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Mortality studies of males and females with chronic obstructive pulmonary disease (COPD) and asthma have suggested that females have a poorer prognosis than males, but the results are either not unanimous or based on poorly characterised patients. The current study analysed the mortality of 279 asthma patients and 869 COPD patients, who were seeking pension due to disability, and compared mortality rates with expected rates derived from the general population. The mean follow-up period was 13.3 yrs (range 2.5-22.4 yrs) during which time 96 (34.4%) and 671 (77.2%) deaths were identified among asthma and COPD patients, respectively. The average age at study entry was 46.8 and 56.6 yrs, and the average forced expiratory volume in one second (FEV1) was 68.8 and 44.1 % predicted in the two diagnostic groups. After adjustment for predictors of survival (age, FEV1 % predicted, chronic bronchitis, body mass index, smoking status, oral prednisolone, ischaemic heart disease, and cor pulmonale), the relative risk of death was 1.21 (95% confidence interval: 0.77-1.89) and 0.98 (0.83-1.16) in females compared with males, in asthma and COPD patients, respectively. The standardised mortality rate (SMR) for males was 1.54 (1.10-2.09) and 2.7 (2.5-3.0), and for females 1.91 (1.44-2.49) and 4.8 (4.2-5.4), in asthma and COPD patients, respectively. Direct comparison of the SMR of males and females showed that females had higher mortality than males, with a rate ratio of 1.24 (0.82-1.84) and 1.8 (1.5-2.0), in asthma and COPD patients, respectively. Poisson regression analysis with control for the confounders did not change this result. Females and males with the same level of obstructive lung disease appear to have the same level of mortality. However, using standardised mortality rates, females have a higher mortality than males, suggesting that the protective effect of being female is lost in chronic obstructive pulmonary disease patients.

Patients with severe hereditary alpha1-antitrypsin deficiency (alpha1-ATD) face a high risk of developing emphysema at a young age. Intravenous augmentation therapy with purified human alpha1-antitrypsin (alpha1-AT) is now available. However, a controlled trial to show its efficacy has never been carried out. The aim of this study was to compare the decline in forced expiratory volume in one second (deltaFEV1) between Danish patients who had never received augmentation therapy and German patients treated with weekly infusion of alpha1-AT. From the files of the Danish alpha1-ATD register, 97 exsmokers, with a PiZ phenotype and for whom results of at least two lung function measurements with an interval of at least 1 yr were available, were identified. From a German group of patients treated with weekly infusions of alpha1-AT, 60 mg x kg(-1) body weight, 198 exsmokers, with biannual lung function measurements were identified. The deltaFEV1 was compared between the two treatment groups by random effects modelling. The deltaFEV1 in the treated group was significantly lower than in the untreated group, with annual declines of 53 mL x yr(-1) (95% confidence interval (95% CI) 48-58 mL x yr(-1)) and 75 mL x yr(-1) (95% CI 63-87 mL x yr(-1)), respectively (p=0.02). The two groups differed with respect to gender and initial FEV1% predicted. Gender did not have any influence on the deltaFEV1. Stratification by initial FEV1% pred showed a significant effect of the treatment only in the group of patients with an initial FEV1% pred of 31-65%, and deltaFEV1 was reduced by 21 mL x yr(-1). This nonrandomized study suggests that weekly infusion of human alpha1-antitrypsin in patients with moderately reduced lung function may slow the annual decline in forced expiratory volume in one second.

In 16 patients with pulmonary fibrosis, an artificial pneumothorax was introduced using the Veress cannula and the Saugman water manometer. Atmospheric air was introduced by fractionated insufflation to a total volume of 800 ml (median). The interpleural space was found on the first attempt, and in all cases, fractionated insufflation of atmospheric air was conducted while the intrapleural pressure was controlled with the water manometer. In one case, the procedure was stopped because of a rise in the pleural pressure after insufflation of only 50 ml air. This was undoubtedly caused by pleural adhesions not visible on chest X-ray. The main concern with air insufflation is air embolism but this was not observed clinically in any of the present cases. The patients in the present study all suffered from pulmonary fibrosis judged by clinical examination, chest X-ray and pulmonary function tests. Despite a diffusion capacity (DCO/VA) with a median value of 48% expected, the procedure was well tolerated. It has previously been shown that artificial pneumothorax preceding thoracoscopy is well tolerated due to hyperventilation, with an increase in respiratory frequency and a fall in arterial CO2 concentration (PaCO2), while pH and arterial O2 concentration (PO2) remain constant. This probably also explains the tolerance of the patients in this material. Insufflation of air as described here should be restricted to senior pulmonologists because it is an infrequent procedure. The present authors found the procedure to be uncomplicated and easy to perform with little discomfort to the patients.

The pharmacology and safety of substitution treatment intraveneously withα1-antitrypsin (AAT) in patients deficient of AAT has been thoroughly investigated. The clinical efficacy of the treatment has so far not been established. The difficulties and uncertainties involved in defining the right persons for treatment, and determining the right time for a possible start of treatment are discussed. A controlled trail with participation of several European countries is suggested.

