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 immunological aspects of allergic disorders of the lung (Type I-IV by Gell and Coombs, drug hypersensitivity, auto-immune diseases) and non-allergic lung diseases (emphysema in alpha 1-antitrypsin deficiency, bronchial carcinoma) are described. The short review is closed with remarks about the immunological defence in the bronchial mucosa.
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PMID:[Immunological aspects in lung diseases (author's transl)]. 13 14

It is well known that incidence of chronic obstructive lung disease in adult patients with alpha 1-antitrypsin deficiency (ATD) is high. Adult carriers of this genetic trait with cirrhosis of the liver, and also with fibrosis of the liver and hepatoma, have been reported. A causal relationship between ATD and liver lesions has been suspected. In most cases liver disease has been recognized at post morten, - in a few cases, however, intra vitam, when severe symptoms of the liver disease had become apparent. The case of a 59 year-old patient is reported with PIZZ-homozygous ATD, moderate pulmonary emphysema and with marked portal fibrosis and focal transition in cirrhosis of the liver without any sequelae. The clinical course has been rather benign so far.
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PMID:[Alpha 1-antitrypsin deficiency, liver cirrhosis and pulmonary emphysema (author's transl)]. 16 Apr 81

The cytoplasmic bodies in hepatocytes thought to indicate possession of the Z allele for alpha 1-antitrypsin deficiency were found in necropsy in 10 of 64 adults with cirrhosis, four of nine with hepatic fibrosis, and four of 15 with hepatocellular carcinoma. They were also found in six of 76 adults with severe panacinar emphysema, and in four of a control series of 110 adults with neither emphysema nor liver disease. The association of the bodies with each of the three liver diseases was statistically significant, but the association of the bodies with emphysema was not. It is considered probable that heterozygous (PiMZ) alpha 1-antitrypsin deficiency is associated with an increased incidence of cirrhosis, hepatic fibrosis, and hepatocellular carcinoma.
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PMID:Alpha-1-antitrypsin bodies in the liver. 19 72

Chowdhury and Louria [1] reported that cadmium could reduce in vitro the concentration and the trypsin inhibitory capacity of plasma alpha 1-antitrypsin. They suggested that this could explain the emphysema observed in some workers exposed to cadmium. Using the same experimental approach as these authors, we could not reproduce their observations. Furthermore, in vivo results obtained on workers excessively exposed to cadmium during more than 20 years and exhibiting obvious signs of chronic cadmium intoxication did not reveal a decrease in the concentration and the activity of plasma alpha 1-antitrypsin.
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PMID:alpha 1-antitrypsin in cadmium toxicity: an evaluation of its suggested role. 20 88

Methods are described for the covalent attachment of succinoyl-Ala-Ala-Pro-ValCH2Cl, an active site-directed inhibitor of human leukocyte elastase (EC 3.4.21.11), to microspheres of human albumin. The insertion of side arms of various lengths revealed that maximum inhibition of this enzyme was obtained when the spacer arm was at least 24.3 A in length. Approximately 30 molecules of the inhibitor could be attached to each molecule of albumin. Such derivatized microspheres were capable of inhibiting approximately one mole of elastase per mole of albumin, which is comparable to the inhibitory activity of alpha 1-antitrypsin. Experiments in vivo in which rats were injected intravenously with radiolabeled microspheres to which the inhibitor had been attached showed a rapid and exclusive uptake by the lungs. About 40--50% of the injected microspheres subsequently remained in the lungs with a half-life of approximately 17 days. These derivatized microspheres thus appear to offer promise as a therapeutic agent for emphysema.
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PMID:Albumin microspheres as carrier of an inhibitor of leukocyte elastase: potential therapeutic agent for emphysema. 28 51

