Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glomerular changes of 70 cases of pulmonary diseases and 25 control cases among 1100 consecutive autopsy cases were studied by light, immunofluorescence, and electron microscopy. These pulmonary diseases consisted of 11 cases of chronic obstructive bronchiolitis (COB), 15 cases of bronchopneumonia, 4 cases of acute interstitial pneumonia, 22 cases of idiopathic interstitial pneumonia (IIP), and 18 cases of lung cancer free from IIP. Bacteriological examination of the lung was performed in these cases including control cases on autopsy. Mesangial IgA deposition was predominant in 25 out of the 70 study cases (36%) frequently accompanied by C3, whereas slight mesangial IgA deposition was observed in one of the control cases. Incidence of IgA deposition was 64% in IIP, 54.5% in COB, 13.3% in bronchopneumonia, 16.7% in lung cancer and 25% in acute interstitial pneumonia. The results of the present study suggest that recurrence or persistence of inflammatory processes of the lung leads to IgA-mediated immune abnormalities and to mild mesangial changes with predominant IgA deposition, which are similar to the immunopathologic features of IgA nephropathy.
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PMID:Glomerular IgA deposition in pulmonary diseases. 370 13

Lung cancer and chronic interstitial pneumonia associated with systemic sarcoidosis was detected in a 66-year-old woman at autopsy. Histologically, hyalinized sarcoid lesions were scattered in cervical lymph nodes, thoracic lymph nodes, abdominal lymph nodes, and spleen. Scattered non-caseating epithelioid cell granulomas with giant cells were observed in both lungs demoting cancer and chronic interstitial pneumonia. A tumor mass occupying right hilar portion was well-differentiated squamous cell carcinoma involving right upper lobe and right hilar lymph nodes. In the lower lobe of the left lung, a small nodule of poorly differentiated squamous cell carcinoma was detected. Alveolar septa, especially in both lower lobes of the lungs were thickened diffusely with fibrosis, edema, and inflammatory cell infiltration. Alveolar cavities contained hyaline membrane and large mononuclear cells. Atypical bronchiolar epithelial proliferation and squamous metaplasia associated with squamous cell carcinoma were detected. The clinical and pathological characteristics among eight reported cases of lung cancer associated with sarcoidosis and three reported cases of interstitial pneumonia associated with sarcoidosis were reviewed separately. There is no report describing both lung cancer and chronic interstitial pneumonia associated with sarcoidosis.
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PMID:Lung cancer and chronic interstitial pneumonia associated with systemic sarcoidosis. 400 90

The effect and toxicities of Cis-containing combination chemotherapy were tested in 28 patients with primary lung cancer. All patients were treated with 80 mg/m2 Cisplatinum on the first day and 750 mg ftorafur p.o. every day. In addition to these drugs, patients with squamous cell cancer were treated with continuous subcutaneous infusion of 4 mg/m2 Peplomycin for 5 days and one shot i.v. of 4 mg MMC. Patients with adeno- and large cell cancer were treated with 30 mg/m2 Adriamycin and 4 mg MMC, while patients with small cell cancer were given 150 mg/m2 VP-16 p.o. for 5 days. The following results were obtained. Of 22 evaluable patients, overall response rate was 50%. In each histologic type, response rate was 50% (5/10) for squamous cell carcinoma 50% (4/8) for adenocarcinoma 33% (1/3) for large cell carcinoma and 100% (1/1) for small cell carcinoma. No CR was obtained in this series. Main side effects due to Cisplatinum were nausea, vomiting, loss of appetite, mild leukopenia and thrombocytopenia, mild elevation of serum creatinine and BUN and alopecia, all of which were transient. Interstitial pneumonitis was observed in 40% of patients with squamous cell cancer. Two patients with adenocarcinoma died within 3 weeks after treatment due to embolism of the abdominal aorta and myocardial infarction probably caused by treatment with Adriamycin.
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PMID:[CDDP-containing combination chemotherapy for advanced lung cancer]. 621 53

