Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal tissues of 208 autopsied cases were examined. Malignant neoplasm with hematological malignancies often accompanied DIC. Tissue sections were stained with hematoxylin and eosin and Mallory's phosphotungstic acid hematoxylin (PTAH), and were applied for immunoperoxidase method (IP), using antisera against human fibrinogen, FDP-D and FDP-E. Histologically in 80 cases (38%) fibrin or fibrinogen related materials (FRMs) were observed in the glomerular capillary or the intratubular area or in both. FRMs were PTAH or IP positive or both in 23 of the 26 cases (88%) clinically diagnosed as DIC. In the remaining three cases anticoagulants probably interfered with FRMs observation. This study showed the PTAH stain was nonspecific and insensitive to FRMs, and that IP was necessary for a pathological diagnosis of DIC. The presence of FRMs in the renal tubuli is an important finding in confirming DIC. DIC may be present histologically in the absence of clinical DIC symptoms.
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PMID:Disseminated intravascular coagulation (DIC). Immunohistochemical study of fibrin-related materials (FRMs) in renal tissues. 243 64

Metastasization may be associated with activation of haemostatic processes resulting in increased levels of circulating factor VIII-related antigen (FVIIIRAg) (von Willebrand factor antigen). To evaluate the relevancy of this in prostate cancer (PCa), the level of FVIIIRAg in the serum of patients with PCa, benign prostatic hypertrophy (BPH) and non-prostatic diseases was quantitated by a modified micro enzyme-linked immunosorbent assay. Significant (P less than 0.05) differences were noted between the level of FVIIIRAg in PCa and patients with BPH and other than prostatic disease. Noteworthy were elevated levels of FVIIIRAg in PCa patients with metastatic vs. localized disease. Consideration of the "unorthodox", but possibly more convenient use of routine serum specimens commonly available in the non-haematological laboratory vs. plasma for the quantitation of FVIIIRAg, in situations where an "absolute" level is not required, and of disseminated intravascular coagulation as contributory to the present observations, is given. Pending evaluation of a larger patient population these observations may be of prognostic value.
Cancer Lett 1988 Jun 30
PMID:Immunoquantitation of factor VIII-related antigen (von Willebrand factor antigen) in prostate cancer. 245 28

A cerebral infarct due to a thrombosis of the left pericallosal artery was the first manifestation of an ovarian adenocarcinoma in a 42-year-old woman. A paraneoplastic origin was suggested by the observation that this patient had chronic intravenous coagulation and subsequently developed migratory thrombophlebitis (Trousseau's syndrome) despite high dose vitamin K antagonists therapy. This was supported by the fact that all manifestations of the hypercoagulable state disappeared following surgical cure of the cancer. Because cerebral infarction can be the first manifestation of a potentially curable cancer, patients with a cerebral infarct of an unknown etiology should be investigated for a malignant process, if there is laboratory or clinical evidence od disseminated intravascular coagulation.
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PMID:Ischemic stroke as the presenting manifestation of localized systemic cancer. 245 36

In the present study plasma fibronectin levels were determined in patients with hematopoietic malignancy, particularly leukemias, in an effort to clarify their clinical implications. Among leukemia patients, those with AML, ALL, ATL or CLL had various plasma fibronectin levels that were higher in some cases, while lower in others, as compared to normal control values. An elevation of the fibronectin level was noted often in APL, while lower fibronectin values were observed in many instances of CML. In these types of leukemia, acute exacerbation as well as supervention of infection tended to be associated with lower than normal levels of fibronectin. An especially marked depression of fibronectin occurred, when leukemia was complicated by sepsis or DIC, in which a good parallel was noted between the progress of disease and the fibronectin level. In lymphoproliferative diseases, the fibronectin value varied widely, but low fibronectin levels were frequently associated with intercurrent infection or an extreme deterioration of the general physical conditions.
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PMID:Variation of plasma fibronectin levels in leukemia patients. 248 45

