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)

A quantitative study of alpha-1-antirypsin and alpha-2-macroglobulin in the sputum showed an increase in both during attacks of asthma and in patients with chronic obstructive bronchitis. The levels were much lower in asthma patients during remissions, in emphysema and in patients with chronic simple bronchitis, without associated bronchospasm. The parallel variations in levels of alpha-1-antitrypsin, albumin and transferrin in the sputum, contrasts with the course of secretory IgA and are in favour of a transudation process of alpha-1-antitrypsin across the respiratory mucosa.
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PMID:[Quantitative study of alpha 1 antitrypsin and alpha 2 macroglobulin in the sputum]. 5 36

We describe a patient in whom selective IgA deficiency and homozygous alpha1-antitrypsin deficiency were discovered. Clinically, the patient suffered from chronic sinopulmonary infections, destructive emphysema, and bronchiectasis. The interrelation of IgA and alpha1-antitrypsin was studied. Twenty-three alpha1-antitrypsin-deficient sera were screened for IgA deficiency. None of these sera were deficient in IgA. Fifteen IgA-deficient sera were screened for alpha1-antitrypsin deficiency. In this group, three patients were found to have variant alpha1-antitrypsin phenotypes. Respiratory infections were a prominent complaint in all three of these patients, with bronchiectasis in two patients. We believe that the combination of IgA and alpha1-antitrypsin deficiencies should be considered in the evaluation of any patient with idiopathic bronchiectasis.
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PMID:Selective IgA deficiency and Pi ZZ-antitrypsin deficiency. Association with recurrent sinopulmonary infections, emphysema, and bronchiectasis. 30 13

Fifty-three patients with bronchiectasis (chronic bronchial suppuration) of unknown cause, in whom the chronic production of purulent sputum was the prominent clinical feature, were investigated for possible immunological abnormalities. They were compared with two control groups comprising 50 patients with chronic bronchitis and emphysema and 33 patients with bronchial asthma. Forty-two patients with bronchiectasis(79%) had at least one abnormality of immunoglobulin, usually elevation of IgA, IgG or IgM. Eight patients had all three immunoglobulin levels raised and this was related to severity of disease. Similar increases in immunoglobulin levels were observed in the control groups, but the frequency and severity of these changes were significantly greater in the bronchiectasis patients. Two patients had IgA deficiency. There was a very high prevalence of rheumatoid factor (52%) and an increased prevalence of antinuclear factor (10%) in the bronchiectasis patients compared with the control groups. The presence of these autoantibodies did not correlate closely with severity of disease. Ten patients with bronchiectasis (19%) had one or more autoimmune disorders, and the association of severe bronchiectasis, Hashimoto's thyroiditis and pernicious anaemia in one patient is described in detail. The immunoglobulin changes, high incidence of autoantibodies and association with autoimmune disorders raises the possibility that in some patients with bronchiectasis (chronic bronchial suppuration) of apparent unknown cause abnormal immune mechanisms may be important in causing or perpetuating the condition.
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PMID:Immunological abnormalities in bronchiectasis with chronic bronchial suppuration. 30 9

In patients with chronic cor pulmonale caused by pulmonary emphysema, circulating autoantibodies against the heart tissue were investigated by the HA and HI techniques using the myocardium as antigen. Quantitative analysis of serum IgG, IgA and IgM were carried out by use of the radial immunodiffusion method. These results were compared with clinical findings, especially cardiopulmonary hemodynamics and pulmonary function tests and with the prognosis. Circulating anti-heart antibodies were found in 15 of 29 (51.7 per cent) patients with chronic cor pulmonale. The titers of circulating anti-heart antibodies indicated a good correlation with pulmonary hypertension, hypoxia and respiratory impairment. Furthermore, a good correlation was noted between anti-heart antibody titers and the serum IgG level. Five of 15 (33.3 per cent) patients with positive results for anti-heart antibodies died, while one of 13 (7.7 per cent) with negative results died. In this investigation, circulating anti-lung antibodies were also searched in sera from patients with chronic cor pulmonale, but they showed no cross reaction with anti-heart antibodies, of which the specificity was found in the patients. These data could be utilized in evaluation and discussion of the pathophysiological findings of the patients with chronic cor pulmonale.
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PMID:Anti-heart antibodies in patients with chronic cor pulmonale. 112 Oct 59

