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Purpose: To study the short-term reproducibility of lung density measurements by multi-slice computed tomography (CT) using three different radiation doses and three reconstruction algorithms., Material and Methods: Twenty-five patients with smoker's emphysema and 25 patients with alpha1-antitrypsin deficiency underwent 3 scans at 2-week intervals. Low-dose protocol was applied, and images were reconstructed with bone, detail, and soft algorithms. Total lung volume (TLV), 15th percentile density (PD-15), and relative area at -910 Hounsfield units (RA-910) were obtained from the images using Pulmo-CMS software. Reproducibility of PD-15 and RA-910 and the influence of radiation dose, reconstruction algorithm, and type of emphysema were then analysed., Results: The overall coefficient of variation of volume adjusted PD-15 for all combinations of radiation dose and reconstruction algorithm was 3.7%. The overall standard deviation of volume-adjusted RA-910 was 1.7% (corresponding to a coefficient of variation of 6.8%). Radiation dose, reconstruction algorithm, and type of emphysema had no significant influence on the reproducibility of PD-15 and RA-910. However, bone algorithm and very low radiation dose result in overestimation of the extent of emphysema., Conclusion: Lung density measurement by CT is a sensitive marker for quantitating both subtypes of emphysema. A CT-protocol with radiation dose down to 16 mAs and soft or detail reconstruction algorithm is recommended.

This study reports the smoking habits in a Danish population, evaluates plasma cotinine and thiocyanate levels in the detection of 'slips' (subjects participating in smoking cessation trials who begin to smoke a few cigarettes per week) and provides distribution scores on questionnaire measures of nicotine dependence. A total of 599 subjects with a mean age of 41 years participated in the study. Of these 46% were current smokers with no difference in the proportion of males(46%) and females(45%) and with a mean cigarette consumption of 12.7 daily. Plasma samples were analyzed for cotinine and thiocyanate, and the smokers completed two questionnaires to measure nicotine dependence: the Fagerström Tolerance Questionnaire and the modified Horn-Russell scale. The mean plasma cotinine was 207 micrograms/l for smokers, 14.4 micrograms/l for occasional smokers and 8.0 micrograms/l for non-smokers (ex-smokers and never-smokers). For plasma thiocyanate the levels were 130 mg/l, 54.8 mg/l, and 54.3 mg/l, respectively. The mean Horn-Russell score was 7.4 and the mean Fagerström score was 5.9. The two tests correlated with a t-value of 0.61 (p < 0.001) and the scores in both tests increased with increasing cigarette consumption. In conclusion, 75% of the smokers consumed 10 or more cigarettes per day and males smoked more cigarettes than females. It was impossible to distinguish occasional smokers (slips) from non-smokers using plasma cotinine or thiocyanate levels. We suggest that studies are needed to evaluate if light smokers benefit from nicotine replacement therapy because they achieve plasma cotinine levels which are similar to those seen when using patches for nicotine replacement therapy.

For patients with COPD, FEV1 has been shown to be the single most important factor to influence survival. Patients with alpha 1-antitrypsin deficiency (alpha 1ATD) develop emphysema at a young age, especially if they smoke, and the purpose of this study was to calculate survival with respect to the initial FEV1 and smoking history. For this study, patients with Pi-type ZZ were analyzed. FEV1 was divided in four groups: below 25%, 25 to 49%, 50 to 74%, and more than 75% of predicted. A total of 347 patients with 107 deaths were available for analysis. Three patients were lost to follow-up, and 17 had received a lung transplant. There was no significant difference in survival between males and females. The median survival time for patients with an initial FEV1 below 25% was 6.3 yr (95% CI 5.2-8.0). For the FEV1 groups 25 to 49% and 50 to 74%, median survival times were: 10.5 (9.2-11.9) and 14.2 (12.4-infinity) yr, respectively. The median survival for the above 75% group was not calculable. For patients with an initial FEV1 less than 50%, smokers had a poorer survival rate than patients who quit smoking during the study period (p < 0.01). We conclude that for patients with severe alpha 1ATD, FEV1 is a very strong predictor of survival regardless of sex. Patients who quit smoking had a better survival rate than patients who continued to smoke.

Background: The hereditary disorder alpha 1-antitrypsin deficiency is characterised by development of severe emphysema at an early age with smoking being the most significant additional risk factor. The purpose of the present paper was to analyse potential risk factors other than smoking for emphysema and to estimate the prognosis of life time non-smokers.Methods: Patients were identified through the files of the Danish alpha 1-antitrypsin deficiency register which contains information on more than 700 persons with the condition. Many of the patients, the non-index cases, were identified from family studies.Results: There were 75 life time non-smokers with PiZ (27 index cases and 48 non-index cases) aged 20 years or more at entry. Twenty one subjects died during the follow up period. The Standardised Mortality Ratio (SMR) was 3.0 (95% confidence intervals (CI) 1.9 to 4.6). There was no significant difference in SMR between males and females. The SMR was 8.8 (95% CI 5.0 to 14) for the index cases and 0.96 (95% CI 0.3 to 2.3) for the non-index cases based on five deaths. The overall mean % predicted forced expiratory volume in one second (FEV1) at entry was 83% with a significant difference between index cases (54%) and non-index cases (100%) (p < 0.001). The difference in the ratio of FEV1 to forced vital capacity (FVC) was also highly significant with values of 0.57 and 0.79 for index and non-index cases, respectively (p < 0.001). In the non-index group only three had an FEV1% predicted of less than 70%.Conclusions: Occupational exposure to airway irritants did not have any significant influence on the development of emphysema. Only a few life time non-smokers develop severe emphysema; most never develop pulmonary symptoms and thus remain undetected unless family members of index cases are screened. [ABSTRACT FROM AUTHOR]