Alcohol and drugs in epilepsy: pathophysiology, presentation, possibilities, and prevention.

The potentially serious outcomes from ingestion of and dependence on toxins make this an important topic for epileptologists. We must be aware of the potential for harm from compounds that may be freely available, yet patients may try to conceal their use. Problematic compounds may cause seizures either acutely or on withdrawal: Their use may reduce effectiveness of antiepileptic drugs, or may simply promote and enhance chaotic lifestyles. Any or all of these factors may worsen seizure control or even directly cause seizures. This article highlights the pathophysiology behind provoked seizures, provides clues to diagnosis, and then outlines the steps that clinicians should take to reduce the deleterious effects of toxic compounds.

Smoke-free legislation and hospitalizations for acute coronary syndrome.

BACKGROUND: Previous studies have suggested a reduction in the total number of hospital admissions for acute coronary syndrome after the enactment of legislation banning smoking in public places. However, it is unknown whether the reduction in admissions involved nonsmokers, smokers, or both. METHODS: Since the end of March 2006, smoking has been prohibited by law in all enclosed public places throughout Scotland. We collected information prospectively on smoking status and exposure to secondhand smoke based on questionnaires and biochemical findings from all patients admitted with acute coronary syndrome to nine Scottish hospitals during the 10-month period preceding the passage of the legislation and during the same period the next year. These hospitals accounted for 64% of admissions for acute coronary syndrome in Scotland, which has a population of 5.1 million. RESULTS: Overall, the number of admissions for acute coronary syndrome decreased from 3235 to 2684--a 17% reduction (95% confidence interval, 16 to 18)--as compared with a 4% reduction in England (which has no such legislation) during the same period and a mean annual decrease of 3% (maximum decrease, 9%) in Scotland during the decade preceding the study. The reduction in the number of admissions was not due to an increase in the number of deaths of patients with acute coronary syndrome who were not admitted to the hospital; this latter number decreased by 6%. There was a 14% reduction in the number of admissions for acute coronary syndrome among smokers, a 19% reduction among former smokers, and a 21% reduction among persons who had never smoked. Persons who had never smoked reported a decrease in the weekly duration of exposure to secondhand smoke (P<0.001 by the chi-square test for trend) that was confirmed by a decrease in their geometric mean concentration of serum cotinine from 0.68 to 0.56 ng per milliliter (P<0.001 by the t-test). CONCLUSIONS: The number of admissions for acute coronary syndrome decreased after the implementation of smoke-free legislation. A total of 67% of the decrease involved nonsmokers. However, fewer admissions among smokers also contributed to the overall reduction.

Validity of self-reported smoking status: Comparison of patients admitted to hospital with acute coronary syndrome and the general population.

Many studies rely on self-reported smoking status. We hypothesized that patients with acute coronary syndrome (ACS), a smoking-related condition, would be more prone to misclassify themselves as ex-smokers, because of pressure to quit. We compared patients admitted with ACS with a general population survey conducted in the same country at a similar time. We determined whether ACS patients who classified themselves as ex-smokers (n = 635) were more likely to have cotinine levels suggestive of smoking deception than self-reported ex-smokers in the general population (n = 289). On univariate analysis, the percentage of smoking deceivers was similar among ACS patients and the general population (11% vs. 12%, p = .530). Following adjustment for age, sex and exposure to environmental tobacco smoke, ACS patients were significantly more likely to misclassify themselves (adjusted OR = 14.06, 95% CI 2.13-93.01, p = .006). There was an interaction with age whereby the probability of misclassification fell significantly with increasing age in the ACS group (adjusted OR = 0.95, 95% CI 0.93-0.97, p<.001), but not in the general population. Overall, smoking deception was more common among ACS patients than the general population. Studies comparing patients with cardiovascular disease and healthy individuals risk introducing bias if they rely solely on self-reported smoking status. Biochemical confirmation should be undertaken in such studies.

A randomised controlled trial of a smoking cessation intervention delivered by dental hygienists: a feasibility study.

