We measured serum levels of carbohydrate deficient transferrin (CDT) in 420 subjects: 100 healthy blood donors, 82 healthy employees, 70 abstaining patients with different chronic nonalcoholic liver disease, 16 abstaining patients with alcoholic fatty liver, 50 abstaining patients with alcoholic liver cirrhosis, 25 abusing patients with alcoholic fatty liver, 41 abusing patients with alcoholic liver cirrhosis, and 36 patients with alcohol dependence syndrome with a daily ethanol consumption of 173 +/- 120 g the last 4 weeks before blood was drawn. In controls the serum level of CDT was significantly higher in females compared with males (17.7 +/- 5.1 and 13.7 +/- 3.8 units/liter, respectively), and the upper normal limit was defined as 27 and 20 units/liter. Sixty-two of 102 (60.8%) abusing patients with alcoholic liver disease had increased levels of CDT compared with 1 of 66 abstaining (1.5%) patients with alcoholic liver disease, and 10 of 70 (14.3%) abstaining patients with nonalcoholic liver disease among them 3 with primary biliary cirrhosis and 2 with chronic autoimmune hepatitis. No correlation was found between serum CDT and gamma-glutamyltranspeptidase (GGT), AST, ALT, and mean red cell volume (MCV). The sensitivity and specificity for serum CDT was 61 and 92%, respectively, compared with 85 and 18% for GGT and 70 and 66% for MCV. No advantage was gained by using the CDT/transferrin ratio. Our study confirms that CDT is a specific marker for chronic alcohol abuse, except in few patients with other chronic liver diseases. Serum CDT seems to be a better indicator of abstention than GGT; AST and MCV in patients with alcoholic liver disease. However, in our hands CDT is not so sensitive for alcohol abuse in patients with liver disease as reported earlier in unselected alcoholics.
Aims: To examine whether asthma induced by exposure to aluminium potroom emissions (potroom asthma) is associated with inflammatory changes in the airways. Methods: Bronchial biopsy specimens from 20 asthmatic workers (8 non-smokers and 12 smokers), 15 healthy workers (8 non-smokers and 7 smokers), and 10 non-exposed controls (all non-smokers) were analysed. Immunohistofluorescent staining was performed to identify mucosal total leucocytes (CD45 + leucocytes), neutrophils, and mast cells. Results: Median RBM thickness was significantly increased in both asthmatic workers (8.2 mm) and healthy workers (7.4 mm) compared to non-exposed controls (6.7 mm). Non-smoking asthmatic workers had significantly increased median density of lamina propria CD45+ leucocytes (1519 cells/mm 2 v 660 and 887 cells/mm 2 ) and eosinophils (27 cells/mm 2 v 10 and 3 cells/mm 2 ) and significantly increased concentrations of exhaled NO (18.1 ppb v 6.5 and 5.1 ppb) compared to non-smoking healthy workers and non-exposed controls. Leucocyte counts and exhaled NO concentrations varied with smoking habits and fewer leucocytes were observed in asthmatic smokers than in non-smokers Asthmatic smokers had significantly increased numbers of eosinophils in lamina propria compared to non-exposed controls (10 v 3 cells/mm 2 ). Both eosinophilic and non-eosinophilic phenotypes of asthma were recognised in the potroom workers and signs of airway inflammation were also observed in healthy workers. Conclusions: Airway inflammation is a central feature of potroom asthma and exposure to potroom emissions induces pathological alterations similar to those described in other types of asthma. Cigarette smoking seems to affect the underlying mechanisms involved in asthma, as the cellular composition of airway mucosa appears different in asthmatic smokers and non-smokers.
IntroductionDifferences in the organisation of idiopathic pulmonary fibrosis (IPF) and interstitial lung diseases (ILDs) in the Nordic countries are not well described. Diagnostic setups, treatment modalities and follow-up plans may vary due to national, cultural and epidemiological features. The aim of the present study was to describe the different organisation of diagnostics and treatment of IPF and ILD in the Nordic countries.MethodsAll university and regional hospitals with respiratory physicians were invited to respond to a questionnaire collecting data on the number of physicians, nurses, patients with ILD/IPF, the presence of and adherence to disease-specific national and international guidelines, diagnosis and treatment including ILD-specific palliation and rehabilitation programmes.ResultsTwenty-four university and 22 regional hospitals returned the questionnaire. ILD and IPF incidence varied between 1.4 and 20/100,000 and 0.4 and 10/100,000, respectively. Denmark and Estonia have official national plans for the organisation of ILD. The majority of patients are managed at the university hospitals. The regional hospitals each manage 46 (5–200) patients with ILD and 10 (0–20) patients with IPF. There are from one to four ILD centres in each country with a median of two ILD specialists employed. Specialised ILD nurses are present in nine hospitals. None of the Nordic countries have national guidelines made by health authorities. The respiratory societies in Sweden, Norway and Denmark have developed national guidelines. All hospitals except two use the ATS/ERS/JRS/ALAT IPF guidelines from 2011. The limited number of ILD specialists, ILD-specialised radiologists and pathologists and the low volume of ILD centres were perceived as bottlenecks for implementation of guidelines. Twenty of the 24 university hospitals have multidisciplinary conferences (MDCs). Pulmonologists and radiologists take part in all MDCs while pathologists only participate at 17 hospitals. Prescription of pirfenidone is performed by all university hospitals except in Estonia. Triple therapy with steroid, azathioprine and N-acetylcysteine is not used. No hospitals have specific palliation programmes for patients with ILD/IPF, but 36 hospitals have the possibility of referring patients for palliative care, mostly based on existing oncology palliative care teams; seven hospitals have rehabilitation programmes for ILD.ConclusionThere are obvious differences between the organisations of ILD patients in the Nordic countries. We call for national plans that consider the challenge of cultural and geographical differences and suggest the establishment of national reference centres and satellite collaborative hospitals to enable development of common guidelines for diagnostics, therapy and palliation in this patient group.
Cigarette smoking may alter bronchial inflammation in asthma. Multicolour immunohistofluorescent examination on bronchial cryosections was used to examine bronchial inflammatory cell infiltrate in patients with occupational asthma. Monoclonal antibodies to CD3, CD4, CD8, T-cell receptor-d1, CD68 and human leukocyte antigen-DR were combined to identify Tcell subsets and macrophages in bronchial biopsies from 20 workers with occupational asthma (12 smokers and eight nonsmokers), 15 healthy workers (seven smokers and eight nonsmokers) and 10 nonsmoking, nonexposed controls.The increased subepithelial CD4+ T-cell density in nonsmoking asthmatics was not present in smoking asthmatics, who had the lowest CD4+ T-cell density of all groups. The decreased subepithelial CD4+ and CD8+ T-cell density correlated with a reduction in lung function, as measured by percentage predicted forced expiratory volume in one second, in smoking asthmatics only. Although smoking asthmatics had a significantly increased number of intraepithelial CD8+ T-cells and macrophages compared with nonsmoking asthmatics, the proportion of cd-T-cells was significantly decreased in both asthmatic groups.Smoking asthmatics had a distinctly different distribution of T-cell subsets compared with nonsmoking asthmatics. The accumulation of subepithelial CD4+ T-cells, which was observed in nonsmoking asthmatics, appeared to be inhibited in smoking asthmatics, suggesting a smokinginduced bronchial immune modulation, at least in occupational asthma in the aluminium industry.
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