Tobacco Smoking In Patients Research Articles

The Association Between Chronic Tobacco Smoking and Brain Alterations in Schizophrenia: A Systematic Review of Magnetic Resonance Imaging Studies.

The high co-occurrence of tobacco smoking in patients with schizophrenia spectrum disorders (SSD) poses a serious health concern, linked to increased mortality and worse clinical outcomes. The mechanisms underlying this co-occurrence are not fully understood. Addressing the need for a comprehensive overview of the impact of tobacco use on SSD neurobiology, we conducted a systematic review of neuroimaging studies (including structural, functional, and neurochemical magnetic resonance imaging studies) that investigate the association between chronic tobacco smoking and brain alterations in patients with SSD. Eight structural and fourteen functional studies were included. Structural studies show widespread independent and additive reductions in gray matter in relation to smoking and SSD. The majority of functional studies suggest that smoking might be associated with improvements in connectivity deficits linked to SSD. However, the limited number of and high amount of cross-sectional studies, and high between-studies sample overlap prevent a conclusive determination of the nature and extent of the impact of smoking on brain functioning in patients with SSD. Overall, functional results imply a distinct neurobiological mechanism for tobacco addiction in patients with SSD, possibly attributed to differences at the nicotinic acetylcholine receptor level. Our findings highlight the need for more longitudinal and exposure-dependent studies to differentiate between inherent neurobiological differences and the (long-term) effects of smoking in SSD, and to unravel the complex interaction between smoking and schizophrenia at various disease stages. This could inform more effective strategies addressing smoking susceptibility in SSD, potentially improving clinical outcomes.

The association between childhood trauma and tobacco smoking in patients with psychosis, unaffected siblings, and healthy controls.

In patients with psychosis, rates of tobacco smoking and childhood trauma are significantly higher compared to the general population. Childhood trauma has been proposed as a risk factor for tobacco smoking. However, little is known about the relationship between childhood trauma and smoking in psychosis. In a subsample of the Genetic Risk and Outcome of Psychosis study (760 patients with psychosis, 991 unaffected siblings, and 491 healthy controls), tobacco smoking was assessed using the Composite International Diagnostic Interview and childhood trauma was measured with the Childhood Trauma Questionnaire. Logistic regression models were used to assess associations between trauma and smoking, while correcting for confounders. Positive associations were found between total trauma, abuse, and neglect, and an increased risk for smoking in patients, while correcting for age and gender (ORtrauma 1.77, 95% CI 1.30-2.42, p < 0.001; ORabuse 1.69, 95% CI 1.23-2.31, p = 0.001; ORneglect 1.48, 95% CI 1.08-2.02, p = 0.014). In controls, total trauma and abuse were positively associated with smoking, while correcting for age and gender (ORtrauma 2.40, 95% CI 1.49-3.88, p < 0.001; ORabuse 2.02, 96% CI 1.23-3.32, p = 0.006). All associations lost their significance after controlling for additional covariates and multiple testing. Findings suggest that the association between childhood trauma and tobacco smoking can be mainly explained by confounders (gender, cannabis use, and education) in patients with psychosis. These identified aspects should be acknowledged in tobacco cessation programs.

Corroborating evidence for the correlation between the MTHFR C677T single nucleotide variant and smoking in Croatian subjects independent of ischemic stroke

Hyperhomocysteinaemia is a risk factor for ischemic stroke development. Single nucleotide variation in the methylenetetrahydrofolate reductase gene (MTHFR, C677T polymorphism, T allele) causes a Ala222Val mutation that is associated with hyperhomocysteinemia, cardiovascular disease and stroke. The homozygous TT genotype of MTHFR may also be linked to tobacco smoking in patients from distinct demographic groups. This study evaluated the association of T allele with smoking in a cohort of 301 Croatian adults, including 187 healthy controls and 114 patients with ischemic stroke (IS) and proven ischemic cerebral infarction based on Computed Tomography (CT). Exclusion criteria were hemorrhagic cerebral infarction on CT scan, medical history of diabetes mellitus, and age (>60 years). Cholesterol, triglycerides (TG), low-density lipoprotein (LDL), high-density lipoprotein (HDL) and C-reactive protein (CRP) were biochemically analyzed. A positive correlation between the TT genotype of MTHFR and smoking was observed within our entire study cohort (p = 0.011). In the control group, the relative frequency of the TT genotype in smokers is complemented by the prevalence of the CC genotype among non-smokers. Hence, our study with Croatian subjects corroborates previous studies indicating that the TT MTHFR variant is linked to smoking. This positive correlation between the TT genotype and smoking represents a confounding parameter that must be accounted for to permit evaluation of statistical associations with stroke and biochemical markers in blood and single nucleotide variations in the MTHFR gene.