Twelve cases of interstitial pneumonitis were seen in 50 patients (24%) treated with cyclophosphamide, methotrexate, and etoposide (VP-16-213) for small cell anaplastic lung cancer. The clinical course and pathologic characteristics were consistent with drug-induced pneumonitis in all 12 cases. One additional patient had concurrent histologic evidence of interstitial pneumonitis, pneumocystis infection, and perivascular metastases. Patients presented with severe dyspnea, hypoxemia, cough, fever, and bilateral interstitial infiltrates on chest films. The onset was rapid and unpredictable, following as little as one month or as much as five months of therapy. Nine patients recovered but there were three deaths in the acute period directly attributable to the drug-induced pneumonitis. Although the use of twice weekly oral methotrexate may have been a causative factor, a previously unsuspected drug interaction with etoposide may be the etiologic factor resulting in this unusually high incidence of pulmonary toxicity. The difficulty in establishing a diagnosis of interstitial pneumonitis in this group of patients with chronic lung disease and lung cancer is well known. The extent of morbidity and mortality seen in this study and the commercial availability of etoposide make earlier clinical recognition of this complication imperative.
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PMID:Chemotherapy-induced interstitial pneumonitis during treatment of small cell anaplastic lung cancer. 672 94

The expression of tenascin, a of extracellular matrix glycoprotein, was studied immunohistochemically in the lungs of 22 autopsy cases, including chronic idiopathic interstitial pneumonia (chronic IIP) associated with lung cancer (5 cases), chronic IIP without lung cancer (6 cases), acute idiopathic interstitial pneumonia (acute IIP; 6 cases) and alveolar pneumonia (AP; 5 cases). In the honeycomb lesion of chronic IIP, tenascin expression was observed in the basement membrane of metaplastic epithelia and in the subepithelial stroma of thickened septa with fibrosis. In the non-honeycomb area of chronic IIP, tenascin was expressed in mildly thickened alveolar walls with fibrosis. The distribution of tenascin expression in chronic IIP associated with lung cancer resembled that in chronic IIP without lung cancer. In acute IIP, tenascin expression was observed in mildly thickened alveolar walls with fibrosis, in organizing hyaline membranes. In AP, tenascin was expressed in organizing exudate of alveoli and was scarcely observed in the alveolar wall. It is very possible that tenascin is associated with the fibrosing process and remodelling in IIP, and has a promoting effect in carcinogenesis in IIP lung.
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PMID:[Tenascin expression in idiopathic interstitial pneumonia]. 752 24

Cord factors are mycoloyl glycolipids in cell walls of bacteria belonging to Actinomycetales, such as Mycobacterium, Nocardia and Rhodococcus. They induce granuloma formation in the lung and interstitial pneumonitis, associated with production of macrophage-derived cytokines. We studied how cord factors induce biological activities in the cells. Cord factors isolated from M. tuberculosis, trehalose 6-monomycolate (mTMM) and trehalose 6,6'-dimycolate (mTDM), enhanced protein kinase C (PKC) activation in the presence of phosphatidylserine (PtdSer), diacylglycerol and Ca2+, and mTMM activated PKC alpha more strongly than PKC beta or gamma under the same assay conditions. Kinetic studies of mTMM in response to PKC activation revealed that mTMM increased the apparent affinity of PKC to Ca2+ in the presence of both PtdSer and diolein. Although this is similar to observations with unsaturated fatty acids, such as arachidonic acid, mTMM was synergistic with PtdSer for PKC activation, but arachidonic acid was not. mTMM was also different as regards PKC activation, as phorbol ester was. A single i.p. administration of mTMM to mouse induced tumor necrosis factor-alpha (TNF-alpha) in serum and in the lung, which is a unique target tissue of cord factors. Based on our recent finding that TNF-alpha is an endogenous tumor promoter, the correlation between lung cancer and pulmonary tuberculosis is discussed.
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PMID:Activation of protein kinase C by mycobacterial cord factor, trehalose 6-monomycolate, resulting in tumor necrosis factor-alpha release in mouse lung tissues. 755 98

The present status of idiopathic interstitial pneumonia (IIP) was evaluated from data collected as part of the Financial Support Program for patients with IIP, conducted in Hokkaido since 1979. The prevalence of IIP in 1992 was 4.08/100,000, and the yearly incidence was 1.23/100,000. The ratio of men to women was 1.85/1.0. Under age 55, women were more numerous than men, and over age 55, men were more numerous than women. Clinical and epidemiological analyses of the patients with IIP, with collagen vascular disease-interstitial pneumonia suggested possible contribution of dust inhalation to the etiology IIP. A prospective study revealed that about 20% of the subjects had systemic signs and symptoms of collagen diseases from 2 months to 10 years after the diagnosis of IIP. In addition, about 15% of the subjects with IIP developed lung cancer during the follow-up period. This incidence was significantly higher than that in the patients with chronic obstructive pulmonary diseases and the same smoking history, which suggests that IIP itself is a risk factor for lung cancer.
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PMID:[Present status of idiopathic interstitial pneumonia--from epidemiology to etiology]. 760 30

