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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis of pulmonary edema that occurs during interleukin-2 therapy has often been attributed to an increase in pulmonary capillary permeability. However, renal insufficiency, fluid overload, and hypotension also develop in many patients. These manifestations of systemic toxicity may contribute to the development of pulmonary edema during therapy. Understanding the cause of pulmonary edema during interleukin-2 therapy could directly affect patients' care. Therefore, we reviewed the chest radiographs and clinical course of 54 patients who received high-dose interleukin-2 therapy and lymphokine-activated killer cells for advanced carcinoma. The type, frequency, and course over time of pulmonary abnormalities were recorded and correlated with clinical measures of renal function, fluid status, and blood pressure. Focal or diffuse parenchymal lung opacities were found on radiographs in 43 (80%) of 54 patients. Findings of interstitial pulmonary edema were most common, occurring in 76% of patients. Weight gain, hypotension, and elevation of the serum creatinine level were not associated statistically with interstitial edema. Diffuse air-space disease developed in 20% of patients. Focal consolidation, which was associated with positive central venous catheter cultures (p less than .03), developed in 28% of patients. Pleural effusion occurred in 48% of patients and was associated with all types of parenchymal disease. These data suggest that the frequent development of pulmonary edema during interleukin-2 therapy is not due to renal insufficiency, fluid overload, or hypotension, but is more likely the result of an interleukin-2-related increase in pulmonary capillary permeability.
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PMID:Pathogenesis of pulmonary edema during interleukin-2 therapy: correlation of chest radiographic and clinical findings in 54 patients. 189 99

This is an autopsy report of multiple primary cancers observed in a patient who had clinically been diagnosed as chronic arsenic poisoning. An 88-year-old man, non-smoker, had worked in an arsenic mine for 6 years from the age of 47. He had undergone operations for Bowen's disease and gastric cancer at ages 80 and 86, respectively. At autopsy, squamous cell carcinoma of the lung and a polypoid lesion in the piriform recess were found. Furthermore, microscopic examination revealed latent prostatic adenocarcinoma and oncocytoma in the kidney. The polypoid lesion of the piriform recess appeared to originate from the duct of the minor salivary gland in the pharynx, showing an adenoid cystic carcinoma-like pattern with squamous cell carcinoma in part. The cause of death was thought to be respiratory failure due to bronchopneumonia and pulmonary edema as well as hydrothorax, and chronic heart failure following ischemic heart disease. Bowen's disease was followed by four internal malignant tumors, even though the etiological relation between these cancers and arsenic is not clear.
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PMID:Multiple primary cancers in a case of chronic arsenic poisoning--an autopsy report. 233 47

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 patient was a 70-year-old male with complaint of macrohematuria at the first visit to our clinic on June 10, 1986. At that time, cystoscopy revealed a thumb sized papillary tumor and a rice sized non papillary tumor, and the biopsy specimen was pathologically diagnosed as undifferentiated carcinoma. But, he refused admission. On January 30, 1987, he came back to our clinic with complaints of dyspnea, general fatigue and weight loss. Moderate lt. gynecomastia was found and the level of serum hCG-beta was detected as high as 101 ng/ml. Excretory urogram and enhanced CT revealed a large mass in the bladder. In the seventeenth day after admission, he died of lung edema and heart failure. The findings of autopsy showed a large light greenish to light brownish tumor of 10 X 10 X 3 cm in the bladder. Distant metastases were observed in internal, common iliac and paraaortic lymph nodes, but without other distant metastasis. In histological and immunohistochemical studies, the final diagnosis is choriocarcinoma of the bladder, containing syncytiotrophoblastic giant cells with hCG-beta granules as an undifferentiated carcinoma. To our knowledge this case is the eighth described in Japan. Herein we report a new case of primary choriocarcinoma of the bladder and make a brief review of the literatures.
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PMID:[Primary choriocarcinoma of the bladder: a case report of autopsy]. 267 66

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

A new approach to cancer treatment has been developed based on the adoptive transfer of activated lymphocytes into cancer patients. Lymphocytes harvested from patients by leukapheresis are converted into lymphokine-activated killer (LAK) cells by incubation with recombinant interleukin-2 (rIL-2). These LAK cells are then infused back into the patients in combination with intravenous IL-2. Among 25 patients treated with this form of adoptive immunotherapy there were 11 patients with measurable tumor reductions, including 1 complete responder. The majority of responses occurred in patients with metastatic renal cell carcinoma, melanoma and colorectal carcinoma. The toxicities of IL-2, including fluid retention and pulmonary edema, limit therapy, and laboratory investigation is now aimed toward understanding the mechanism of IL-2 toxicity. The use of LAK cells and IL-2 in cancer therapy is still in a developmental stage and needs to be refined before its role can be definitely established.
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PMID:Therapy of cancer using the adoptive transfer of activated killer cells and interleukin-2. 312 51

