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

Chronic disseminated intravascular coagulation with secondary hyperfibrinolysis occurred in a patient with metastatic renal carcinoma. In the beginning the treatment with heparin was successfull. Heparindosage up to 35 000 E/day could never suppress this process completely. The value of determining thrombintime, concentration of fibrin splitting products, coagulation factors II, V, VII, IX, X and XIII, antithrombins II and III in controlling heparintherapy is discussed. Besides thrombintime and platelets the determination of fibrin splitting products is another substantial factor in controlling treatment of chronic intravascular coagulation. The patient died of myocardial rupture with heart tamponade, caused by a great intramyocardial metastasis.
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PMID:[Consumption coagulopathy in a patient with metastatic renal carcinoma (author's transl)]. 93 86

We report a case of left renal cell carcinoma extending into vena cava with malignant peritoneal mesothelioma. A 41-year-old man presented to our outpatient clinic with macroscopic hematuria. Upon laparotomy, numerous white nodules were identified on diaphragm and serosa of liver, stomach, small intestine and mesentery. Biopsied specimen showed malignant mesothelioma of peritoneum and renal cell carcinoma of left kidney. He was treated with intraperitoneal cisplatinum and intravenous pirarubicin for mesothelioma, and chemoembolization for renal tumor. After two courses of therapy, he suffered from disseminated intravascular coagulation and died of subarachnoid hemorrhage. Autopsy revealed that intraperitoneal nodules were markedly decreased in number and renal tumor had changed into hemorrhagic necrosis, but tumor thrombus in vena cava had little necrotic change.
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PMID:[Renal cell carcinoma with malignant peritoneal mesothelioma: report of a case]. 141 43

Topical administration of interferon for locally recurrent renal cell carcinoma in 2 cases was reported. Case 1: a 56-year-old woman had undergone radical nephrectomy for left renal cell carcinoma. She had a locally recurrent tumor adjacent to spleen 26 months after the surgery. She received 3 million units of interferon alpha every day intralesionally for almost 3 years without any distant metastasis. Case 2: a 59-year-old man had undergone left radical nephrectomy for renal cell carcinoma. He had recurrent tumor contiguous to spleen 24 months after nephrectomy. With Seldinger method a catheter was indwelled selectively in splenic artery. Two million units of interferon gamma was administered through the catheter, twice a week for 4 weeks, and once a week in subsequent course. The tumor showed necrosis on CT film. He died of DIC 5 months after the initiation of intraarterial administration of interferon gamma. Topical use of interferon showed some favorable effects in both cases even after the failure of systemic administration. Further investigation is warranted to demonstrate the advantage of topical use of interferon over systemic administration.
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PMID:[Intralesional and transarterial administration of interferon for renal cell carcinoma]. 153 Feb 94

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

Autopsy findings were reviewed in 43 patients clinically diagnosed in the last 12 years as having urogenital malignant tumors. Clinical diagnoses were 14 bladder carcinoma, 11 prostatic carcinoma, 6 renal cell carcinoma, 5 renal pelvic carcinoma, and 7 other malignant tumors. Autopsy showed that 31 cases died due to carcinoma and 12 because of other causes. The most common ultimate causes of death were DIC and infection, especially pneumonia and sepsis. Autopsy showed 36 of the 43 cases (83.7%) with metastasis. Clinical diagnosis showed 34 cases of metastasis, but the number of metastasized organs and lymph-nodes was much lower than in subsequent autopsy findings. Autopsy proved 5 cases of clinical misdiagnosis (11.6%) and 4 of undiagnosed malignant tumors (9.3%). In 15 cases (32.6%) the ultimate cause of death as revealed by autopsy had not been clinically diagnosed. Five cases diagnosed as having died due to cancer in fact were found to have died due to other causes. Recent diagnostic techniques are greatly advanced, yet many findings are still revealed for the first time by autopsy. Autopsy continues to be a very important final arbiter of progress and the effect of malignant tumors, and serves to remind us of the ongoing need for constant vigilance and improvement of clinical diagnostic techniques.
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PMID:[Review of 43 autopsy cases of urogenital malignant tumors]. 273 88

Primary renal angiosarcoma is a very rare malignant tumor that closely mimics the more common renal cell adenocarcinoma (hypernephroma) in radiologic appearance. Both tumors are hypervascular masses and the diagnosis must be confirmed histologically. However, in the presence of a tumor with a capsular blood supply, and in the absence of venous invasion, the diagnosis of renal angiosarcoma may be suggested, especially in a patient with a new onset of consumption coagulopathy.
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PMID:Primary renal angiosarcoma mimicking a renal cell carcinoma. 273 70

