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)

Fibrosing alveolitis is a rare, diffuse lung disease characterized by varying combinations of two histological features: thickening of alveolar walls and the presence of large mononuclear cells in the alveolar spaces. Clinical details of 10 children with fibrosing alveolitis are reported. The main symptoms in children are tachypnoea or dyspnoea, cough, poor weight gain, and cyanosis. The condition is similar to that in adults, but it is usually a more acute illness, and if untreated, more predictably fatal. Respiratory failure, pulmonary hypertension, and cardiac failure are the major complications. Less commonly, superimposed bacterial infection and pneumothorax occur. Chest x-rays often show a sequence of changes with a ground-glass appearance and fine mottling in the early stage of the disease, progressing to a picture of mainly hilar linear markings in those children who recover. The histological features at lung biopsy or necropsy are described; these correlated poorly with the radiological features, steroid responsiveness, and clinical course. Lung function tests in 3 older children showed evidence of markedly reduced lung volumes in 2. Static lung compliance in 4 children in the acute stage of the illness was normal in 3 and diminished in one. The response to steroid therapy was analysed in cases from the literature and the 10 reported cases. No spontaneous remissions occurred, all the survivors having been treated with corticosteroids. In children fibrosing alveolitis is almost always a corticosteroid-responsive disease. An appropriate course of prednisolone would be of at least 4 week's, but preferably of 8 weeks' duration, at a minimum daily dose of 2 mg/kg. After improvement the steroid withdrawal should be cautious and protracted, comprising at least a year's continuous treatment.
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PMID:Fibrosing alveolitis in infancy and childhood. 83 51

We present a study of 151 persons working in slate-pencil manufacturing industries located in the Mandsaur district of Madhya Pradesh, India. Cough, dyspnea, and pain in the chest were the important symptoms. Cyanosis, rhonchi, and crepitations were found in varying numbers of cases. The chest x-ray films were abnormal in 85 cases.
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PMID:Silicosis in slate pencil workers. A clinicoradiologic study. 83 63

Using two case-histories it is shown that atypical radiological findings caused the delay in diagnosis of pulmonary embolism depsite clinical signs (such as fever and intermittent dyspnoea; cyanosis, haemoptoe and cough reflex were absent). The exact diagnosis was finally established after having excluded all diseases, which were of greater probability on the grounds of the x-ray findings.
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PMID:[Differential diagnostic problems in pulmonary embolism caused by x-ray findings]. 86 71

Major fracture of the intrathoracic airway following closed chest trauma is a potentially lethal injury which can be repaired successfully if the diagnosis is made early, Cough, dyspnea cyanosis, hemoptysis, mediastinal emphysema, or pneumothorax not responding to drainage via intercostal tube and a deterioration of the patient's clinical condition out of proportion to the apparent closed chest injury, should alert the clinician to the possiblity of this entity. This report describes the findings in a patient with a longitudinal disruption of the entire intrathoracic trachea and the findings in a second patient with complete transection of the right main bronchus. Each was repaired primarily, with eventual recovery, The principles of management of this difficult group of injuries are reviewed.
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PMID:Major airway injury in closed chest trauma. 87 56

The prognostic features of the disease are summed up. The leading symptom of the disease is the dyspnoe followed by a dry hacking cough, loss of weight and fever. Clinically we find rales, cyanosis clubbing and signs of right heart insufficiency. Lung function data point to a decreased vital capacity and diffusing capacity; residual volume and functional residual capacity are about normal. Corticosteroid monotherapy is not an efficient treatment. The combination of prednisolon + azathioprine improves vital capacity but not working capacity. Prednisolone and d-penicillamine improve all parameters including working capacity. This can be enhanced by still adding azathioprine or cyclophosphamide to prednisolone and d-penicillamine.
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PMID:[Idiopathic fibrosing alveolitis]. 91 41

A retrospective analysis of 50 patients who had been observed to aspirate gastric contents was performed to define better the course of patients with this syndrome. The patients invariably had a disturbance of consciousness, most commonly due to sedative drug overdose or general anesthesia. The onset of clinical signs occurred prompty after aspiration and tended to be similar in all patients, irrespective of their subsequent course or outcome. These findings usually included fever, tachypnea, diffuse rales, and serious hypoxemia. Cough, cyanosis, wheezing, and apnea were each seen in approximately one third of the cases. Apena, shock, and early severe hypoxemia were particularly ominous events. Initial roentgenograms revealed diffuse or localized alveolar infiltrates, which progressed during the next 24 to 36 hours. Subsequent clinical courses followed 3 patterns: 12 per cent of the patients died shortly after aspiration; 62 per cent had rapid clinical and radiologic improvement, with clearing, on average, within 4.5 days; 26 per cent demonstrated rapid improvement, but then had clinical and radiographic progression associated with recovery of bacterial pathogens from the sputum and a fatal outcome in more than 60 per cent. Treatment from the outset by adrenocortical steroids or antimicrobial agents had no demonstrable effect on the outcome. The clinical features of aspiration of gastric contents are characteristic and distinguish it from other forms of aspiration-related lung disease.
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PMID:Pulmonary aspiration of gastric contents. 100 48

