The results demonstrate similar allele and genotype frequencies of GC in COPD patients overall and healthy controls. However, there was a higher prevalence of genotypes carrying a GC*1F allele and lower prevalence of genotypes with a GC*2 allele in the CMH patients than in controls. This difference was most notable in the homozygous form: 8.3% vs 1.1% for the GC*1F/*1F, and 0.0% vs 7.6% for the GC*2/*2 genotypes, respectively. When controlled for smoking, only the non-smoking CMH patients demonstrated a significantly altered frequency of the GC*1F/*1F genotype (p = 0.0001). The prevalence of the GC*2/*2 genotype was also significantly lower in patients with bronchial hypersecretion with airflow obstruction compared with the control group (2.9% vs 7.6%). Taken together, these results demonstrate that the GC*1F and GC*2 alleles are associated with sputum hypersecretion in individuals who are at increased risk of developing COPD.

Using Icelandic whole-genome sequence data and an imputation approach we searched for rare sequence variants in CHRNA4 and tested them for association with nicotine dependence. We show that carriers of a rare missense variant (allele frequency=0.24%) within CHRNA4, encoding an R336C substitution, have greater risk of nicotine addiction than non-carriers as assessed by the Fagerstrom Test for Nicotine Dependence (P=1.2 × 10−4). The variant also confers risk of several serious smoking-related diseases previously shown to be associated with the D398N substitution in CHRNA5. We observed odds ratios (ORs) of 1.7–2.3 for lung cancer (LC; P=4.0 × 10−4), chronic obstructive pulmonary disease (COPD; P=9.3 × 10−4), peripheral artery disease (PAD; P=0.090) and abdominal aortic aneurysms (AAAs; P=0.12), and the variant associates strongly with the early-onset forms of LC (OR=4.49, P=2.2 × 10−4), COPD (OR=3.22, P=2.9 × 10−4), PAD (OR=3.47, P=9.2 × 10−3) and AAA (OR=6.44, P=6.3 × 10−3). Joint analysis of the four smoking-related diseases reveals significant association (P=6.8 × 10−5), particularly for early-onset cases (P=2.1 × 10−7). Our results are in agreement with functional studies showing that the human α4β2 isoform of the channel containing R336C has less sensitivity for its agonists than the wild-type form following nicotine incubation.

There has been an increasing consensus worldwide on how to treat asthma, and, simultaneously, an increase in the sales of antiasthma drugs. However, little is known about actual drug use, dosage, combinations of drugs, etc., or about the clinical characteristics of patients using these drugs.All individuals with prescriptions for antiasthma drugs, who came to Icelandic pharmacies during March 1994, were invited to participate. By means of questionnaires, the pharmacists recorded the age and gender of the patient, the speciality of the prescribing doctor, as well as the name of the drug, total amount prescribed, and dosage. The patients were asked to answer another questionnaire on their clinical diagnosis, usage of other antiasthma drugs, etc.The pharmacists registered 2,026 individuals, with 2,687 prescriptions: 1,574 for beta 2 -agonists, 838 for inhaled corticosteroids, 208 for theophylline, 48 for anticholinergic drugs, and 19 for cromoglycates. One thousand, three hundred and fifty one patients answered the questionnaires. The majority (67%) claimed to have asthma, 18% chronic bronchitis, 11% emphysema and 5% other diseases or symptoms. Among those aged ≥16 yrs with asthma, 93% used beta 2 -agonists, 62% inhaled corticosteroids, 19% theophylline, and very few used other drugs. The most commonly used combination (57%) was beta 2 -agonists with inhaled corticosteroids. Thirty one per cent used beta 2 -agonists as monotherapy, and 5% used only inhaled corticosteroids. Theophylline was used mainly in combination with beta 2 -agonists and inhaled corticosteroids.In conclusion, our data suggest that two thirds of antiasthma drug users have asthma and that most are treated according to present guidelines. The use of inhaled corticosteroids, however, seems somewhat less than optimal.

The template bleeding time (TBT), ADP‐induced platelet aggregation, and serum production of TXB2 were measured in healthy young male subjects immediately before, and on days 1, 4 and 6 after the ingestion of 1 single dose of 500 mg acetylsalicylic acid (ASA) in 3 different formulations: Aspirin® (Bayer), and the 2 enteric‐coated formulations Reumyl® (Hässle) and Premaspin® (Lääke). The ingestion of Aspirin® resulted in a significant prolongation of the TBT over a period of 6 d. However, after the ingestion of the same amount of ASA in the 2 enteric coated formulations, the TBT as measured on day 6 had become normalized. After the ingestion of Aspirin®, there was no reappearance of the second wave of ADP‐induced platelet aggregation during the study period; however, after the ingestion of the 2 enteric‐coated formulations, secondary platelet aggregation occasionally returned on day 6. In response to the intake of each of the 3 ASA formulations, the serum TXB2 production as measured 24 h later was almost completely inhibited. In each of the 3 study groups, the TXB2 formation as measured on day 6 was still significantly impaired.