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 teenage girl in bone marrow remission with acute lymphocytic leukemia died suddenly from pulmonary edema. She had taken her first oral dose of methotrexate and cyclophosphamide 10 hours previously when she was feeling well and was asymptomatic. One week previously she had received the last of four intrathecal injections of methotrexate. Autopsy showed marked pulmonary edema as well as chronic lung changes, as previously described in patients with methotrexate pneumonitis. There is usually at least a 12-day interval from the onset of administration of methotrexate to the onset of the lung toxicity. The authors suggest the patient was sensitized by the intrathecal methotrexate and then reacted with angioneurotic edema of the lung when given the first oral dose of methotrexate. Careful examination for infectious agents, including electron microscopy, was negative.
Cancer 1977 Oct
PMID:Methotrexate-induced sudden fatal pulmonary reaction. 26 2

Clonogenic growth (colony-forming efficiency, CFE) of i.v. injected allogeneic W256 tumour cells in the lungs was markedly enhanced by treatment of rats with alpha-naphthyl thiourea (ANTU) injected i.p. from 2 h before to 2 h after the tumour cells. ANTU specifically increases pulmonary vascular permeability in adult rats and causes acute pulmonary oedema and pleural effusion. Inhibition of drug toxicity to the lungs by tachyphylaxis, specific antimetabolites or iodides did not abolish the effect of ANTU on CFE. CFE was not increased when cells were seeded by i.v. injection the lungs affected by advanced pulmonary oedema at 6 to 24 h after treatment with drug. ANTU did not enhance growth of intratracheally injected cells. Although ANTU has no cytotoxic or immunosuppressive action, treatment of tumour-immunized rats with ANTU caused apparent "breakdown" of tumour immunity in 50% of rats, by causing growth of tumour colonies in the lungs. Possible mechanisms for the ANTU-induced decrease in innate resistance to growth of tumour in the lungs are discussed.
Br J Cancer 1978 Jan
PMID:Effect of toxic thioureas on resistance of rats to growth in the lungs of intravenously and intratracheally seeded tumour cells. 61 62

One hundred adults with unilateral diffuse lung opacity have been studied. Seventy cases involve the right lung. Lymphangitic cancer, pneumonia, pulmonary edema, aspiration, and radiation injury account for the majority of cases (90%). Unilateral pulmonary edema is usually right sided, and, frequently, the heart is not enlarged. Unilateral lymphangitic spread of cancer is usually right sided and most often due to a primary lesion in the involved lung. Occasionally a cancer outside the lung may spread unilaterally.
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PMID:Unilateral diffuse lung opacity; Differential diagnosis with emphasis on lymphangitic spread of cancer. 84 83

Although most new 'high tech' industrial processes are developed in industrialized countries, many of these technologies are eventually transferred to the industrializing countries. Many of these new technologies are associated with the use of respiratory toxins. However, there has been little study of acute or chronic health effects of work in these industries. The semiconductor industry illustrates many of these issues. The past decade has been increasing globalization of semiconductor manufacturing. Semiconductor manufacturing uses many chemicals with extremely high respiratory toxicity, including gases such as arsine and phosphine, strong acids and bases, dopants and photoactive chemicals. In semiconductor manufacturing, gases and chemicals are strictly controlled, but little is known about the occurrence of respiratory symptoms or disease in this industry. Potential acute respiratory effects of these exposures include mucous membrane irritation, tracheobronchitis, pulmonary edema and death. Chronic effects may include airway sensitization and possibly respiratory cancer. Movement of 'high tech' industries to less industrialized countries may not be accompanied by the same degree of attention to the control of workplace exposures. The shortage of adequately trained health and safety personnel, greater attention to safety than to health issues, and the unorganized and unskilled workforce in industrializing countries may exacerbate this situation. More research is needed on the health effects of exposures in rapidly changing industries such as semiconductor manufacturing, and the results of this research must be communicated and safe practices implemented worldwide.
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PMID:Occupational lung diseases in the industrializing and industrialized world due to modern industries and modern pollutants. 132 47

The chest roentgenograms of 54 patients receiving high dose interleukin-2 with or without lymphokine-activated killer cell therapy for advanced cancer were retrospectively reviewed. Thirty-nine patients (72 percent) developed chest roentgenographic abnormalities consisting of pleural effusions, 28 (52 percent); diffuse infiltrates (pulmonary edema), 22 (41 percent); and focal infiltrates, 12 (22 percent). These abnormalities resolved in 30 of 39 (77 percent) patients by four weeks after therapy. Simple pleural effusions were the only residual roentgenographic abnormalities seen and were present primarily in patients receiving IL-2 by bolus intravenous injection (8 of 28) (29 percent) as compared to continuous intravenous infusion (1 of 24) (4 percent) (p = 0.03). Only roentgenographic evidence of pulmonary edema appeared to correlate with the degree of clinical pulmonary toxicity (p = 0.001). The development of chest roentgenographic abnormalities correlated with the administration of IL-2 solely by bolus intravenous injection (p = 0.04), a pretreatment FEV1 of less than 3 L (p = 0.04), and treatment associated bacteremia (p = 0.09), but not with prior therapy, the presence of pulmonary metastases or the degree of systemic capillary leak as measured by percentage of weight gain during therapy. Although the roentgenographic abnormalities did not relate to the number of LAK cells received, two patients developed sudden onset of dyspnea and chest roentgenographic evidence of pulmonary edema shortly after the first LAK cell administration, implying that a direct cause-and-effect relationship exists in some patients. Possible mechanisms for these IL-2 related chest roentgenographic abnormalities and pulmonary toxicity in general are discussed.
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PMID:Chest roentgenographic abnormalities in IL-2 recipients. Incidence and correlation with clinical parameters. 154 Nov 42

