Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three patients received respectively 190 mg, 175 mg, and 196 mg of methotrexate and developed bilateral pulmonary infiltrates without evidence of peripheral blood eosinophilia. Sputum in the three cases failed to reveal acid-fast bacilli, pathogenic fungi, or opportunistic organisms by cultures and appropriate stains. Despite discontinuance of the drug and/or institution of corticosteroid therapy, progressive respiratory failure led to death. In all three cases, autopsy revealed gross and microscopic features indistinguishable from those seen in the Hamman-Rich syndrome, and methotrexate hepatotoxicity was present in one. Pulmonary eosinophilia or granulomas, classically seen in previously reported cases of methotrexate pneumonitis, were not observed. It is suggested therefore that methotrexate be added to the list of agents capable of inducing diffuse interstitial pulmonary fibrosis. Conversely, diffuse interstitial pulmonary fibrosis should be considered in the differential diagnosis of patients receiving methotrexate who develop bilateral pulmonary infiltrates seen on chest roentgenograms.
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PMID:Methotrexate-induced diffuse interstitial pulmonary fibrosis. 42 24

Although chronic eosinophilic pneumonia is a well-known disorder, acute eosinophilic pneumonia has not been as well described. We described the clinical features of two patients with acute eosinophilic pneumonia. The patients presented with an acute onset of high fever, severe hypoxemia and diffuse pulmonary infiltrates. Eosinophilic pneumonia was diagnosed by bronchoalveolar-lavage and confirmed by transbronchial lung biopsy. We believe that we have described an acute type of eosinophilic lung disorder which can not be applied to Crofton's classification of PIE, so we reviewed previously reported cases of acute eosinophilic pneumonia and tried to summarize their clinicopathological features. We also emphasized the existence of eosinophil infiltration into the bronchial wall in Acute Eosinophilic Pneumonia.
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PMID:[A case report and literature review of acute eosinophilic pneumonia]. 189 92

106 (15.7%) of 675 artificially ventilated newborn developed interstitial pulmonary emphysema (PIE). Basic lung diseases were: IRDS, neonatal pneumonia, shock lung, meconium aspiration, hypoplasia of the lungs and other miscellaneous disorders of the chest. PIE developed in 68% of patients within 8 hours following artificial respiration. At the beginning of PIE both lungs were concerned in 41.5% of patients, one lobe of both lungs was affected in 32.1%. PIE was located in one lung in 8.5% and in only one lobe in 17.9%. Maximum of PIE was seen within 5 days after initiating respiration in 76.7% of the patients. Persistent PIE developed in 28.7% of the patients. Persistent PIE of both lungs was seen in 11 cases, PIE of one lung in 8 cases and persistent lobar emphysema in another 8. Pulmonary pseudocysts developed in 22 (20.8%) of the patients.
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PMID:[Interstitial pulmonary emphysema in mechanically ventilated newborn infants. Study of the course of the disease]. 301 98

Clinical, roentgenographic and pathologic findings in patients with chronic eosinophilic pneumonia, including 19 additional cases, have been reviewed and summarized. Most patients present with subacute respiratory and constitutional symptoms and have failed to respond to therapy for presumptive pneumonia. A previous history of atopy, most often asthma, will be obtained in one-half. Eosinophilia occurs in most cases and its absence may be the major indication for lung biopsy. Although pulmonary infiltrates are more often peripheral than not, the classic "photographic negative of pulmonary edema" is seen in less than one-third of cases. Pathologic findings include an intra-alveolar and interstitial infiltrate which comprises eosinophils, histiocytes, and exudate. Bronchiolitis obliterans and eosinophilic microabscesses occur less frequently. Open-lung biopsy is preferable when atypical features prevent a confident clinical diagnosis. The exquisite responsiveness of CEP to corticosteroids should encourage use of a therapeutic trial when there is a strong clinical suspicion of the disorder. The rapid clinical response should not deter the clinician from giving a prolonged course of treatment. The differential diagnosis includes other diseases characterized by PIE and the more recently recognized bronchiolitis obliterans and organizing pneumonia, a disorder which is also marked by peripheral pulmonary infiltrates.
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PMID:Chronic eosinophilic pneumonia. A report of 19 cases and a review of the literature. 328 20

Two cases of pulmonary eosinophilia associated with coccidioidal infections are reported. Pulmonary eosinophilia in these cases represents a hypersensitivity reaction to the fungus. Histologically, the pulmonary eosinophilia in these cases closely mimicked or appeared identical to idiopathic chronic eosinophilic pneumonia. Coccidioides immitis organisms were rare or absent in the areas of pulmonary eosinophilia. Recognition of this phenomenon is important for proper care of the patient.
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PMID:Pulmonary eosinophilia in coccidioidal infections. 356 77

