[Securing the therapy management during the leave permissions for the elderly patients]. / Sécurisation de la prise en charge médicamenteuse des patients âgés pendant les permissions de sortie.

Leave permission can be granted over a limited period of hospitalisation during which the patient can return home under the responsibility of the hospital. Despite its frequency, this practice is not evaluated in terms of maintaining the security of medication. This complex process involves several actors, processes and locations. In that case, the drug iatrogenic risk is not at all negligible, especially for the elderly. Patient comprehension of medication is not always easy and must be evaluated before leaving the hospital. Therefore, a risk analysis has been initiated to ensure the medical practice's security of our geriatric hospital. Multidisciplinary working group meetings were dedicated to analyse and overcome 21 unacceptable failure modes. The establishment of traceability nurse/patient for the medication intake, information and evaluation of drug monitoring allowed the patient's medication compliance. In the meanwhile, the role of the working group on the security of the internal drug circuit in the hospital has integrated the harmonization of practices, a unique source of information and a variety of comprehensible, readable and informative materials to propose to the patients. These preventive actions have been formulated to secure, optimize and to individualize drug management during the leave permission. In the context of optimization during transit period home/hospital, this process reorganized by the working group can be integrated in a public health approach to reduce the number of preventable readmissions.

Association of lung function decline with the heme oxygenase-1 gene promoter microsatellite polymorphism in a general population sample. Results from the European Community Respiratory Health Survey (ECRHS), France.

Inducible heme oxygenase (HO-1) acts against oxidants that are thought to play a major role in the pathogenesis of chronic obstructive pulmonary disease (COPD), characterised by impaired lung function. A (GT)(n) repeat polymorphism in the HO-1 gene promoter can modulate the gene transcription in response to oxidative stress. We hypothesised that this polymorphism could be associated with the level of lung function and decline in subjects exposed to oxidative aggression (smokers). We genotyped 749 French subjects (20-44 years, 50% men, 40% never smokers) examined in both 1992 and 2000 as part of the ECRHS. Lung function was assessed by forced expiratory volume in 1 second (FEV1) and FEV1/forced ventilatory capacity (FVC) ratio. We compared long (L) allele carriers ((GT)(n) > or =33 repeats for one or two alleles) to non-carriers. Cross sectionally, in 2000, L allele carriers showed lower FEV1/FVC than non-carriers. During the 8 year period, the mean annual FEV1 and FEV1/FVC declines were -30.9 (31.1) ml/year and -1.8 (6.1) U/year, respectively. FEV1/FVC decline was steeper in L allele carriers than in non-carriers (-2.6 (5.5) v -1.5 (6.4), p = 0.07). There was a strong interaction between the L allele and smoking. In 2000, the L allele was associated with lower FEV(1) and FEV(1)/FVC in heavy smokers (> or =20 cigarettes/day) only (p for interaction = 0.07 and 0.002 respectively). Baseline heavy smokers carrying the L allele showed the steepest FEV1 decline (-62.0 (29.5 ml/year) and the steepest FEV1/FVC decline (-8.8 (5.4 U/year) (p for interaction = 0.009 and 0.0006). These results suggest that a long (L) HO-1 gene promoter in heavy smokers is associated with susceptibility to develop airway obstruction.

Serum carotenoids, vitamins A and E, and 8 year lung function decline in a general population.

BACKGROUND: Oxidative stress is thought to have a major role in the pathogenesis of airway obstruction. A study was undertaken to determine whether subjects with low levels of antioxidants (serum beta-carotene, alpha-carotene, vitamins A and E) would be at a higher risk of accelerated decline in forced expiratory volume in 1 second (FEV1) as their lungs would be less protected against oxidative stress. METHODS: 1194 French subjects aged 20-44 years were examined in 1992 as part of the European Community Respiratory Health Survey (ECRHS); 864 were followed up in 2000 and 535 (50% men, 40% lifelong non-smokers) had complete data for analysis. RESULTS: During the 8 year study period the mean annual decrease in FEV1 (adjusted for sex, centre, baseline FEV1, age, smoking, body mass index and low density lipoprotein cholesterol) was 29.8 ml/year. The rate of decrease was lower for the subjects in tertile I of beta-carotene at baseline than for those in the two other tertiles (-36.5 v -27.6 ml/year; p = 0.004). An increase in beta-carotene between the two surveys was associated with a slower decline in FEV1. No association was observed between alpha-carotene, vitamin A, or vitamin E and FEV(1) decline. However, being a heavy smoker (> or =20 cigarettes/day) in combination with a low level of beta-carotene or vitamin E was associated with the steepest decline in FEV1 (-52.5 ml/year, p = 0.0002 and -50.1 ml/year, p = 0.010, respectively). CONCLUSIONS: These results strongly suggest that beta-carotene protects against the decline in FEV1 over an 8 year period in the general population, and that beta-carotene and vitamin E are protective in heavy smokers.