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)

The measurement of fibrin or fibrinogen degradation products is widely used in clinical practice for the diagnosis and follow up of coagulolytic disturbances. Recently D-dimer assays have become very popular owing to their direct application to plasma. However, in some clinical situations there is a need to differentiate fibrin from fibrinogen degradation products. These are still routinely measured by conventional assays on serum. We tried to develop various monoclonal antibodies specific for the neo-epitopes unmasked during the degradation of fibrin or fibrinogen. Fifteen mice hybridomas producing the expected antibodies were obtained and ten were extensively characterized. They could be classified in three reactivity classes: D and D-dimer, D-dimer and early fibrinogen or fibrin degradation products. These monoclonal antibodies were used to develop latex slide assays and ELISA techniques. Two types of assays were obtained; those which were specific for fibrin-related products and those evaluating the totality of fibrin or fibrinogen degradation products. Assays discriminating the fibrinogen split products from those derived from fibrin, and performed directly on citrated plasma can be proposed. They provide complementary information in clinical states such as DIC, pulmonary embolism, leukaemias, thrombolysis, etc.
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PMID:Monoclonal antibodies to different neo-epitopes on fibrinogen and fibrin degradation products. 172 2

Protein C (PC) is the central component of a major antithrombotic regulatory system with both anticoagulant and profibrinolytic properties. A deficiency of PC is one of several hereditary abnormalities of haemostatic proteins that have been described in patients with a propensity for thromboembolic complications. Major morbidity is often seen in these patients. The various aspects of hereditary PC deficiency in terms of clinical presentation, genetics, diagnosis and treatment of both homozygous and heterozygous states will be presented. In heterozygous deficiency, the levels of plasma PC are usually between 35% and 65% of normal, whereas the majority of normal individuals have levels between 70% and 130%. PC-deficient patients usually develop venous thrombotic complications between the ages of 15 and 40 years with a high incidence of DVT and pulmonary embolism. The majority of thrombotic lesions appear to develop spontaneously; others are associated with trauma, surgery or pregnancy. Treatment of symptomatic patients is initial heparin therapy followed by coumadin. After multiple thrombotic events, lifelong oral anticoagulant therapy is necessary. The potential complications of treatment are coumadin-induced skin necrosis, heparin-induced thrombocytopenia and bleeding. Homozygous PC deficiency, a rare but fatal hereditary condition, manifests itself with massive DIC and purpura fulminans in the newborn period. Effective treatment for these infants can be instituted with either oral anticoagulant therapy or PC replacement. The heterozygous deficiency of PC is similar to that found in other inherited disorders in that several genetic mechanisms are responsible for the expression of the disease. Both quantitative and qualitative decreases in PC exist, the former being type I deficiency and the latter, type II. The best initial diagnosis of either form involves a clotting (functional) assay while differentiation between the two also requires an antigenic (immunological) assay. Autosomal inheritance with significant variable penetrance is found with profound clinical implications. In summary, PC deficiency is one of a group of inherited disorders termed hereditary thrombotic disease, which may have serious implications for patient morbidity and mortality.
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PMID:Hereditary protein C deficiency: a review of the genetics, clinical presentation, diagnosis and treatment. 210 16

We report a fatal case of occult pulmonary embolism complicating bronchogenic carcinoma which presented with rapidly progressive pulmonary miliary shadows and respiratory failure. A clotting profile abnormality compatible with disseminated intravascular coagulation was noted. Postmortem examination showed extensive clots occluding the major pulmonary vessels and areas of pulmonary infarcts. Histologic examination revealed fibrin deposition in the microvasculature compatible with DIC. Cases of pulmonary embolism with DIC have previously been reported, but this is the first case with pathologic confirmation. Thus, unusual presentation with diffuse lung shadow and DIC should not deter the clinician from correct diagnosis so that appropriate treatment can be promptly started.
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PMID:Occult fatal pulmonary embolism with disseminated intravascular coagulation. An unusual case masquerading as miliary tuberculosis. 222 85

