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Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acute intravenous and oral toxicity of single doses of paraquat dichloride was studied in the cynomolgus monkey. Renal handling and effects upon renal function were also investigated following an oral dose of [14C]paraquat. Clinical signs consisted of vomiting, anorexia and dyspnoea. By 48 h all animals showed signs of acute renal failure with oliguria, high plasma urea and SGPT levels and metabolic acidosis. Animals dosed orally showed similar, though less severe, signs to those dosed intravenously. The oral LD50 was approx. 70 mg paraquat cation/kg. Following an oral dose plasma levels peaked by 2 h, but were constant from 12 h to 24 h. Paraquat clearance was high initially and exceeded the creatinine and urea clearance, but fell off markedly after 14 h as renal failure developed. By 18 h urine production had ceased. It is concluded that acute renal failure and acute pulmonary damage are the main causes of death, with interstitial pulmonary fibrosis being a factor in animals surviving the acute phase.
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PMID:The toxicity and renal handling of paraquat in cynomolgus monkeys. 12 Jun 23

Four children aged 31/2 to 13 years, who developed allergic alveolitis as a result of antigenic exposure in a domestic situation are described. The clinical symptoms consisted of gradual onset of increasing dyspnoea, chronic cough and weight loss. Lung function tests showed characteristic reduction in vital and diffusion capacity. Serologically, antibodies against animal antigens were demonstrated in all patients. Radiologically there were pronounced reticular changes in both lungs affecting mostly the middle and lower zones. Occasionally there were miliary and sometimes confluent shadows. In differential diagnosis, virus infections, pneumocystis carinii, fungus infections, dermatomyositis, sarcoidosis and tuberculosis had to be considered. Apart from a short course of steroid treatment, it is necessary to make certain that the children are no longer exposed to the causal antigen. Under these conditions the prognosis is good, but otherwise the disease, as in adults who are continuously exposed to the antigen, results in pulmonary fibrosis.
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PMID:[Exogenous allergic alveolitis during childhood (author's transl)]. 14 24

An uncommon, but lethal, toxic side effect of busulfan (Myleran) therapy for chronic myelogenous leukemia is pulmonary fibrosis. A 16-month-old male infant treated for 11 months with busulfan for chronic myelogenous leukemia is, we believe, the first case of "busulfan lung" in the pediatric age group to be reported. Progressive roentgenographic changes in the lung of a diffuse intra-alveolar and interstitial pattern were noted. The patient died after a four-day episode of cough, fever, and progressive dyspnea. At autopsy, no evidence of infection or leukemic infiltrates were seen in the lungs. Characteristic histologic findings as a result of busulfan therapy were observed in the lung and pancreas.
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PMID:Busulfan lung. 26 39

Ten patients developed pulmonary fibrosis after bischloroethylnitrosourea (BCNU) therapy for malignancy. This was lethal in seven patients, four of whom had no evidence of tumor at autopsy. Presenting symptoms were either the insidious onset of cough and dyspnea or the sudden onset of respiratory failure. Physical findings were unremarkable. Chest roentgenogram usually showed interstitial infiltrates. Pulmonary function studies showed resting hypoxia with diffusion and restrictive defects. This complication of therapy does not appear to be dose related and may be made more likely by the concomitant administration of cyclophosphamide. Prednisone therapy did not benefit most patients. The literature and the implications of the use of BCNU alone or in combination are reviewed.
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PMID:Pulmonary toxicity associated with bischloroethylnitrosourea (BCNU). 44 51

Dyspnea is the medical term for the patient's or subject's complaint of shortness of breath. It encompasses the respiratory discomfort experienced in many different diease states as well as the shortness of breath felt by a normal subject during or after strenuous exercise. Several parameters which have been shown to correlate with the onset or severity of dyspnea are described, including reduced vital capacity, the ratio of minute ventilation to vital capacity, reduced breathing reserve, the work of breathing, and the oxygen cost of breathing. Attempts at quantitation of dyspnea have usually consisted of measuring physiological parameters associated with the sensation, such as the "dyspneic index". The direct measurement of respiratory sensations using modern psycho-physical methods is at an early stage of development. Since the observation that the existence of dyspnea is often unrelated to any disturbance of arterial blood gas composition, it has been generally held that the mechanism of dyspnea is primarily neurophysiological. The neural pathways may conceptually be divided into those which transmit the "dyspnea message" from the respiratory apparatus to integrating centers in the brain, and those concerned with subsequently bringing the sensation to the level of consciousness. It seems likely that there is no single sensing mechanism and neural pathway which will be able to explain dyspnea in the diverse populations of patients and subjects who experience unpleasant respiratory sensations. Three theories concerning mechanisms of dyspnea are briefly described: "length-tension inappropriateness", vagal afferent activity especially from the J-receptors, and the recent concept of diaphragmatic fatigue. Some specific characteristics of the shortness of breath experienced in certain disease states are described, including chronic bronchitis and emphysema, bronchial asthma, pulmonary fibrosis and congestive heart disease.
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PMID:Dyspnea. 50 81