Eight patients who developed interstitial pneumonia after surgery for primary lung cancer were reviewed to investigate its causes and the key points in treatment. These patients accounted for 1.8% of 633 operated lung cancer patients at our institution over the last 9 years. Risk factors such as bilateral recurrent laryngeal nerve palsy, preoperative chemoradiotherapy, and extensive mediastinal involvement were present in all of them. Pneumonia developed on the nonoperated side in all patients between the 2nd and 45th postoperative day (mean: 18 days). In most of the patients, faint reticular shadows initially appeared in the lower lobe of the nonoperated lung, rapidly spread to the upper lobe, and finally affected the whole lung. Among these eight patients, the initial five patients died because steroids were only administered after the pneumonia had become widespread, whereas the last three patients received early steroid therapy and were saved. The findings that 1) this pneumonia originated from the lower lobe of the nonoperated lung where blood flow is highest postoperatively, 2) the eosinophil count increased just before the onset of pneumonia, and 3) early steroid therapy and immunosuppressive therapy were effective suggest that an allergic or autoimmune mechanism may play some role in its development. When characteristic reticular shadows appear in the lower lobe on the nonoperated side in a lung cancer patient, even if not associated with any symptoms, an early diagnosis of interstitial pneumonia and initiation of steroid therapy is mandatory to ensure survival.
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PMID:[Postoperative interstitial pneumonia in primary lung cancer patients--its causes and management]. 760 93

Of 12 patients who underwent lung resections for lung cancer with idiopathic interstitial pneumonia (IIP), eight patients survived and four patients died due to acute exacerbation of IIP after the operation. The preoperative values for percent forced vital capacity, predicted postoperative percent vital capacity, percent one-second forced expiratory volume index and serum level of C-reactive protein were significantly different between the group of patients who survived and that of having died. Three days after the operation, the percentage of lymphocytes among leukocytes and serum level of lactate dehydrogenase in the two groups were both significantly different. These findings showed that the operative strategy for patients with lung cancer and IIP needs specifically careful consideration for operative procedure, and preoperative serum levels of C-reactive protein and postoperative lactate dehydrogenase and the percentage of lymphocytes in leukocytes would be useful in evaluation of the severity of IIP.
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PMID:[Lung resection for lung carcinoma with idiopathic interstitial pneumonia]. 779 11

Obstetrician-gynecologists reviewed patient records of women delivering during January 1986-December 1992 to determine the maternal mortality rate and trends and the causes of maternal deaths in the maternity ward at the National University of Singapore. There were 26,173 deliveries and 9 maternal deaths (a maternal mortality rate of 22.9/100,000). The causes of maternal deaths were pulmonary embolism (underlying condition, systemic lupus erythematosus [SLE]), hemorrhage from multiple sites (thrombotic thrombocytopenia), acute exacerbation of SLE with interstitial pneumonitis, pulmonary fibrosis (systemic sclerosis), fulminant hepatitis (prior hepatitis and liver disease), and cerebral embolism (rheumatic heart disease with mitral valve replacement). There were also three incidental maternal deaths bringing the maternal mortality rate up to 34.4/1000. The incidental causes of death included septicemia from perforated peptic ulcer (uncontrolled thyrotoxicosis), multiple metastases from lung cancer, and suicide (family dispute over adoption of newborn). A cesarean section preceded 4 (44%) of the 9 maternal deaths. Two of these deaths were incidental maternal deaths. Cesarean section was related to two of the remaining six (33%) deaths. These findings show that traditional direct causes of maternal death (hemorrhage, sepsis, embolism, or hypertension) were not responsible for the maternal deaths at this tertiary facility. Instead, the women tended to have medical conditions that placed them at high risk of death regardless of pregnancy status.
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PMID:Maternal mortality: evolving trends. 781 Nov 98


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