In patients with chronic obstructive pulmonary disease, quantitative analysis of serum IgG, IgA and IgM were carried out by use of the radial immunodiffusion method. The concentration of IgE in sera was also determined by the radioactive radial immunodiffusion method. The mean value of serum IgG level in the group of cor pulmonale was higher than that in groups of emphysema, asthma and normal subjects. The mean value of serum IgA level was higher in two groups of cor pulmonale and emphysema than in the group of asthma and of normal subjects. There was no difference of serum IgM levels between these four groups. The mean value of serum IgE in the group of allergic asthma was higher than that in the group of non-allergic asthma or normal subjects and an elevated serum IgE level was also found in patients with cor pulmonale. Findings of this study suggested that the raised level of serum IgG in patients with chronic cor pulmonale might reflect production of antiheart antibodies against cardiac tissue.
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PMID:Quantitative determination of serum immunoglobulins in chronic obstructive pulmonary diseases with special reference to cor pulmonale. 125 20

We studied the pulmonary diseases which had developed as consequent deformities after healing of tuberculosis, which we called tuberculosis sequelae. Results are described as follows. 1. The frequency of tuberculosis sequelae was about 6% in the patients with pulmonary diseases admitted to our hospital. 2. 93 cases of them consisted of 4 groups, which were 39 of repeated bacterial infection of lower respiratory tract, 23 of pulmonary aspergilloma, 13 of atypical mycobacteriosis and 28 of chronic respiratory failure. 3. Patients with tuberculosis sequelae were distributed more in the younger age group than others with resembled pulmonary diseases. The men to women ratio was about 2:1. Patients with pulmonary aspergilloma were younger than those with atypical mycobacteriosis. 4. Death rate in tuberculosis sequelae was about 5% per year. 46% of patients with atypical mycobacteriosis and 44% with chronic respiratory failure died within 4 years. 5. In chest X-ray findings, fibrosis and shrinkage of the lung, compensatory pulmonary emphysema, deformity or dilatation of bronchi, bulla formation and residual tuberculous cavities were recognized in 40 to 65% of the cases. Severe pleural thickness or past thoracoplasty were frequently recognized in the patients with chronic respiratory failure. All the patients with pulmonary aspergilloma had one or more residual cavities. 6. The frequency of systemic complications was not more than in the control population matched by age. Comparatively, serum IgG and IgA were elevated and PHA-induced lymphocyte activation was not lowered in the patients with pulmonary aspergilloma and atypical mycobacteriosis. From these results, the main factor in the development of tuberculosis sequelae seemed to be local defects of the chest.
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PMID:[Tuberculosis sequelae: clinical aspects]. 207 59

Nephelometric assays (LN) are known since several years ago. Laser beam immunonephelometric analysis (He-Ne: 640 nm), are a sophistication of the spectrophotometers. Nephelometry was the first method to make use of narrow-angle light scattering and a laser beam. It was made 2500 +/- 200 determinations of human fluids for IgG, IgA, IgM, C3 and C4, both LN and RID (radial immunodiffusion method). Human patients had the following characteristics: 18-55 years old, both sexes and with different pulmonary pathologies (Bronchial asthma, Bronchitis, Tuberculosis, Emphysema, Fibrosis, Extrinsic allergic alveolitis). We found a greater sensitivity and a shorter analysis time for LN than for RID. On the other hand, Nephelometry gave different values to the radial immunodiffusion method for all the proteins evaluated.
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PMID:[Laser nephelometry. A better methodology?]. 212 76

