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)

The authors prospectively studied 113 consecutive patients with deep venous thrombosis of the lower extremities to determine the most appropriate workup study for searching for a hidden cancer. After a careful physical examination, the following routine tests were performed: erythrocyte sedimentation rate (ESR), whole blood counts, biochemistry, carcinoembryonic antigen (CEA) levels, chest radiograph, upper gastrointestinal endoscopy, abdominal ultrasound and computed tomography (CT) scan. If a malignant lesion was suspected, further appropriate studies were performed. After discharge, periodic follow-up was performed on all patients in the outpatient clinic. A malignant neoplasm was detected in 12 patients. Of these 12 patients, six were asymptomatic with the exception of experiencing thrombophlebitis. Cancer was found more commonly in patients with idiopathic deep vein thrombosis (DVT) (7 of 31 versus 5 of 82 patients with secondary DVT; P = 0.012), and in those patients with abnormal lactic dehydrogenase (LDH) levels (6 of 23 versus 6 of 90; P = 0.007). Abnormal CEA levels allowed diagnosis of two cases of colonic cancer (on colonoscopy). Both ultrasound and CT scan of the abdomen showed two cases of urinary bladder carcinoma at a very early stage. Furthermore, two cases of adenomatous polyps in colon were found, a condition considered by most authors to be a colorectal cancer precursor. In addition, there were five patients with large benign pelvic tumors, and two patients with absent inferior vena cava. The most striking finding was that some cases of cancer were at a very early stage. It was concluded that blood cell counts, LDH, CEA, chest radiograph, and abdominal ultrasonography (or CT scan) should be routinely performed on all patients with deep venous thrombosis (particularly those with idiopathic DVT). Malignancy would not have been recognized in some patients if these tests had not been performed.
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PMID:Occult cancer in patients with deep venous thrombosis. A systematic approach. 198 47

Deep vein thrombosis (DVT) and subsequent pulmonary embolism (PE) is a major source of mortality and morbidity in stroke patients. This study was designed to determine the effectiveness of different prophylactic treatments in the prevention of DVT after a stroke in patients undergoing rehabilitation. An additional objective was the identification of risk factors for DVT in stroke in patients during rehabilitation. Three hundred and sixty patients, over a 3-year period, were randomly assigned to one of four groups: adjusted dose heparin, intermittent pneumatic compression (IPC), functional electrical stimulation (FES), or control. There was no significant difference in the development of DVT by treatment group. Patients with DVT on admission (prevalent, n = 61) were compared with the study patients (n = 360). Time interval (from stroke to admission) and lactic dehydrogenase (LDH) concentration were significant risk factors, as well as predictors, for development of DVT (p < .000). These results suggest that the longer a patient remains without DVT prophylaxis after a stroke, the greater the risk of developing DVT and this supports early prophylaxis before rehabilitation.
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PMID:Deep vein thrombosis: prevention in stroke patients during rehabilitation. 771 32

The influence of methylmethacrylate monomer (MMA) on the cellular integrity of monocytes, granulocytes and endothelial cells in vitro was investigated. Clinically relevant blood concentrations of MMA (i.e., 5-10 micrograms/mL) were clearly cytotoxic to all cell types studied, as evidenced by the release of lactic dehydrogenase (LD) and 51Cr, and increased uptake of trypan blue (vital staining). Scanning electron microscopic examination of cells treated with 10 micrograms/mL MMA showed marked signs of cytotoxicity after 1 min incubation, and after 30 min the majority of the cells were totally disintegrated. These findings may have clinical bearing on intraoperative cardiorespiratory dysfunction and deep vein thrombosis in MMA-fixed joint replacement surgery.
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PMID:Toxic effects of methylmethacrylate monomer on leukocytes and endothelial cells in vitro. 819 46

Bleeding and thrombosis are major causes of morbidity and mortality in patients with chronic myeloproliferative disorders. We retrospectively evaluated 101 consecutive patients affected by primary thrombocytosis (46 male, 55 female, aged 18-84 years; mean +/- SD 61 +/- 15) followed for a period ranging from 6 months up to 10 years (median 5 years) at our hematological unit. At the time of diagnosis 48 patients were asymptomatic; 26 had clinical evidence of atherothrombosis (cerebral ischemic attacks, ischemic heart disease, peripheral occlusive arterial disease), ten had venous thrombosis, four experienced major hemorrhages, 23 presented microvascular ischemic manifestations namely erythromelalgia, paresthesias, acrocyanosis and dizziness. At presentation 51.2% of the patients had elevated serum lactic dehydrogenase, 34.5% hyperuricemia, and 23.4% serum creatinine > 1.2 mg/dL. Color Doppler ultrasound provided evidence of vascular stenosis or medium-intimal hyperplasia of epiaortic vessels in 48.9% of patients studied, and similar alterations of lower limb arteries in 23.8% of cases. Therapy modality included an antiplatelet agent (picotamide 300 mg/bid); a cytoreductive agent (busulphan, hydroxyurea, pipobroman or melphalan) was used when platelet count was > 800000/microL. Symptoms due to microvascular ischemia promptly regressed after picotamide and cytoreductive therapy. During follow-up. nine patients suffered from atherothrombotic events (transient ischemic attacks, ischemic stroke, unstable angina pectoris) and five developed deep vein thrombosis or superficial thrombophlebitis. Five patients experienced major hemorrhages (two melena, two hematuria, one perioperative bleeding); the two gastrointestinal hemorrhages occurred in patients self-medicated with non steroidal anti-inflammatory drugs, and the two episodes of hematuria occurred on oral anticoagulant therapy and aspirin respectively. No major bleeding occurred in patients on continuative therapy with picotamide, even in the presence of upper digestive tract disorders. Seven patients died: mortality resulted from one sudden coronary death, three solid neoplasia, one blast crisis, one anile, and one massive hemorrhage due to abdominal aortic prosthesis tearing. Our study suggests that a long-term antithrombotic prophylaxis with picotamide may be of benefit in patients affected by primary thrombocytosis; a controlled clinical trial is warranted to assess whether picotamide can ameliorate the natural history of the disease.
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PMID:Thrombotic and hemorrhagic complications in chronic myeloproliferative disorders. 895 59

