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)

Intranasal administration of a 4% solution of cromolyn sodium for the treatment of ragweed hay fever was tested in an 8-week double-blind matched-pair study involving 66 patients. Patients on active drug received 5.2 mg into each nostril 6 times daily; control patients received a placebo spray. The treated group showed a significant reduction in mouth breathing (p less than 0.001), stuffy nose (p less than 0.002), runny nose (p less than 0.003), and postnasal drip (p less than 0.035). Patients receiving the active drug also reported fewer sneezing episodes (p less than 0.003) and nose blowing episodes (p less than 0.015). One patient using cromolyn solution developed nasal ulceration, tongue swelling, coughing, and wheezing. Other side effects were minimal and occurred with equal frequency in both groups. In the treated group relief of symptoms was most marked in patients with high preseasonal levels of IgE ragweed antibody. Intranasal 4% cromolyn solution appears to be an effective drug for the treatment of ragweed hay fever; measurement of the preseasonal level of IgE ragweed antibody is a useful screening test to identify patients most likely to achieve a maximal beneficial response to treatment.
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PMID:Preseasonal IgE ragweed antibody level as a predictor of response to therapy of ragweed hay fever with intranasal cromolyn sodium solution. 40

A 28 year old veterinary medical student experienced spiking fever, cough, peripheral blood eosinophilia and an eosinophilic pulmonary infiltrate. Corynebacterium pseudotuberculosis was isolated from a transtracheal aspirate and bronchoscopy washings. C. pseudotuberculosis, a pathogen responsible for lymphadenitis in livestock, has never been reported to cause pneumonia in man. In the four cases of C. pseudotuberculosis previously reported, lymphadenitis was the chief clinical presentation. In our patient specific antibodies against the isolated C. pseudotuberculosis developed but not against the other corynebacteria. With erythromycin therapy, the peripheral blood eosinophilia and IgE anti-C. pseudotuberculosis titer decreased whereas the IgG titer continued to increase.
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PMID:Corynebacterium pseudotuberculosis. A new cause of infectious and eosinophilic pneumonia. 46 27

The anatomical distribution of plasma cells and other cells containing immunoglobulin in the respiratory tract, and the relative proportions of the immunoglobulin classes have been estimated on necropsy tissues from nine adult human subjects without respiratory disease, five non-smokers and four smokers, none of whom had cough or sputum. Cell counts on multiple sections stained by immunofluorescent methods for the presence of immunoglobulin were carried out on the upper trachea, main bronchus, and lower lobe bronchus. Cells containing immunoglobulin were found mostly in the submucous glands but were also present in the lamina propria of the tracheal and bronchial epithelium. These cells were present in the greatest concentration in the main bronchus and were always present in the lobar bronchus and, in most subjects, in the upper trachea. The cells were not always present round small bronchi and bronchioles and were virtually absent from alveolar walls. Cells containing IgA were much more numerous than those containing other immunoglobulin classes in all subjects except one, in whom IgG and IgE cells were equally numerous. Two subjects appeared to be significantly different from the rest. One non-smoking subject had a marked deficiency of IgA cells at all sampling sites, and one smoker had a marked excess of IgA cells. In spite of these two subjects there was no significant difference between smokers and non-smokers except in the lobar bronchus where the smokers had significantly more IgA cells than the non-smokers.
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PMID:Distribution of plasma cells and other cells containing immunoglobulin in the respiratory tract of normal man and class of immunoglobulin contained therein. 78 99

Eighteen patients showing hypersensitivity to nitrofurantoin with symptoms like sudden fever, malaise, cough, pleuritis, leucocytosis and sometimes eosinophilia were analysed for immune reactions, i.e. lymphocyte transformation and specific antibodies. In addition, thirty-three individuals treated with the drug but with no clinical signs of the described reactions were included as controls. The lymphocyte transformation test (LTT) was found positive in ten out of the eighteen sensitive patients while one to three out of fourteen tested control patients were positive, depending on test conditions. An incubation period of 4 days in culture medium supplemented with autologous serum gave stimulation to a greater extent than did isologous serum and/or incubation for 6 days. The antibody determinations, with the enzyme-linked immunosorbent assay (ELISA), showed no IgE antibodies to nitrofurantoin in any of the patients. In contrast, most of the hypersensitive and even the control patients had specific IgG antibodies. The mean value of the antibodies of the sensitive group was higher than of the control group, but considerable overlapping between the groups was noted. In adverse reactions to nitrofurantoin a positive LTT and/or a high antibody titre to the drug favours an allergic mechanism and contributes to a more reliable diagnosis.
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PMID:Adverse reactions to nitrofurantoin in relation to cellular and humoral immune responses. 89 Oct 20

