Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

A case is reported of fatal recurrent unilateral reexpansion pulmonary edema following thoracentesis in a woman with stage IV ovarian adenocarcinoma. Reexpansion pulmonary edema is a rare complication resulting from reexpansion of a collapsed lung after treatment of pleural effusion, pneumothorax, or atelectasis. The etiology is unknown, and there are no guaranteed measures of prevention. The clinical presentation varies from asymptomatic to rapidly progressive fatal pulmonary edema. The diagnosis is established by chest x-ray. Depending on the severity of the clinical symptoms, treatment varies from monitoring with serial chest x-rays to mechanical ventilation. Reexpansion pulmonary edema is fatal in 20% of cases. Gynecologists should be aware of this rare entity because it may require immediate diagnosis and aggressive treatment.
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PMID:Fatal recurrent reexpansion pulmonary edema. 276 41

Mitomycin C associated Hemolytic Uremic Syndrome (HUS) is a potentially fatal but uncommon condition that is not yet widely recognised. It consists of microangiopathic hemolytic anemia, thrombocytopenia and progressive renal failure associated with mitomycin C treatment and affects about 10% of patients treated with this agent. The renal failure usually develops about 8-10 mth after start of mitomycin C treatment and the mortality is approximately 60% from renal failure or pulmonary edema. Renal lesions are similar to those seen in idiopathic HUS and include arteriolar fibrin thrombi, expanded subendothelial zones in glomerular capillary walls, ischemic wrinkling of glomerular basement membranes and mesangiolysis. The mechanism of action is postulated as mitomycin C-induced endothelial cell damage. We describe the clinical course and pathological findings in a 65 yr-old man with gastric adenocarcinoma who developed renal failure and thrombocytopenia while on treatment with mitomycin C and died in pulmonary edema.
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PMID:Mitomycin C associated hemolytic uremic syndrome. 310 39

An autopsy case of MAHA induced by MMC is reported. The patient received MMC and tegafur following operation for colon adenocarcinoma. Five months after the operation, the patient developed MAHA, thrombocytopenia, and renal impairment. MAHA was exacerbated by blood transfusions and he died of extensive pulmonary edema. Autopsy findings showed no residual carcinoma but microangiopathies of the kidney, such as fibrinoid necrosis of the small arteries, arterioles, and glomerular capillaries, and intimal proliferation in the small arteries were evident. As renal impairment is usually irreversible in MAHA by MMC, careful follow-up of renal function should be emphasized in patients receiving MMC.
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PMID:[Microangiopathic hemolytic anemia (MAHA) observed after administration of mitomycin C (MMC)]. 311 42

Human recombinant interleukin-2 (rIL-2) was administered to normal and tumor-bearing BDF mice for 1 to 3 weeks, and the hematologic, clinical chemistry, gross and histopathologic findings were evaluated. Vascular leak syndrome (pulmonary edema, pleural effusion, ascites), hepatocyte necrosis, elevated hepatic serum transaminases, hypoalbuminemia, tissue and peripheral eosinophilia, thrombocytopenia, and prerenal azotemia were the detrimental effects of rIL-2 treatment. Vascular leak syndrome and hepatocyte necrosis were causally associated with vascular-oriented lymphocytic infiltration of pulmonary and hepatic parenchyma. Pleural effusions contained up to 99,000 cells/mm3, most of which were large granular lymphocytes. Antiserum to the glycolipid asialo GM1 (ganglio-n-tetrosylceramide), given simultaneously with rIL-2, prevented overt toxicity of rIL-2 (mortality, vascular leak syndrome, and hepatic damage) and substantially reduced infiltration of pulmonary and hepatic vasculature by asialo GM1+ lymphocytes. Asialo GM1 antiserum did not inhibit lymphoid hyperplasia, tissue infiltration by Lyt 2+ lymphocytes, tissue and peripheral eosinophilia, or thrombocytopenia in rIL-2 treated mice. Additionally, asialo GM1 antisera prevented toxicity, but not anti-tumor efficacy, of high dose rIL-2 therapy in BDF mice bearing the colon 38 adenocarcinoma. These results suggest that, in BDF mice and with this tumor model, vascular leak syndrome and hepatocyte necrosis are mediated by an endogenous subset of rIL-2-stimulated lymphocytes which are asialo GM positive, that mechanisms of toxicity and efficacy associated with high dose rIL-2 therapy are not necessarily the same, and that these mechanisms can be therapeutically separated.
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PMID:Toxicity of human recombinant interleukin-2 in the mouse is mediated by interleukin-activated lymphocytes. Separation of efficacy and toxicity by selective lymphocyte subset depletion. 326 43