Human and bovine respiratory syncytial viruses resemble each other closely. During annual winter outbreaks, they cause similar respiratory tract disease in infants and calves. The disease is most severe in children and calves between 1 and 3 months old, when maternal antibodies against the virus are usually present. Reinfections, which are common, are accompanied by progressively milder illnesses in children, but are symptomless in calves. Because maternal antibodies suppress serum and mucosal antibody responses of all isotypes, the development of a vaccine that is effective in young children and calves with high levels of maternal antibodies has been severely hampered. Although virus administered intranasally to young calves with maternal antibodies does not evoke antibody responses, it can prime these calves for a protective memory response upon reinfection. Protection appears to be associated with the capacity to mount a mucosal memory IgA response. There are several indications that one or more immunopathologic mechanisms contribute to the disease. An Arthus reaction (type III) may have a role in the pathogenesis, because activated complement may cause most of the pathologic lesions, including edema and emphysema in uninfected parts of the lung. Lungs from calves with severe or fatal disease have depositions of complement component C3 and a low histamine content. The most immunogenic and protective antigen of the virus is the fusion (F) glycoprotein, which evokes a strong antibody response and is a target for cytotoxic T cells. On the F protein, epitopes that induce neutralizing and non-neutralizing antibodies, both of which may enhance complement activation, were identified. Immunity to the F protein may have beneficial and harmful effects.
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PMID:Immunity to human and bovine respiratory syncytial virus. 219 33

Thirty patients of chronic obstructive pulmonary disease (COPD; all smokers) and an equal number of controls (15 smokers) were studied. The COPD patients were further divided into group A (predominantly emphysema) and group B (predominantly bronchitis) of 15 patients each. Serum and sputum IgG, IgA and IgM and serum C3 and C4 were estimated. IgG, IgA, IgM and C3 and C4 were similar in smoker and non-smoker controls. Mean (+/- SD) serum IgG (IU/ml) was significantly higher in COPD patients (207.78 +/- 62.73) than in control (177.25 +/- 43.5; P less than 0.05), serum IgA (IU/ml) was also significantly higher in COPD (205.04 +/- 46.56) than in control (108.21 +/- 33.3; P less than 0.01). IgM was similar in the 2 groups. Sputum IgA (IU/ml) was higher in COPD (4.68 +/- 3.51) than in control (2.25 +/- 1.03; P less than 0.05). IgG and IgM were similar in the 2 groups. Both serum C3 (IU) and C4 (IU) were lower in COPD patients (C3 = 95.9 +/- 33.11, C4 = 113.6 +/- 62.4) than in control (C3 = 167.3 +/- 25.42, C4 = 205 +/- 76.5; P less than 0.05). Serum IgA in type B COPD (212.25 +/- 50.06) was higher than in type A (197.52 +/- 43.3; P less than 0.05) IgG and IgM were similar in these 2 groups. In COPD patients, immunoglobulins were either normal or higher indicating that deficiency of immunoglobulin is not a predisposing factor in development of COPD. Similar immunoglobulin values in smoker and nonsmoker controls indicated that smoking was not the cause of rise of immunoglobulins in COPD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alterations in immunoglobulin & complement levels in chronic obstructive pulmonary disease. 222 68

To investigate the influence of smoking on the aging immune system, the following parameters were determined in elderly smokers and non-smokers: presence of emphysema; absolute number of leucocytes, lymphocytes, T cells and B cells bearing membrane-bound IgG; serum IgG, IgA, IgM levels, occurrence of rheumatoid and antinuclear factors, and natural antibody level (against different bacteria). Ultrastructural disorders in lymphocytes were also investigated. The number of leucocytes, the levels of serum IgA, and the prevalence of autoantibodies were higher, and the natural antibody level was lower in smokers than in non-smokers. Giant mitochondria and cytoplasmic disorders were found more frequently in smokers than in non-smokers, and in an even higher rate in smokers with emphysema. These findings suggest that smoking may accelerate the appearance of age-dependent (especially disease-related) immunological changes.
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PMID:The effect of smoking on peripheral blood lymphocytes and on some immunological parameters in old age. 239 75


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