Low-molecular weight dextran is commonly used to prevent thrombosis after microvascular procedures; however, the potential complications of this drug are not well known. We report a case of acute pulmonary edema in a healthy person after elective microsurgery for treatment of a malignant tumor of the forearm. The mechanism of action of dextran and the pathophysiology of two potential adverse reactions to this drug are discussed. It is thought that in this patient pulmonary edema was caused by dextran toxicity.
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PMID:Acute pulmonary edema associated with use of low-molecular weight dextran for prevention of microvascular thrombosis. 170 97

Besides general complications of immunosuppression such as increased susceptibility to opportunistic infections or malignancy, individual immunosuppressive agents are associated with specific side effects. Nephrotoxicity is the major side effect of cyclosporine (CsA). Various attempts have been made to minimize this toxicity, such as monitoring drug blood levels, modifying the protocol, and coadministering other agents. Other side effects caused by CsA are hepatotoxicity, hyperkalemia, hypertension, tremor, gum overgrowth, and hirsutism. Azathioprine (AZA) causes dose-related bone marrow suppression, commonly leading to leukopenia. Careful monitoring of complete blood cell count and dosage adjustment according to white blood cell count are usually adequate to prevent serious leukopenia. The side effects of corticosteroids are numerous and include slow wound healing and de novo insulin-dependent diabetes mellitus. Many complications are dose related, and with low dosage or discontinuation of steroids, their frequency rapidly decreases. Antilymphoblast and antithymocyte globulins (P-ALG) are foreign antibodies and may cause allergic-type reactions such as fever, chill, and hypotension. The initial side effect of monoclonal antibody (muromonab-CD3, OKT3) is similar to that of P-ALG. It includes high fever, shaking chills, headache, rigors, and hypotension. To prevent it, acetaminophen, an antihistamine, and a steroid usually are administered before injection. Because this agent is also associated with high frequency of pulmonary edema, it should not be given to any patient who has more than 3% body weight gain during the week prior to therapy. In rare case, it causes aseptic meningitis or encephalopathy, which is manifested by fever, severe headache, and seizure.
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PMID:Complications associated with immunosuppressive therapy and their management. 174 17

Fifteen patients with refractory B-cell lymphoma were treated in a Phase I dose escalation clinical trial with a highly potent immunotoxin consisting of the Fab' fragment of a monoclonal anti-CD22 antibody (RFB4) coupled to chemically deglycosylated ricin A chain. All patients had low, intermediate, or high grade non-Hodgkin's lymphoma. The immunotoxin was administered i.v. in two to six doses at 48-h intervals. The peak serum concentration and the t1/2 were not dose dependent among patients and averaged 1.3 micrograms/ml and 86 min, respectively. Three patients made antibody against A chain, and a fourth made antibody against both A chain and mouse immunoglobulin. Antibody responses were low (less than or equal to 85 micrograms/ml) in three patients and were not detected until 1 mo after treatment. The maximum tolerated dose of the immunotoxin was 75 mg/m2. Dose-related toxicities included vascular leak syndrome, fever, anorexia, and myalgia. Dose-limiting toxicities included pulmonary edema and/or effusion, expressive aphasia, and rhabdomyolysis (resulting in reversible kidney failure). There was no evidence of liver dysfunction. Partial responses were achieved in 38% of evaluable patients, and in those patients who had greater than 50% CD22+ tumor cells, 50% of the patients achieved a partial response. Clinical responses were not related to tumor grade and were generally transient, lasting between 1 and 4 mo.
Cancer Res 1991 Aug 01
PMID:Phase I immunotoxin trial in patients with B-cell lymphoma. 185 19

A 73-year-old woman with ureteral cancer and multiple systemic metastasis was admitted complaining of dyspnea on exertion after administration of recombinant human tumor necrosis factor (rH-TNF). On chest examination, coarse crackles were heard during inspiration throughout the lungs. Chest roentgenogram revealed a ground glass infiltration, an air bronchogram in the right lung field and an ill-defined right pulmonary artery. Her symptom and chest roentgenological finding improved and coarse crackles were not heard after discontinuation of rH-TNF. Neutrophils and lymphocytes of bronchoalveolar lavage fluid increased and transbronchial lung biopsy specimens showed slight thickening of alveolar septa with infiltration of inflammatory cells. The pulmonary edema was thought to be caused by rH-TNF which induces adherence of neutrophils to endothelium and stimulates them to increase lysosomal enzyme release and oxygen radical production. As a results, it is thought pulmonary permeability might be increased.
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PMID:[Ureteral cancer resembling pulmonary edema induced by recombinant human tumor necrosis factor]. 203 98

We reviewed the charts of the cancer patients admitted in a medical oncology ICU during an 11-month period. Among 330 admissions (55% for a medical complication, 45% for monitoring during administration of an intensive or potentially toxic treatment), 49 patients died and 34 autopsies were performed. Every autopsied case was reviewed by a group of oncologists and pathologists. The direct cause of death was neoplasia itself in only four patients. Six deaths remained unexplained after post mortem examination. In 23.5% of cases, the direct cause of death was a major infection (four aspergillosis, two candidemia, one CMV pneumonia, one acute cholecystitis). Overall, the clinical diagnosis of the immediate cause of death was correct in only 41% of the cases. Lesions of pulmonary edema (PE) were found at autopsy in 68% of the cases. No predictive factors for PE were determined.
Eur J Cancer 1990 Mar
PMID:Causes of deaths in an oncologic intensive care unit: a clinical and pathological study of 34 autopsies. 214 96


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