Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 49-year-old woman complained of cough and a purulent sputum (about 40 ml/day). She kept budgerigars for a period of 30 years, she first noticed a productive cough 10 years previously. Her chest roentgenogram revealed a diffuse reticulonodular pattern. She was diagnosed as having a chronic type of budgerigar breeder's lung associated with chronic bronchitis. Peptostreptococcus anaerobius was cultured from her sputum, bronchoalveolar lavage fluid, as well as from droppings of her budgerigar. This is the second case of hypersensitivity pneumonitis presenting as chronic bronchitis with much sputum in Japan.
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PMID:Budgerigar breeders' hypersensitivity pneumonitis presenting as chronic bronchitis with purulent sputum. 749 84

Hypersensitivity pneumonitis or extrinsic allergic alveolitis is an immunologically mediated lung disease caused by repeated inhalations of organic antigens. The basic histological lesion consists of a diffuse mononuclear cell infiltration of alveolar wall, alveoli, terminal bronchioles, and neighboring interstitium. The inflammation is often followed by granulomas, which then may progress to fibrosis. Unlike other infectious and noninfectious granulomatous disorders, hypersensitivity pneumonitis is limited to the lung. The disease occurs more frequently in men than in women and children. The acute form of hypersensitivity pneumonitis, characterized by fever, chills, myalgias, cough, and dyspnea, may be confused with acute pneumonitis. Although there is no single radiological, physiological, or immunologic test specific for hypersensitivity pneumonitis, the diagnosis can often be suspected on the basis of a compatible temporal relationship between pulmonary symptoms and a history of environmental or occupational exposure. Once the diagnosis is suspected, the presence of serum precipitating antibodies (immunoglobulin [lg] G), suppressor cytotoxic lymphocytosis in bronchoalveolar lavage (BAL) fluid, and granulomatous alveolitis in lung biopsy specimens is extremely helpful in confirming the diagnosis. For patients in whom the diagnosis is confirmed, avoidance of the causative antigen is the best therapy, although corticosteroids are used to suppress inflammation. Once the fibrosis has developed, the patient may gradually develop respiratory failure or cor pulmonale, possibly resulting in death.
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PMID:Hypersensitivity pneumonitis: a noninfectious granulomatosis. 756 4

A 49-year-old woman used an automatic bed cleaner on October 18, 1990. Eight hours later, she was admitted to a hospital complaining of coughing and fever. The chest X-ray film showed small granular shadows in both lower lung fields. After a few days of antibiotic therapy, these symptoms had disappeared. She used the bed cleaner again on the afternoon of November 15, 1990. The next day, she was admitted to our hospital because of coughing and fever. An environmental provocation test with the bed cleaner induced the same symptoms. Dust from the bed cleaner stimulated her lymphocytes. Hypersensitivity pneumonitis from the dust of a bed cleaner was diagnosed.
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PMID:[Hypersensitivity pneumonitis induced by dust from an automatic bed cleaner]. 760 45

Six auto parts manufacturing workers were referred for evaluation of a 6-week history of work-related dyspnea, cough, and fatigue. Two workers also reported fever and weight loss. All six worked in a machining area where a waterbased metalworking fluid was used and recirculated under high pressure, thereby creating an aerosol. Chest radiographs revealed pulmonary interstitial infiltrates in four workers. Lung function tests showed that four workers had decreased diffusing capacity. After removal from the work area, all workers recovered. The metalworking fluid was cultured for bacteria and fungi. Isolates from broth cultures were sonicated to obtain antigen extracts. Serum precipitins to one or more of the microbial isolates were identified in all six workers but not in eight of nine nonexposed control subjects. The most frequent precipitin response (six of six workers) was against antigens of Pseudomonas fluorescens, which was cultured from the metalworking fluid. In all workers, precipitins to at least one other cultured organism were detected; these included Aspergillus niger, Staphylococcus capitas, an acid-fast Rhodococcus sp, and Bacillus pumilus. This represents the first report of hypersensitivity pneumonitis associated with industrial exposure to aerosolized metalworking fluid. Observed precipitin responses to a variety of microbial contaminants in metalworking fluid strongly suggest a causative role for microbial antigens in the induction and elicitation of this manifestation of hypersensitivity pneumonitis.
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PMID:Machine operator's lung. A hypersensitivity pneumonitis disorder associated with exposure to metalworking fluid aerosols. 765 98

A 64-year-old man was admitted complaining of cough, hemoptysis, dyspnea, and fever. His chest X-ray film on admission showed reticulo-granular shadows in both lung fields. Ausculation of his chest revealed fine crackles in both lower zones. After admission, he was treated with antibiotics, but his chest-radiographic appearance worsened temporarily, and sputum cytology results were repeatedly positive. Diagnosis was difficult. Differential cell count of the bronchoalveolar lavage fluid showed lymphocytosis, with a high CD 4/8 ratio. Transbronchial lung biopsy specimens revealed Masson bodies and alveolitis. With antibiotic therapy alone, his condition improved, and he was discharged. Five and a half hours later, his symptoms worsened and he was readmitted. His chest X-ray film on the second admission was almost the same as that on the first admission. His symptoms became less severe, and his condition improved without treatment. Hypersensitivity pneumonitis was diagnosed. Because the onset was in February, this was not considered to be a case of so-called summer type hypersensitivity pneumonitis a provocation test was done with water from the humidifier he had been using at home. The white blood cell count increased and PaO2 decreased significantly, so the result of the provocation test was thought to be positive. Therefore, so-called humidifier lung was strongly suspected. The results of sputum cytology on the first admission were probably falsely positive.
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PMID:[A case of hypersensitivity pneumonitis probably caused by a humidifier in winter]. 773 Nov 29

