Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From July, 1973, to June, 1977, 25 patients in an immunosuppressed state from underlying reticuloendothelial neoplasm or associated chemotherapy, underwent open biopsy of the lung at the University of Maryland Hospital for diagnosis of unilateral diffuse pulmonary infiltrates. Eight patients were in marked respiratory distress, 13 in moderate distress, and 4 in little or no distress at the time of open lung biopsy. There were 3 postoperative deaths (12%). The operation-related morbidity was 1 out of 25 (4%). Two of the patients who died were found to have irreversible pulmonary fibrosis secondary to bleomycin drug therapy. The subsequent treatment of all 25 patients was influenced by the biopsy findings as follows: upgrading the disease stage or establishing treatment failure in 11 patients; establishing the presence of inflammatory disease in 3 patients; establishing the diagnosis of fibrosis associated with drug treatment without recurrent disease or infection in 11 patients. The preferability of open lung biopsy as opposed to transbronchial or percutaneous techniques is discussed.
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PMID:Open lung biopsy in diagnosing pulmonary infiltrates in immunosuppressed patients. 50 82

A light and electron microscopic study was carried out in 21 infants in whom the pathologic diagnosis of bronchopulmonary dysplasia had been made. All the infants except two had the respiratory distress syndrome at birth, and all 21 had been treated with respirator and oxygen therapy for various periods of time. The pathologic alterations observed in all the infants studied were primarily damage of the bronchial and bronchiolar ciliary apparatus and mucous membranes, severe necrotizing bronchiolitis, and marked bronchiolar and alveolar fibrosis. These changes were more pronounced in infants who survived the longest period of time. Such inflammatory and fibrotic changes are known to predispose to destruction of lung tissue, emphysema, and pulmonary hypertension. Six of these 21 infants developed symptoms and signs of cardiac atrial or ventricular stress, including cor pulmonale, prior to their demise. These infants were among those that survived the longest periods of time, had the longest exposure to supplemental oxygen, and showed histopathologically severe pulmonary fibrosis and emphysema.
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PMID:Bronchopulmonary dysplasia: the pulmonary pathologic sequel of necrotizing bronchiolitis and pulmonary fibrosis. 99 46

The authors report ten cases of drug induced lung diseases, complicated by respiratory failure of whom five were attributed to cytotoxic drugs and five to non cytotoxic drugs. The drug induced lung disease presented as acute respiratory distress syndrome in two cases, alveolar interstitial lung disease in three cases, purely interstitial in five cases. There was acute respiratory failure (ARF) in eight cases and chronic respiratory failure (CRF) in two cases. Among the five patients admitted for cytotoxic drug induced lung disease and ARF, four recovered and one died of diffuse destructive pulmonary fibrosis. Among the five patients having non cytotoxic drug induced lung disease, three were in ARF and recovered. The other two had CRF and died of diffuse pulmonary fibrosis. The diagnostic of drug induced lung disease was established in each case with the chronology of the clinical events, the exclusion of other possible causes of the lung disease and the evolution after removal of the incriminated drug. Broncho-alveolar lavage (BAL) had a major diagnostic value. It was contraindicated by respiratory failure in five cases. The predominant alveolar cell type was lymphocyte (four cases), eosinophil (three cases) and neutrophil (one case), BAL was realized with a provocation test and demonstrated the pathogenic role of cyclothiazide in one case. No specific information was given by histology. The prognosis did not seem to be linked to the severity of the initial clinical picture, or to the nature of the underlying neoplastic disorder, but to the degree and evolution of the pulmonary fibrosis.
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PMID:[Drug-induced pulmonary diseases: diagnostic, therapeutic and prognostic aspects. Apropos of 10 personal case reports]. 128 22

Sixteen beagles were allocated into 4 groups, each group consisting of 2 males and 2 females, which were injected sc with 1,3,5 or 7 mg paraquat/kg. The beagles were observed for 2 w after the administration. At the end of the observation period all the dying and surviving dogs were studied pathologically. The LD50 was calculated as 1.8 (1.0-6.1) in males and 3.5 (2.4-10.1) mg/kg in females. Clinical laboratory tests showed increases in segmented neutrophils and monocytes, decreases in lymphocytes, slight decreases in chloride, moderate increases in BUN, GOT, GPT and phospholipids, slight increases in uric acid, total protein, creatine, total cholesterol and total bilirubin, and prolonged prothrombin times. Marked edema, congestion and hemorrhage of lungs, as well as slight congestion in various organs, were observed grossly. In histopathological examination, marked pulmonary hemorrhage and congestion, fibroblast-like cells in alveolar septa, breakdown of alveolar walls, thickening of alveolar walls and pleura, mild congestion and degeneration of the liver, and mild degeneration of renal tubules were observed. The cause of death was respiratory distress and renal failure. The surviving animals had mild atelectasis of the lungs. Electromicroscopic examination on the surviving animals revealed the appearance of spindle-shaped cells, proliferation of type II alveolar cells and fibroblasts, mitosis of fibroblasts, and abundant collagen fiber in the lung, calcium deposition, stratification and thickening of basement membranes, and localized necrotic epithelial cells in the proximal tubules of kidneys, and stratification of intramitochondrial cristae of the liver. Pulmonary fibrosis in the switchover stage was present with participation from type II alveolar cells, fibroblasts and myofibroblasts.
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PMID:Acute toxicological studies on paraquat: pathological findings in beagle dogs following single subcutaneous injections. 150 67

