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)

Previously, we showed that nitric oxide (NO) plays a major role in the pathogenesis of IL-2-induced capillary leak syndrome in healthy or mammary adenocarcinoma-bearing C3H/HeJ mice. NO synthase (NOS) inhibitors, such as NG-nitro-L-arginine methyl ester (L-NAME) reduced all the manifestations of IL-2-induced capillary leakage, without compromising the antitumor effects of IL-2. The present study was carried out on healthy C3H/HeJ mice subjected to one or two 4-day rounds of systemic IL-2 therapy with or without oral L-NAME therapy to: (a) identify the tissue source of NOS activity and NOS protein induced by IL-2 therapy; (b) identify histologically the nature of the structural damage to the lungs associated with IL-2 therapy-induced pulmonary edema; and (c) evaluate the effects of additional L-NAME therapy on the above-mentioned parameters. Results revealed that IL-2 therapy in healthy mice resulted in the expression of inducible NOS in numerous tissues including the endothelium and muscles of the anterior thoracic wall as well as splenic macrophages. One round of IL-2 therapy resulted in high levels of inducible NOS (iNOS) activity in the anterior thoracic wall accompanied by pleural effusion. After two rounds of IL-2 therapy, there was neither pleural effusion nor high iNOS activity in the thoracic wall. IL-2-induced pulmonary edema after one round of therapy correlated to both a significant rise in NO production measured in the serum and structural damage to the lungs and its capillaries. Addition of the NOS inhibitor L-NAME totally eradicated NOS activity but not necessarily iNOS expression. It also reduced IL-2-induced pulmonary edema and pleural effusion, restrained the rise in the levels of NO metabolites (nitrites and nitrates) in the serum and pleural effusion, and significantly restored the structural integrity of the lungs after one round of therapy. Thus, NOS inhibitors may be beneficial adjuncts to IL-2 therapy for cancer and infectious diseases.
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PMID:The role of active inducible nitric oxide synthase expression in the pathogenesis of capillary leak syndrome resulting from interleukin-2 therapy in mice. 901 Apr 49

A 74 year old patient with diabetes mellitus was hospitalized because of nausea, recurrent vomiting and increasing fatigue. Shortly before admittance the patient had diarrhea. He also reported a recent onset of aversion against meat consumption. Clinical investigation revealed a possible right-sided paraumbilical abdominal tumor, normal bowel sounds, a vascular bruit and a normal white blood count with increased band forms. During hospitalisation the general condition of the patient deteriorated rapidly with fever and increasing numbers of immature granulocytes. The patient finally died under the symptoms of a paralytic ileus with hypotonia and hypoglycemia. Autopsy revealed a fist-sized stenosing tumor in the cecum with the histology of a mainly well differentiated, cylindrocellular adenocarcinoma. As immediate cause of death a bilateral paracentral lung embolism with pulmonary edema was found, the latter probably as immediate consequence of preterminal heart failure.
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PMID:[Intestinal paralysis in long-term diabetes mellitus]. 965 91

In adults, the haemolytic-uraemic syndrome (HUS) is associated with probable causative factors in the minority of all cases. Cytotoxic drugs are one of these potential causative agents. Although metastatic cancer by itself is a recognized risk-factor for the development of HUS, therapy with mitomycin-C, with cis-platinum, and with bleomycin carries a significant, albeit extremely small, risk for the development of HUS, compared with all other cytotoxic drugs. Gemcitabine is a novel cytotoxic drug with promising activity against pancreatic adenocarcinoma. We are reporting on one patient with metastatic duodenal papillary carcinoma developing HUS while on weekly gemcitabine therapy. The presenting features in this patient were non-cardiac pulmonary oedema, renal failure, thrombocytopenia and haemolytic anaemia. The diagnosis of HUS was made on the day of admission of the patient to this institution. Upon aggressive therapy, including one single haemodialysis and five plasmaphereses, the patient recovered uneventfully, with modestly elevated creatinine-values as a remnant of the acute illness. Re-exposure to gemcitabine 6 months after the episode of HUS instituted for progressive carcinoma, thus far has not caused another episode of HUS.
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PMID:Elevated reticulocyte count--a clue to the diagnosis of haemolytic-uraemic syndrome (HUS) associated with gemcitabine therapy for metastatic duodenal papillary carcinoma: a case report. 1018