A thrombotic microangiopathy resembling the hemolytic uremic syndrome was diagnosed in 12 patients with adenocarcinoma, in whom the tumor was in complete or near-complete remission after treatment with mitomycin C-containing drug regimens. Microangiopathic hemolytic anemia, thrombocytopenia, and renal failure were initially present in all cases. All patients eventually developed pulmonary edema and systemic arterial hypertension, and three experienced neurologic complications. Blood transfusions exacerbated the syndrome in nine patients. High titers of platelet-aggregating plasma immune complexes were present in all six cases in which they were measured. The constituent antibody of each complex failed to react with mitomycin C antigen preparations, whereas in vitro reactivity to endodermally derived neoplasms was demonstrated. Plasmapheresis was associated with amelioration of the syndrome in only one patient. In patients receiving mitomycin C chemotherapy, the development of anemia and thrombocytopenia or azotemia may represent the initial manifestations of this newly defined thrombotic microangiopathy. A consistently effective form of management of this syndrome has not as yet been defined.
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PMID:Carcinoma-associated hemolytic-uremic syndrome: a complication of mitomycin C chemotherapy. 392 62

A bolus of 1000 mg of 5-FU intravenously was given to a 54-year-old patient with adenocarcinoma of colon, a month after hemicolectomy. He had not received irradiation therapy. Five hours later he complained of severe chest pain; after 24 hours ecg. changes of pericarditis were seen and on heart auscultation a pericardial friction rub was heard. After 6 day the ecg. returned to the pattern of that on day of admission to the ICCU. Two further injections of 1000 mg of 5-FU were also followed by severe precordial pain and the same ecg. pattern. The pulmonary edema 14 hours after the second injection and the slight elevation of CPK value after the third injection strongly suggest myocardial cell damage. For the strictly temporal relationship between the clinical and electrocardiographic pattern with 5-FU administration intravenously, we are of the opinion that the perimyocarditis was due to the direct toxic action of 5-FU on pericardium and myocardium.
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PMID:[Early cardiotoxicity of 5-fluorouracil]. 734 80

4-Ipomenaol (IPO) has been shown to induce P-450-mediated necrosis of Clara cells in experimental animals, and clinical trials were initiated to treat people with bronchioloalveolar cancers with this novel drug. We therefore performed experiments to examine two different animal lung tumor models for acute IPO cytotoxicity: hamster Clara-cell-derived adenocarcinomas and mouse alveolar type II cell tumors. Clara cells serve as stem cells for airway cell renewal and, therefore, tumors derived from Clara cells may likewise differentiate into various bronchiolar cell types, or undergo squamous cell metaplasia. Bronchiolar cell tumors were induced in Syrian hamsters by a single weekly gavage with 6.8 mg N-nitrosomethyl-n-heptylamine (NMHA)/animal for 35 weeks. NMHA-induced bronchiolar tumors were classified as well-differentiated lepidic bronchioloalveolar carcinomas, acinar adenocarcinoma, adenosquamous carcinoma, and squamous-cell carcinoma. After 35 and 46 experimental weeks, control and carcinogen-treated hamsters were injected once with doses of 40-110 mg IPO/kg i.p. and necropsied 15-48 h later. Solid and papillary tumors with alveolar cell features were induced transplacentally in C3H/HeNCr mice, by treating pregnant animals on gestation day 16 with 0.5 mmol N-nitrosoethylurea/kg, i.p. Offspring of control and carcinogen-treated mice were injected at 2-3 months of age with 35 mg or 50 mg IPO/kg i.p. and necropsied either 24-48 h or 5 and 12 days after injection. Light microscopic studies were carried out to assess cytotoxic effects in various tissues in both hamsters and mice; in hamsters, additional ultrastructural studies were performed. When administered to hamsters, IPO induced moderate to severe cytotoxicity in normal and dysplastic bronchiolar lining cells, in most lepidic bronchioloalveolar carcinomas, and in some glandular areas of adenosquamous cell carcinomas. Susceptible cells included normal, anaplastic, and neoplastic nonciliated and some ciliated bronchiolar cells. Undifferentiated and squamous tumor cells were resistant to IPO, as were resident normal alveolar type II cells. However, some adenocarcinomas composed primarily of ciliated and mucous cells also showed no IPO-induced necrosis, indicating a deficiency in appropriate activating enzymes. In the mice, IPO induced bronchiolar cell necrosis and, at the high dose, also severe pulmonary edema. No cytotoxicity was observed in normal or hyperplastic alveolar epithelium, nor in either solid or papillary growth forms of mouse alveolar cell tumors.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute effects of 4-ipomeanol on experimental lung tumors with bronchiolar or alveolar cell features in Syrian hamsters or C3H/HeNCr mice. 827 Jun 7