A registry of suspected cases of cancer-associated hemolytic-uremic syndrome (C-HUS) was established in May 1984. Records of 85 patients from the registry, all with history of cancer, hematocrit less than or equal to 25%, platelet count less than 100,000, and serum creatinine greater than or equal to 1.6 mg/dL were subjected to in-depth analysis. Eighty-nine percent of patients had adenocarcinoma, including 26% with gastric cancer. Microangiopathic hemolysis was reported in 83 patients; coagulation studies were normal with rare exception. Bone marrow examination ruled out chemotherapy-induced myelosuppression in 68 of 85. Thirty-five percent of patients were without evident cancer at time of syndrome development. Mitomycin (MMC) was part of the treatment regimen in 84 patients; all but nine received a cumulative dose greater than 60 mg. Pulmonary edema, generally noncardiogenic, developed in 65% of patients, often after blood product transfusions. C-HUS has a high mortality: over 50% of patients died of or with syndrome, most within 8 weeks of syndrome development. Conventional treatment was ineffective, although ten of 21 treated with staphylococcal protein A (SPA) immunopheresis showed significant responses. Statistical analysis found only absence of obvious tumor and treatment with SPA to suggest favorable prognosis. C-HUS is distinguishable from related syndromes such as childhood HUS, thrombotic thrombocytopenic purpura (TTP), consumption coagulopathy, and microangiopathic hemolysis associated with advanced carcinoma. MMC is likely involved in the development of C-HUS; the risk of developing C-HUS after treatment with MMC is between 4% and 15%. However, possible bias in patients referred to the registry and reports of non-MMC C-HUS cases must be remembered. Recommendations include careful monitoring of renal and hematologic function in patients treated with MMC, aggressive nontransfusion in patients with suspected C-HUS, and consideration of treatment with SPA immunopheresis in patients with definite syndrome.
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PMID:Cancer-associated hemolytic-uremic syndrome: analysis of 85 cases from a national registry. 251 Dec 78

The combination of tumor necrosis factor (TNF) and interferon-gamma has synergistic bioactivity in numerous preclinical model systems. We have tested this potential synergism in vivo by administration of both cytokines to patients with advanced cancer using overlapping 24-hour continuous intravenous (IV) infusions in a phase I trial. Thirty-six patients were treated with a fixed dose of interferon-gamma (200 micrograms/m2/d) with interpatient dose escalation of TNF (from 5 to 205 micrograms/m2/d). The dose-limiting toxicity at the maximal-tolerated dose (MTD) of TNF (205 micrograms/m2) with interferon-gamma was hypotension. Other toxicities noted included an influenza-like syndrome, transient decreases in circulating leukocyte and platelet counts, subclinical evidence of disseminated intravascular coagulation, and the sporadic occurrence of acute pulmonary toxicity. The recommended phase II dose for this combination schedule is TNF, 136 micrograms/m2, with interferon-gamma, 200 micrograms/m2. The addition of interferon-gamma to TNF resulted in a greater than three-fold increase in toxicity compared with TNF administered as a single agent, supporting the hypothesis that the combination of these cytokines may induce synergistic effects in vivo.
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PMID:A phase I trial of recombinant human tumor necrosis factor and interferon-gamma: effects of combination cytokine administration in vivo. 250 16

Activated protein C (APC) is inhibited by two major plasma inhibitors (PCIs). To find evidence for in vivo complexation of APC, immunoblotting studies were performed on plasmas of 85 patients with suspected disseminated intravascular coagulation (DIC). Samples from 62 of these patients contained 5% to 35% of protein C antigen in APC:inhibitor complexes, indicating that protein C activation and inhibition had occurred. In 24 normal plasmas, no detectable APC:PCI complexes were observed (less than 5%). Patients with higher levels of complexes had more abnormal coagulation test data for DIC. The major band of APC complexes detected by anti-protein C antibodies did not react with antibodies to the heparin-dependent protein C inhibitor (PCI-1) previously described. Rather, APC was complexed with another recently described plasma protein C inhibitor, PCI-2. Immunoblotting studies for protein S, the cofactor for APC, revealed that the majority of the DIC patient plasmas contained a higher than normal proportion of protein S in cleaved form, suggesting that protein S may have been proteolytically inactivated. Protein S total antigen levels were also found to be low in DIC patients, excluding those with malignancy. These studies support the hypothesis that the protein C pathway is activated during DIC.
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PMID:Activation and complexation of protein C and cleavage and decrease of protein S in plasma of patients with intravascular coagulation. 252