Early recognition and treatment of immunologically mediated diseases of the lung are vital to prevent irreparable damage. Extrinsic allergic alveolitis and allergic bronchopulmonary aspergillosis are often confused but should not be difficult to distinguish. The former is nonatopic and is marked by chills, fever, chest pains, cough, dyspnea, and restrictive pulmonary function. The immunologic hallmark is the presence of precipitating antibody to the suspected antigen. Allergic bronchopulmonary aspergillosis is atopic and is marked by low-grade fever, obstructive pulmonary function, markedly elevated serum IgE levels, and positive immediate and late response on skin tests. Both diseases respond well to early corticosteroid therapy. Prophylactic measures are also important in controlling extrinsic allergic alveolitis.
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PMID:Immunologically mediated lung diseases. Extrinsic allergic alveolitis and allergic bronchopulmonary aspergillosis. 94 40

A 47-year-old woman was admitted to our hospital because of dry cough and throat discomfort. Chest X-ray film showed reticular shadows with Kerley B line and scattered nodular shadows. Blood examination revealed normal WBC count (5100/mm3) with eosinophilia (21%), negative CRP, elevated ESR (49 mm/l hr), normal IgE level and positive antinuclear antibody with speckled pattern. Skin tests and precipitating antibodies for common allergens were negative. Results of arterial blood gas analysis and respiratory function test were almost normal. Bronchoalveolar lavage fluid yields 85.7% eosinophils, which suggested eosinophilic lung disease. To establish the diagnosis, thoracotomy was performed and lung specimens were obtained from S3a and S8a. In the area of the nodule, the alveolar spaces were filled with eosinophils and mononuclear cells, with no evidence of vasculitis, granuloma or parasites. Alveolar spaces were almost preserved in residual areas. The walls of air ways, pleura and lobular septa were heavily infiltrated with eosinophils and mononuclear cells. Thus, open lung biopsy confirmed the diagnosis of idiopathic eosinophilic pneumonia. The areas of intraalveolar filling with eosinophils and mononuclear cells were found to correspond to the nodular shadows on chest X-ray film. The relationship between the findings of chest X-ray films and lung histology are discussed.
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PMID:[A case of eosinophilic pneumonia with diffuse reticular shadows and scattered nodular shadows on chest X-ray film--comparison of findings of chest X-ray and lung histology]. 128 40

We describe two patients demonstrating a granulomatous inflammation of bronchial mucosa characterized clinically by a persistent dry cough, lack of manifestations of bronchial asthma, normal level of serum IgE and serum ACE, inflamed bronchial mucosal appearance consisting of edema, erythema, bleeding and narrowing and recovering without specific treatment. Histopathological findings of the bronchial inflammation of our patients were characterized by noncaseating granuloma formation consisting of epithelioid cells and multinucleated giant cells with infiltration of lymphocytes, plasma cells and eosinophils. The bronchial granulomatous inflammation of our patients was thought to differ from that of diseases which have been known, to our knowledge, as diseases demonstrating a granulomatous inflammation of bronchial mucosa. Although the pathogenesis of the disease could not be clarified by a careful search of special staining and culturing for the infective agent, it was most suggestive of non-specific inflammation with a granulomatous response to some sort of inhaled agents.
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PMID:Idiopathic granulomatous bronchitis. An unusual form of known granulomatous lung diseases or an unknown disease? 134 46

The upper and lower airways have complimentary roles in the ultimate object of supplying the body with oxygen whilst removing waste products of metabolism. Pathology in one area may trigger a response in another, the physiology of which, in the case of virus-induced asthma exacerbations remains poorly characterized. Viral infection of the upper airways by common cold viruses frequently triggers a response in the lower airways leading to prolonged morbidity, especially in subjects with significant pre-existing airway disease. The induction or amplification of BHR may be an important mechanism whereby asthmatic symptoms are produced although the cellular and tissue events or reflex mechanisms activated by viral illnesses and underlying BHR changes are poorly defined and may be dependent on the type and the severity of infection. Children and asthmatics tend to develop frequent colds setting in motion a sequence of events culminating in airway obstruction and symptoms of wheezing, coughing and chest tightness. This may reflect independent inflammatory changes caused by a simply additive effect of viral damage to the mucosa superimposed upon pre-existing allergic inflammation (Fig. 1). Few if any symptoms will develop in normal subjects with a mild cold whereas significant symptoms may ensue if the cold is severe and induces marked lower airway swelling, secretions and smooth muscle contraction; pathology to which children who have small calibre airways may be particularly susceptible. In asthmatics even a mild cold frequently induces exacerbation of symptoms, while serious life-threatening asthma attacks may occur associated with a severe cold. Some studies have suggested that this effect is not only additive but also synergistic and brought about by release of the mediators already present in increased quantities, the induction of IgE synthesis, or by the potentiation of neural and epithelial damage. The combined effect of both asthma and viruses may thus be amplified and result in a sustained and refractory period of airway obstruction, severe symptoms and unstable asthma. As most hospital admissions for asthma occur over the winter months and soon after the start of the school terms [115], spread of viruses through the community to susceptible individuals may be the single most important cause of sustained exacerbations of asthma. Definition of the pathological and physiological mechanisms involved will lead to better understanding and may thus provide a basis for prevention and the development of effective forms of treatment for virus-induced asthma.
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PMID:Viruses as precipitants of asthma symptoms. II. Physiology and mechanisms. 135 15

