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

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

Chest radiographs of 39 patients with ankylosing spondylitis were studied. Three showed apical pulmonary fibrosis, two with cavitary lesions. Other known causes of lung disease were excluded. Symptoms and roentgenographic evidence of spondylitis were present for many years prior to the onset of pulmonary symptoms, which variably included shortness of breath, cough, hemoptysis, pleuritic chest pain, fever, and chills. Apical pulmonary lesions of unknown cause were absent in 53 age, sex, and racematched osteoarthritis control patients. The findings suggest that apical pulmonary fibrosis may be an extra-skeletal manifestation of ankylosing spondylitis, the frequency of which approaches that of spondylitic heart disease.
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PMID:Pulmonary manifestations of ankylosing spondylitis. 120 76

We present the clinical and biopsy findings of a 63-yr-old white male with interstitial pulmonary fibrosis and a long history of extensive exposure to mica while working in the rubber industry. The patient presented 30 yr after the initial exposure with complaints of progressive shortness of breath and a chronic nonproductive cough. Pulmonary function testing revealed restrictive lung function with a mild reduction in the total lung capacity (80% of predicted) and a moderate-to-severe reduction in the diffusing capacity of carbon monoxide (50% of predicted). The chest radiogram and high-resolution chest CT scan showed diffuse fibrosis and focal honeycombing involving the upper and lower lung zones bilaterally. Bronchoalveolar lavage revealed 20% neutrophils in the lavage fluid with abundant rectangular flaking crystals. Open-lung biopsy exhibited extensive fibrosis and architectural remodeling with abundant sheets and fragments of engulfed polarizable crystalline material. Energy-dispersive spectroscopy and electron diffraction studies confirmed the material to have the features of mica. Asbestos and other silicates were not identified. The documentation of prolonged exposure to mica, the clinical and radiographic features of severe interstitial fibrosis, and the histopathologic delineation of the interstitial lesion, including spectroscopic and crystallographic verification of crystalline mica, support the causal relationship between mica and interstitial fibrosis.
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PMID:Mica-associated pulmonary interstitial fibrosis. 189 15

A 63 year old woman developed progressive shortness of breath, pulmonary hypertension, and respiratory failure and died from pulmonary fibrosis 45 years after thoracic fistulography with Thorotrast. Bouts of acute respiratory failure occurred with features of noncardiogenic pulmonary oedema. Lung tissue obtained by biopsy and at necropsy showed abundant radioactive particles of thorium dioxide in the lungs. The particles were congregated in the walls of blood vessels and in perivascular fibrous zones, consistent with a causal role of Thorotrast in the development of lung fibrosis. It is suggested that the fibrosis was due to the combined effects of alpha radiation on the interstitial perivascular zones and of recurrent pulmonary oedema due to endothelial damage.
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PMID:Lung fibrosis induced by Thorotrast. 225 23

A 61-year-old man was admitted to our hospital because of persisting cough, sputum and shortness of breath for four months. Brushing specimens and BALF bronchoscopically obtained revealed acid-fast bacilli and TBLB showed pathological findings consistent with interstitial pneumonia. Based on these results, clinical symptoms, chest roentgenograms on admission and identification of M. kansasii, a diagnosis of M. kansasii lung infection occurred in idiopathic pulmonary fibrosis was made. The patient's symptoms consistent with M. kansasii lung infection and his sputum became negative 6 weeks after antituberculosis chemotherapy with INH, SM and RFP. Because of an increasing dyspnea due to pulmonary fibrosis, however, the patient received oxygen therapy. This case suggested an increasing tendency of compromised hosts associated with M. kansasii lung infection.
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PMID:[M. kansasii lung infection occurring in a compromised host with idiopathic pulmonary fibrosis]. 258 49

A 71-year-old man with a long-standing history of rheumatoid arthritis required methotrexate treatment since 1986, with a total dose of 210 mg. In April 1987, before arthroplastic surgery, methotrexate was discontinued. Four weeks later a syndrome of fever, dry cough, shortness of breath, and diffuse air-space consolidations on the chest radiograph evolved. An antibiotic therapy had no beneficial effect, and a bronchoscopy yielded no pathogens. An open lung biopsy led to the diagnosis of methotrexate-induced pneumonitis. This is the first report of a case where methotrexate-induced pneumonitis developed several weeks after cessation of the treatment. Methotrexate can cause four types of pulmonary adverse reactions: pneumonitis, pulmonary edema, pulmonary fibrosis, and pleuritis. Possible pathogenetic mechanisms, symptoms, treatment, and prognosis are discussed.
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PMID:Methotrexate-induced pneumonitis: appearance four weeks after discontinuation of treatment. 280 69

Despite having fixed changes in lung structure, patients with chronic obstructive pulmonary disease and interstitial pulmonary fibrosis can be helped by pulmonary rehabilitation. They learn that shortness of breath is not to be feared but rather accepted and tolerated as a step toward eventual successful rehabilitation. They are taught to accept the reality of their disease but not to dwell on its limitations. They learn to fight depression and anxiety and to overcome their disability within a realistic framework. From the exercise program they build strength, endurance, and confidence and become more independent and mobile. Even very compromised patients can benefit from an intensive inpatient rehabilitation program.
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PMID:Inpatient pulmonary rehabilitation. A team approach to the more fragile patient. 281 9

Three patients who developed pulmonary fibrosis following prolonged treatment with nitrofurantoin for chronic urinary tract infections are presented. They had received the drug for 3--4 years; all gave histories of 2--3 years of progressive shortness of breath and an unproductive cough. On examination, all 3 patients had bilateral crackles and 1 had finger clubbing. Chest radiographs showed bilateral shadowing and lung function tests a restrictive defect with reduced gas transfer. Lung biopsies showed extensive fibrosis in 2 patients and advanced honeycomb formation in 1. The response to steroid therapy in 2 patients was excellent, with resolution of symptoms, clearing of the chest radiographs and improvement in lung function. It is proposed that nitrofurantoin has no place in the long-term treatment of chronic urinary tract infections and that its use in acute infections should be questioned.
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PMID:Pulmonary fibrosis following long-term nitrofurantoin therapy. 707 74

Six patients with breast cancer developed pulmonary toxicity following mitomycin therapy. The presenting symptoms were shortness of breath and a dry cough. The radiological pictures varied from a normal chest x-ray to extensive bilateral pneumonitis. The histological findings consisted of diffuse alveolar damage progressing to interstitial pulmonary fibrosis. Corticosteroid therapy resulted in complete resolution of pneumonia in one patient. Respiratory symptoms improved in 3 patients following discontinuation of the drug. Two patients with extensive bilateral pneumonitis, who were not treated with steroids, died of respiratory failure. Mitomycin-induced lung toxicity appears to be reversible with the discontinuation of drug and the administration of corticosteroids. Lung biopsy is necessary in order to rule out other diagnoses.
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PMID:Pulmonary toxicity of mitomycin. 735 Oct 10

A 48-year-old man with no history of pulmonary disease developed acute lung disease after the intensive exposure of fly ash. He subsequently had progressive worsening of shortness of breath and hypoxemia to the point of requiring mechanical ventilation. Fly ash is a compound consisting of silicon dioxide and various other substances and is used in industrial settings to generate electricity. Exposure to fly ash may cause irritation to the mucous membrane of the respiratory tract and even pulmonary fibrosis in humans. To our knowledge, this is the first case report described in the medical literature of acute lung disease developing after fly ash exposure.
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PMID:Acute lung disease after exposure to fly ash. 802 Mar 1


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