Allergic alveolitis is the immunologic response of the alveolar wall and the interstitial spaces of lung to inhalation of different organic, antigenic substances. This paper presents the case of a 12 1/2-year old girl with a pulmonary disease caused by inhalation of protein contained in the excrement dust from budgerigars. In the paat few years several reports already described this disease in breeders of pigeons and budgerigars. During some years our patient had recurrent episodes of a subacute illness with severe cough, dysponea, cyanosis of lips, tachycardia, and weakness. Auscultation showed only discrete crepitant rales at both lung bases. In contrast the chest roentgenogram demonstrated marked changes with soft fine patchy densities and reticulation dispersed through the lung parenchyma. The histological examination of lung biopsy showed a thickening of alveolar walls and of interstitial spaces with lymphocytic infiltration, fibrosis, and multinuclear giant cells. In accordance with this findings pulmonary function tests revealed a restriction and a decrease in diffusing capacity; furthermore there was a middle-grade obstruction. The presence of precipitating antibodies in the serum against extracts of excrements from budgerigars confirmed the relation between pulmonary disease and domestic allergen. Our experience indicates that perferential therapy is the avoidance of contact with birds.
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PMID:[Allergic alveolitis due to inhalation of avian proteins (author's transl)]. 116 83

A life-threatening respiratory disease, characterized by fever, cough, dyspnoea, cyanosis and wide-spread bilateral pulmonary infiltrates, developed in a 40-year-old patient receiving intermittent methotrexate therapy for psoriasis. Blood eosinophilia accompanied the illness. A prominent feature in the clinical picture was a discrepancy between auscultatory findings and the pronounced changes in the chest X-ray. Systemic corticosteroids produced rapid improvement. It is suggested that the pulmonary syndrome represents a hypersensitivity reaction.
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PMID:Methotrexate pneumonitis in a psoriatic. 119 23

Hypersensitivity pneumonitis due to the inhalation of Shiitake mushroom spores was demonstrated in a 38-year-old woman. Symptoms of cough, nausea and malaise, and clinical findings of cyanosis, bibasilar crackles, reduced lung volumes, hypoxemia, leukocytosis, elevated ESR, positive C-reactive protein, and bilateral diffuse reticulonodular shadows on chest roentgenogram improved after the patient was removed from exposure. Alveolitis was demonstrated by transbronchial lung biopsy, as well as an increase in lymphocytes in bronchoalveolar lavage. Serum precipitins and specific IgG antibodies to an extract of Shiitake mushroom spores, but not to other common molds or mushroom body, were detected in serum. Provocative inhalation test with the extract of mushroom spores caused the same clinical symptoms and signs as experienced in the workroom. This is the first report of typical hypersensitivity pneumonitis induced by Shiitake mushroom spores. Mushroom spores as well as thermophilic actinomycetes must be considered a causative agents for mushroom worker's lung.
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PMID:Hypersensitivity pneumonitis induced by Shiitake mushroom spores. 128 27

Five patients with neurogenic pulmonary edema (NPE) were reported. The edemas were caused by head injuries in four patients and by a craniotomy in the fifth. The onset of NPE was either acute (3 hours after injury) or was slow to develop (4 days later). Clinical symptoms included the sudden onset of coughing, tachypnea, tachycardia, and pink bubbly sputum. Moreover, the patients also suffered cyanosis, confusion, or respiratory failure. The distribution of the resulting pulmonary edema was diffuse in 4 cases and localized within a single lobe of the lung in 1 case. Treatment of the NPE included reducing intracranial pressure (glycerol), diuresis (furosemide and mannitol), narcotics (morphine, phenobarbital), and blocking the peripheral effect of sympathetic reflex activity (hydralazine, sodium nitroprusside). Mechanical ventilation support (CPU-1) in combination with controlled hyperventilation may also be necessary. The inability to correct hypoxemia without toxic levels of oxygen necessitates the use of PEEP (positive end-expiratory pressure, +5-10 cmH2O). Resolution of symptoms was noted 24 to 48 hours after treatment in 4 patients. Early diagnosis and intensive care of the pulmonary edema may have a significant bearing on the recovery of lung functions. Unfortunately, 4 of the patients failed to survive because of central nervous system failure. We therefore want to emphasize that NPE can cause secondary deterioration of neurological functions. In conclusion, when dealing with respiratory distress patients with CNS injuries, the possibility of additional damage from a NPE must be taken into consideration.
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PMID:[Neurogenic pulmonary edema: five cases report]. 129 67


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