A 73-year-old female developed pulmonary disease during treatment with chlorambucil for polycythemia vera. Cough and dyspnea were prominent symptoms. A chest roentgenogram revealed interstitial fibrosis. The diffusing capacity was markedly reduced. Pathologic findings included alveolar lining cell dysplasia, interstitial round cell infiltrates and interstitial fibrosis. Resolution of the pulmonary symptoms and partial clearing of the fibrosis on chest roentgenogram followed discontinuation of the chlorambucil and institution of steroid treatment. Chlorambucil may cause pulmonary fibrosis similar to busulfan and cyclophosphamide and this may be a potential complication of all alkylating agents.
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PMID:Pulmonary disease with chlorambucil therapy. 63 May 32

The major difference between heart disease in the old and the young is that elderly people almost have one or more other major, even life-threateninng conditions. These associated diseases challenge the physician in establishing a diagnosis and prognosis, understanding the pathogenesis of the symptoms and signs, and determining the best managemnt. Another important difference is that old persons have senescent changes in all organ systems, whether the heart is normal or diseased. Dyspnea, especially on exertion, is common, and so is edema of the feet and ankles. Chest x-rays show changes typical of old age, e.g., small lung fields, mild to moderate pulmonary fibrosis, and calcium plaques in the aorta. In the absence of cardiac disease, the heart is normal in size or even small. Translationg experience in managing heart disease in young patients to elderly patients must be done cautiously. Old people tend to be confused, delicate, mentally and physically slow, feeble, and unreliable, and they are more sensitive to most-if not all-drugs, especially digitalis. The physician should see them often and question them routinely about their symptoms, signs, and medication. Decisions on management should not be hurried, except in an emergency situation.
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PMID:The special problems of heart disease in old people. 83 77

The clinical histories of 81 patients with hypersensitivity reactions to nitrofurantoin, 66 of whom had pulmonary reactions, were studied. Of all patients, 94% were women and of these, 43% were between 40 and 59 years of age. The nitrofurantoin preparation that contained vitamin c caused significantly fewer hypersensitivity reactions than the others. Acute pulmonary reactions appeared a mean of 8.7 days after the start of nitrofurantoin treatment. Typical for these were high fever, dyspnoea, cough, blood eosinophilia, bilateral pneumonic or pleuro-pneumonic infiltrations, a reduced transfer factor of the lung and, as revealed in pulmonary biopsy specimens, vasculitis, interstitial inflammation and alveolar exudation. Symptoms of subacute and chronic pulmonary reactions developed after at least 1 and 6 months of treatment, respectively. Findings of interest were anti-nuclear antibodies in serum, capillary sclerosis, interstitial fibrosis and inflammation in pulmonary tissue. Most patients with an acute pulmonary reaction recovered within 15 days, but in more than half of those with chronic reactions slight signs of pulmonary fibrosis persisted on follow-up. The findings suggest that the interstitial pulmonary changes caused by nitrofurantoin are largely the result of an Arthus-type immune complex-mediated reaction.
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PMID:Nitrofurantoin-induced acute, subacute and chronic pulmonary reactions. 84 Dec 94

Pulmonary veno-occlusive disease has recently been recognized as a distinct pathological entity and a cause of pulmonary arterial hypertension. Twenty previously reported cases and a new patient are here reviewed. The majority presented with breathlessness and in the early stages of the disease, when the abnormal signs were not striking, some patients were wrongly diagnosed as suffering from an anxiety state. The condition usually has an insidious onset but is remorselessly progressive and since no effective treatment is available at present, invariably fatal and the majority of patients have died within two years. The fully developed clinical picture is dominated by symptoms and signs of pulmonary arterial hypertension, similar to those found with other diseases causing a raised pulmonary arterial blood pressure. However, some patients with pulmonary veno-occlusive disease show, in addition, signs of pulmonary venous and capillary hypertension, which can lead to its clinical recognition when associated with a normal left atrial blood pressure. In this condition the pulmonary wedge pressure would appear to be unreliable as a record of the left atrial blood pressure. Pulmonary angiography and lung scanning will differentiate pulmonary veno-occlusive disease from massive thromboembolic pulmonary arterial hypertension but not from primary pulmonary arterial hypertension or micro thromboembolism. Although in some patients it should now be possible to recognise pulmonary veno-occlusive disease in life, there will be others where, even after full investigation, it will still be impossible to differentiate the condition from primary pulmonary arterial hypertension or micro thromboembolism and in these the diagnosis will only be made when the distinctive histological pattern of the disease is demonstrated. In pulmonary veno-occlusive disease there is a widespread occlusion of the pulmonary veins and venules by a loose intimal fibrosis which is often basophilic. Recanalization of the occluded veins is common and in some cases may be very striking. These occlusive lesions in the pulmonary veins lead to an elevation of pulmonary arterial pressure with associated disease of these vessels, and are also responsible for chronic oedema of the elveolar walls with subsequent development of interstitial pulmonary fibrosis. In the present case organised thrombi were present in the pulmonary arteries in addition to the pulmonary venous lesions.
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PMID:Pulmonary veno-occlusive disease. 115 89

A 38-year-old patient with effort dyspnea, somnolence, cianosis and cor pulmonale is presented. Chest roentgenograms and lung function studies suggested the diagnosis of pulmonary fibrosis. The patient showed also severe hypercapnia with normal resting ventilation and ventilatory response to exercise lower than usual for this condition. Autopsy confirmed the clinical diagnosis. This subject may belong to the growing group of patients where CO2 retention is not explained by their pulmonary pathology.
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PMID:Idiopathic interstitial pulmonary fibrosis with hypercapnia. 117 39


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