Eriksson's method was analysed and an attempt was made to determine the probability of the occurrence of phenotypes predisposing to emphysema and obstructive catarrhs, when low alpha-1-AT values were found using gelatinous film or immunochemical methods. The authoresses propose a three-stage system for the detection of all those susceptible to emphysema.
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PMID:[Laboratory procedures in the detection of deficiencies and the determination of alpha 1-antitrypsin phenotypes in the blood serum]. 31 59

alpha 1-antitrypsin (alpha 1AT) of the Pi type Z is associated with two diseases: pulmonary emphysema and cirrhosis of the liver. We report 23 families with both parents heterozygous for the PiZ allele, characterized from our own analysis and from world literature sources. All families were identified through members expressing disease. From the extended pedigrees, 18 backcross families (parents with Pi types MM and MZ) were identified. Analysis of the backcross families reveals a significant increase in Pi MZ offspring (.73) among families where the male is heterozygous. The distortion is not detected among families where the female is heterozygous. Among the matings where both parents are heterozygous, we found 0.43 Pi ZZ from families where one or more members expressed hepatic cirrhosis, and 0.40 Pi ZZ for total families studied. This contrasts to the 0.25 Pi ZZ expected, but is consistent with the distortion observed in backcross matings. The implications of various statistical approaches are discussed, and we point out why our findings differ from previous reports. We suggest a possible biological explanation residing in the fertilization process.
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PMID:Segregation distortion of the alpha 1-antitrypsin Pi Z allele. 31 54

Leukocyte elastase and alpha 1-antitrypsin have been implicated in the pathogenesis of pulmonary emphysema. The relationship between these proteins has been studied in sputum both qualitatively and quantitatively in bronchitic patients with and without chest infections. Leukocyte elastase was found in 75% of the noninfected samples but was enzymatically inactive, suggesting complete inhibition. During infection, leukocyte elastase and alpha 1-antitrypsin concentrations increased, although the enzyme was only partially inactivated. The proportion of alpha 1-antitrypsin present as "complex" was smaller in the presence of infection, suggesting damage of the protein by excess enzyme.
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PMID:Alpha,-antitrypsin and leukocyte elastase in infected and noninfected sputum. 31 41

There is now overwhelming evidence that lung destruction resulting in emphysema is largely due to enzymatic action on pulmonary connective tissues, mainly elastin. These enzymes are probably derived from neutrophil polymorphonuclear leucocytes and alveolar macrophages. Arguments are advanced to show that release of these enzymes is related to cigarette smoking. This explanation for the pathogenesis of emphysema is compatible with the distribution of the disease within the lung noted in epidemiological studies. If this conclusion with regard to the role of cigarette smoking is correct it must follow that, apart from patients with alpha 1-antitrypsin deficiency, emphysems is a disease which could be almost entirely eliminated if the smoking habit was abandoned.
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PMID:Aetiology of emphysema. 31 6

Beagle dogs exposed to cigarette smoke for 600 d experience a significant change in pancreatic elastase levels, as measured in tissue homogenates, compared with their sham-exposed controls. Greater elastase activity was found in the high-nicotine cigarette smokers than in the low-nicotine cigarette smokers. Levels of serum alpha 1-antitrypsin, an antiprotease capable of complexing the excess elastase, were also investigated. Animals smoking high-nicotine cigarettes had significantly lower serum alpha 1-antitrypsin activities than controls. Low-nicotine smokers showed alpha 1-antitrypsin activities that were not significantly different from those of controls. The importance of these observations is reinforced by a number of studies suggesting that proteases, their inhibitors, and an imbalance thereof may be related to the onset of neoplastic lesions. Studies have indicated that antiprotease levels follow the patterns of Mendelian inheritance. Severe deficiency states predispose human subjects to emphysema. A similar relationship may exist between antiprotease levels and susceptibility or resistance to neoplasms of the pancreas, a concept that deserves investigation in light of the findings reported here.
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PMID:Pancreatic elastase and serum alpha 1-antitrypsin levels in beagle dogs smoking high- and low-nicotine cigarettes: possible mechanism of pancreatic cancer in cigarette smokers. 31 12


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