The first Danish experience of treatment of the respiratory distress syndrome (RDS) in preterm infants with exogenous surfactant is described. Fifteen infants with birthweights of 645-1,865 g and gestational ages of 25-32 weeks, all receiving artificial ventilation with at least 60% oxygen for severe RDS, were treated with purified porcine surfactant (Curosurf) within the first 28 hours of life. Pulmonary function improved immediately in all of the infants. Four infants (27%) died, four (27%) developed bronchopulmonary dysplasia (pulmonary fibrosis) and two (13%) had late neurological sequelae. These preliminary results are considered to be promising and they are in complete agreement with the results of randomised, controlled investigations from abroad. Systematic registration is, however, still necessary.
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PMID:[Treatment of severe respiratory distress syndrome with surfactant]. 163 99

We reported earlier in the 1st report the use of treadmill walk apparatus and transcutaneous blood gas measurement apparatus as a newly designed exercise test. In this report, test was carried out in 90 persons (4 healthy, 66 recovered from pulmonary tuberculosis, 3 recovered from silico-pulmonary tuberculosis, 12 of COPD, and 5 of pulmonary fibrosis et bronchiectasis). The changing curves of transcutaneously measured O2 partial pressure (tPo2) were, as previously reported, classified into 4 types: 1. unchange-6, 2. slightly decreased-38, 3. moderately decreased-24, 4. markedly decreased-21. And unexpected odd curves were seen in 4 patients, 3 of whom were retested the other day, and their changing curves of tPo2 in the second test were corrected and classified into slightly or moderately decreased type. The decreasing slopes of 4 types of tPo2 curves were subclassified, in each type, into 3 to 4 forms. In recovered pulmonary tuberculosis patients, in general, when the spread of pathologic changes in the lungs was wider, the more decreased types of tPo2 curves were seen. But in COPD patients, such was not the case. In the exercise test, total tolerance time (minutes) against the definite load was significantly shorter in the more decreased type; unchanged-13.5-14.5, slightly decreased -7-10, moderately decreased-6-9, and markedly decreased-3-5. The recovering time of tPo2, pulse rate, blood pressure etc. from the records in the end of the exercise to the pre-exercise records, was longer in the more decreased type. On the other hand, usually the lower Pao2 of the patients were, the more their changing curves of tPo2 decreased. Pao2 was previously measured in blood taken from brachial artery in supine position before the test. But exceptionally in some patients with high Pao2 value, the curves belonged to markedly decreased type. The changes of oxygen values of some patients during exercise test were individually different, showing that this exercise test reflected their comprehensive respiratory function. Prognosis was especially bad in patients with markedly decreased type, 8 of whom had died from respiratory failure within 2 years after the test. In conclusion, it can be said that this exercise test was effective in judging the pulmonary reserve function and the prognosis in recovered pulmonary tuberculosis patients, but more detailed investigations are necessary, especially in more COPD patients, for the understanding of the respiratory distress.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Blood gas changes during treadmill exercise in convalescents from pulmonary tuberculosis. 2. Clinical results]. 192 Oct 94

Clinical records and thoracic radiographs of 19 horses with a confirmed pathologic diagnosis of silicosis were reviewed. These horses had histories of varying degrees of chronic weight loss, exercise intolerance, and respiratory distress. At the time of presentation, two horses were asymptomatic. Ten horses were geldings and nine were female. The mean age of the 19 horses was 10.7 +/- 5.5 years. Fourteen horses were identified as being from the Monterey-Carmel Peninsula of midcoastal California. An abnormal, structured interstitial pulmonary pattern was identified on thoracic radiographs in each horse. The interstitial pulmonary changes were classified as miliary (13 horses), reticulonodular (4), or linear interstitial (2), and were best visualized dorsally and caudodorsally. In addition to the abnormal interstitial pulmonary pattern, areas of pulmonary consolidation were evident caudodorsally in seven horses. Other thoracic radiographic features included: hilar lymphadenopathy (4 horses), pleural effusion/thickening (4), cranial mediastinal lymphadenopathy (2), hyperinflation (1), and a discrete pulmonary mass (1). Necropsy findings in eight horses and results of lung biopsies in an additional five horses showed a diffuse, multifocal, granulomatous pneumonia with areas of pulmonary fibrosis. Cellular infiltrates included predominantly macrophages with intracellular and/or extracellular crystalline material, occasional lymphocytes, and giant cells. Similar cellular changes were also identified, during necropsy, in the hilar and tracheobronchial lymph nodes in each of the eight horses, although gross enlargement of the lymph nodes was present in only six horses. The radiographic and pathologic findings of these 19 horses are consistent with chronic or the accelerated forms of silicosis that are recognized in humans.
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PMID:Thoracic radiographic features of silicosis in 19 horses. 194 58

