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)

Adoptive immunotherapy, the administration of interleukin-2 (IL-2) and interleukin-2 activated cells, leads to tumor regression in some patients with advanced cancer. Although this new therapeutic modality offers hope for the future, at present, a multitude of toxicities limit the total dose and duration of therapy. Among the toxic side effects a purported third space or vascular leak syndrome is the most serious. In this review, we detail the evidence for a third space syndrome (peripheral edema, ascites, oliguria, elevated serum creatinine levels) and cardiopulmonary dysfunction (hypotension, respiratory distress, pulmonary edema, hypoxemia) with adoptive immunotherapy in human and animal studies. We conclude that IL-2 administration is associated with increased pulmonary microvascular permeability, infiltration of the lung parenchyma with large esterase negative lymphoid cells, hypoxemia, systemic hypotension, positive fluid balance and, in animals, transient pulmonary hypertension. These abnormalities do not seem to be caused by IL-2 directly; the causes may be mediated by IL-2 activated lymphocytes or other IL-2 activated cellular mediators.
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PMID:Cardiopulmonary toxicity of adoptive immunotherapy. 306 15

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

Neoplasms are rare cardiac findings of which myxomas comprise about 75%. We report of 15 patients, predominantly female (60%) with a mean age of 58.8 years. Male patients (40%) were 20 years younger on average. 80% of these tumors developed in the left atrium fixed to the atrial septum. In 2 patients the right ventricle and in 1 patient the right atrium was involved. No left ventricular or bilateral tumors were found. Clinical findings showed a great variety of symptoms. Often misdiagnosis was established until echocardiography was performed. Major symptoms were dyspnea (80%), elevated erythrocyte sedimentation rate (73%), arrhythmias (53%), lung edema (47%), embolization (40%) and anemia (40%). Pathological examination and tumor genesis are still in discussion. Several theories are reported in literature: a true thrombus, thrombus organization with malignant potential, true neoplasms as well as a familiar myxoma complex may explain clinical and histological features. Our findings did not confirm only one theory but emphasize different possibilities.
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PMID:Cardiac myxoma. Clinical and pathologic features in 15 cases. 317 79

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

The recombinant cytokines IFN-gamma and TNF-alpha stimulate several macrophage-mediated functions important in host defense. However, systemic administration of cytokines may be limited by significant host toxicity. We investigated whether aerosolized cytokines can stimulate alveolar macrophage and blood monocyte function, and whether they induce an inflammatory response in the lungs of normal rats. We found that aerosolized murine rIFN-gamma or recombinant human TNF-alpha increased IL-1 production by both alveolar macrophages and blood monocytes for at least 5 days after administration. Furthermore, murine rIFN-gamma increased the expression of Ia Ag on alveolar macrophages and human rTNF-alpha increased alveolar macrophage- and blood monocyte-mediated tumor lysis. Sequential aerosolization of IFN-gamma and TNF-alpha significantly increased both IL-1 release and Ia expression compared to either cytokine administered alone. Aerosolized human rTNF-alpha achieved lung levels comparable to those produced by an i.v. TNF-alpha dose reported to cause diffuse organ injury and death in rats. However, plasma TNF-alpha levels were several thousand-fold lower after aerosol administration. Aerosolized cytokines did not induce lung edema or an inflammatory cell infiltrate within the airways or alveoli. Aerosolized human rTNF-alpha alone, or murine rIFN-gamma and human rTNF-alpha, induced margination of leukocytes in pulmonary blood vessels 1 day after aerosolization, and a few small foci of pulmonary hemorrhage 5 days later. We conclude that aerosol administration of IFN-gamma or TNF-alpha enhances both pulmonary and systemic monocyte function, and that the combination of IFN-gamma and TNF-alpha produce additive or synergistic effects. Aerosolized cytokines induce only a minimal pulmonary inflammatory response. Aerosolized TNF-alpha produces high cytokine levels in the lung but very low uptake into the circulation.
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PMID:Lung-specific delivery of cytokines induces sustained pulmonary and systemic immunomodulation in rats. 328 35

