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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent progress in elucidating the complex and heterogeneous interactions between malignancy and coagulation or fibrinolysis reactions in humans has clarified the pathogenesis of disseminated intravascular coagulation that occurs with malignancy and has revealed evidence for two distinct pathways of growth regulation based on production by tumor cells of initiators of thrombin formation versus plasminogen activators. We have proposed a preliminary classification of tumors (see Table 2) based on these interactions. Type I tumors are those in which the tumor cells are associated with an intact coagulation pathway that leads to thrombin formation at the tumor periphery but in which the tumor cells lack u-PA. Examples of tumors in this category include SCCL, malignant melanoma, and renal cell carcinoma. Type II tumors are those in which the tumor cells express u-PA but lack an associated coagulation pathway leading to thrombin formation. Examples of type II tumors include prostate cancer, colon cancer, breast cancer, and N-SCLC. Type III tumors are those that express neither of these pathways, or exhibit some other pattern of interaction. Obviously, this formulation must be regarded as hypothetical. However, this concept fits with the limited data available to date from clinical trials. More importantly, this hypothesis can be tested further by means of intervention aimed at interrupting pathways relevant to specific tumor types. Characterization of additional tumor types by the methods described should permit amplification of this classification of tumors and other patterns of interaction may be defined. Exploration of the coagulation-cancer interaction holds considerable promise for gaining new understanding of both the coagulation mechanism and tumor biology. Most intriguing is the prospect that imaginative approaches to cancer treatment may be devised that are not only relatively nontoxic and low cost, but also effective.
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PMID:Pathways of coagulation/fibrinolysis activation in malignancy. 157 11

Platelet counts were evaluated in 714 patients with advanced non-small cell lung cancer (N-SCLC), small cell carcinoma of the lung (SCCL), and colon cancer entered to a clinical trial. Patients had not received prior chemotherapy. Platelet counts were not different in patients who had received radiation therapy prior to entry to the study. In comparison to the other tumor types, patients with N-SCLC demonstrated an increased prevalence of thrombocytosis (counts greater than 400,000/mm3), higher platelet counts at the time of entry to the study, higher over all mean platelet counts, relative preservation of high platelet levels during disease progression, and no relationship between platelet numbers and the amount of chemotherapy given. By contrast, platelet counts in patients with SCCL were negatively correlated with the absolute amount of cyclophosphamide and adriamycin given, and declined most dramatically with disease progression and death. Platelet numbers did not correlate with fibrinopeptide A or fibrin split product levels suggesting that disseminated intravascular coagulation or fibrinolysis may have had less influence on platelet numbers than certain other factors. By contrast, significant correlations were found for all three tumor types between platelet numbers and other indicators of bone marrow function including anemia, total leukocyte count, and absolute neutrophil count; and the fibrinogen level. Based upon these findings, we postulate that the host response to malignancy, possibly in the form of production of bone marrow-stimulating cytokines, may play a prominent role in regulation of platelet counts in these (and perhaps other) neoplasms, and that a particularly prominent and persistent degree of marrow stimulation exists in patients with N-SCLC.
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PMID:The platelet count in carcinoma of the lung and colon. 196 50

A 53-year-old man with a prior history of myocardial infarcts and small cell lung cancer presented with lower limb ischemia. Laboratory tests revealed acute consumption coagulopathy and echocardiography showed massive intracavitary thrombi in the right atrium and both ventricles. Despite the administration of heparin, the patient died 3 weeks later of ventricular fibrillation. Autopsy demonstrated no relapse of lung cancer but large old myocardial infarcts.
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PMID:Intracardiac thrombosis associated with an acute consumption coagulopathy. 381 55

The clinical manifestation of disseminated intravascular coagulation (DIC) as paraneoplastic phenomenon is common in patients with lung cancer (especially in those with non small cell lung cancer).Surprisingly, only few data have been published on the prevalence of this phenomenon. Herein we present the case of a patient with metastatic giant-cell carcinoma of the lung complicated by DIC leading the patient to death. We also review the literature regarding the incidence, the pathogenesis and the therapy of DIC in NSCLC. As more effective therapy for lung cancer becomes available and patients live longer, DIC can be expected to be encountered more frequently. Because of this fact clinicians should be alert to the occurrence of such clotting disorders and should be familiar with their diagnosis and management.
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PMID:Disseminated intravascular coagulation (DIC) and non-small cell lung cancer (NSCLC): report of a case and review of the literature. 1907 Mar 99

A 76-year-old woman was admitted to our hospital with infiltrations evident in the right lower lobe on chest computed tomography. Bronchoscopic biopsy showed lymphoma of mucosa-associated lymphoid tissue (MALT). Lymphoma of the pulmonary MALT became enlarged at 8 months after diagnosis and dyspnea developed. Four courses of chemotherapy(rituximab+ cladribine)resulted in a partial response. However, 14 months after the chemotherapy, she developed multiple lung and liver tumors accompanied by disseminated intravascular coagulation syndrome. A histological examination of bone marrow aspiration showed small cell carcinoma. We administered one course of carboplatin and etoposide, but bone marrow suppression was so severe that further chemotherapy was precluded. To our knowledge, this is a rare case of small cell lung cancer arising from the treatment of lymphoma of pulmonary MALT.
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PMID:Small-cell lung cancer arising after chemotherapy for a patient with lymphoma of pulmonary mucosa-associated lymphoid tissue-a case report. 1983 33