The combination of dacarbazine (DTIC, 220 mg/m2) and cisplatin (DDP, 25 mg/m2) IV daily for 3 days every 3 weeks, carmustine (BCNU, 150 mg/m2) IV every 6 weeks, and tamoxifen (TAM, 10 mg orally twice daily) produced a 50% objective response rate in patients with metastatic melanoma. Associated with this treatment, there was a high incidence of deep venous thrombosis (DVT) and pulmonary embolism (PE). In an effort to reduce this toxicity, this regimen minus TAM was studied, and the results are reported. Twenty of twenty patients are evaluable for response and toxicity. There was one complete response (CR) lasting 5+ months and one partial response (PR) lasting 4+ months for an overall response rate of 10% (95% confidence limits, 1.23% to 31.70%). Two patients exhibited a mixed response and three patients developed disease stabilization lasting 4 to 10 months. Toxicity was similar to the original study except that no patients developed DVT or PE. This statistically significant (Fisher's exact test [two-tail] P = 0.008) decrease in the response rate by comparison with that achieved with the TAM-containing regimen may signal an essential role of TAM in this regimen. TAM may be acting in synergy with cisplatin through its calcium channel-blocking properties. TAM should be included as described in the initial reports, and the patients should be carefully observed for vascular complications.
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PMID:The importance of tamoxifen to a cisplatin-containing regimen in the treatment of metastatic melanoma. 292 Mar 58

Plasmas from patients with a wide variety of thrombotic and presumed prethrombotic conditions were examined for high molecular weight crosslinked fibrin degradation products (known as X-oligomers) using a two-site enzyme-linked immunospecific assay (ELISA). This assay employed a catcher-tag principle using two monoclonal antibodies (mabs) directed towards different epitopes on the complex X-oligomer fraction. In general, thrombotic events (pulmonary embolism, PE, myocardial infarction, MI, peripheral vascular disease, PVD, and disseminated intravascular coagulation, DIC) were accompanied by elevated levels of X-oligomers in the plasma. During pregnancy the value of X-oligomer assays was demonstrated to be a clear-cut marker for pre-eclampsia. Patients following a variety of forms of surgery present with heterogeneous plasma levels of X-oligomers and this may merely reflect the formation and lysis of the fibrin formed during and after surgery. The possible value of this ELISA procedure in monitoring thrombolytic therapy is discussed with a critical analysis of the data presented herein. While the assay of X-oligomer was demonstrated to be a valuable marker of fibrinolysis in plasma, more extensive data are required in order to assess whether such an assay is of diagnostic value in thrombosis-related conditions.
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PMID:Monoclonal antibodies to crosslinked fibrin degradation products (XL-FDP). II. Evaluation in a variety of clinical conditions. 334 98

Denver type peritoneo-venous (PV) shunting for intractable ascites was performed in 16 patients also treated with endoscopic injection sclerotherapy (ST) for variceal haemorrhage. Indications, timing and results of shunt insertion are detailed and discussed. Serial ST for eradication of varices could be completed in 10 patients a median of 7 months before PV shunting. The postoperative risk of bleeding was increased four times, i.e. the number of GI bleedings per month of follow-up, was 0.05 and 0.21 (p less than 0.05) respectively, before and after shunt operation. Two patients experienced their first variceal bleeding and 6 patients rebled during a median follow-up of 3 months after PV shunting. The Denver shunt succeeded in resolving ascites clinically in 13 patients within 7 days with a median decrease in weight of 10 kg, parallel to increased urinary output and reduced serum-creatinine. Three patients did not benefit from the shunt procedure due to terminal neoplastic disease (one patient), and severe hepatorenal failure, although the shunts were proven patent. Serious complications included clinically important consumptive coagulopathy, DIC-syndrome (two patients), myocardial infarction (one), pulmonary embolism (three), and sepsis following intervention of obstruction (one).
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PMID:Peritoneo-venous shunting and endoscopic sclerotherapy in patients with portal hypertension. 349 19