A case of extensive bone marrow necrosis due to cancer metastasis is reported. A 55-year-old female, who had a history of subtotal gastrectomy for signet ring cell carcinoma of the stomach 7 years ago, was admitted to our hospital with a complaint of lumbago on October 25, 1987. Red blood cell count was 92 X 10(4)/microliters, hemoglobin 2.7 g/dl, hematocrit 8.0%, platelet 6.4 X 10(4)/microliters, and white blood cell count 13,400/microliters with leukoerythroblastosis. Bone marrow aspiration of the sternum, left iliac crest, and bilateral posterior superior iliac supine showed extensive bone marrow necrosis. Serum ALP was increased to 7410IU/l, dominated isozyme of bone type. Hemostatic findings suggested a complication of consumption coagulopathy. Skull, vertebrae, iliac and pelvic bone X-ray showed multiple osteolytic lesions, and irregular isotope uptake was recognized on the bone scintigraphy using 99mTc. Sixth bone marrow examination at the right iliac crest revealed signet ring cell carcinoma metastasis. In spite of detailed examinations, there was no evidence of primary carcinoma, including the remnant of stomach. We speculated that the signet ring cells were originated from the respected gastric cancer. The patient has received anti-cancer chemotherapy with UFT and OK432, and is still alive 9 months after diagnosis.
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PMID:[Extensive bone marrow necrosis associated with carcinomatosis 7 years after operation for gastric cancer]. 254 85

Although a 39-year-old male received the curative operation of total gastrectomy for advanced scirrhous carcinoma of the stomach, recurrence of cancer was occurred soon after the surgery, accompanied by hemorrhagic diathesis from DIC. The abdominal CT scan examination revealed the rapid enlargement in the size of the several lymphnodes around the abdominal aorta, and the blood chemistry tests showed marked increase of the serum CEA value. The sequential chemotherapy with intermediate dose of MTX and 5-FU in conjunction with OK-432 was started to treat the case. This chemotherapy was carried out once a week for 5 times and consequently DIC was led to the perfect remission. Furthermore, CEA level decreased within normal range, and the size of the enlarged lymphnodes at paraaortic area diminished remarkably. Although he complained of nausea and loss of appetite during the treatment, no severe adverse effects such as granulocytopenia, diarrhea, or loss of hair were observed. The successful result in this patient suggests that sequential therapy of intermediate dose of MTX and 5-FU with administration of OK-432 may be effective in the treatment of advanced scirrhous carcinoma of the stomach.
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PMID:[Effect of sequential MTX/5-FU therapy for a case of disseminated intravascular coagulation syndrome associated with recurrence of gastric cancer--a case report]. 255 83

Malignant ascites is often refractory to therapy and rapidly deteriorating the nutritional and physical state of the cancer patient. Nevertheless, ascites does not always implicate preterminal state of the cancer process (e.g. ovarian carcinoma). A short review is made of the pathophysiology of ascites in cirrhosis and in malignancy, and different modes of treatment are discussed. The results of medical therapy of malignant ascites (salt and water restriction, diuretics, intraperitoneal cytostatics or radiocolloids) are not convincing. The immunotherapy with OK-432, as worked out by Katano (16-46) has to prove its value. The best and most hopeful results in cases of massive previously resistant ascites, are obtained with a peritoneojugular shunt, improving immediately the nutritional status and life condition, providing excellent palliation. The superiority of the Denver shunt versus the Le Veen shunt has been assessed recently, especially for malignant ascites. Some technical and perioperative details merit more attention, to limit the high risk ratio. Control of the intrathoracic position of the catheter tip, the maintenance of the bloodflow in the jugular vein, the intramuscular tunnelisation of the peritoneal catheter, the discard of 3 or 5 liters ascitic fluid and the substitution of part of it by physiological fluid, perioperative prophylactic antibiotics and heparinisation, flow-rate control in the postoperative period by changing patients position, respiratory exercises, daily flushing, all those measures limit the risk of fibrinolysis (DIC), shunt occlusion, fluid overload and infection. The fear of metastasis by shunt is unfounded, since the survival of the primary tumor is mostly too short (41). The postoperative follow up in an intensive care unit is necessary during 24-72 hours.
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PMID:[The Denver shunt in malignant ascites]. 258 Apr 8


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