Tobacco smoking in patients with heart failure and coronary artery disease: A 20-year experience at Duke University Medical Center

We performed a retrospective analysis of HF patients undergoing coronary angiography from 1990-2010. Patients with coronary artery disease (CAD) and HF were stratified by EF (< 50% vs. ≥50%), smoking status (prior/current vs. never smoker), and level of smoking (light/moderate vs. heavy). Time-from-catheterization-to-event was examined using Cox proportional hazard modeling for all-cause mortality (ACM), ACM/myocardial infarction/stroke (MACE), and ACM/HF hospitalization with testing for interaction by HF-type (HFrEF vs. HFpEF). Of 14,406 patients with CAD and HF, 85% (n = 12,326) had HFrEF and 15% (n = 2080) had HFpEF. At catheterization, 61% of HFrEF and 57% of HFpEF patients had a smoking history. After adjustment, there was a significant interaction between HF-type and the association between smoking status and MACE (interaction P = .009). Smoking history was associated with increased risk for MACE in patients with HFrEF (adjusted hazard ratio [HR] 1.18 [1.12-1.24]), but not HFpEF (HR 1.01 [0.90-1.12]). Active smokers had increased mortality following adjustment compared to former smokers regardless of HF-type (HFrEF HR 1.19 [1.06-1.32], HFpEF HR 1.30 [1.02-1.64], interaction P = .50). Heavy smokers trended towards increased risk of adverse outcomes versus light/moderate smokers; these findings were consistent across HF-type (interaction P > .12). Smoking history was independently associated with worse outcomes in HFrEF but not HFpEF. Regardless of HF-type, current smokers had higher risk than former smokers.

T82. THE IMPACT OF SMOKING ON LIFE EXPECTANCY IN PSYCHOTIC DISORDERS, AN ELECTRONIC CASE REGISTER COHORT STUDY

BackgroundSchizophrenia, schizoaffective disorder and bipolar affective disorder are associated with a life expectancy at birth that is 10–20 years shorter than in the general population. The prevalence of cigarette smoking in people with these disorders is very high, but the extent to which this accounts for differences in mortality is unclear. We addressed this issue by examining the effect of smoking on life expectancy and survival in a large electronic healthcare database of patients receiving secondary mental healthcare in South East London.MethodsData on all patients with a diagnosis of schizophrenia, schizoaffective disorder or bipolar affective disorder from 1st January 2007 to 31st December 2018 was obtained. Smoking status was determined using unstructured text data extracted from electronic health records. Chiang’s method of abridged life tables was used to calculate estimates of life expectancy at birth according to gender and most commonly recorded smoking status. Cox proportional hazards models were used to estimate mortality risk and adjusted for a broad range of demographic and clinical variables.Results21,588 patients were included in the study of which 20,155 (93.4%) were classified as either smokers (16,717 [77.4%]) or non-smokers (3,438 (15.9%]). 2,434 (11.3%) participants died by the end of the observation period. In female patients, life expectancy at birth was 67.6 years in current smokers (95% CI: 66.4 to 68.8) and 74.9 years in non-smokers (95% CI: 72.8 to 77.0). In male patients, life expectancy at birth was 63.5 years in current smokers (95% CI: 62.5 to 64.5) and 68.5 years in non-smokers (95% CI: 64.4 to 72.6). Adjusted survival models showed that current smoking was associated with an increased risk of death, in both females (aHR = 1.42; 95% CI: 1.21–1.66) and males (aHR = 1.49; 95% CI: 1.25–1.79).DiscussionSmoking may account for a substantial proportion of the reduced life expectancy in patients with psychotic disorders. Interventions to reduce tobacco smoking in patients with psychosis may therefore improve life expectancy in this group.

