Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 57-year-old male with primary intracranial malignant melanoma who survived 9 years and 6 months is reported. He underwent surgical removal of the tumour three times during the decade 1978 to 1988, and received chemo-immuno-radiotherapy during that time. Acute tumour growth, suggesting tumour dissemination, was seen in the CT scans after the third removal of recurrent tumour, but then it disappeared after combined chemoradiotherapy with DTIC. He gradually became inactive, probably because of brain atrophy caused by high-dose radiotherapy and chemotherapy, and died of renal failure without any sign of recurrence on CT scans.
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PMID:Long-term survival after removal of primary intracranial malignant melanoma. Case report. 260 74

With the aim of temporarily assisting deterioration of liver function developing after surgery, extracorporeal blood purification therapy (EBPT) (plasma exchange and/or hemofiltration) was carried out in 26 postoperative patients. Initiation of EBPT was instituted according to the criteria of either a serum bilirubin greater than 15 mg/dl or Grade 2 or more coma. Plasma exchange was carried out 235 times in 23 patients and hemofiltration was performed 28 times for seven patients. In addition, hemodialysis and CAPD were linked in eight cases. Plasma exchange was found to control the progression of DIC and endotoxemia. Nine patients (35%) were weaned from EBPT. In the survivors the levels of blood ammonia and number of major complications were significantly lower compared to the nonsurvivors. Three patients treated only with hemofiltration were all lost. Among co-morbid factors present, incidences of renal failure, respiratory failure, and associated liver cirrhosis significantly increased poor clinical outcome on EBPT for postoperative liver failure.
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PMID:Temporary metabolic support by extracorporeal blood therapy for liver failure after surgery. 319 18

Two patients who had cerebral aspergillosis with massive intracerebral hemorrhage were presented. Case I was a 59-year-old woman who had slight mental retardation. There was swelling in the left forehead, from which mucosal cysts of frontal sinus had been removed 2 years before her admission. She had a diagnosis of subdural abscess and radical operation was performed. Aspergillus was found in the abscess histologically. Three months after the operation, CT scan revealed multiple abscess in bilateral frontal lobe. When she lost consciousness suddenly 4 months after the operation, CT scan showed a huge intracerebral hematoma. Case 2 was a 16-year-old girl who suffered from immunological dysfunction caused by more than 6 months antibiotics-steroid treatment for pneumonitis. She lost her consciousness after complaints of severe headache. CT scan showed a heterogeneous high density area with severe brain edema in the left temporal lobe. The removal of hematoma was performed immediately. The level of her consciousness improved, but she died of the complication of DIC and renal failure 14 days after the hemorrhage. Autopsy revealed a number of aspergillomas in lungs, kidneys, gastrointestinal tract, liver and pancreas. Marked necrosis and a number of aspergillus hyphae which invaded and penetrated the wall of cerebral vessels were found in the brain tissue. It was presumed that such a huge intracerebral hematoma was caused by direct invasion and penetration into the brain of aspergillus from the blood vessels. The diagnosis of cerebral aspergillosis is made mainly by the pathological examination of the tissue obtained at surgery or autopsy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two cases of cerebral aspergillosis with intracerebral hemorrhage]. 322 71

The toxicity of a new chemotherapeutic regimen for CNS tumors using eight anticancer agents administered in a 12-hour period was evaluated in 34 children with newly diagnosed and recurrent tumors treated at the Children's Hospital and Medical Center in Seattle. The chemotherapy included methylprednisolone, vincristine, lomustine (CCNU), procarbazine, hydroxyurea, cisplatin (CDDP), and either cyclophosphamide or imidazole carboximide (DTIC). The first five patients additionally received high-dose methotrexate (HDMTX), but because of excessive toxicity this was replaced by cytarabine. Of 125 courses administered without HDMTX, red cell transfusions were required in 15% of the courses and platelet transfusions were required in 8%. Hospitalization for empiric treatment of fever associated with neutropenia occurred in 6% of courses. Three episodes of documented sepsis occurred. Virtually all hematologic toxicity occurred in patients with recurrent disease. Renal toxicity occurred in 14% of patient courses. One patient died of renal failure and sepsis following therapy. Neurologic and hepatic complications were infrequent. High-frequency hearing loss above the voice range was common, but clinically significant hearing loss occurred in only three patients. Severe nausea and vomiting were infrequent. Overall, the toxicity of "eight in one" chemotherapy in newly diagnosed patients was minimal; toxicity was greater in patients with recurrent disease.
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PMID:Eight drugs in one day chemotherapy in children with brain tumors: a critical toxicity appraisal. 337 69

In addition to the typical manifestations of thrombotic-thrombocytopenic purpura like thrombocytopenia, haemolysis, fever, coma and renal failure, signs of a beginning DIC could be seen in a patient after abdominal surgery. Haemostatic, cardiovascular and respiratory data are presented. Pulmonary angiography by using a Swan-Ganz-catheter revealed multiple filling defects reversible with therapy. Treatment with fresh whole blood aggravated thrombocytopenia. Daily infusions of fresh frozen plasma combined with heparinisation and antithrombin III because of DIC, induced haematologic remission. Renal failure and cerebral symptoms could not be influenced. Diagnosis, monitoring and therapy are discussed.
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PMID:[Partial remission of fulminant thrombotic-thrombopenic purpura (Moschcowitz syndrome) by infusion of fresh plasma]. 375 26

