Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mortality experience of 5971 members of the British Diabetic Association (BDA) was followed-up for between five and eight years to mid-1973. Overall, 1207 deaths occurred compared with 778 expected from the mortality of the population of England and Wales in 1972. This excess of deaths was due almost entirely to diabetes mellitus and ischaemic heart disease. Deaths from cancer (128) were significantly fewer than expected (168), mainly because of a deficit in the number of deaths from cancers related to smoking (cancers of the buccal cavity and pharynx, oesophagus, respiratory system, and bladder). There was also a lower than expected mortality from chronic bronchitis and emphysema. Data on saccharin consumption by BDA members showed that more than half of them used saccharin tablets daily, with an overall daily intake of three to six tablets, depending on age and sex. Information on a small sample of survivors from the mortality study suggested that about 23% of them would have taken saccharin daily for 10 years or more and 10% for 25 years or more by the end of the follow-up. It was concluded that these relatively high levels of saccharin intake had not increased the risk of cancer in general among BDA members.
Br J Prev Soc Med 1976 Sep
PMID:Cancer mortality and saccharin consumption in diabetics. 97 34

Ventilatory function was studied by the authors in 43 subjects affected with obstructive respiratory disease. The research was performed both at rest and during two exercise tests -- 60 and 100 watts, respectively. The subjects were divided into three groups on the basis of tidal volume (at 30 1 ventilation) / vital capacity ratio. It was found that during muscular effort subjects with major impairment of spirometric indexes hypoventilated, whereas the opposite occurred in patients with lesser impairment. Moreover, subjects hyperventilating during muscular work were found to have brandypnea, whereas the opposite occurred in hyperventilating patients. It is suggested that progressing and worsening of obstructive emphysema lead to a relative hypoventilation during muscular work, which is due to an "inability" to increase the frequency of breathing.
Lav Um 1976 Sep
PMID:[Assessment of working capacity in a group of subjects affected with obstructive respiratory disease (author's transl)]. 102 80

In order to evaluate low serum alpha-1-antitrypsin level as a contributory factor of combined emphysema in silicotic patients, serum alpha-1-antitrypsin analysis was carried out in 80 patients with silicosis. Low serum alpha-1-antitrypsin level was found in 5 patients. Large opacities were observed roentgenologically in only 1 out of these 5 cases in contrast to 31 of the other 75 cases. Also the suggestive findings for the emphysema were showed in 4 of these 5 cases while such findings were found on their chest X-ray films in only 43 of the other 75 cases. FEV 1.0% below 50 were calculated in 3 of the 5 cases, on the contrary in 22 of the 75 cases. RV above 50% predicted value was showed by all the 5 low antitrypsin patients, in contrast to only 25 of other 74 cases. The silicotic patients with low serum alpha-1-antitrypsin concentration are most likely to have an association with a high incidence of complicated emphysema.
Tohoku J Exp Med 1975 Sep
PMID:Low serum alpha-1-antitrypsin level as a contributory factor of combined emphysema in silicosis. 108 Dec 85

Alpha1-antitrypsin deficiency is a genetic model that predisposes to pulmonary emphysema or a form of hepatic cirrhosis in man. The antitrypsin protein protects the tissues from proteolytic digestion by lysosomal proteases from inflammatory cells. The three causes of antitrypsin deficiency demonstrated to date are: 1) A defect in synthesis and release of the Z variant from the liver. 2) Presence of an inactive (null) gene for antitrypsin production, and 3) Increased lability of certain variants associated with the in vivo degradation of antitrypsin.
Pathol Biol (Paris) 1975 Sep
PMID:The multiple causes of alpha1-antitrypsin deficiency. 110 Nov 53