An eosinophilic granulomatous pneumonia is described in a German shepherd dog. On thoracic radiographs and at post mortem examination disseminated pulmonary tumour-like nodules had been seen. Histologically the nodules consisted of macrophages, eosinophils, plasma cells and occasionally giant cells. In plasma cells and macrophages, large amounts of immunoglobulin G and immunoglobulin M could be demonstrated. An aetiology could not be determined, but vasculitis and cytology made an allergic reaction of type 1 and, or, type 3 most likely. The classification of pulmonary infiltration with eosinophilia (PIE-syndrome) is discussed.
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PMID:Eosinophilic granulomatous pneumonia in a dog. 373 55

Five patients with eosinophilic lung diseases and blood hypereosinophilia (PIE syndrome) were investigated clinically and by bronchoalveolar lavage (BAL). Comparative studies on blood and alveolar eosinophils were carried out after purification and selection of eosinophil subpopulations according to their density. A predominant 'hypodense' alveolar eosinophil population was found in BAL fluids of active chronic eosinophilic pneumonia (CEP). In addition, supernatants of alveolar macrophages obtained from CEP are able to enhance spontaneously the generation of eosinophil oxygen metabolites. Such eosinophil stimulation emphasizes a probable tissue cell cooperation. In addition, BAL permitted the study of membrane immunological markers on eosinophilic inflammatory cells endowed with migratory properties. An increase in eosinophils carrying surface IgE was demonstrated in alveolar cells from PIE Syndrome particularly with hypodense eosinophils from CEP patients. Although no specific stimulus is known at the present time, this work underlines the potential implication of IgE-mediated hypersensitivity processes in the pathogenesis of eosinophilic lung diseases.
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PMID:Eosinophilic lung disease: immunological studies of blood and alveolar eosinophils. 395 85

Pulmonary eosinophilia is a disease entity which is characterized by an increase of eosinophils in the bronchoalveolar lavage fluid or in tissue. While there are several disease states encountered in pulmonary eosinophilia, some have a definite cause and diagnosis, while others are of unknown etiology. The diagnosis of idiopathic eosinophilic pneumonia is given when other pulmonary eosinophilia with known cause and diagnosis are excluded. Simple pulmonary eosinophilia and chronic eosinophilic pneumonia are well established disease entities, but recent papers have clarified a new concept of acute eosinophilic pneumonia. In this article, the clinical features of three idiopathic eosinophilic pneumonias simple pulmonary eosinophilia as a self-limiting lung infiltrates, chronic eosinophilic pneumonia as a disease with longstanding symptoms requiring steroids administration and a tendency to relapse, and acute eosinophilic pneumonia as an acute respiratory distress which responds dramatically to steroids administration and without relapse after discontinuation of therapy are discussed.
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PMID:[Pulmonary eosinophilia]. 849 56

A 76-year-old woman was admitted to our hospital because of productive cough, fever and anorexia in January 1995. She had suffered from bronchial asthma for 25 years. From 1983, exacerbation of PIE was recorded three times, on which occasions prednisolone and antibiotics were quite effective. On admission, marked leukocytosis (28,000/microliters) and eosinophilia (18,000/microliters) were found. However, plasma IgE level was normal, and specific antigen for eosinophilia was not detected by RAST or the skin allergic reaction test. Chest X-ray film and CT scan revealed extensive bilateral pulmonary infiltration. Increase in eosinophils (33%) was demonstrated in bronchoalveolar lavage. Furthermore, biopsy specimen of the affected lung revealed diffuse infiltration of eosinophils into alveolar septa. On the basis of these findings, the patient was diagnosed as chronic eosinophilic pneumonia (PIE syndrome). Hyponatremia (117 mEq/l) was persistent after the hydration with normal saline. Plasma ADH was not suppressed (2.29 pg/ml) in spite of hypoosmolality of plasma. Laboratory examination showed that renal, adrenal and thyroid function as well as plasma renin activity were normal. Taking these findings together, she was diagnosed as having SIADH. Treatment with prednisolone improved not only the PIE syndrome but also SIADH.
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PMID:[A case of pulmonary infiltration with eosinophilia (PIE) syndrome associated with syndrome of inappropriate secretion of ADH (SIADH) in the elderly patient]. 855 92

We encountered a 23-year-old woman with allergic granulomatous angiitis (AGA) associated with cerebral infarction, myo-pericarditis, and acute respiratory failure due to extended eosinophilic pneumonia. She underwent emergency treatment at our hospital because of right hemiparesis and impaired consciousness. AGA was suspected because the patient had a history of bronchial asthma accompanied by pulmonary infiltrations with eosinophilia, and presented with diffuse pulmonary infiltrates, pericardial effusion, diffuse hypokinesis of myocardium, cerebral infarction and marked peripheral eosinophlia. Pulmonary eosinophilia was confirmed by examination of broncho-alveolar lavage fluid. Myocardial tissue biopsy specimens revealed fibrous granulation indicative of myocarditis. The patient responded well to corticosteroid therapy.
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PMID:[Allergic granulomatous angiitis associated with cerebral infarction, myo-pericarditis and acute respiratory failure due to eosinophilic pneumonia]. 991 84


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