A case study report is presented of a 20 year old black woman with a past history of oral contraceptive (OC) use who developed Budd-Chiari syndrome (hepatic vein thrombosis) associated with decreased levels of antithrombin 3. This combination has not been previously reported. The woman presented on December 28, 1979 with midepigastric pain. She had no previous illnesses, but OCs had been used up to 2 years prior to admission. Shortly after admission the patient became hypotensive, developed oliguric renal failure, and began to rapidly accumulate ascites. During this admission, the patient's transaminase levels abruptly declined. A percutaneous liver biopsy obtained on January 9, 1980 showed centrilobular hemorrhagic necrosis of a severe degree. An inferior vena cavagram was repeated on January 14, 1980 demonstrating hepatic vein thrombosis. Streptokinase, followed by heparinization, was given in an effort to lyse the thrombi, but repeat inferior cavagram on January 24th proved this to be unsuccessful. Thrombosis of the left iliac and left femoral vein then appeared. Because of her apparent "hypercoagulable state," the antithrombin 3 level was measured on January 31st and found to be 27%. A simultaneous serum fibrinogen was 255 mg/dl. Family members (father, mother, and 4 children) were studied. All had normal antithrombin 3 levels, thus excluding a familial defect. The patient gradually improved and was discharged on February 25, 1980 on Coumadin, diuretics, and a 3 g sodium diet. Because of ascites and peripheral edema, a LeVeen shunt was placed on March 25, 1980. At surgery, she was noted to have obstruction of the right internal jugular and right cephalic veins. Because of possible thrombosis in the superior inferior vena cava branches, venography was performed on March 31st and demonstrated thrombosis of the right subclavian, inferior vena cava, and internal iliac veins. Despite the therapy, patient again began to reaccumulate ascites and was readmitted on May 17th. The then nonfunctioning shunt was repositioned in the patient's right atrium. Postoperatively, the patient's course was complicated by DIC. Because heparin induced thromboycytopenia was suspected, heparin was discontinued and Coumadin begun. On June 6th the patient became suddenly short of breath. A lung scan was consistent with pulmonary embolism. She could not be adequately ventilated and died on June 8th. Although the patient discontinued OC use 2 years prior to initial presentation of the disease, the morphologic features of the venous thrombosis and hepatic damage were indicative of a chronic, ongoing process of longer than 6 months' duration, thus raising the possibility of a cause-effect relationship between the OC and thrombotic process. Prospective studies are needed to substantiate the view of a relationship between OC use, antithrombin 3 deficiency, and the Budd-Chiari syndrome.
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PMID:Budd-Chiari Syndrome and antithrombin III deficiency. 710 23

Case report about death due to veno-occlusive liver disease following Dacarbazine treatment: 9 years after surgical treatment of malignant melanoma of the trunk a 68-years old patient developed lymph node metastases in the right axilla, which were removed immediately by surgical excision. One month before the patient had undergone surgical treatment of empyema of the gallbladder: Cholecystectomy and appendectomy were performed, postoperative recovery was uncomplicated. On account of the second lymph node metastasis within nine months adjuvant treatment with Dacarbazine was agreed and started one month later. After having performed the first course of treatment without any hints to intolerance the patient suddenly exhibited severe shock symptoms on the fourth day of the second course. Clinically residual myocardial infarct or pulmonary embolism were assumed, but could not be verified. The patient delivered increasing hepatomegaly. A massive increase in transaminase values was noted. Hemostasiologic changes with decreased Quick value occurred. The patient died of cerebral hemorrhage five days after beginning the second Dacarbazine cycle. Autopsy findings were severe liver cell necroses as well as liver vein thromboses, no metastases of melanoma could be found. Hepatotoxicity of Dacarbazine and the mechanism of liver vein thrombosis are discussed with special regards to possible hemostasiologic changes and sensibilisation due to Dacarbazine and/or previous liver cell damage.
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PMID:[Veno-occlusive syndrome with acute liver dystrophy following decarbazine therapy of malignant melanoma (author's transl)]. 721 35

A low-D-Dimer concentration has a high negative predictive value for thromboembolic events. Actual and proposed applications include exclusion diagnosis of DIC, DVT and pulmonary embolism (1-7), follow up of cancer therapy (8) and diagnosis of abruptio placentae(9). A variety of tests are commercially available. Unfortunately, due to differences in standardization protocols, the cut-off normal/pathological of one test can usually not be used for another(10). As was shown by Nieuwenhuizen, one way to at least reduce these discrepancies is to use patient material as a reference(11). We have used this approach to standardize the latex test Tinaquant a D-Dimer against the ELISA test Asserachrom D-Dimer.
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PMID:Pooled patient samples as reference material for D-Dimer. 857 41

The incidence and clinical significance of pulmonary embolism (PE) in pulmonary malignancy were analysed among 111 autopsy cases including: 65 primary and 24 metastatic lung cancer, 8 hematological malignancies and 14-malignant pleural mesothelioma. In 34 (31%) cases PE was found, in 4 (12%) patients cancer tissue emboli was documented. In nonsmall cell lung cancer the frequency of PE was 40%, compared to 24% in small cell, 25% in metastatic lung cancer and 14% in mesothelioma. Deep venous thrombosis of lower extremities was the source of thrombotic material in 35% cases. In remaining cases the sources of thrombotic material were different (caval vein inferior, superior, and their main branches, right heart cavities, pulmonary artery). In 8 patients with PE the acute form of DIC was observed. In 15 (44%) patients the clinical ante mortem diagnosis of PE was done. In 26% of all analysed cases PE was the direct cause of death. We concluded that PE is a frequent and dangerous complication of lung neoplasms. Clinical diagnosis can be extremely difficult.
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PMID:[Pulmonary embolism in malignancy of the lung: a retrospective clinical evaluation and pathomorphologic personal material]. 898 39


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