Positive pressure during expiration by face masks applied by the patient has gained wide acceptance in the treatment of chronic bronchitis, but the efficacy is still unproven. The effect of 6 months of treatment with PEEP-masks (positive end-expiratory pressure) was therefore studied in 47 patients with severe irreversible obstructive pulmonary disease (forced expiratory volume in one second (FEV1) about 1 l), and mucus hypersecretion. Patients were double-blindly randomized to at least 45 min daily treatment with PEEP-masks with either 10 or 0 cm water pressure. After 6 months of treatment, no statistical difference was found between the two groups in change of median values (month 6 - month 0) of FEV1, forced vital capacity (FVC), arterial oxygen tension (PaO2), amount of sputum or dyspnoea. Median values of arterial carbon dioxide tension (PaCO2) decreased significantly (0.03 kPa) in the placebo group. Cough intensity and dyspnoea during walking on staircases improved significantly in the placebo group. No difference among groups was found in number of days bedridden, hospitalized, number of exacerbations or antibiotic consumption. We conclude, that the use of PEEP-masks in these patients is without clinical documentation and cannot be recommended.

The aim of this investigation was to quantify dissemination of Mycobacterium tuberculosis infection in patients with pulmonary tuberculosis and to show the pattern of eradication during treatment. The study is based on 98 out of the 113 patients with pulmonary tuberculosis who died during their admission to hospital in the Municipality of Copenhagen from 1963 to 1971. These patients had cultures for M. tuberculosis performed from different organs at autopsy: 78% treated=100 days had dissemination of bacteria, cultured with decreasing frequency in the lungs, spleen, liver, and kidneys, respectively. In comparison, 23% treated100 days had dissemination of bacteria, among which 50% occurred in patients with records of poor treatment compliance, 14% in patients with good treatment compliance. 81% of all patients had at least one chest x-ray judged to be without a miliary pattern. This study emphasizes that M. tuberculosis is often disseminated to organs other than the lungs in severe pulmonary tuberculosis. Eradication of bacteria in these organs can take several months. This observation adds to our understanding of the natural history of tuberculosis: M. tuberculosis is a resilient organism that can adapt to a wide variety of environmental conditions.

About half of all patients on home oxygen therapy receive non-continuous oxygen therapy (less than 15 h daily) (NCOT). The goal of NCOT is to improve well-being during daily activities and to improve sleep quality. The aim of this study was to evaluate the effect of NCOT on pulmonary symptoms and sleep quality, and to determine whether patients with a subjective beneficial effect differed from those without effect in terms of patients' characteristics, utilization of oxygen, hospitalization and survival. Furthermore, the relationship between the reported beneficial effect of NCOT on dyspnoea and physical activity during domestic activities was examined. During the period November 1994 to July 1995, 254 Danish patients were prescribed oxygen less than 12 h daily or ‘on demand’. Of these patients, 142 (55·9%) answered a questionnaire on hours spent with oxygen and symptomatic effect of oxygen treatment. While on oxygen, 76·3% of the patients reported improved dyspnoea score (0–10) more than 0·5 points, 78·3% had improved quality of life, 59·5% improved sleep, 48·5% increased physical activity, 49·3% felt less tired and 40·0% reported improved thinking. Fifty-seven (43·2%) patients reported both improved dyspnoea and physical activity, whereas seven (5·3%) patients reported that oxygen had no effect on dyspnoea but a beneficial effect on physical activity. Only 11 (7·7%) patients reported no subjective improvement on oxygen. The subjective effect of NCOT was not significantly associated to hours spent with oxygen, the underlying disease, gender, hospitalization or survival. During daily activity and regardless of daily number of hours spent with oxygen, NCOT improved well-being in nearly all patients. The most pronounced improvement was reported on dyspnoea, sleep and quality of life. Very few patients sensed improved physical activity without relief in breathlessness.

Many studies of asthma mortality rely on official registration. The aim of this study was to evaluate the accuracy of death certificates, where asthma was coded as cause of death. In a 12-month period, medical information on all subjects with asthma officially coded as the underlying cause of death in Denmark, was obtained by reviewing hospital records, contacting general practitioners and sometimes close relatives. A panel of four pulmonologists each examined the obtained information and independently assessed the cause of death. Of a total of 218 death certificates, 39 were excluded as the cause of death could not be validated. In 16 (9%) of the subjects death from asthma was judged to be the definite cause of death and in 12 (7%) death from asthma was possible. Of 151 non-asthma deaths coded as due to asthma, 109 were judged to have suffered or died from COPD and 14 from heart disease. The accuracy of Danish death certification in asthma deaths is poor, especially in the elderly, where COPD is often classified as asthma. We conclude that the true asthma mortality in Denmark is substantially lower than officially recorded.

