Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hemostatic abnormalities are present in a majority of patients with metastatic cancer. These abnormalities can be categorized as 1) increased platelet aggregation and activation, 2) abnormal activation of coagulation cascade, 3) release of plasminogen activator, and 4) decreased hepatic synthesis of anticoagulant proteins like Protein C and antithrombin III. The abnormal activation of coagulation cascade is mediated through release of Tissue Factor, Factor X activators, and other miscellaneous procoagulants from the plasma membrane vesicles of tumor cells. Macrophages of a tumor-bearing host also produce increased amounts of Tissue Factor. Production of Factor X activators and macrophage Tissue Factor is decreased by warfarin. The ability of the tumor cells to produce platelet-aggregating activity and plasminogen activator parallels their metastatic potential in animal and experimental systems. These studies also show that antiplatelet agents and antibodies against plasminogen activator can suppress the metastatic process. One or more laboratory abnormalities of hemostasis can be shown in up to 95% of patients with metastatic cancer. These abnormalities, however, are unable to predict subsequent development of thromboembolic or hemorrhagic complications. Clinical complications occur in 9-15% of the patients in the form of thrombotic or hemorrhagic disorders. The therapy of tumor-related coagulopathy should be guided by its clinical expression. Subclinical DIC should not be treated. Coumadin is generally ineffective for therapy of thrombosis in cancer patients. There is no consensus regarding the use of heparin in acute promyelocytic leukemia (APL). The defibrination in APL may be from disseminated intravascular coagulation as well as systemic fibrinolysis, as shown by decreased alpha 2 antiplasmin levels. In such cases, epsilon aminocaproic acid plus heparin therapy may be of benefit.
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PMID:Hemostasis in malignancy. 174 46

A case is reported of a 60 year-old patient with chronic disseminated intravascular coagulation (DIC) which was increased by the therapeutic embolization of a renal tumour. The patient had 2 primary carcinomas (renal and prostatic) with vertebral metastases, severe chronic anaemia (due to haematuria), and chronic DIC, with thrombocytopaenia, soluble complexes, and fibrinogen and fibrin degradation products. Therapeutic embolization of the renal artery was carried out with fragments of dura mater. Although the result was anatomically very satisfactory, the patient's condition worsened, with continuing haematuria, and development of an haematoma in the lumbar fossa. Coagulation factors and antithrombin III (AT III) concentrations decreased, whereas the activated partial thromboplastin, thrombin and reptilase times increased. The patient also suffered from acute renal failure (creatinine: 690 mumol.l-1). Treatment consisted in fluid replacement, red blood cell and platelet transfusions, 150 IU.kg-1.d-1 heparin and 20 IU.kg-1.d-1 AT III. Haematological tests returned to pre-embolization values on the ninth day. The sudden worsening in the patient's condition was probably due to the sudden massive release of tissue thromboplastins related to the renal necrosis induced by the therapeutic embolization. The use of heparin AT III in the management of this patient is discussed.
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PMID:[Worsening of chronic disseminated intravascular coagulation after embolization of the renal artery]. 233 Oct 88