BACKGROUND: Tobacco use continues to be a global public health problem. Helping patients to quit is part of the preventive role of all health professionals. There is now increasing interest in the role that the dental team can play in helping their patients to quit smoking. The aim of this study was to determine the feasibility of undertaking a randomised controlled smoking cessation intervention, utilising dental hygienists to deliver tobacco cessation advice to a cohort of periodontal patients. METHODS: One hundred and eighteen patients who attended consultant clinics in an outpatient dental hospital department (Periodontology) were recruited into a trial. Data were available for 116 participants, 59 intervention and 57 control, and were analysed on an intention-to-treat basis. The intervention group received smoking cessation advice based on the 5As (ask, advise, assess, assist, arrange follow-up) and were offered nicotine replacement therapy (NRT), whereas the control group received 'usual care'. Outcome measures included self-reported smoking cessation, verified by salivary cotinine measurement and CO measurements. Self-reported measures in those trial participants who did not quit included number and length of quit attempts and reduction in smoking. RESULTS: At 3 months, 9/59 (15%) of the intervention group had quit compared to 5/57 (9%) of the controls. At 6 months, 6/59 (10%) of the intervention group quit compared to 3/57 (5%) of the controls. At one year, there were 4/59 (7%) intervention quitters, compared to 2/59 (4%) control quitters. In participants who described themselves as smokers, at 3 and 6 months, a statistically higher percentage of intervention participants reported that they had had a quit attempt of at least one week in the preceding 3 months (37% and 47%, for the intervention group respectively, compared with 18% and 16% for the control group). CONCLUSION: This study has shown the potential that trained dental hygienists could have in delivering smoking cessation advice. While success may be modest, public health gain would indicate that the dental team should participate in this activity. However, to add to the knowledge-base, a multi-centred randomised controlled trial, utilising biochemical verification would be required to be undertaken.

A randomized, controlled trial of C0- Vs C2-guided therapeutic drug monitoring of cyclosporine in stable heart transplant patients.

BACKGROUND: Cyclosporine monitoring using 2-hour post-dose samples (C2) is thought to be more efficacious than using pre-dose levels (C0) in managing immunosuppression for transplant patients. We evaluated the effect of C2 monitoring on cyclosporine dose and clinical parameters in stable heart transplant patients. METHODS: 125 stable heart transplant patients were randomized to C0 or C2 monitoring of cyclosporine levels for a period of six months. All patients had both C0 and C2 samples taken, and clinicians were blinded to one of the samples depending on randomization. The primary endpoint was the relative change in cyclosporine (Neoral) dose during the study period and secondary endpoints were change in creatine clearance, mortality, infection, and acute rejection. RESULTS: There was a significant decrease in the cyclosporine dose for the C2 group as compared with the C0 group (-11 mg/day and -26 mg/day respectively, p = 0.0025). No proven rejection episodes occurred in either group and there was no significant difference in the incidence of infection (C0 6, C2 10; p = 0.14), the change in renal function (change in creatine clearance C(0) +0.54 ml/min; C2 -0.16 ml/min; p = 0.61), the number of blood tests or dose adjustments between groups over the study period. Analysis of the blinded samples revealed that the reduction of cyclosporine dose in the C2 group could not be accounted for by reduced immunosuppression . CONCLUSION: C2 monitoring allows a significant cyclosporine dose reduction without compromising patient outcome in stable heart transplant patients. Further studies are required to ascertain whether this dose reduction can be translated into clinical benefit.

Cigarette smoking impairs the therapeutic response to oral corticosteroids in chronic asthma.

The study was designed to assess the effect of cigarette smoking on the therapeutic response to oral corticosteroids in chronic stable asthma. We performed a randomized, placebo-controlled, crossover study with prednisolone (40 mg daily) or placebo for 2 weeks in smokers with asthma, ex-smokers with asthma, and never-smokers with asthma. All subjects had reversibility in FEV1 after nebulized albuterol of 15% or more and a mean postbronchodilator FEV1% predicted of more than 80%. Efficacy was assessed using FEV1, daily PEF, and an asthma control score. There was a significant improvement after oral prednisolone compared with placebo in FEV1, ml (mean difference, 237; 95% confidence intervals, 43, 231; p = 0.019), morning PEF L/m (mean difference, 36.8; 95% confidence intervals (CI), 11, 62; p = 0.006), and asthma control score (mean difference, -0.72; 95% CI, -1.2, -0.3; p = 0.004) in never-smokers with asthma but no change in smokers with asthma (mean differences of 47, 6.5, and -0.05 with p values of 0.605, 0.47, and 0.865, respectively). Ex-smokers with asthma had a significant improvement in morning and night PEF (mean difference, 29.1; CI, 2.3, 56; p = 0.04 and 52.4; CI, 26, 79; p = 0.003, respectively), but not in FEV1 or asthma control score. We conclude that active smoking impairs the efficacy of short-term oral corticosteroid treatment in chronic asthma.