A 37-year-old woman had worked for 4 years in a shell-processing factory where considerable airborne dust was produced cutting and polishing fresh water shells into pearl nuclei. She had a dry cough and dyspnea. Transbronchial lung biopsy showed noncaseating granulomas and cellular intraalveolar infiltrates. High-resolution lung computed tomography (HRCT) showed diffuse small nodules and ground-glass opacities. Hypersensitivity pneumonitis caused by shell dust should be considered in the appropriate clinical setting in a patient with the appropriate radiographic abnormalities.
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PMID:Hypersensitivity pneumonitis in a pearl nucleus worker. 776 29

Pneumoconiosis from inorganic dusts is very common worldwide and has been studied by many experts in Taiwan. However, pneumoconiosis due to organic dusts, i.e. hypersensitivity pneumonitis, seems rather uncommon in Taiwan, and to our best knowledge there has been no related report so far. In this study, we shall report five cases of bagassosis. These five patients all were men, ranging in age from 29 to 52 years. One of them worked at a sugarcane factory, and the remaining four all worked at the paper mills. The exposure history to organic dusts ranged from 2 days to 15 years. Their chief complaints were cough, dyspnea, and fever. The chest roentgenographic manifestations in our patients could mainly be subdivided into three patterns; i.e. reticulonodular infiltrates (three cases), reticular infiltrates (one case), and miliary nodular infiltrates (one case). These lesions were located diffusely with predilection for both lower lung fields. Three patients received bronchoalveolar lavage (BAL), which revealed a predominantly lymphocytic population. Arterial blood gas determinations in room air showed hypoxemia in most of them, but none of them were hypercapnic. Pulmonary function testing typically showed a restrictive ventilatory pattern in all of our cases, and the most sensitive diffusion capacity of carbon monoxide (DLco) ranged from 43% to 78% of the normal value. All of our patients received corticosteroid therapy after establishment of the diagnosis and had rather satisfactory responses. In addition, we also present possible preventive measures in the field of industrial hygiene.
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PMID:Hypersensitivity pneumonitis: bagassosis. 780 12

Diagnosing of alveolitis is a puzzle of many pieces, based on clinical experience and keeping in mind the criteria of extrinsic allergic alveolitis. They are antigen-exposure, typical delayed postexpositional symptoms (cough, chills, fever, dyspnea, tiredness), and serological tests of precipitating antibodies. Helpful findings are X-ray of the chest, high resolution computer tomography, auscultation findings, lowered diffusing capacity, bronchoalveolar lavage with lymphocytes > 50% and low T4/T8-ratio, histology of periphere lung specimens, and occasional inhaled provocation. Differential diagnosis are toxic lung disorders, drug adverse effects, sarcoidosis, silicosis, autoimmune alveolitis, idiopathic fibrosing alveolitis. The most frequent failure in diagnosis are common viral cold, bronchopneumonia, sarcoidosis, chronic bronchitis, and miliar tuberculosis.
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PMID:[Diagnostic process of alveolitis--state of the art]. 787 67

An episode of fever, cough, shortness of breath and leucocytosis developed in a 31-year-old atopic housewife from mould exposure in her home environment is evaluated. A chest radiograph revealed diffuse tiny nodular infiltrations in both whole lung fields. Spirometry revealed a severe restrictive type of ventilation impairment. Bronchoalveolar lavage (BAL) showed an increased lymphocyte count with reversed CD4+/CD8+ ratio and transbronchial lung biopsy showed markedly increased lymphocytic infiltration in alveolar septa. Fungal cultures in the air of her home were positive for Penicillium expansum and other fungi. Double immunodiffusion test with the patient's serum showed two precipitin bands to P. expansum antigens. Her symptoms, abnormal findings of radiograph, and spirometric abnormalities disappeared after 2 months' avoidance. The serum precipitin disappeared after 1 month's avoidance. This study indicates that the patient had hypersensitivity pneumonitis (HP) on exposure to P. expansum in her home environment.
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PMID:Hypersensitivity pneumonitis induced by Penicillium expansum in a home environment. 803 26

A 34 year old sawmill maintenance engineer developed a dry cough that was associated with widespread wheezes and crackles in his lungs. His symptoms worsened, with work related lethargy, fever, and breathlessness, and the loss of a stone in weight. At that time, while still at work, he had a neutrophil leucocytosis and increased concentration of gamma globulins. When seen subsequently some two months after stopping work, his chest radiograph and lung function tests were normal, but the cells recovered at bronchoalveolar lavage showed an increase in lymphocytes and mast cells, a pattern consistent with extrinsic allergic alveolitis. Serum precipitins were identified to extracts of sawdust, wood chips, and bark from the sawmill, and to eight species of mould grown from these samples. Specific IgG binding inhibition studies suggested that a common epitope present on Trichoderma koningii might be responsible for the cross reactivity of the patient's serum with the wood and fungal extracts. A diagnosis of wood associated extrinsic allergic alveolitis was made and since changing his job the patient has remained well. Wood associated allergic alveolitis has not previously been described in British sawmill workers, but has been reported in Sweden, with a prevalence of 5%-10% in exposed workers. A review of published data suggests extrinsic allergic alveolitis in wood workers is primarily caused by inhalation of the spores of contaminating fungi, but inhaled wood dust may exert a synergistic effect.
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PMID:Extrinsic allergic alveolitis and asthma in a sawmill worker: case report and review of the literature. 813 Aug 43


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