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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A follow-up study of eight Mayo Clinic patients with chronic eosinophilic pneumonia (also called Carrington's eosinophilic pneumonitis) was done in order to ascertain, if possible, the long-term prognosis of this entity, since it has not been delineated clearly in the literature. Chronic eosinophilic pneumonia is a subacute-to-chronic pulmonary disorder occurring most commonly in nonatopic women with cough, fever, dyspnea, weight loss, and night sweats. The typical chest roentgenogram shows peripheral non-migratory infiltrates, and the characteristic pulmonary histologic finding is eosinophilic infiltration of the interstitium and alveolar spaces. Peripheral eosinophilia is seen in most cases but not all. At the time of follow-up, two of eight patients were continuing to take corticosteroids after 5 1/2 and 8 years. Five patients have been able to discontinue corticosteroid treatment after an average of 4 years, and one patient never required corticosteroids. Chronic eosinophilic pneumonia is added to previous classifications of pulmonary infiltrate with eosinophilia.
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PMID:Chronic eosinophilic pneumonia (Carrington's): a follow-up study. 62 61

A 75-year-old man developed dyspnea, cough, peripheral radiographic infiltrates, eosinophilia, and severe hypoxemia requiring mechanical ventilation. An open lung biopsy revealed chronic eosinophilic pneumonia, and the patient recovered with corticosteroid therapy. Chronic eosinophilic pneumonia is a disease that should be included in the different diagnosis of treatable causes of acute respiratory failure.
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PMID:Chronic eosinophilic pneumonia: an unusual cause of acute respiratory failure. 741 25

A 64-year-old women presented with a dry cough. The common cold was diagnosed and she was given medication, but the symptom did not resolve. She came to our hospital, and multiple patchy shadows were seen on a chest X-ray film. Bronchoalveolar lavage fluid contained an abnormally high percentage of eosinophils. Microscopic examination of transbronchial lung biopsy specimens showed infiltration of eosinophils into the alveoli and alveolar septa. Chronic eosinophilic pneumonia was diagnosed. Analysis of bone marrow cells showed high percentages of mature eosinophilic cells, and blood serum had a high concentration of eosinophil cationic protein. An inhalation challenge test with methacholine revealed bronchial hypersensitivity and hyperresponsiveness. Prednisolone (30 mg/day) was given and the symptoms resolved. After steroid treatment, the patient was asymptomatic, although airway hyperresponsiveness remained. The concentration of eosinophil cationic protein in serum and the results of the methacholine inhalation test reflected the degree of chronic eosinophilic pneumonia, and the production of eosinophils in bone marrow was suppressed by steroid medication.
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PMID:[Chronic eosinophilic pneumonia involving eosinophil cationic protein and bone marrow cells]. 895 6

Chronic eosinophilic pneumonia is characterized by infiltration of eosinophils into alveolar spaces. Patients with this condition may also have asthmatic episodes, chronic coughing, and bronchorrhea, even after the infiltrative opacity on the chest roentgenogram resolves. We used computed tomography, pulmonary function tests, and biopsies to evaluate the airways of 11 patients with chronic eosinophilic pneumonia. The tomograms showed bronchial wall thickening in all patients at the time of the onset of symptoms and ten months later. Centrilobular peribronchovascular interstitial thickening was detected in four patients, 10 months after the onset. Pulmonary function tests showed that small airway dysfunction remained 13 months after the onset. Pathological analysis revealed airway abnormalities that included basement membrane thickening and cellular infiltration 2 years after the onset. These results show that airway changes had not resolved even after roentgenographic opacities had disappeared. More attention should be given to treatment of airway disease associated with chronic eosinophilic pneumonia, and to whether these changes in the airway are similar to those seen in bronchiolitis obliterans organizing pneumonia.
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PMID:[Clinico-pathological analysis of airway abnormalities in patients with chronic eosinophilic pneumonia]. 902 17

Chronic eosinophilic pneumonia (CEP) is a disorder, characterized by a history of pneumonia (> 2 months) and eosinophilic pulmonary infiltration without any organic causes. We describe a 28-year-old woman who presented with cough, dyspnea and fever for 2 months. She was diagnosed with mild asthma and allergic rhinitis 2 years before being diagnosed with CEP. For a period of 9 months she took no medication. Her chest roentgenogram at this admission revealed patchy infiltration in both upper lung fields. Laboratory data revealed blood eosinophilia (4,284/mm3), and her serum IgE was mildly elevated (245.8 IU/ml). A computerized tomography of the chest did not show bronchiectasis. CEP was diagnosed from significant eosinophilia in bronchoalveolar larvage fluid and transbronchial biopsy revealed eosinophilic infiltration without any demonstrable infectious agent. The patient was treated with prednisolone 45 mg/day. Her symptoms disappeared and her chest roentgenogram showed nearly complete resolution in 2 and 4 days, consecutively.
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PMID:Chronic eosinophilic pneumonia: a case report. 1099 53

Chronic eosinophilic pneumonia (CEP) is a disease of unknown cause. The hallmark of CEP is eosinophil accumulation in the lungs. While the triggering factor is unknown, eosinophil accumulation in the lungs is now believed to be secondary to the actions of eosinophil-specific chemoattractants, including eotaxin and regulated upon activation, normal T-cell expressed and secreted (RANTES), and IL-5 released from Th2 lymphocytes in the lungs. There is a female preponderance in CEP, with a peak incidence in the 5th decade; the onset is insidious with weight loss, cough, and dyspnea. An atopic history is common, but asthma is not a prerequisite for the development of CEP. Airways obstruction may develop during the course of CEP, but may also result from CEP. The chest x-ray usually shows bilateral peripheral shadows, which may be migratory. Peripheral eosinophilia is usual. Standard treatment of CEP is with oral steroids, usually with dramatic resolution of symptoms and radiographic changes; however, relapses are common when the daily steroid dose is reduced below 15 mg. Current data suggest that when treatment is stopped, relapse is common in the majority of patients (>80%) followed for a sufficiently long period of time. Some recent reports suggest that treatment with inhaled steroids may be of some value in this condition.
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PMID:Chronic eosinophilic pneumonia: a review. 1726 25