A 66-year-old female with bilateral ureteral tumors associated with chronic renal failure is presented. She received pan-hysterectomy due to uterine cancer in 1957. She was first referred to our clinic to make internal shunt under a diagnosis of chronic renal failure. In 1979, the diagnosis of neurogenic bladder and bilateral vesicoureteral reflux (rt; grade 3, lt; grade 1) was made. She was admitted to our clinic with complaints of macroscopic hematuria and a temperature of 39 degrees C on April 28, 1983. Cystoscopically, pyuria from the right ureteral orifice was found. Right retrograde pyelography revealed severe dilatation of the right ureter and renal pelvis with some filling defects. For drainage of pus retaining in the right renal pelvis, right percutaneous nephrostomy was made under the guidance of ultrasonography. After her general condition improved, right nephroureterectomy was performed under the diagnosis of right pyonephrosis on June 8, 1983. Right pyelonephritis and right ureteral tumor, grade 3, were pathologically demonstrated. After the operation, an invasive bladder tumor was detected on cystoscopy and ultrasonography, subsequently a total of 3,900 rad irradiation was given to the bladder tumor. She died of pulmonary edema 7 months later. Autopsy demonstrated a transitional carcinoma, grade 3, of the left ureter. Bilateral urothelial tumors of the upper urinary tract is rare, and to our knowledge only 29 cases have been reported in Japan.
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PMID:[Bilateral ureteral tumors associated with chronic renal failure: a case report]. 332 59

Following gastrectomy for locally advanced adenocarcinomas, three patients developed microangiopathic hemolytic anemia and renal failure shortly after completing courses of adjuvant chemotherapy with mitomycin and 5-FU. These complications progressed despite cessation of chemotherapy, and all three patients died of noncardiogenic pulmonary edema precipitated in two cases by blood transfusions. At autopsy, two patients had no residual carcinoma and all had a diffuse microangiopathy involving mainly the kidneys and lungs. There was intimal hyperplasia of many arterioles sometimes associated with complete occlusion of the lumen, prominent nuclear atypia in many capillary cells, and numerous capillary fibrin thrombi. Direct immunofluorescence studies revealed extensive fibrinogen-fibrin deposits in the vascular lesions. Chemotherapy-induced microangiopathic hemolytic anemia and renal failure may predispose patients to fatal episodes of noncardiogenic pulmonary edema that can be triggered by blood transfusions.
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PMID:Microangiopathic hemolytic anemia, renal failure, and noncardiogenic pulmonary edema: a chemotherapy-induced syndrome. 640 59

We have discussed several diseases that diffusely affect the pulmonary parenchyma. The diagnostic problem is to separate cardiac pulmonary edema from noncardiac pulmonary edema, diffuse interstitial fibrosis, and lymphangitic spread of carcinoma. Frequently, this may not be possible by radiographic means alone, and additional historic and physiologic information must be obtained. It is also important to know that cardiac pulmonary edema may present in a focal or regional distribution in patients with chronic obstructive pulmonary disease. Several additional radiographic tests may be used to evaluate abnormal pulmonary parenchymal densities seen on the portable chest radiograph, when the differential diagnosis includes increased extravascular water, pneumonia, and pulmonary fibrosis. The easiest of these tests to perform is the gravitational shift test.
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PMID:The ICU chest film: cardiac versus pulmonary disease. 654 46

Collected from the Annuals of Pathological Autopsy Cases in Japan (1958-1980), autopsy findings of diabetic patients under dialysis were studied in 103 cases on peritoneal dialysis and 103 cases on hemodialysis. Direct causes of death in 13 cases (12.6%) of the 103 diabetic patients on peritoneal dialysis and in 8 cases (7.8%) of the 103 diabetic patients on hemodialysis was infections, and in seven cases (6.8%) on peritoneal dialysis and 19 cases (18.4%) on hemodialysis was bleeding. The incidence of bleeding in diabetic patients on hemodialysis was significantly higher than that in peritoneal dialysis cases (p less than 0.025). Other direct causes of death in diabetic patients on dialysis included myocardial infarction, uremia, pulmonary edema, liver cirrhosis and carcinoma. No significant difference was seen between peritoneal dialysis and hemodialysis, except the incidence of complications of bleeding and pericarditis.
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PMID:Autopsy findings in diabetic nephropathy patients under dialysis, collected from the annuals of pathological autopsy cases in Japan. 654 81


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