The influence of smoking on the formation of airway hyperresponsiveness to cold and the course of destructive-cytological processes in the goblet cells of the bronchial epithelium in patients with asthma

Tobacco smoking in patients with asthma can intensify the bronchi mucosa damage and significantly worsen the course of the disease.Aim. To assess the influence of tobacco smoking on the clinical manifestations of the disease, airway response to cold air exposure and destructive-cytological processes in the goblet cells of bronchial epithelium in patients with asthma.Materials and methods. In 145 patients with asthma their asthma control level was determined by the Аsthma Control Test, lung function (FEV1 , %) and airway response (∆FEV1 , %) to a 3-minute isocapnic hyperventilation (–20 °С) of cold air (IHCA) were evaluated, and induced sputum (IS) was collected. In cytograms of IS a percentage content, the index of cell destruction (ICD) and the index of cytolysis intensiveness (IC) were assessed; histochemically the activity of myeloperoxidase (MPO) and the contents of glycoproteins were identified. The 1st group included 102 non-smokers and the 2nd group included 43 smokers.Results. In IS of patients of the 2nd group in comparison with the 1st one we found intensification of the destructive (ICD = 0.47 ± 0.02 and 0.40 ± 0.02, respectively, р = 0.044) and cytolytic activity of goblet cells (IC = 0.22 ± 0.03 and 0.15 ± 0.02, respectively, р = 0.047) with the domination of the number of completely destroyed cells (21.7 ± 2.4 vs. 14.5 ± 1.6%, р = 0.043) and the decrease in the number of cells with a normal structure (52.5 ± 2.1 vs. 60.5 ± 3.1%, р = 0.047). For smokers it was typical to have high contents of neutrophils in IS (34.1 ± 3.0 vs. 23.9 ± 1.4%, respectively, р = 0.0006) and high level of myeloperoxidase in granulocytes of bronchi (94.3 ± 5.4 vs. 80.7 ± 3.6 pixels, р = 0.037). Smokers responded more actively to IHCA (∆FEV1 was –13.7 ± 2.6 vs. –7.9 ± 1.2%, respectively, р = 0.032), and the degree of the response correlated with the indices of destructive-cytological activity of IS cells.Conclusion. Tobacco smoking in patients with asthma leads to the disturbance of the structure of goblet epithelium in the bronchi with the intensification of destructive-cytological processes, which is accompanied by a decrease in the level of glycoproteins in cytoplasm, an increase in the secretory activity of the goblet cells, neutrophilia, growth of oxidative peroxidase activity of granulocytes, worsening of the bronchial conductance, and intensification of airway response to cold air.

Tobacco Smoking in Patients of Therapeutic Hospital in Izhevsk, Russia

Sergei Pakriev* Author Affiliations Department of Psychiatry, Russia Received: May 13, 2019 | Published: May 20, 2019 Corresponding author: Sergei Pakriev, Department of Psychiatry, Russia DOI: 10.26717/BJSTR.2019.18.003114

Smoking as a factor of immune deficiency deepening in patients with chronic obstructive pulmonary disease and chronic pancreatitis

The objective of the work – to study the state of humoral link of the immune system in patients with chronic pancreatitis with concomitant COPD and without it. There were examined 90 patients with COPD in combination with chronic pancreatitis (45 women and 45 men) aged 35–86 years, mean age – (56.42 ± 4.11 years) and 43 – with chronic pancreatitis. Among the examined individuals there were 32 persons with chronic pancreatitis and COPD I st. (35.5 %), and 58 persons with chronic pancreatitis and COPD II st. (64.5 %). Duration of the disease – from 1 to 25 years, the combination of diseases – from 1 to 10 years. There were 20 (22.2 %) active smokers among surveyed patients. The duration of the smoking 10–30 years, middle duration – (22.75 ± 1.20) years. The smoking experience of 9 patients was 10–20 packs/years, 11 – more than 20 pack/years. Methods of examination: general clinical, laboratory, instrumental, questioning, testing, statistical methods. In patients with chronic pancreatitis without COPD, the level of all studied classes of Ig was significantly increased (IgG 10.4 %, IgA 13.1 %, IgM 45.9 %; P &lt; 0.05). Disbalance in immunoglobulines level was detected in patients with COPD with a significant decrease (P &lt; 0.05) in IgG and IgA levels (by 7.9 % and 27.3 % respectively) and IgM increased (by 76.7 %). This indicates an imbalance in the functioning of the cellular immune system with the formation of a secondary immune deficiency. The increase in the level of immune complexes in both groups (2.6 and 3.2 times, respectively) showed the presence of torpid inflammatory process in COPD. The presence of tobacco smoking in patients with chronic pancreatitis and COPD significantly deepened the changes in the immune system in comparison with non-smokers.