The complication of thrombotic thrombocytopenic purpura or hemolytic uremic syndrome (TTP/HUS) can occur in cancer patients. It is characterized by a microangiopathic hemolytic anemia, severe thrombocytopenia, and renal failure. Pulmonary manifestations, especially pulmonary edema, are a common observation. Neurologic changes are also frequently seen. The etiology is unknown at this time. It has been observed in many different types of cancer and is most commonly seen in gastric adenocarcinoma followed by carcinoma of the breast, colon, and small cell lung carcinoma. The hemolysis can be massive and is due to red cell fragmentation, as schistocytes are present in all the cases. Though immune complexes are present in the plasma, the antiglobulin (Coomb's) test is negative. Chemotherapeutic agents, especially mitomycin C, have been implicated as causative factors. There is a correlation of this complication with the cumulative dose. However, chemotherapy cannot account for all the cases as the syndrome can occur in untreated patients. It can be differentiated from disseminated intravascular coagulation by the absence of a coagulopathy. Management should consist of plasma exchange, use of a Staphylococcus aureus column (Prosorba), and control of hypertension. Because of the susceptibility to pulmonary edema, blood volume overloading should be avoided.
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PMID:Thrombotic microangiopathy manifesting as thrombotic thrombocytopenic purpura/hemolytic uremic syndrome in the cancer patient. 1035 89

We present a rare case of a synchronous primary lung cancer adjacent to a hamartoma. A 71-year-old woman was admitted with congestive heart failure due to acute myocardial infarction. A chest radiogram on admission showed pulmonary edema with a tumor shadow in the right upper lung field. Because histological diagnosis was not obtained preoperatively, a wedge resection of the lung was conducted using video-assisted thoracoscopic surgery. The histopathological examination confirmed the coexistence of an adenocarcinoma with a chondromatous hamartoma. Right upper lobectomy was performed followed by excision of the mediastinal lymph nodes. Although hamartoma is generally considered to be a benign neoplasm, there have been several reports of increased risk to lung cancer in patients with a chondromatous hamartoma. Therefore, we recommend that patients with a hamartoma should be submitted to a complete evaluation and to regular follow-up, considering the risk to associated synchronous malignancy.
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PMID:Coexistence of lung cancer and hamartoma. 1135 62

Acute pulmonary thromboembolism is fatal if the diagnosis and treatments are delayed. Here we present a case of acute thromboembolism to the right and left pulmonary arteries after right lung lobar resection. A 52-year-old woman who admitted to our hospital with lung cancer was performed right upper lobectomy with mediastinal lymph node dissection (pT1N0M0, well differentiated adenocarcinoma). Two days after surgery, she complained sudden chest discomfort and dyspnea. The blood pressure and oxygen saturation were rapidly decreased. Because there was no lung edema or atelectasis in the chest portable roentgenogram and no ischemic change in the electrocardiogram, pulmonary thromboembolism was suspected and emergency chest computed tomography (CT) was performed. The CT showed left and right pulmonary arterial thromboembolism and immediate anti-coagulator therapy was started. Her condition was improved and chest CT, which was performed three days after the onset of the thromboembolism, showed decreased but still remained thrombus. The anti-coagulator therapy was continued and one month after the onset of the thromboembolism, thrombus was disappeared on chest CT. She is doing well 17 months after surgery. Early diagnosis and treatments are critical for the pulmonary thromboembolism.
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PMID:[Acute pulmonary thromboembolism complicating lung lobectomy; report of a case]. 1247 69