Vitronectin, also known as serum-spreading factor or S-protein, mediates cell adhesion and inhibits formation of the membrane-lytic complex of complement and the rapid inactivation of thrombin by antithrombin III in the presence of heparin. Vitronectin is normally present in plasma at a concentration of approximately 300 micrograms/mL. The investigators quantified plasma vitronectin with an enzyme-linked immunosorbent assay and visualized reduced and nonreduced vitronectin by immunoblotting after separation of plasma or serum by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The concentration of plasma vitronectin was markedly reduced in some patients with disseminated intravascular coagulation, especially in those with liver failure; it was near normal in patients with metastatic cancer and acute leukemia. Patients with vitronectin levels less than 40% normal invariably had low fibrinogen and antithrombin III and a prolonged prothrombin time. In both normal and patient plasmas there was heterogeneity in the ratio of the 75,000- and 65,000-mol wt polypeptides of reduced vitronectin: 18% had mostly the 75,000-mol wt polypeptide, 59% had roughly equal amounts of the two polypeptides, and 22% had mostly the 65,000-mol wt polypeptide. This polymorphism is inherited and appears to be due to two alleles that are present with approximately equal frequency. The blotting patterns of vitronectin in reduced and nonreduced plasmas were largely unaltered in plasma of patients with defibrination syndrome, fibrinolysis, liver failure, sepsis, metastatic cancer, and acute leukemia. There was no evidence of fragmentation of vitronectin or formation of the disulfide-bonded complex of vitronectin and thrombin-antithrombin III that is found when blood is clotted. Thus these results corroborate in vitro observations that the liver is the major source of plasma vitronectin, suggest that vitronectin may become depleted during disseminated intravascular coagulation, and define a genetic polymorphism of vitronectin.
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PMID:Plasma vitronectin polymorphism in normal subjects and patients with disseminated intravascular coagulation. 245 67

Spontaneous extracranial metastases of glioblastoma multiforme in the absence of previous surgery have been rarely reported (Table 1). We presented an autopsy case of glioblastoma multiforme which spontaneously metastasized to the lungs, bronchial lymph nodes, liver, kidney, heart and spleen. A 68-year-old man was admitted to the Department of Neurosurgery at our hospital with chief complaints of right sided weakness in July 1984. He was well until November 1983, when he noticed weakness of right lower extremity followed one month later by the weakness in the right arm. He was treated at another hospital under the diagnosis of cerebral infarction, but his right sided weakness gradually progressed. In June 1984, a diagnosis of brain tumor was made by the neurological findings and CT scan, and he was transferred to our hospital for further evaluation and treatment. Neurological examination revealed disorientation, bilateral papilledema, right hemiparesis, right hyperreflexia and right hemisensory disturbance. CT scan revealed abnormal low density area in the left fronto-parietal lobe (Fig. 1) with irregular enhanced lesions on contrast CT scan (Fig. 2). Chest x-ray showed abnormal shadow in the right middle and lower lobe (Fig. 3) and a diagnosis of pulmonary infarction was suspected. The clinical states of this patient took downhill course and he expired on July 13, 1984 by the complication of disseminated intravascular coagulation syndrome. The brain weight was 1400 gr. Dura mater and falx cerebri were tightly adherent to the left parietal lobe (Fig. 4). Primary brain tumor was found in the left fronto-parietal region. The tumor was poorly defined with necrosis and hemorrhage (Fig. 5).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Glioblastoma multiforme with extracranial metastases without previous surgery: demonstration of extracranial metastases by peroxidase antiperoxidase staining and clinicopathological study]. 282 54

Two patients, a 58-year-old male and a 41-year-old female, who had poorly differentiated adenocarcinoma with signet ring cells of the stomach, developed progressive multiple organ failure following their surgical treatment, even though they did not have any direct surgical complications. Their abdominal explorations revealed primary gastric tumors with deep infiltration and metastases to the regional lymph nodes. Their clinical courses were characterized by acute renal failure and respiratory distress associated with disseminated intravascular coagulation. Histopathological examination at autopsy revealed diffuse cortical necrosis of the kidneys and marked congestion, edema, and hemorrhage with or without alveolar fibrosis of the lungs. Fibrin thrombi in the lesions of the kidneys and lungs strongly suggested the existence of disseminated intravascular coagulation. It is likely that the widely spreading cancer cells themselves produced the subclinical background for disseminated intravascular coagulation, which appeared to play an important role in the development of the multiple organ failure.
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PMID:Multiple organ failure without sepsis following surgical treatment of advanced gastric carcinoma. 285 82