Retrospective evaluation of the state of hemostasis in 20 patients dying with pulmonary artery thromboembolism (PATE) after combined treatment of renal carcinoma (10) and urinary bladder carcinoma (10) was performed. The signs of intravascular blood coagulation (IVBC) in the initial condition were determined in all the patients. After a course of pre-operation actin therapy with large fractions (totally 20 g) activation of IVBC was observed both in renal and urinary bladder carcinoma. In the postoperation period, on the day of PATE development in patients with renal carcinoma the state of hemostasis corresponded to stage I of disseminated intravascular coagulation syndrome. In patients with urinary bladder carcinoma after operation the state of hemostasis corresponded to stage II of DIVC-syndrome with signs of local hemorrhage of the urinary bladder wound. The therapy of this condition with fibrinolysis inhibitors (aminocaproic acid) with hemotransfusion without heparin facilitated thrombus formation in these patients in deep pelvic veins followed by PATE.
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PMID:[Mechanism of development of fatal pulmonary artery thromboembolism during the treatment of kidney and bladder cancer]. 663 95

In 40 patients with non-metastasising (n = 31) and metastasising (n = 9) renal cell carcinoma, evidence of Stauffer's syndrome (increase in alkaline serum phosphatase and prolongation of prothrombin time) was found in 18 patients. Prolongation of prothrombin time was not due to depletion of vitamin K-dependent coagulation factors or manifest fibrinolysis, but due to the presence of circulating fibrinogen fibrinmonomer-FDP complexes. Ethanol gelation test was found to be positive in 28/40 subjects and soluble fibrin monomer complexes were increased in 38/40 patients. The resulting disturbance of fibrinogen-fibrin conversion was reflected by an increase in thrombin coagulase time and reptilase time. These findings suggests a state of latent compensated intravascular coagulation (presumably triggered within the vascular tumor). For diagnostic purposes the most sensitive indicator is thrombin coagulase time. Thrombin coagulase time normalised after tumor resection and was positive in patients with recurrent metastases. The increase in alkaline serum phosphatase was due to an increase in the hepatic isoenzyme. Such an increase was much more common than the elevation of total alkaline serum phosphatase. Regan's isoenzyme was only found in 1 subject. In parallel, gamma-GT was elevated in 24 patients. The study shows that Stauffer's syndrome occurs more frequently than commonly assumed when thrombin coagulase time, gamma-GT and the hepatic isoenzyme of alkaline serum phosphatase are determined in patients with renal cell carcinoma. DIC and low grade fibrinolysis may account for the coagulation abnormalities of the syndrome.
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PMID:Stauffer's syndrome in renal cell carcinoma evidence for intravascular coagulation. 736 22

A 41-year-old man incidentally found to have a right renal and left large lung tumor in the course of screening for liver dysfunction was admitted to our hospital. Needle biopsy of each tumors revealed histologically renal cell carcinoma and pulmonary blastoma. The renal tumor grew rapidly and soon he died of DIC. Autopsy was performed and the final diagnosis was adult Wilms' tumor and its metastasis to the lung. Histological findings of each large tumors showed different histologic pattern. The renal tumor revealed diffuse nephroblastic subtype and the lung tumor showed epitherial type. This is a rare case of Wilms' tumor in terms of its adult onset and different histologic pattern between the primary tumor and its metastatic lesion.
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PMID:[Adult Wilms's tumor with histologically dissisimilar lung metastasis]. 817 84

A 7-year-old male German Shepherd dog in poor body condition had a 3-month history of intermittent hematuria. Nonregenerative anemia, mild leukocytosis, marked hypoalbuminemia, and hematuria were observed. Subsequently, marked neutrophilia and moderate monocytosis were noted; anemia, hypoalbuminemia, and hematuria persisted; and the dog developed disseminated intravascular coagulation. Ultrasonographic examination of the abdomen revealed the presence of an enlarged and irregularly shaped right kidney with a large area of cavitation, and a nephrectomy was performed 30 days after initial examination. Cytologic examination of fine-needle aspirates and imprints of the right kidney revealed a neoplastic cell population suggestive of renal carcinoma. The histopathologic diagnosis was chromophobic cystic-papillary renal carcinoma. The tumor cells expressed granulocytic/macrophage-colony-stimulating factor (GM-CSF), detected by immunohistochemical staining, and elaboration of GM-CSF by the tumor may have mediated the leukocytosis in this dog. Following excision of the tumor, neutrophil and monocyte counts were only mildly increased. The dog died 135 days after initial presentation, and a necropsy was not permitted. Paraneoplastic neutrophilic leukocytosis is an uncommon finding and may be caused by elaboration of CSF by neoplastic cells.
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PMID:Paraneoplastic leukocytosis in a dog with a renal carcinoma. 2163 65


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