We have investigated whether restoration of the balance between neutrophil elastase and its inhibitor, alpha(1)-antitrypsin, can prevent the progression of pulmonary emphysema in patients with alpha(1)-antitrypsin deficiency. Twenty-six Danish and 30 Dutch ex-smokers with alpha(1)-antitrypsin deficiency of PI*ZZ phenotype and moderate emphysema (FEV(1) between 30% and 80% of predicted) participated in a double-blind trial of alpha(1)-antitrypsin augmentation therapy. The patients were randomized to either alpha(1)-antitrypsin (250 mg/kg) or albumin (625 mg/kg) infusions at 4-wk intervals for at least 3 yr. Self-administered spirometry performed every morning and evening at home showed no significant difference in decline of FEV(1) between treatment and placebo. Each year, the degree of emphysema was quantified by the 15th percentile point of the lung density histogram derived from computed tomography (CT). The loss of lung tissue measured by CT (mean +/- SEM) was 2.6 +/- 0.41 g/L/yr for placebo as compared with 1.5 +/- 0.41 g/L/yr for alpha(1)-antitrypsin infusion (p = 0.07). Power analysis showed that this protective effect would be significant in a similar trial with 130 patients. This is in contrast to calculations based on annual decline of FEV(1) showing that 550 patients would be needed to show a 50% reduction of annual decline. We conclude that lung density measurements by CT may facilitate future randomized clinical trials of investigational drugs for a disease in which little progress in therapy has been made in the past 30 yr.

The launching of cheap, pocket-sized spirometers, with data storage capability, has made patient-administered sequential spirometry (PASS) an attractive method of monitoring ventilatory capacity. At present, little information is available on the quality of PASS, compared to laboratory spirometry. The aim of this study was to investigate whether patients could perform PASS without loss of reliability and reproducibility as compared with traditional laboratory spirometry. Ten healthy volunteers performed spirometry for 1 month and 10 emphysematous patients with α 1 -antitrypsin deficiency (type PiZ) performed spirometry twice daily for up to 2 yr. To fulfil Good Clinical Practice criteria on full data documentation, a traditional direct recording spirometer, the Vitalograph R-model, was used. A decompression device was used for calibration and a 3·8% annual drift in volume registration was noted. This drift was largest for the first year. After training, all patients were able to perform unsupervised spirometry, producing technically correct forced expiratory curves. Reproducibility of FEV 1 and FVC obtained by PASS was found to be as good as for laboratory spirometry. After adjustment for the diurnal variation, the residual variation of FEV 1 was 2·5% (range 1·6-4·2%) for healthy volunteers and 5·6% (range 4·2–7·7%) for emphysematous patients. Forced vital capacity showed the same pattern. In conclusion, PASS is possible in highly motivated individuals without loss of reliability and reproducibility when compared to laboratory spirometry.

During the years 1975-1985, 25 Danish children (less than 15 years) and 40 children of immigrants in the Municipalities of Copenhagen and Frederiksberg had tuberculosis for the first time. The children were assessed at the time of diagnosis and were retraced in 1987. The incidence of tuberculosis among foreign children was 10-40 times that among Danish children. Pronounced differences in the localizations of tuberculosis in Danes and foreigners were observed. Whereas the Danish children had exclusively pulmonary tuberculosis, 13 of the foreign children had either extrapulmonary tuberculosis or pulmonary and extrapulmonary tuberculosis simultaneously. Two of the foreign children had tuberculosis meningitis and one miliary tuberculosis. Significantly more patients with bacillary tuberculosis were present among foreigners than among Danes. No significant differences were found between the occurrence of symptoms, Mantoux-positive reactions, previous Calmette vaccination or known contact with a person with tuberculosis in Danes and foreigners. Treatment was followed as prescribed and all were cured from tuberculosis. One child with tuberculosis meningitis developed slight sequelae while the remainder of the children developed somatically normally.

Sixty-five patients with severe alpha 1-antitrypsin (AAT) deficiency (phenotype PiZ) were followed with spirometry at regular intervals of one year and a median observation period of four years. The annual decline in pulmonary function was adjusted for sex, age and height by division with the predicted normal pulmonary function. The median decline in FEV1 was 1.9% predicted/year. The rate of decline was independent of age and pulmonary function, except for patients with FEV1 below 25% of predicted normal. There was a tendency towards a slower median decline in FEV1 in ex-smokers (1.7% predicted/year) compared to smokers (3.8% predicted/year) and never-smokers (3.7% predicted/year), however, this difference was not significant (p greater than 0.01). At the time of diagnosis smokers and ex-smokers had a lower FEV1 (44 and 38% predicted) than never-smokers (85% predicted) (p less than 0.02), and smokers and ex-smokers were generally younger (median age 44 and 42 years, respectively) than never smokers (median age 55 years) (p greater than 0.1). Our data indicate that smokers as well as nonsmokers with severe AAT deficiency are at risk of developing pulmonary emphysema. The disease seems to appear later in nonsmokers, though once initiated it progresses at the same rate.

The inflammatory nature of a tumour-like lesion not formerly observed in the parietal pleura was confirmed histologically using immunohistochemical analysis and clinically by spontaneous regression. A study of the literature revealed that the histological picture of the lesion was consistent with that of the rarely described inflammatory pseudotumour.