Tài liệu Interview chronic obstructive pulmonary disease (copd)

Chronic obstructivepulmonary disease Chronic Obstructive Pulmonary Disease, or COPD, encompasses a group of airway diseases of which the predominant defect is difficulty in getting air out of the lungs. That is what is meant by the term obstructive. The main disorders are chronic bronchitis, emphysema and bronchial asthma, less commonly cystic fibrosis and bronchiectasis. Chronic obstructive pulmonary disease is a very common condition and it is the most common cause of absenteeism from work and social disability payment. Peter Howard, Professor of Respiratory Medicine at the University of Sheffield, England, talked about the risk factors for chronic obstructive pulmonary disease and discussed current and future approaches to its treatment. The risk factors, Pr Howard said, were essentially environmental, but genetic factors could also be important. The major risk factors are the smoking of cigarettes, but atmospheric pollution and occupational environmental pollution with dust and fume is also of great importance. And the latter, at least in the United Kingdom, is of increasing importance at the moment as smoking in the male population is declining and the Clean Air Acts are forcing a very much cleaner general environment. The major risk factor is cigarette smoking There has always been an urban factor in chronic bronchitis, in that it’s very much more common as a disease in industrial manufacturing towns. In a town like Sheffield for example, where I come from, there’s been an extraordinarily high incidence of chronic bronchitis and its terminal phases of respiratory failure. But we still have a lot to do to clean up the working environment in manufacturing companies. There’s also a genetic factor for some cases of emphysema. Some families are deficient in a protective enzyme in the lungs called alpha-1-antitrypsin. And this is a very interesting new development because it has been recently possible to synthesize this enzyme and to inhale it through a nebulizer to replace the deficiency. For bronchial asthma there are familial factors and there are also environmental factors for allergic varieties such as pollens and various dusts to animals such as dogs and cats, horses, house dust mite and feathers. These sorts of things are risk factors for allergic asthma and there’s a familial predisposition. In the early phases of chronic bronchitis and emphysema, the treatment is based on combatting infection and improving airway function with bronchodilator drugs. The treatment of chronic bronchitis and emphysema when it becomes symptomatic is to treat infection. And the best way of treating infection is to give antibiotics for the individual exacerbations as they occur. It has been shown many times that this is the best policy rather than giving continuous antibiotics throughout say a winter season. The next treatment is to achieve whatever bronchodilatation you can. Chronic bronchitis and emphysema are characterized by a progressive decline of spirometric airway function. However, all patients have a certain amount of reversibility to bronchodilator drugs. That is that you can improve the spirometric tests by the administration of these compounds. The amount that can be achieved is very variable from one patient to another. It is for this reason that at the presentation it’s worth having a full respiratory function evaluation. This will guide therapy as to how much bronchodilatation is required. It’s very much more common in industrial manufacturing towns In the early phases, simple metered dose inhalers of beta-2-agonists such as salbutamol, terbutaline or fenoterol are very useful. More recently it has been realized that the doses of beta-2-agonists or the alternative compound ipratromium bromide that can be achieved through metered dose inhalers does not necessarily give full benefit. And that by increasing the dose either through spacer devices, nebuhalers or even nebulizers in a number of patients you can get added benefit. And this is particularly so as the breathlessness increases and the severity of airways obstruction develops. In advanced disease, treatment is much more difficult and the critical question is whether declining airway function can be prevented from progressing to end-stage respiratory failure. There were some interesting new developments in this area, Pr Howard commented. The question arises as to whether in fact you can, even in advanced disease, reverse the airways obstruction or even arrest the decline. And there’ve been a number of new developments, or new thoughts in this area which are not yet fully established treatment but are quite interesting. In the early phases, a small number of bronchitic patients have benefit from corticosteroid therapy, but it’s a very small number. There’s been some question as to whether corticosteroids given by oral tablets or through aerosols will reduce the decline of airway function by combatting airway inflammation, which is a characteristic feature of the disease. Here medical opinion is very sharply divided. Medical opinion is divided on the usefulness of corticosteroids The Dutch feel that corticosteroids given orally in a dose of 10mg of prednisolone daily will help to stem the decline of airway function. In other countries, particularly in the UK, we haven’t been able to observe such an effect. But there are a number of studies, particularly in the United States, at the present time to look at this point further. There are one or two other interesting developments on the horizon as well to try and prevent the decline of airway function, one of which is to use a substitute alpha-1- antitrypsin. The mechanism of emphysema is now considered to be due to an antagonism of this important enzyme in the alveolar space by tobacco smoke. This antagonism is more severe if the patient is congenitally deficient. But most patients are not congenitally deficient of the enzyme. But, since the smoking antagonizes it, would it be possible by the use of a replacement aerosol to prevent the effects of smoking in causing emphysema? The answer to this question cannot yet be given. However, it has been shown that it is possible to aerosolize a genetically engineered alpha-1-antitrypsin and to increase serum levels of this enzyme. This is really quite an exciting development because it could mean that the progression of emphysema could be reduced or even stopped. It will be a number of years before this question can be answered. The only other difficulty is that the replacement enzyme at present is extraordinarily expensive and better means of producing it, if it is shown to be efficacious, will have to be found. Genetically engineered alpha 1antitrypsin is an exciting development Another approach is to use a compound such as ambroxol hydrochloride which replaces and stimulates the production of surfactant in the alveolus. The dosages of this compound which have been used so far, have been too small, but it illustrates that a number of approaches are being tried in order to reduce the decline of airway function in this disease. Lung transplantation is an option for selected patients. There are still many problems to be overcome Pr Howard warned and the technique is still very much in an early phase. Lung transplantation is a very active consideration for patients who are serious respiratory cripples below the age of 60 years. Lung transplantation is very much in its early phases. A number of units in each European country are transplanting lungs. This is done in several ways: either as a total heart-lung transplant, as a dual lung transplant or as a single lung transplant. It’s not possible at this moment to decide for pulmonary disease the best option. But clearly in view of the difficulty of getting enough donor lungs, the single lung transplant option offers the greatest possibility of transplanting the greatest number of patients. Experiments have been done with a number of patients with cystic fibrosis and with bronchial asthma and just one or two with bronchiectasis. Lung transplantation is still in an early phase Technically, it is now possible to achieve lung transplantation without too much difficulty. There is however a very great problem of controlling the rejection of the tissue in the immediate post-transplant phase. The great problem is bronchiolitis. Balancing the immunosuppression therapy is very difficult. It requires repeated bronchoscopy, repeated lung biopsy to monitor the tissue rejection. Only 20 to 30 % of transplanted single lungs survive to give the patient a reasonable standard of life for 2 or 3 years. The remainder are rejected to a greater or lesser degree. It is very difficult to put in a further donor lung because of the poor availability of material if a single lung is rejected. One can only consider that transplantation at the present time is therefore an experimental science but one can hope that in the future there will be developments and the whole science will become a lot easier.