The authors studied 79 patients with chronic obstructive lung disease. (COLD) (FEV1/VC less than 70%). Patients with chronic asthma were excluded from the series. These patients with COLD were divided up into 2 groups, depending on radiological and clinical criteria: (1) Type A, primary emphysema, 24 patients; (2) Type B, chronic bronchitis, 49 patients. 6 patients of type X (intermediate type) were excluded. Their respiratory function tests were studied together with clinical and radiological findings and blood gases. Furthermore, were studied in each patient, the antitrypsic activity and the serum concentrations of alpha-1-antitrypsin and phenotype Pi. Group A were, on average, more obstructive than group B. The ratio FEV1/VC was 31% +/- 7% in group A, against 46% +/- 13% in group B. The serum antitrypsin activity and the serum concentration in alpha-1-AT were on average close to normal in both groups. However, group A was divided up into two populations: a small population with a low concentration of alpha-1-AT, and a large population with normal alpha-1-AT. A study of the incidence of various phenotypes in groups A and B showed a significantly higher frequency of phenotype ZZ in group A (12.5%) than in group B (10%). All ZZ subjects were of clinical type A. There was no significant difference in the incidence of other phenotypes encountered. Serum alpha-1-antitrypsin concentration was very low in 3 ZZ patients. One case with phenotype SZ and one MM showed intermediate levels. The authors emphasize the low percentage of cases of pulmonary emphysema which may be explained by an alpha-1-antitrypsin deficiency. Nevertheless, this preliminary report should be completed by a study of a larger sample of patients with COLD with control of the phenotype.
Pathol Biol (Paris) 1975 Sep
PMID:[Phenotype Pi and alpha 1 antitrypsin deficiency in types A and B chronic obstructive bronchopneumopathies]. 110 Nov 55

Intraruminal and intravenous administration of 3-methylindole (3MI; skatole) caused interstitial pulmonary edema and emphysema in cattle. In 3 adult heifers given the intraruminal dose of 0.2 g of 3 MI per kilogram of body weight, clinical signs of respiratory disease appeared between 6 and 12 hours after dosing, and death due to pulmonary edema and emphysema occurred at 33, 69, and 72 hours. The mean plasma concentration of 3MI became maximal (18.5 mug/ml) at 3 hours and then decreased to low concentrations by 48 hours. In 2 heifers given an intraruminal dose of 0.1 g of 3MI/kg, clinical signs developed, but they did not die during the 96-hour experiment. The mean plasma concentration of 3 MI became maximal (16.8 mug/ml) at 3 hours and decreased to 1.6 and 0.4 mug/ml at 12 and 36 hours, respectively. At necropsy of the heifers, the lung were large, firm, dark red, and heavier than normal. Diffuse pulmonary edema was the predominant change in cattle which died early, and interstitial emphysema was more severe at later stages of the disease. During the early stages, alveoli were overdistended, and a few more ruptured. Most alveolar spaces were filled with proteinaceous residue, but the alveolar septums were smooth and of normal thickness. At later stages, proliferation of alveolar cells was observed, and alveolar septums were thickened. In 3 cows given 0.06 g of 3MI/kg by jugular infusion, clinical signs appeared in all cows, and 1 cow died of pulmonary edema and emphysema 56 hours after the infusion was started. Severe pulmonary lesions seen in all of the cows given a 3MI infusion were similar to those in the cows given an intraruminal dose of 3MI. The mean plasma concentration of 3MI increased to 10.7 mug/ml at 9 hours after starting the infusion and decreased to 0.5 mug/ml at 18 hours. The results indicate that 3MI, a product of ruminal tryptophan fermentation, can cause pulmonary edema and interstitial emphysema in cattle and support the hypothesis that 3MI is the causative agent in tryptophan-induced pulmonary disease.
Am J Vet Res 1975 Sep
PMID:Pulmonary edema and emphysema in cattle after intraruminal and intravenous administration of 3-methylindole. 116 73