Patients with Paragonimiasis westermani show a typical ring form or nodular shadow on chest X-ray, cough, sputum, and hemosputum. Recently, case reports of Paragonimiasis westermani, accompanied by pneumothorax and pleural effusion, as for Paragonimiasis miyazakii, have been increasing. Paragonimus westermani often causes an ectopic infection in various organs such as the peritoneal cavity, pleural cavity, pericardium, liver, adrenal gland and brain. Cutaneous paragonimiasis is considered one of the typical forms of ectopic infection in its earlier phase, but a few unexpected cases of cutaneous Paragonimiasis westermani have also been reported. A 68-year old man, who had never eaten fresh-water crab or raw sliced meat of wild boar, noticed subcutaneous induration of the abdominal wall. The induration had been gradually moving upwards and to the right from the infraumbilical region for over 20 days, and then disappeared at the right upper lateral abdominal wall. Eight months later, he developed severe pain in the right lower chest, and a chest X-ray showed right pleural effusion. Laboratory examinations revealed eosinophilia (WBC 3940/mm3, eosinophil 9%), elevated ESR, and an elevated serum total IgE level (5517 IU/ml). Ouchterlony's double diffusion test performed with the patient's serum in agarose showed strong bands toward Paragonimus westermani antigen, compared to Paragonimus miyazakii antigen. Immunoelectrophoresis with the patient's serum showed specific bands toward Paragonimus westermani antigen. This patient was finally diagnosed as having Paragonimiasis westermani infection, and he responded to praziquantel administration. The clinical course of this patient appears to be rare in cases of Paragonimiasis westermani infection. The clinical course of this case resembled some cases of Paragonimiasis miyazakii infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of Paragonimiasis westermani with pleural effusion eight months after migrating subcutaneous induration of the abdominal wall]. 138 80

Of 113 methyl isocyanate (MIC)-exposed subjects studied initially at Bhopal, India, 79, 56, 68, and 87 were followed with clinical, lung function, radiographic, and immunologic tests at 3, 6, 12, 18, and 24 months. Though our cohort consisted of subjects at all ages showing a varied severity of initial illness, fewer females and young subjects were seen. Initially all had eye problems, but dominant symptoms were exertional dyspnea, cough, chest pain, sputum, and muscle weakness. A large number showed persistent depression mixed with anxiety, with disturbances of personality parameters. The early radiographic changes were lung edema, overinflation, enlarged heart, pleural scars, and consolidation. The persistent changes seen were interstitial deposits. Lung functions showed mainly restrictive changes with small airway obstruction; there was impairment of oxygen exchange. Oxygen exchange improved at 3-6 months, and spirometry improved at 12 months, only to decline later. The expiratory flow rates pertaining to large and medium airway function improved, but those for small airways remained low. There were changes of alveolitis in bronchoalveolar lavage fluid on fiber optic bronchoscopy, and in 11 cases positive MIC-specific antibodies to IgM, IgG, and IgE were demonstrated. On follow up, only 48% of the subjects were clinically stable, while 50% showed fluctuations. Thirty-two percent of the subjects had lung function fluctuations. Detailed sequential behavior over 2-4 years was predicted for dyspnea, forced vital capacity, maximum expiratory flow rate (0.25-0.75), peak expiratory flow rate, VO2, and depression score. A model for clinical behavior explained a total variance of 52.4% by using the factors of cough, PCO2 and X-ray zones in addition to above five parameters. The behavior of the railway colony group (1640 patients) revealed a similar pattern of illness. When this observed pattern of changes was transferred to the affected Bhopal city sections (with an equitable age-sex distribution), our model results were again validated. Thus the picture of MIC-induced disease seems similar despite the differences for age-sex and initial severity of illness in our cohort and in the population of Bhopal city as predicted by our model.
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PMID:Sequential respiratory, psychologic, and immunologic studies in relation to methyl isocyanate exposure over two years with model development. 139 63


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