ABSTRACT
Los factores familiares en los adolescentes se relacionan con el inicio y la experimentación del consumo de sustancias legales o ilegales; sin embargo, la influencia de la familia ha sido un tema poco abordado. OBJETIVO: determinar los factores familiares asociados al consumo de cigarrillo en estudiantes de Cartagena, Colombia. METODOLOGÍA: se diseñó un estudio transversal con estudiantes de colegios públicos y privados. Se investigaron las características demográficas, el consumo de cigarrillo durante el último mes, los antecedentes familiares de personas fumadoras y el funcionamiento familiar. La funcionalidad familiar se valoró con el cuestionario de apgar familiar. Resultados: se encuestaron 1.014 estudiantes con edades entre 11 y 22 años. El 6,9% (70 estudiantes) informó fumar al menos un cigarrillo durante el último mes y el 48,4% (491) informó tener disfunción familiar. Las variables familiares padre fumador (OR = 2,40) y hermano fumador (OR = 2,06), mostraron asociación estadísticamente significativa al consumo de cigarrillo. Conclusión: el consumo de cigarrillo en estudiantes se asoció con tener padre fumador y hermano fumador. No existe relación con la condición de madre fumadora u otro familiar, ni con el funcionamiento familiar. En próximas investigaciones se deberían incluir otras variables familiares como la estructura y la comunicación.
Family factors in adolescents are related to the initiation and experimentation with the consumption of legal or illegal substances, but the influence of the family has been a subject little discussed. OBJECTIVE: To identify family factors associated with cigarette consumption among students from Cartagena, Colombia. METHODOLOGY: A cross sectional study was designed with students in public and private schools. We investigated the demographic characteristics, cigarette consumption during the last month, family history of smokers and family functioning. Family functioning was assessed with the Family apgar questionnaire. Results: We surveyed 1014 students aged between 11 and 22 years. 6.9% (70 students) reported smoking at least one cigarette during the last month and 48.4% (491) reported having family dysfunction. The family variables fathers who smoked (OR = 2.40) and sibling smoking (OR = 2.06) showed significant association to smoking. Conclusion: Cigarette consumption among students was associated with having a father and brother smoker. There is no relation to maternal smoking status or other family or with family functioning. In future research should include other variables such as family structure and communication.
Subject(s)
Tobacco Use , SmokersABSTRACT
AIM: The purpose of this study was to estimate the effect sizes of drug interactions on plasma clozapine concentrations, adjusting for potentially confounding factors such as smoking. METHODS: The estimation was performed by using a mixed model, and a combination of unpublished (N=83) and published (N=172) data that included patients taking phenobarbital, valproic acid, fluvoxamine, fluoxetine, paroxetine, sertraline, citalopram and reboxetine, and patients not taking co-medications. RESULTS: The 255 patients provided a total of 415 steady-state trough plasma clozapine concentrations. Each patient provided 1 to 15 measures of plasma clozapine concentrations. Total plasma clozapine concentration, defined as the sum of plasma clozapine and norclozapine concentrations, was also investigated. A random intercept linear model of the natural log of plasma clozapine concentration with the natural log of dose and other variables as independent variables was built. The model confirmed that phenobarbital induces clozapine metabolism (effect size, E=-28%), and that fluoxetine (E=+42%), fluvoxamine (E=+263%) and paroxetine (E=+30%) inhibit it. Valproic acid appeared to inhibit clozapine metabolism in non-smokers (effect size, E=+16%), whereas it appeared to induce clozapine metabolism in smokers (E=-22%). The effect sizes of smoking on plasma clozapine concentration were -20% in patients not taking valproic acid, and -46% in patients taking valproic acid. Thus, smoking induces clozapine metabolism, and this induction may be stronger when the patient is taking valproic acid. The effect sizes allowed the computation of clozapine dose-correction factors for phenobarbital, 1.4 [95% confidence interval, CI, (1.1, 1.7)]; paroxetine, 0.77 (0.67, 0.89); fluoxetine, 0.70 (0.64, 0.78); fluvoxamine, 0.28 (0.22, 0.35); and valproic acid [0.86 (0.75, 1.0) in non-smokers, and 1.3 (0.96, 1.73) in smokers]. Sertraline, reboxetine and citalopram had no obvious effects. DISCUSSION: The results for total plasma clozapine concentrations are similar to those for plasma clozapine concentrations. The main limitations of this study were that the computed effect sizes reflect only the doses and treatment-durations of the co-medications studied, and that the substantial "noise" of the clinical environment may make it difficult to detect the effects of some variables, particularly those with small effect sizes. Gender was not significant probably due to its relatively small effect size in the studied population, and age was not significant probably due to the limited age variability. CONCLUSION: This article contributes to the clozapine literature by describing a possible interaction between taking valproic acid and smoking, which modifies plasma clozapine concentrations, by estimating the effect sizes of other compounds on plasma clozapine concentrations after correcting for confounders, and by providing dose-correction factors for clinicians.