We tested whether treatment with an inhibitor of nitric oxide synthesis (Ng-methyl-L-arginine, MeArg) can ameliorate interleukin-2(IL-2)-therapy-induced capillary leak syndrome in healthy or tumor-bearing mice without compromising the antitumor effects of IL-2 therapy. Healthy or C3-L5-mammary-adenocarcinoma-bearing C3H/HeJ mice were treated with one or two rounds of various doses of IL-2 (ten injections, i. p., every 8 h) or MeArg (ten injections s. c., every 8 h) or their combination. In an additional experiment, MeArg was given chronically in the drinking water, rather than s. c. to healthy mice subjected to one round of therapy as above. Mice were killed 1 h after their last IL-2 injection to measure the water content of the lungs and pleural cavities (markers of capillary leakage), NO production (given by NO2- and NO3- levels in the serum and pleural effusion), as well as the effect of therapies on the primary tumor size and number of spontaneous lung metastatic nodules. Results revealed that all doses of IL-2 (7500-35000 Cetus U/injection), as well as both rounds of IL-2 therapy, caused capillary leakage. However, no pleural effusion was seen after the second round in any of the IL-2-treated groups. MeArg therapy, given subcutaneously (5-20 mgkg(-1) injection(-1) in healthy and 20 mgkg(-1) injection(-1) in tumor-bearing mice), did not ameliorate IL-2-induced capillary leakage in either group of mice, and did not compromise antitumor effects of IL-2. However, subcutaneous MeArg therapy alone reduced the growth of the primary tumors, the occurrence of lung metastases and the amount of tumor-induced pulmonary edema. When MeArg therapy was given orally (1 mg/ml drinking water), a substantial drop in NO production, as well as reduction in capillary leakage was noted in IL-2-treated healthy mice. These findings suggest that NO inhibitors could be a valuable adjunct to IL-2 therapy of cancer and infectious diseases.
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PMID:Effects of N(g)-methyl-L-arginine, an inhibitor of nitric oxide synthesis, on interleukin-2-induced capillary leakage and antitumor responses in healthy and tumor-bearing mice. 862 65

To examine intensive care unit (ICU) admission rates and diagnoses of patients with HIV infection, and to determine the outcomes of different critical illnesses, we analyzed data derived from the 63 patients who were admitted to an ICU from among the 1,130 adults with HIV infection who did not have AIDS at the time of enrollment in a multicenter prospective study. Patients were admitted and treated according to the judgment of their physicians. During 4,298 patient-years of follow-up for the entire cohort, there were 1,320 hospital admissions, of which 68 (5%) included admission to an ICU. Twenty-five (40%) of the patients admitted to the ICU died during that admission. Twenty-four patients (38%) were admitted with a principal diagnosis of lung disease; 11 had Pneumocystis carinii pneumonia (PCP), one of whom was coinfected with Aspergillus fumigatus and Legionella pneumophilia, and six of them (55%) died. Four had bacterial pneumonia, two had pulmonary edema caused by renal failure, and one each had pulmonary tuberculosis, pulmonary Kaposi's sarcoma, pneumothorax, adult respiratory distress syndrome, severe pulmonary fibrosis, cytomegalovirus pneumonitis, and metastatic adenocarcinoma to the lungs. Eleven of these 14 patients (79%) died. Thirty-nine patients had 44 admissions for nonpulmonary diagnoses, including gastrointestinal disorders (14 admissions), cardiovascular disorders (nine), sepsis syndrome (six), neurologic disorders (four), monitoring and ICU nursing care during or after a procedure (four), metabolic disorders (three), trauma (two), drug overdose (one), and unknown reasons (one). Nine (23%) of these patients died. Twenty-eight patients underwent mechanical ventilation, and 16 (57%) died. Seven (25%) had PCP (five died), seven had other primary pulmonary diseases (six died), and 14 were placed on mechanical ventilation for nonpulmonary disorders (five died). Survival did not correlate with CD4 count determined within 6 mo of admission to the ICU. In conclusion, the range of indications for critical care in patients with HIV infection is diverse. PCP accounted for only 16% of the ICU admissions, and mechanical ventilation for PCP and other pulmonary disorders was associated with a high mortality rate. In contrast, mechanical ventilation for nonpulmonary disorders, and admission to the ICU for nonpulmonary diagnoses was associated with a more favorable outcome.
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PMID:Intensive care of patients with HIV infection: utilization, critical illnesses, and outcomes. Pulmonary Complications of HIV Infection Study Group. 900 Dec 91


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