Investigating the Predictive Role of Health Beliefs and Cardiac Self-Efficacy in History of Tobacco Smoking in Patients with Coronary Artery Disease (CAD)

Investigating the Predictive Role of Health Beliefs and Cardiac Self-Efficacy in History of Tobacco Smoking in Patients with Coronary Artery Disease (CAD)

Tobacco smoking is associated with antipsychotic medication, physical aggressiveness, and alcohol use disorder in schizophrenia: results from the FACE-SZ national cohort.

Tobacco smoking is common in schizophrenia and is one of the main causes of premature mortality in this disorder. Little is known about clinical correlates and treatments associated with tobacco smoking in patients with schizophrenia. Still, a better characterization of these patients is necessary, in a personalized care approach. Aggressiveness and childhood trauma have been associated with tobacco smoking in general population, but this association has never been explored in schizophrenia. Our study examines the clinical and therapeutic characteristics of tobacco smoking in schizophrenia. 474 stabilized patients (mean age = 32.2; 75.7% male gender; smokers n = 207, 54.6%) were consecutively included in the network of the FondaMental Expert centers for Schizophrenia and assessed with valid scales. Current tobacco status was self-declared. Aggressiveness was self-reported with Buss-Perry Aggressiveness Questionnaire and Childhood Trauma with Childhood Trauma Questionnaire. Ongoing treatment was reported. In univariate analysis, tobacco smoking was associated with lower education level (p < 0.01), positive syndrome (p < 0.01), higher physical aggressiveness (p < 0.001), alcohol dependence (p < 0.001), and First Generation Antipsychotics (FGAs) use (p = 0.018). In a multivariate model, tobacco smoking remained associated with physical aggressiveness (p < 0.05), current alcohol dependence (p < 0.01) and FGA use (p < 0.05). No association was observed with childhood trauma history, mood disorder, suicidal behavior, psychotic symptom, global functioning or medication adherence. Patients with tobacco use present clinical and therapeutic specificities, questioning the neurobiological links between tobacco and schizophrenia. They could represent a specific phenotype, with specific clinical and therapeutic specificities that may involve interactions between cholinergic-nicotinic system and dopaminergic system. Further longitudinal studies are needed to confirm the potential efficacy of second generation antipsychotics (SGAs) on tobacco use in schizophrenia and to develop effective strategies for tobacco cessation in this population.

The impact of tobacco smoking in patients taking long-action injection drugs – A retrospective comparative study between haloperidol and risperidone

IntroductionSmoking rate seems to be higher among patients with schizophrenia, comparing to other psychiatric entities, mainly in those who are on typical antipsychotics. Tobacco is known to have enzyme inducer properties, due to cytochrome P450 complex activity: CYP1A1, CYP1A2, CYP2E1 and CYP2D6. CYP2D6 and CYP1A2 play an important role in antipsychotics metabolism, mainly in the first generation ones, like haloperidol, despite its importance in risperidone metabolism.AimTo analyze the importance of tobacco smoking in patients taking long-action injections.ObjectivesTo investigate how sexual dysfunction varies with tobacco smoking, in patients taking long-action injections.MethodsIndividuals from both sexes, from 18 to 55 years old, taking antipsychotic long-action injections, answered the Arizona Sexual Experience Scale (ASEX).ResultsIn the studied population (n = 44), there were 20 individuals on haloperidol and 24 individuals on risperidone. In a total of 18 (40.9%) positive results for sexual dysfunction, 6 were on haloperidol (30%), 12 (50%) were on risperidone. Seventeen individuals of the 20 who were on haloperidol were smokers, but only 4 were considered to have sexual dysfunction, 35.3%; 12 of the 24 individuals who were on risperidone were smokers, but only 5 were considered to have sexual dysfunction, 41.7%.ConclusionsPatients treated with haloperidol smoke more, comparing to risperidone. Sexual dysfunction is more frequent in patients taking risperidone than in patients taking haloperidol. This data supports that CYP2D6-CYP1A2 induction by tobacco, mainly interacts with haloperidol, which may be helpful for patients to try less side effects.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Opioid Use and Tobacco Smoking in Patients With Rheumatic Diseases