In spite of all the scientific and technical advances in recent years, shock that is not rapidly correctable with fluid can have a morbidity rate exceeding 80%. Consequently awareness of such precipitating factors as sepsis and early diagnosis and treatment are essential. Treatment should be rapid and should follow a previously outlined protocol. Such protocols should include correction of the precipitating problem and aggressive resuscitation to assure adequate ventilation and oxygenation of the blood and optimal oxygen delivery to the tissues. Fluid and blood should be given as needed until filling pressures begin to rise rapidly with further fluid infusion. With hemorrhagic shock in previously healthy individuals, a hemoglobin level of 10.0 g/dL is usually adequate. In older, septic, or cardiogenic shock patients, a hemoglobin level of 12.5 to 14.0 may be preferable. If an optimal preload does not increase cardiac output to normal or higher levels, inotropic agents should be used. If shock still persists, one must be sure that the arterial pH is not excessively high or low. Glucocorticoids may then be given in low dose (200 mg hydrocortisone) in case some degree of adrenal insufficiency is present. They can also be given in high doses (equivalent to 150 mg/kg hydrocortisone) early in septic shock primarily to prevent excess complement activation and to preserve membrane integrity. Vasopressors may occasionally be required if there is excessive vasodilation, especially if there is persistent hypotension in the presence of high-grade coronary or cerebral artery stenosis. Vasodilators may be used to try to correct myocardial ischemia (nitroglycerin), excessive preload (nitroglycerin), or excessive afterload (nitroprusside or hydralazine). Combinations of vasodilators and inotropic agents may be required in some patients with high systemic vascular resistance and persistently low cardiac outputs. Mechanical assist with IABP can be of great value in persistent cardiogenic shock. Diuretics may occasionally help prevent renal failure in patients who are persistently oliguric after blood flow and pressure are restored. Heparin is occasionally of value if DIC develops with no concomitant fibrinolysis. Antibiotics are important in septic shock and may also be important if persistent shock has reduced gastrointestinal mucosal integrity so that bacteria and bacterial products can enter the portal system.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Science and shock: a clinical perspective. 389 56

The records of 27 cases of disseminated intravascular coagulation with burn, trauma, perforated peritonitis or leakage of gastrointestinal anastomoses at the Second Department of Surgery and Intensive Care Unite, Toho University Hospital from 1977 to 1982 were reviewed. In this series, multiple organ failure (MOF) occurred in 20 cases and single organ failure occurred in 4 cases. Lung failure occurred in 20 out of 27 cases. Renal failure occurred in 18 out of 27 cases. Then, correlation was observed between decrease in platelet count and decrease in PaO2/FiO2. Serum creatinine level and total bilirubin level were elevated according to the progress of DIC. Twenty death cases with DIC out of 21 had MOF. However, 3 survived cases out of 6 cases had only single organ failure and other 3 survived cases out of 6 cases had not organ failure. Therefore, close correlation was observed between DIC and MOF in the prognosis of DIC. Earlier and active support of organ failure was important for clinical management of DIC.
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PMID:[The role of multiple organ failure in DIC]. 667 59

Factor VIII-related antigen (VIIIR:Ag) was consistently higher than factor-VIII procoagulant activity (VIII:C) in 57 patients with clinical conditions characterized by acute-phase reactions. Two different methods for measuring VIII:C (one- and two-stage assays) and VIIIR:Ag (electroimmunodiffusion and immunoradiometric assay) gave concordant results in the majority of cases. In 43% of plasma samples, crossed immunoelectrophoresis in agarose gel was characterized by the appearance of an additional, fast-moving precipitin peak which was immunologically identical with the major, slower-moving VIIIR:Ag peak. The fast-moving peak was detected in all the patients with clinical conditions typically associated with increased plasma proteolysis (DIC, acute pancreatitis, during thrombolytic therapy). It was present in a smaller proportion of cases with liver and renal failure and malignancies and in the post-operative period. The additional VIIIR:Ag peak is thought to be the result of in vivo factor VIII/von Willebrand factor fragmentation by proteolytic enzymes.
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PMID:Alterations of factor VIII von Willebrand factor in clinical conditions associated with an increase in its plasma concentration. 679 81

This patient had many of the clinical features described in the literature as characteristic of DIC, an uncommon disease. These included the acute systemic infection precipitating the tissue pathology, ecchymotic skin lesions progressing to amputation, shock, anemia, and renal failure. The literature reported two case studies that resulted in amputation. During prosthetic training, both the patients developed skin problems that required prosthetic modification before they could wear their prostheses. The patient in our case study also required careful prosthetic modification with continual monitoring of the status of the skin. After three skin grafts and two surgical procedures to remove heteroptic ossification, the patient became a limited community ambulator (Fig. 4). When he attains full growth and the heteroptic bone formation subsides, we believe he should become a community ambulator, as long as he receives proper prosthetic care and follow-up.
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PMID:Disseminated intravascular coagulation resulting in amputation. A case report. 687 39

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


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