Thalidomide has antiangiogenic properties and was found to be effective in patients with multiple myeloma (MM) when used in the setting of posttransplantation relapse. We have now analyzed risk factors associated with development of deep vein thrombosis (DVT) in a cohort of 535 patients treated with thalidomide with cytotoxic chemotherapy (VAD [vincristine/doxorubicin/dexamethasone], CAD [cyclophosphamide/doxorubicin/dexamethasone], DCEP [dexamethasone/cyclophosphamide/etoposide/cisplatin], or DT-PACE [dexamethasone/thalidomide/cisplatin/doxorubicin/cyclophosphamide/etoposide] or without cytotoxic chemotherapy (thalidomide and dexamethasone only). A total of 82 patients developed DVT, and the frequency was affected by a number of baseline characteristics. On multivariate analysis, the combination of thalidomide with chemotherapy including doxorubicin was associated with the highest odds ratio (OR) for DVT (4.3; P < or = 0.001); in addition, newly diagnosed disease (OR, 2.5; P = 0.001) and chromosome 11 abnormality (OR, 1.8; P = 0.048) were also independent predictors for DVT. With a median follow-up of 2.9 years, survival was inferior in patients with chromosome 13 abnormalities (P = 0.001), age > 60 years (P = 0.001), lactate dehydrogenase level > or = 190 IU/L (P = 0.002), and creatinine level > or = 2 mg/dL (P < 0.001). However, the development of DVT did not adversely affect survival when examined as a time-dependent variable and adjusted for standard risk features (hazard ratio, 0.8; P = 0.162).
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PMID:Thalidomide and deep vein thrombosis in multiple myeloma: risk factors and effect on survival. 1283 52

Venous thromboembolism (VTE) constitutes a common cause of hospital-related morbidity and mortality, with the proverbial clinical feature of deep venous thrombosis (DVT). Endothelial cell injury and dysfunction comprise the critical contributor for the development of DVT. Lipoxin A4 (LXA4) fulfills pleiotropic roles in injury repair. However, its role in DVT remains poorly elucidated. In the present study, LXA4 supplementation dampened H2O2-evoked cytotoxic injury in human umbilical vein endothelial cells (HUVECs) by increasing cell viability, suppressing cell apoptosis and caspase-3 activity. Moreover, treatment with LXA4 afforded cytoprotective effects against oxidative stress damage in response to H2O2 by abrogating ROS, lactate dehydrogenase (LDH) and MDA leakage, and elevating anti-oxidant SOD levels. Notably, LXA4 administration attenuated pro-vasoconstriction factor endothelin-1(ET-1) expression in HUVECs exposed to H2O2, but enhanced the productions of vasodilatation factor NO and prostacyclin (PGI2). Simultaneously, H2O2-induced high expression of pro-thrombotic Von Willebrand Factor (vWF) was also inhibited by LXA4. Mechanism analysis substantiated that LXA4 further augmented activation of the Nrf2-HO-1 pathway. Nevertheless, blocking this signaling via si-Nrf2 transfection or HO-1 antagonist ZnPP both reversed LXA4-mediated effects against oxidative stress injury and thrombotic potential. Cessation of the LXA4 receptor pathway by its inhibitor Boc2 not only counteracted LXA4-evoked activation of the Nrf2-HO-1, but also reversed LXA4-mediated anti-oxidative stress and thrombosis-related factor expression. Accordingly, this study suggests that LXA4 may ameliorate vascular endothelial cell oxidative stress injury and subsequent thrombotic response via LXA4 receptor-dependent activation of the Nrf2-HO-1 signaling, implying a promising strategy for DVT and its complication.
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PMID:Lipoxin A4 restores oxidative stress-induced vascular endothelial cell injury and thrombosis-related factor expression by its receptor-mediated activation of Nrf2-HO-1 axis. 3105 86