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

The surgical challenge of resection of renal cell carcinoma with vena caval invasion may require close cooperation between the urologist and cardiovascular surgeon. From 1977 to 1986, 13 patients with renal cell carcinoma and tumor thrombus invading the inferior vena cava (IVC) underwent radical surgical resection. In three of 13 patients the thrombus extended into the heart (right atrium two patients and right ventricle one patient). The tumor originated in the right kidney in 10 patients and in the left kidney in three patients. There were 10 men and three women with a mean age of 64 years (range, 46 to 75 years). Surgical management included midline incision, seven, with median sternotomy, four, and thoracoabdominal, two. After exposure of the renal vessels and IVC, all patients underwent radical nephrectomy. Two patients had caval sleeve resection, one had a partial caval resection, and seven had a 1 cm caval cuff. Planned cardiopulmonary bypass was used in three patients. The tumor thrombus was extracted by simultaneous atrial and caval approaches. One patient underwent unplanned emergency cardiopulmonary bypass after intraoperative cardiac arrest caused by a large tumor embolus of the pulmonary artery. No operative deaths occurred. Postoperative morbidity was significant in five of 13 patients, caval thrombosis in one, lower limb swelling in two, renal failure in one, and pulmonary edema in one patient. Two patients required long-term anticoagulation therapy for confirmed pulmonary emboli within 1 month of surgery. These complications resolved. The follow-up period ranged from 7 to 64 months with a mean of 36 months. Two patients died of metastatic disease at 24 and 48 months after surgery. Three patients are alive with metastatic disease at 6 to 64 months while one patient had a solitary metastatic lesion removed from the frontal lobe 4 years after nephrectomy and has been disease free a subsequent 18 months. Eight of 11 patients are disease free at 7 to 64 months (four patients greater than 52 months). Our 83% survival rate at a mean follow-up of 36 months suggests that this group of patients should not be denied aggressive resection. Documentation of tumor source and caval extension are essential to plan operative procedures, including use of cardiopulmonary bypass.
 ...
PMID:Caval tumor thrombus complicating renal cell carcinoma: a surgical challenge. 366 Feb 38

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.
 ...
PMID:Carcinoma-associated hemolytic-uremic syndrome: a complication of mitomycin C chemotherapy. 392 62

Forty-three peritoneovenous shunts have been inserted to palliate malignant ascites in 33 patients. Ascites was controlled for a time in every patient, but 18 shunts eventually blocked. Further shunt revision successfully controlled ascites until death in five of these patients and for prolonged periods in another five. The authors observed a marked difference between the performances of the two available shunts, but emphasize that the two groups of patients were not selected at random and therefore may not be comparable. Twelve postmortem examinations have been performed in the 33 patients to ascertain causes of shunt malfunction and to identify possible evidence of abnormal or accelerated tumor spread. The postmortem findings highlight great variability in the capacity of iatrogenically introduced showers of tumor cells to seed. There was a spectrum of tumor growth in the lung from a complete absence of tumor cells through dormant tumor clumps to developing metastases. The authors found no evidence either clinically or at autopsy, that the procedure had adversely affected the prognosis, except in one patient who died from pulmonary edema immediately after the operation.
 ...
PMID:Surgical and pathologic complications associated with peritoneovenous shunts in management of malignant ascites. 397 77

Fatal pulmonary toxicity can be consistently produced in L1210 leukemia-bearing mice by single therapeutic doses of cyclophosphamide, BCNU, and mitomycin C but not by adriamycin. Lung toxicity is principally determined by an existing tumor burden at the time of drug administration. Thus when any of the four chemotherapeutic agents was given 5 days after L1210 transplantation there was no mortality. Pulmonary pathology in these mice was equivalent to that noted in normal mice receiving identical drug treatment or to that noted in untreated L1210-bearing mice sacrificed 7, 8, or 10 days after tumor transplantation. When chemotherapy was delayed to day 7 after L1210 transplantation for mitomycin C or to day 8 after transplantation for BCNU and cyclophosphamide, more severe pulmonary toxicity was found. Mortality within the first 5 days of treatment was 38, 50, and 80%, respectively. Pulmonary pathology included moderate to severe vascular congestion and interstitial pneumonitis, diffuse pulmonary hemorrhage often involving the entire pulmonary parenchyma, pulmonary edema, and alveolar cell metaplasia. A unique finding, associated with cyclophosphamide treatment, was the occurrence of perivascular-intramural edema of the walls of medium-size pulmonary vessels. It is hypothesized that stasis within the pulmonary capillary circulation, resulting from advanced tumor growth and from drug treatment, may contribute to the development of chemotherapy-related toxicity.
 ...
PMID:Chemotherapy-induced pulmonary toxicity in mice bearing L1210 leukemia. 640 46

Many nonpulmonary diseases may present with respiratory manifestations or may involve the lungs later in the disease course. The mechanisms by which such involvement occurs are almost as diverse as the diseases themselves and include the following. Hematogenous spread of disease is one of the most common mechanisms of lung involvement, for example, lung involvement by metastatic malignant disease. Cytotoxic factors from another anatomic location may be deposited in the alveolar basement membranes and cause pulmonary damage, for example, pulmonary hemorrhage associated with Goodpasture's syndrome. The pulmonary vasculature may prominently manifest generalized disease, as frequently occurs in Wegener's granulomatosis. Toxins accumulated as a result of disease in another organ system may damage the alveolar capillaries and result in pulmonary edema, as can occur in patients with severe azotemia due to renal failure. Depletion of lung surfactant as a consequence of disease in another organ system may produce alveolar collapse and respiratory failure; a disease that can have this effect is acute pancreatitis. The lungs may be the first organs to exhibit, through unknown mechanisms, underlying systemic diseases such as the collagenoses. Humoral factors released in another anatomic site may cause pulmonary problems; for example, bronchospasm may develop in patients with carcinoid of the intestine as a result of serotonin released by the tumor. Injury to another organ system can produce lung damage by complex mechanisms; an excellent example is the occasional development of neurogenic pulmonary edema in patients with trauma to the brain.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Respiratory manifestations of systemic disease. 3. Neurologic, skeletal, dermatologic, gynecologic, and gonadal diseases and disorders of pregnancy. 647 14