A 64-year-old man complained of irritable cough of 3 months' duration and 1 episode of hemoptysis and dyspnea related to effort. The radiograph revealed a mass in the upper right lobe. Adenocarcinoma of the lung was diagnosed by mediastinoscopy. After removal of the right lung, the patient was admitted to the recovery unit for 36 hours and transferred out without complications. The clinical course in 48 hours on the ward included increasing dyspnea, tachypnea and greater respiratory effort with hypoxemia in spite of increased FiO2. A radiograph showed pulmonary edema and the patient was readmitted to the recovery unit. We describe this case of postpneumonectomy edema and discuss the possible origins of the clinical picture, differential diagnosis, preventive measures and possible treatments.
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PMID:[Post-pneumonectomy edema]. 1270 11

We present the case of a 74-years old man with subtotal gastrectomy for adenocarcinoma, whose postoperative course is complicated by a prolonged fever. Despite extensive diagnostics, the origin of the postoperative fever remains unexplained for 47 days, when the patient is transferred to the ICU because of lethargy, hemodynamic instability, lung edema and abdominal symptoms. The diagnosis of Addison crisis is established and under substitution with hydrocortisone all the symptoms rapidly resolve. Postoperative fever is relatively frequent and infectious causes account for about half of the cases only. An infectious origin has imperatively to be excluded when the fever arises later than 48 hrs after surgery. In case of prolonged fever we suggest to extend the differential diagnosis to other than infectious causes by means of special lists (e.g fever of unknown origin).
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PMID:[Non infectious postoperative fever]. 1743 96

The putative cardiovascular risks and benefits of the ingestion of wine and alcohol-containing spirits have been well publicized; however, less attention has been focused upon the health effects of wine and spirits consumption on the respiratory system. This paper will highlight epidemiologic, clinical and experimental data on the effects of wine and distilled spirits [and the chemical components thereof] on lung function, chronic obstructive pulmonary disease progression, lung cancer risk, risk of developing acute respiratory distress syndrome, high altitude pulmonary edema and wine [sulfite] associated asthma. Several studies have demonstrated a positive [beneficial] effect of light-to-moderate wine consumption on pulmonary function, while chronic ingestion of distilled spirits may have either no effect, or a negative effect. Studies in Scandinavia, Europe and South America have suggested a possible protective effect of wine ingestion against lung cancer, especially adenocarcinoma. Resveratrol [3,5,4'-trihydroxystilbene] a polyphenolic compound found in red wine, has anti-oxidant, anti-inflammatory and estrogen agonist effects and may be responsible for some of the health benefits of wine. The spectrum of potentially beneficial clinical effects of resveratrol and other wine-derived compounds is discussed.
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PMID:Wine, spirits and the lung: good, bad or indifferent? 1852 69

Nanoparticles are now emerging as a novel class of autophagy activators. Functionalized single-walled carbon nanotubes (f-SWCNTs) are valuable nanomaterials in many industries. This article is designed to assess the autophagic response for f-SWCNTs exposure in vitro and in vivo. A few types of f-SWCNTs were screened in human lung adenocarcinoma A549 cells for the autophagic response and related pathways in vitro. Formation of autophagosomes and LC3-II upregulation were confirmed on the basis of electron microscopy and LC3 western blotting for COOH-CNT, but not for PABS-CNT and PEG-CNT. MTT assay showed marked increase in cell viability, when COOH-CNT was added to cells in the presence of autophagy inhibitor 3MA, ATG6 or TSC2 siRNA. Consistent with the involvement of the Akt-TSC1/2-mTOR pathway, the phosphorylation levels of mTOR, mTOR's substrate S6 and Akt were shown significantly decreased in A549 cells on treatment with COOH-CNT using western blotting. What's more, autophagy inhibitor 3MA significantly reduced the lung edema in vivo. In a word, COOH-CNT induced autophagic cell death in A549 cells through the AKT-TSC2-mTOR pathway and caused acute lung injury in vivo. Inhibition of autophagy significantly reduced COOH-CNT-induced autophagic cell death and ameliorated acute lung injury in mice, suggesting a potential remedy to address the growing concerns on the safety of nanomaterials.
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PMID:A functionalized single-walled carbon nanotube-induced autophagic cell death in human lung cells through Akt-TSC2-mTOR signaling. 2159 91


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