Background: Rheumatic diseases are chronic diseases, which may be associated with severe and debilitating pain. Objectives: The purpose of this study was to examine the prevalence of tobacco and opioid use among rheumatic patients. Patients and Methods: In this cross-sectional study, 1042 patients referred to a major rheumatology clinic of Kerman city, in south east of Iran, were interviewed. Patients were divided into seven groups of disease, including rheumatoid arthritis (330 persons) osteoarthritis (313 persons), systemic lupus erythematosus (149 persons), back pain (146 persons), spondyloarthropathies (62 persons), Behcet’s disease (25 persons), and scleroderma (17 persons). The questionnaire consisted of demographic variables, disease-related variables (e.g. duration of disease), the severity of pain on the VAS scale and use of opioids and tobacco based on self-reporting. Results: The mean age of the patients was 49.3 ± 15.0 years and mean disease duration in the whole sample was 7.1 ± 5.1 years. Opium consumption was reported by 104 persons (9.9%), codeine, by 185 persons (17.7%), cigarette smoking by 49 persons (4.7%) and waterpipe smoking by 34 persons (3.3%). Conclusions: In this study, codeine consumption is the most frequently used substance. The consumption of opium is not much different from the general population. Also, the rate of cigarette and waterpipe smoking was less than that in the general population. The prevalence of opium use and tobacco smoking was higher in men than in women. There was no significant relationship between type of rheumatic diseases, disease-related variables, and substance use.

P.3.d.087 Tobacco smoking in patients taking antipsychotic long-acting injections and sexual dysfunction

P.3.d.087 Tobacco smoking in patients taking antipsychotic long-acting injections and sexual dysfunction

Do We Need Tailored Smoking Cessation Interventions for Smokers with COPD? A Comparative Study of Smokers with and without COPD Regarding Factors Associated with Tobacco Smoking

Background: The prevalence of tobacco smoking in patients with chronic obstructive pulmonary disease (COPD) is high. It is assumed that this group of smokers has more difficulties quitting than smokers without COPD. In order to increase the effectiveness of smoking cessation treatments in smokers with COPD it is important to identify any smoking-related factors which are specific to this group of smokers. Objective: To compare smokers with COPD with smokers without COPD regarding factors associated with tobacco smoking and quitting. Methods: We conducted a questionnaire survey in all smoking patients with a recorded diagnosis of COPD from a large Dutch primary health care network. We compared this group with twice as many age-, sex- and health care centre-matched smokers without COPD. Results: Respondents were 107 smokers with COPD and 86 smokers without COPD. The number of attempts to quit was similar in both groups but more smokers with COPD had ever used pharmacological, behavioural and alternative smoking cessation treatments. Furthermore, smokers with COPD more often received triggers to quit from their environment and from their general practitioner, and they were more concerned about, and aware of, the health risks of smoking. Importantly, smokers with COPD reported higher levels of depression and cigarette dependence and a lower self-efficacy to refrain from smoking than smokers without COPD. Conclusion: Smokers with COPD differ from smokers without COPD on several factors which are associated with tobacco smoking and quitting. Taking into account these differences may help to increase the effectiveness of smoking cessation treatments for the specific group of smokers with COPD.

PRS15 - The Prevalence of Tobacco Smoking in Patients With Diabetes in Hospital Pulau Pinang, Malaysia

PRS15 - The Prevalence of Tobacco Smoking in Patients With Diabetes in Hospital Pulau Pinang, Malaysia

FEV1 inversely correlates with metalloproteinases 1, 7, 9 and CRP in COPD by biomass smoke exposure.

BackgroundMatrix metalloproteinases (MMPs) and C-reactive protein (CRP) are involved in chronic obstructive pulmonary disease (COPD) pathogenesis. The aim of the present work was to determine plasma concentrations of MMPs and CRP in COPD associated to biomass combustion exposure (BE) and tobacco smoking (TS).MethodsPulmonary function tests, plasma levels of MMP-1, MMP-7, MMP-9, MMP-9/TIMP-1 and CRP were measured in COPD associated to BE (n = 40) and TS (n =40) patients, and healthy non-smoking (NS) healthy women (controls, n = 40).ResultsPlasma levels of MMP-1, MMP-7, MMP-9, and MMP-9/TIMP-1 and CRP were higher in BE and TS than in the NS healthy women (p <0.01). An inverse correlation between MMP-1, MMP-7, MMP-9, MMP-9/TIMP-1 and CRP plasma concentrations and FEV1 was observed.ConclusionsIncrease of MMPs and CRP plasma concentrations in BE suggests a systemic inflammatory phenomenon similar to that observed in COPD associated to tobacco smoking, which may also play a role in COPD pathogenesis.