Four patients developed an acute respiratory distress syndrome characterised by clinical and radiological signs of pulmonary oedema, a protein-rich oedema, severe hypoxemia refractory to oxygen therapy, contrasting with normal left ventricular filling pressures and indicating increased permeability of the alveolo-capillary membrane, 24 to 72 hours after the onset of acute myocardial infarction. After having excluded the usual causes of the acute respiratory distress syndrome, the authors suggest that acute myocardial infarction, especially when extensive, may cause a lesion of the alveolo-capillary membrane by an unknown mechanism. Treatment consisted in mechanical ventilation with positive expiratory pressures in 3 cases and with continuous positive pressure during spontaneous respiration in the third patient and in relay with controlled ventilation in the other two. These techniques of ventilation improved the hypoxemia and led to complete cure in all cases without evolution to pulmonary fibrosis. In addition to mechanical ventilation, all patients were given systematic antibiotic therapy because of the possibility of an infectious etiology while waiting for the results of microbiological and serological testing and because of the high risk of superinfection which plays an essential part in the outcome of the condition. The immediate response to treatment was favourable in all cases. One patient died suddenly of cardiogenic shock two weeks after this episode. The other patients are still alive 39, 38 and 20 months after infarction. The importance of the diagnosis of the acute respiratory distress syndrome in the acute phase of myocardial infarction resides in its therapeutic implications which are quite different to those of cardiogenic shock.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute respiratory distress syndrome in the initial phase of myocardial infarction in adults]. 212 17

Various anomalies of pulmonary surfactant have been described in relation to acute respiratory distress syndromes, hypersensitivity lung disease and pulmonary sarcoidosis. Phosphatidylcholine (PC) is the essential phospholipid component of pulmonary surfactant. Cytidine diphosphocholine (CDP-choline) is an essential intermediary in the biosynthesis of PC. The authors studied two groups of patients: one group consisted of diffuse interstitial pulmonary fibrosis and the other consisted of pulmonary sarcoidosis with parenchymal involvement. They observed quantitative and qualitative abnormalities of the phospholipid fractions of surfactant and more particularly of PC. The finding of a marked decrease in this phospholipid, especially in the cases of pulmonary fibrosis, justified the study of the therapeutic effects of CDP-choline. After one month of treatment with this substance, at a dose of 1 g I.M. per day, the PC fraction had returned to normal and, at the same time, there was an improvement in the PaO2 at rest and after exercise. Long term administration of CDP-choline appears to be valuable in the maintenance of the phospholipid equilibrium of pulmonary surfactant and in the improvement of the quality of alveolar gas exchange.
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PMID:[Respiratory function and alveolar biological changes under the effect of CDP-choline in pulmonary interstitial pathology: pulmonary fibrosis and sarcoidosis]. 383 93

Plasma for fibronectin determinations was obtained from 39 neonates with uncomplicated respiratory distress syndrome (RDS) and from 15 infants with RDS who developed bronchopulmonary dysplasia (BPD). Tracheal lavage fibronectin and albumin concentrations were measured in 15 infants with RDS and 15 with BPD. Control plasma fibronectin values were obtained from 20 healthy preterm infants on days 1, 2, 3, 14, and 30 of life. Control tracheal lavage fibronectin and albumin concentrations were measured in 17 neonates of various gestational ages who required tracheal intubation for nonpulmonary indications. Mean plasma fibronectin concentrations from patients with RDS was 121 +/- 11 micrograms/ml on days 1, 2, and 3, versus control level of 163 +/- 12 micrograms/ml (P less than 0.01). Mean tracheal lavage fibronectin/albumin ratio was 3.8 +/- 0.6 ng per microgram of albumin on days 1 to 5 for infants with RDS, versus control level of 5.6 +/- 3.6 (P = NS). Tracheal lavage fibronectin/albumin ratio from patients with BPD was elevated at 16.3 +/- 5.0 ng fibronectin per microgram of albumin on days 14 to 21, and 23.6 +/- 7.4 on day 30 (P less than 0.05 versus control and and versus RDS days 1 to 10). Low plasma fibronectin concentrations early in RDS may contribute to the development of pulmonary capillary leak. High tracheal lavage fibronectin levels may foster the development of pulmonary fibrosis in patients with BPD.
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PMID:Tracheal lavage and plasma fibronectin: relationship to respiratory distress syndrome and development of bronchopulmonary dysplasia. 395 35


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