The case of a 25-year-old man who had periosteal osteogenic sarcoma with intravascular metastases in unusual locations is reported. The patient presented with acute renal failure, unilateral pulmonary edema, functional mitral stenosis, and low cardiac output. After successful surgical removal of a left atrial metastasis with subsequent improvement in cardiac output, renal function improved only transiently and urinary output varied markedly. At autopsy, metastatic osteogenic sarcoma was discovered within the lumen of the abdominal aorta obstructing both renal arteries. The case is the first report of a neoplasm metastatic to the aorta causing intermittent bilateral renal arterial obstruction; it illustrates the diagnostic difficulties presented by intravascular metastatic disease.
 ...
PMID:Metastatic periosteal osteosarcoma causing cardiac and renal failure. 657

2'-Deoxycoformycin, a tight-binding adenosine deaminase inhibitor, was administered to 11 adult patients with refractory lymphoproliferative diseases. Total doses ranged from 1.0 to 13.5 mg/kg. Inhibition of lymphoblast adenosine deaminase was obtained in all cases and tumor cytoreduction was noted in eight of ten cases, but no clinically meaningful remissions were obtained. Major toxicities occurred in five patients and included pulmonary edema, renal failure, central nervous system toxicity, hypotension, and death. Toxicity prevented retreatment in several cases in which marked cytoreduction occurred. Deoxyadenosine triphosphate accumulated to a variable extent in the red blood cells of all patients, and a reciprocal decrease in erythrocyte adenosine triphosphate was noted in all cases but one. All patients who suffered major organ toxicity had red blood cell deoxyadenosine triphosphate/adenosine triphosphate ratios greater than 1.3. These data suggest that the degree of replacement of adenosine triphosphate by deoxyadenosine triphosphate in erythrocytes reflects the biochemical milieu which may result in systemic toxicity following treatment with 2'-deoxycoformycin.
 ...
PMID:Alterations in erythrocyte adenine nucleotide pools resulting from 2'-deoxycoformycin therapy. 660 Jun 52

Misinterpretation of confusing cardiac, constitutional, and embolic symptoms delayed the diagnosis of cardiac myxoma and caused two of 18 patients to undergo acute operations during cardiogenic shock with pulmonary edema. In recent cases echocardiographic screening of unclear cardiac symptoms gave the correct diagnosis early. Despite the simple surgical procedure (excision of tumor and underlying endocardium), the postoperative course was complicated by cardiac failure, arrhythmias, and systemic reactions. Prosthetic valve thrombosis and malignancy caused two early deaths. Two patients died later of cerebrovascular insults. Both belonged to a group of five patients having preoperative emboli from fragile myxomas. Four of these five had coronary or cerebral myxomatous pseudoaneurysms. A 6 year follow-up, including recatheterization, showed no tumor recurrence and generally normalization of the clinical condition, heart size, and catheterization findings. Even pronounced mitral insufficiency accompanying left atrial myxomas had subsided spontaneously. Tricuspid insufficiency in two patients with right atrial myxomas persisted, necessitating reoperation in one. When diagnosed, a cardiac myxoma should be removed promptly to reduce cardiac and embolic complications, including myxomatous pseudoaneurysm formation, which might be more frequent than previously recognized.
 ...
PMID:Surgical considerations in the treatment of cardiac myxoma. 669 16

Thiono-sulfur-containing compounds cause a wide variety of toxic effects in mammals. These toxic effects of thiono-sulfur-containing compounds appear to be at least partially the result of their metabolism to reactive intermediates by the cytochrome P-450-containing monooxygenase enzyme systems. Covalent binding of (atomic) sulfur released in the cytochrome P-450 monooxygenase catalyzed metabolism of certain thiono-sulfur compounds appears to be responsible for the inhibition of monooxygenase activity and the loss of cytochrome P-450 seen on administration of these thiono-sulfur compounds in vivo or incubation with cytochrome P-450 monooxygenase enzymes in vitro. Liver necrosis and perhaps the induction of lung edema and neoplasia as well as other effects of thiono-sulfur-containing compounds are more likely the result of the covalent binding of the electrophilic S-oxides or S-dioxides or carbene derivatives of these S-oxides and S-dioxides to tissue macromolecules. The rationale for implicating metabolites of thiono-sulfur compounds other than atomic sulfur in these effects derives from the experiments with thioacetamide and the fact that atomic sulfur is highly reactive and appears to bind predominantly or exclusively to cytochrome P-450. It is difficult to rationalize why binding to and inhibition of cytochrome P-450 would lead to the production of, for examples, liver necrosis.
 ...
PMID:Toxicology of thiono-sulfur compounds. 704 88

Carcinoma of the bronchus was detected following the onset of cardiac rhythm disorders, and a pneumopericardium with associated, radiologically detected, unilateral pulmonary edema. The tumor extended mainly around the bronchus and in the mediastinum, and a bronchopericardial fistula was present together with invasion of the left auricle and pulmonary veins. Pneumopericardium is a rare lesion and it is exceptional to observe it during the course of bronchial cancer. The relationships between unilateral interstitial edema and tumoral obstruction of the ipsilateral pulmonary veins are discussed.
 ...
PMID:[Unilateral pulmonary edema, pneumopericardium and bronchial cancer (author's transl)]. 745 44


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>