sarcomas are usually of poorly differentiated mesenchymal malignancy, most reported cases are immunohistochemically positive for vimentin, alpha-smooth muscle actin (SMA), and/or desmin, therefore resembling leiomyosarcomas. However, the diagnosis of leiomyosarcoma should not be made on the basis of immunostains in the absence of typical morphologic features, and PAS, like the present case, should be more appropriately classified as intimal sarcoma according to the new WHO Classification of Tumours of Soft Tissue and Bone published in 2002.
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PMID:Intimal sarcoma of the pulmonary artery: report of an autopsy case. 1613 54

A 49-year-old man was admitted to our hospital for an expanding tumor in the pulmonary artery. He had visited a previous hospital complaining of dyspnea on effort and had syncope 4 months before admission, and pulmonary embolism was diagnosed because enhanced chest CT showed filling defects, with calcification in the pulmonary trunk and left pulmonary artery. Despite thrombolytic and anticoagulant therapy, the filling defects grew and expanded into the extravascular portion. Additionally, CT showed multiple pulmonary nodules and a small calcified nodule in a right-sided back muscle also appeared. At our hospital, FDG-PET showed abnormal uptake in each lesion shown on CT. We then performed a CT-guided needle biopsy of the nodule of the back muscle, which was pathologically diagnosed as osteosarcoma. He was finally given a diagnosis of osteosarcoma of the pulmonary artery. We administered cisplatin and doxorubicin with partial inhibitory effect on tumor growth. Osteosarcoma of the pulmonary artery is extremely rare, and its diagnosis is difficult before surgery or autopsy. To the best of our knowledge there have been no reports of chemotherapy for osteosarcoma of the pulmonary artery.
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PMID:[Case of osteosarcoma of the pulmonary artery]. 2122 99

Patients with cancer are at high risk of developing venous thromboembolism (VTE), including deep venous thrombosis and pulmonary embolism. Compared to non-cancer patients, VTE in cancer is more frequently associated with clinical consequences, including recurrent VTE, bleeding, and an increase in the risk of death. Low-molecular-weight heparins (LMWHs) are commonly recommended for the prevention and treatment of VTE in cancer patients because of their favorable risk-to-benefit profile. Indeed, compared with vitamin K antagonists, LMWHs are characterized by a reduced need for coagulation monitoring, few major bleeding episodes, and once-daily dosing, which make these drugs more suitable in the cancer setting. Guidelines have been published recently with the aim to improve the clinical outcomes in cancer patients at risk of VTE and its complications. Coagulation activation in cancer may have a role not only in thrombosis but also in tumor growth and dissemination. Hence, inhibition of fibrin formation has been considered a possible tool against the progression of malignant disease. Clinical studies show that anticoagulant drugs may have a beneficial effect on survival in cancer patients, with a major role for LMWHs. Recently a number of prospective randomized clinical trials to test LMWHs to improve cancer survival as a primary endpoint in cancer patients have been conducted. Although the results are controversial, the interest in this research area remains high.
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PMID:Comparative assessment of low-molecular-weight heparins in cancer from the perspective of patient outcomes and survival. 2291 78

Anti-angiogenic therapy, targeting vascular endothelial growth factor (VEGF)-A/VEGF receptors (VEGFRs), is beneficial for tumor growth prevention in a malignant glioma. A simultaneous blockade using both bevacizumab (Bev), which targets circulating VEGF-A, and a multi-kinase inhibitor on VEGFRs was more effective for advanced solid cancers, including melanoma and renal cell carcinoma. However, previous clinical trials demonstrated a high adverse event rate. Additionally, no studies previously assessed treatment efficacy and safety using both VEGF-A and VEGFR-targeted agents for malignant gliomas. We had conducted clinical trials investigating VEGFRs peptide vaccination in patients with malignant gliomas, in which the treatment exhibited safety and yielded therapeutic effects in some patients. The combined use of Bev and VEGFRs vaccination may enhance the anti-tumor effect in malignant gliomas. In this pilot study, the adverse event profile in patients treated with Bev after the vaccination was investigated to establish this treatment strategy, in comparison to those treated with Bev collected from the published data or treated with the vaccination alone. In our previous clinical studies on patients with malignant gliomas, Bev was administered to 13 patients after VEGFRs vaccinations. One patient had a Grade 4 pulmonary embolism. Two patients had Grade 2 cerebral infarctions. There were no significant differences in the adverse event rates among patients treated with Bev, with the vaccination, or with Bev after the vaccination. Although careful observation is imperative for patients after this combination treatment strategy, VEGFRs-targeted vaccination may coexist with Bev for malignant gliomas.
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PMID:A Pilot Study of the Adverse Events Caused by the Combined Use of Bevacizumab and Vascular Endothelial Growth Factor Receptor-Targeted Vaccination for Patients with a Malignant Glioma. 3288 69