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

Infection, hemorrhage and adult respiratory distress syndrome (ARDS) are pulmonary complications occurring after remission induction therapy for acute leukemia. The aim of this study was to analyze the incidence of these causes by serial roentgenogram, clinical, microbiological and laboratory tests in 21 patients (pts) with relapsed acute leukemia (18 X myeloid, 3 X lymphoblastic), an AML-pt (acute myeloid leukemia) suffering from secondary leukemia, and three pts with primary refractory leukemia following treatment with intermediate (IM) and high-dose cytosine arabinoside (HD-Ara C), in combination with amsacrine (AMSA)(n = 19), etoposide (VP 16) (n = 5) or Mitoxantrone (n = 1). Eleven out of 25 pts developed pulmonary complications, one of them with massive hemoptysis and roentgenographic signs of pulmonary bleeding, one suffering from protracted shock after a tumor lysis syndrome, two pts showing symptoms of a cardiogenic pulmonary edema complicating severe Candida pneumonia in one case and legionnaires' disease in the other. Seven of the eleven pts had a non-cardiogenic pulmonary edema with respiratory failure 1-14 days after cessation of induction or consolidation therapy. In six of the seven, there were no signs of cardiogenic, infectious or metabolic reasons, including fluid overload, for the pulmonary edema, one had as a contributing factor a Candida infection of the lung. Three of the seven patients recovered, four died (two following IM and two after HD-Ara C). Other adverse side effects, clearly attributable to HD-Ara C, included delirious state (n = 3), generalized erythema (n = 3), acute pancreatitis (n = 2), acute abdomen (n = 1) and conjunctivitis in almost all patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Med Oncol Tumor Pharmacother 1988
PMID:Non-cardiogenic pulmonary edema complicating intermediate and high-dose Ara C treatment for relapsed acute leukemia. 336 72

A 47-year-old woman presented with the chief complaint of gait disturbance and pain of bilateral lower limbs. She was diagnosed as having necrotizing myelitis because myelography was normal and incidentally bilateral adrenal tumor was recognized by ultrasonography and computed tomography. Left adrenalectomy was performed under the diagnosis of bilateral non-functioning adrenal tumor or metastasis to the adrenal glands with unknown origin. The tumor was 10 x 6 x 3 cm in size and 175 g in weight. The pathological diagnosis was non-Hodgkin lymphoma (diffuse large cell type). After combination chemotherapy of vincristine, cyclophosphamide, prednisolone and adriamycin, residual right adrenal mass showed a remarkable reduction, but unfortunately she died 5 months later postoperatively because of complications of lung edema and pneumonitis.
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PMID:[A case of bilateral adrenal non-Hodgkin lymphoma]. 337 94

A study of 30 cases of pheochromocytoma encountered at our department between 1959 and 1986 is presented. Fourteen patients were males and 16 were females. Their ages ranged from 18 to 72 years with a peak incidence in the fifties. Hypertension was present in 87% of the patients. The incidence of extra-adrenal tumors was 30% and that of malignancy 7%. The 24-hr urinary level of catecholamine was to a certain degree in accord with the location of the tumor and type of hypertension. Computed tomography and venous sampling were very useful for the diagnosis which had an accuracy rate of 100% in this series. Preoperative management using an alpha-blocker was effective in controlling blood pressure and circulating blood volume in most cases. Postoperative blood pressure was normalized within a week after operation in 85% of the patients who had been suffering from hypertension, although elevated levels of norepinephrine in urine were still noted in 56% of the patients one week after operation. Of the 27 follow-up cases, 21 cases (78%) were in good health and 2 cases were alive with hypertension with a mean follow-up period of 8.1 years. Four patients died, one during angiography, one of pulmonary edema one day after operation and the other 2 of metastases of malignant pheochromocytoma.
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PMID:[A clinical review of 30 pheochromocytoma patients]. 340 May 41

A syndrome of pulmonary alveolar septal calcinosis, pneumothorax, and pneumomediastinum, leading to rapidly progressive acute respiratory insufficiency and death was observed in 2 children with acute lymphoblastic leukemia (ALL). Primary clinical and radiological considerations in these patients were pulmonary edema and infection, and the diagnosis of pulmonary alveolar septal calcification was established only at autopsy. One patient, a 15-year-old girl, was found also to have parathyroid hyperplasia typical of familial hyperparathyroidism. The other, a 16-month-old girl, showed osteitis fibrosa of the bones and parathyroid hyperplasia of secondary type, suggesting that the pulmonary calcinosis resulted from hypercalcemia caused by a parathormone or prostaglandin-secreting tumor. The cause of pneumothorax and pneumomediastinum may have been rupture of calcified alveolar septa induced by high PEEP during ventilation of these patients. Other possible mechanisms contributing to hypercalcemia and pulmonary calcinosis in children with acute leukemia include bone resorption due to marrow infiltration, immobilization syndrome, renal failure, and administration of calcium, phosphate, or bicarbonate. This complication of acute leukemia in childhood is rare (2 patients in 430 autopsied over the period 1961-1982 at Childrens Hospital of Los Angeles). How often the process can be reversed if diagnosed before severe respiratory insufficiency is present is not known.
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PMID:Pulmonary alveolar septal calcinosis causing progressive respiratory failure in acute lymphoblastic leukemia in childhood. 347 56


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