Eosinophils may infiltrate the lung tissue, thus impairing gas exchange and causing several symptoms as dyspnea, fever, and cough. This process may be secondary to several factors, including drugs or parasite migration, or primary (idiopathic). Acute eosinophilic pneumonia is life-threatening and presents frequently in young smokers as an acute hypoxemic respiratory failure of generally less than a week with bilateral lung infiltrates, frequently misdiagnosed as severe community-acquired pneumonia. This patients present without peripheral eosinophilia but usually have more than 25% eosinophils on bronchoalveolar fluid. Chronic eosinophilic pneumonia is a protracted disease of usually more than a month before presentation, with a predilection for middle aged asthmatic patients. Hypoxemia is mild-moderate, and there are usually more than 1,000 eosinophils/mm3 of peripheral blood. Bronchoalveolar fluid has high eosinophil levels (usually more than 25%). Migratory peripheral infiltrates are seen in the chest x-ray film. Both acute and chronic eosinophilic pneumonia are treated by glucocorticoids and respiratory support as well as avoidance of any recognized trigger.
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PMID:Pulmonary eosinophilia. 1819 81

We report a case of a 13-year-old girl with an asymptomatic isoniazid-resistant tuberculosis contact. Six months after the contact had been made, chest radiography showed left upper lobe infiltrates without hilar lymphadenopathy, which led to the start of an antituberculous treatment. Tuberculin skin test remained negative and blood tests showed hypereosinophilia. One month after the onset of the treatment, she presented with asthenia, weight loss, and cough. She was admitted to our unit with a diagnosis of drug-resistant tuberculosis. Blood tests showed the persistence of hypereosinophilia. Chest radiograph and high-resolution lung computed tomography (CT) scan showed alveolar peripheral condensations on both upper lobes without significant hilar lymphadenopathy. Bronchoalveolar lavage (BAL) showed a normal total cell count with 44% of eosinophils. Microbiological analyses were all negative. Chronic eosinophilic pneumonia (CEP) was confirmed after the elimination of other different eosinophilic lung diseases. The patient was highly responsive to high doses of oral corticosteroids. Dyspnoea and cough disappeared within one week and chest CT scan showed regression of the lung infiltrates within one month. No relapse occurred during the following nine months.
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PMID:Chronic eosinophilic pneumonia in a 13-year-old child. 1820 53

A 54-year-old woman complained of dyspnea, cough, and productive sputum. Auscultation detected a wheeze in the left and right lung fields. Chest x-ray and computed tomographic films showed non-segmental infiltration in the left upper lung field. Laboratory data revealed eosinophilia in peripheral blood and sputum, elevated levels of serum interleukin-5 (IL-5), airflow limitation, hypoxemia, and heightened airway sensitivity to methacholine (D min : 0.42 units). Bronchoalveolar lavage disclosed an increase in the total number of cells, a 32% increase in eosinophils, and a decreased CD 4/CD 8 ratio of 0.7. Transbronchial lung biopsy specimens revealed infiltrations of eosinophils in the alveolar and interstitial compartments. The histologic features of bronchial biopsy specimens included increased eosinophils in the submucosa and squamous metaplasia. In addition, blood glucose and HbA 1 c levels were elevated. Chronic eosinophilic pneumonia complicated by bronchial asthma and diabetes mellitus was diagnosed. Because the patient was diabetic, she was given suplatast tosilate to reduce the production of IL-5, and high-dose inhaled corticosteroid (beclometasone dipropionate, 1,600 mcg/day) instead of oral corticosteroid therapy. Her symptoms were relieved, peak expiratory flow rates increased, serum IL-5 levels became undetectable, airway sensitivity to methacholine decreased (D min : 4.64 units), and the radiographic abnormalities disappeared. Furthermore, treatment with beclomethasone dipropionate was progressively reduced to 1,200 mcg/day over the subsequent year without relapse. It was concluded that suplatast tosilate and high-dose inhaled corticosteroid therapy may be an effective alternative therapeutic approach to chronic eosinophilic pneumonia in some cases.
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PMID:[Chronic eosinophilic pneumonia complicated by bronchial asthma and diabetes mellitus successfully treated with suplatast tosilate and high-dose inhaled corticosteroid therapy]. 1821 13

The eosinophilic pneumonias are a heterogeneous group of pulmonary disorders, which may compromise only the air ways, the pulmonary parenchyma, or both, characterised by alveolar eosinophils and infiltration of pulmonary tissue, with or without peripheral blood eosinophilia. Idiopathic Chronic Eosinophilic Pneumonia (ICEP), detailed description was by Carrington in 1969, is a rare eosinophilic lung disease, of unknown aetiology, characterised by peripheral blood eosinophilia, chest radiograph infiltrates and prompt response to corticosteroid therapy. ICEP most commonly affects women of middle age and usual symptoms are cough, dyspnea, fever and weight loss. The authors present a case of ICEP in a young woman, 21 years old, non-smoker and previously healthy.
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PMID:[Idiopathic chronic eosinophilic pneumonia--a clinical case report]. 1862 33


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