Five Hereford cows were given an intraruminal dose of L-tryptophan (0.35 g/kg of body weight), and 2 cows were used as controls. Of the 5 treated cows, 3 developed clinical signs of interstitial pul monary edema, and emphysema and severe pulmonary lesions were seen at necropsy after 96 hours. Another cow developed moderate clinical signs and pulmonary lesions, and the remaining cow had few clinical signs and mild pulmonary lesions. The severity of clinical signs in each cow was related to the severity of pulmonary lesions at necropsy. The 3-methylindole (3MI) was present in ruminal fluid and plasma within 6 hours after administration of tryptophan, and the concentrations increased to 3.0 and 9.0 mug/ml within 12 to 24 hours. Severity of pulmonary lesions was related to maximal concentration and duration of 3MI in the plasma. At necropsy, gross lesions were characterized by diffuse, pulmonary edema and interstital emphysema; and the lungs were dark red, firm, and heavier than normal. Predominant microscopic changes included accumulation of proteinaceous residue, hypertrophy and hyperplasia of alveolar lining epithelium, thickening of alveolar septums, and emphysematous thickening of interstitial tissues. These changes were similar to previously reported 3MI-induced pulmonary lesions. The presence of 3MI in ruminal fluid and plasma after administration of tryptophan and the relationship between concentration of 3MI and severity of clinical signs indicate that 3MI is the principal metabolite of ruminal fermentation which leads to the development of acute pulmonary edema and emphysema in cattle given tryptophan.
Am J Vet Res 1975 Sep
PMID:Ruminal and plasma concentrations of 3-methylindole associated with tryptophan-induced pulmonary edema and emphysema in cattle. 116 74

To investigate the effect of a papain-induced emphysema-like condition on pulmonary absorption of drugs, rats were exposed to either papain aerosol or distilled water aerosol (control) intermittently for 2 wk, and rates of drug absorption from damaged and control lungs were compared. To measure absorption rates, 0.1 ml of drug solution (0.1-10 mM) was administered through a tracheal cannula to anesthetized animals, and after various times lungs were assayed for unabsorbed compound. In absorption experiments with the lipoid-insoluble compounds, mannitol, p-aminohippuric acid, and procaine amide ethobromide, all three drugs were absorbed from the lungs about twice as rapidly in papain-treated rats as in control. In contrast, procaine amide, a relatively lipoid-soluble drug, was absorbed at the same rate in both control and papain-treated animals. The results suggest that papain-induced lung damage increases the porosity of the pulmonary epithelium.
Proc Soc Exp Biol Med 1975 Sep
PMID:Effect of papain-induced emphysema on permeability of rat lung to drugs. 116 92

A single dose of crystalline, porcine pancreatic elastase injected intratracheally into hamsters induces widespread alveolar enlargement with subpleural bullae. A uniformly severe lesion is consistently induced by 0-2 mg elastase per 100 g body weight and with negligible mortality. Compared with controls, which showed no lesion, elastase-damaged lungs show a highly significant (P less than or equal to 0-001) increase in alveolar size and a decrease in internal surface area. Taken with the associated physiological abnormalities, these findings closely simulate human emphysema of the panlobular (panacinar) type. Histologically it appears that elastase converts the fine elastic fibres in alveolar walls and pleura into thickened, nodular fibres which may also be broken along their length. With higher doses of elastase, i.e., 0-5 mg/100 g body weight, many pulmonary arteries showed segmental loss of inner and outer elastic laminae, usually with thrombosis on the overlying endothelium. The mechanism of this thrombosis is unclear. These experiments suggest that damage to elastic fibres may be an important element in the development of human panacinar emphysema, and that the damage could be one pathogenetic mechanism which produces damage of elastic fibres.
J Pathol 1975 Sep
PMID:The pathology of elastase-induced panacinar emphysema in hamsters. 119 57

We have reviewed the spectrum of gaseous densities in the soft tissues secondary to a perforated viscus. All patients presented late and most were elderly. The most common surgical procedure was diversion of the fecal stream proximal to the perforation. In our series 4 of 7 patients died in the immediate postoperative period. Knowledge of the mechanism and differential diagnosis of this entity will prevent overlooking this possibility, as occurs too frequently, particularly with subcutaneous emphysema of the leg.
Am J Roentgenol Radium Ther Nucl Med 1975 Sep
PMID:Perforated viscus presenting with gas in the soft tissues (subcutaneous emphysema). 120 Feb 13


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