Evidence indicates that progression of the Lewis lung carcinoma in mice and small cell carcinoma of the lung in humans is retarded by warfarin administration. This suggests that vitamin K-dependent pathways are of importance in the pathogenesis of these tumors. Available data were reviewed for these tumor types in an attempt to explore mechanisms and to gain insights that might guide the selection of other coagulation-reactive drugs for testing in future controlled clinical trials in small cell carcinoma of the lung. While many differences exist between the Lewis lung tumor and small cell carcinoma of the lung, both are rapidly growing malignancies of pulmonary origin that metastasize early to kill the host after a short time. Both are favorably influenced by combination chemotherapy and radiation therapy as well as anticoagulant treatment. Peripheral blood changes indicative of disseminated intravascular coagulation occur in each of these tumor types, and tumor cells from both are capable of interacting with the coagulation mechanism. While many details concerning the host-tumor interaction remain to be elucidated, the considerable and diverse information available for these tumor types provides a secure base for future investigation. It is postulated that certain drugs in addition to warfarin might reasonably be studied in controlled clinical trials of small cell carcinoma of the lung and that drugs other than warfarin might be effective for tumor types that are not responsive to this agent.
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PMID:Basis for selection of anticoagulant drugs for therapeutic trials in human malignancy. 301 48

Disseminated intravascular coagulopathy is a serious complication of numerous pathological conditions, particularly metastatic cancer. It is rarely encountered in orthopaedic surgery. Prompt recognition and treatment is required to prevent death. We describe two patients with pathological fractures of the proximal femur due to metastatic disease who died from disseminated intravascular coagulation after operation. A high index of suspicion, careful monitoring of the clotting mechanism and prompt treatment are required.
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PMID:Disseminated intravascular coagulopathy in patients with cancer undergoing operation for pathological fractures of the hip. 362 52

The cases of 42 patients with malignant ascites treated with a peritoneal venous shunt over a 5-year period are reviewed to establish the incidence of surgical and postsurgical complications. Although the yield of malignant cells found in the peripheral blood was increased after shunting, no new hematogenous metastases were observed after the operation. No evidence of disseminated intravascular coagulation was observed after shunt placement. While the shunt effectively relieved the discomfort due to abdominal distention and respiratory impairment, no restoration of cutaneous hypersensitivity was observed in the nine patients who were anergic prior to surgery. The median survival of patients with breast and gynecological cancer, after surgery, was significantly longer than the survival of patients with primary gastrointestinal neoplasma. In conclusion, peritoneal venous shunt appears to be an effective and safe method to improve the quality of life of patients with malignant ascites.
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PMID:Peritoneovenous shunt and neoplastic ascites: a 5-year experience report. 376 70

Twelve autopsy cases of carcinomatosis of the bone marrow were examined clinicopathologically. Among them, 7 were gastric adenocarcinoma, and the other 5 were a rectal carcinoid and carcinomas of the lung, prostate, maxilla and kidney, respectively. The gastric cancers were almost all poorly differentiated adenocarcinoma with mucin production and presented poorer prognoses than the other cancers. Leukoerythroblastic anemia, microangiopathic hemolytic anemia and DIC were found more frequently in the gastric cancers than in the others. It is concluded that the evolution of these critical hematologic disorders may be dependent on differences of histologic type, original focus and cancer-host interactions as well as wide-spread skeletal metastases of cancer cells.
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PMID:[Clinicopathological examination of 12 autopsy cases of carcinomatosis of the bone marrow]. 398 85

During the period 1975 to 1984, a histopathologic diagnosis of primary cardiac hemangiosarcoma was made in 38 dogs at Angell Memorial Animal Hospital. The diagnosis was confirmed by exploratory thoracotomy in 16 cases and at necropsy in 22 cases. At the time of exploratory thoracotomy, 7 dogs were euthanatized because of nonresectability of the primary tumor and/or gross metastatic disease. In 9 dogs, the tumor was resected by removing part of the right atrium. Complications included atrial and ventricular arrhythmias, anemia, disseminated intravascular coagulation, and pneumonia. Prolonged and multiple hospitalizations were a common feature of the postoperative period. Adjuvant therapy was not utilized in any case. The mean survival time was 4 months (2 days to 8 months).
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PMID:Cardiac hemangiosarcoma in the dog: a review of 38 cases. 405 16


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