Genetic Variation of the Mu Opioid Receptor (OPRM1) and Dopamine D2 Receptor (DRD2) is Related to Smoking Differences in Patients with Schizophrenia but not Bipolar Disorder.

It is not known why mentally ill persons smoke excessively. Inasmuch as endogenous opioid and dopaminergic systems are involved in smoking reinforcement, it is important to study mu opioid receptor (OPRM1) A118G (rs1799971), dopamine D2 receptor (DRD2) Taq1A (rs1800497) genotypes, and sex differences among patients with schizophrenia or bipolar disorder. Smokers and nonsmokers with schizophrenia (n=177) and bipolar disorder (n=113) were recruited and genotyped. They were classified into three groups: current smoker, former smoker, and never smoker by tobacco smoking status self-report. The number of cigarettes smoked per day was used as the major tobacco smoking parameter. In patients with schizophrenia, tobacco smoking prevalence was greater in males than in females as expected, but women had greater daily cigarette consumption (p<0.01). Subjects with schizophrenia who had the OPRM1 *G genotype smoked more cigarettes per day than the AA allele carriers with schizophrenia (p<0.05). DRD2 Taq1A genotype differences had no effect on the number of cigarettes smoked per day. However, female smokers with schizophrenia who were GG homozygous of the DRD2 receptor smoked more than the *A male smokers with schizophrenia (p<0.05). In bipolar patients, there were no OPRM1 and DRD2 Taq1A genotype differences in smoking status. There also were no sex differences for smoking behavior among the bipolar patients. The results of this study indicate that single nucleotide polymorphism (SNP) of the less functional mu opioid receptor increases tobacco smoking in patients with schizophrenia. Alteration of DRD2 receptor function also increased smoking behavior in females with schizophrenia.

P03-134 - Does the frequency of tobacco smoking in patients with schizophrenia varies with regard to the type of antipsychotic drugs?

BackgroundTobacco smoking is considered as one of leading preventable causes of death. High prevalence of tobacco smoking was reported among individuals with mental illnesses, and it is extremely high among patients with Schizophrenia. It is possible that antipsychotic drugs side effects are contributing to this negative trend. Objective of this paper was to establish frequency of cigarette smoking among patients with Schizophrenia hospitalized at the psychiatry clinic and to determinate the difference in frequencies of cigarette smoking among patients with Schizophrenia treated with first or second generation antipsychotics.MethodsStudy included 60 patients with Schizophrenia treated with antipsychotics for period of six months or longer. Experimental group included 30 patients treated with second generation antipsychotics, and control group included 30 patients treated with first generation antipsychotics. Descriptive statistical methods are used. The levels of statistical significance between parametric data were determined by t- test, and between nonparametric data by chi square test. Level of significance was established at P &lt; .05.ResultsIn this sample was 75% smokers, and out of this 46.6% consume up to 20 cigarettes per day, 40% consume 20 to 40 cigarettes, 8.8% between 40-60 cigarettes, and 4.4% consume over 60 cigarettes per day. There was no significant differences between groups of patients treated with first and second generation antipsychotics.ConclusionTobacco smoking is very frequent among patients with Schizophrenia. In this study we did not found significant difference in frequency of tobacco smoking between groups of patients treated with first or second generation antipsychotics.

Morphological and immunological analysis of the oral mucosa in tobacco smoking and odontopreparation

Tobacco smoking causes pronounced structural reorganization of the gingival mucosa and its atrophic changes. Odontopreparation stimulates destructive processes in the gingival mucosa promoting activation of local immunity (stimulation of immunoglobulin synthesis). Significant differences in the local humoral immunity (IgG dysimmunoglobulinemia) and cytokine spectrum in nonsmoking and tobacco-smoking patients were detected. Subcompensated level of immune resistance in tobacco smokers prompts referring them to a group at a high risk of chronic pathological processes of the oral cavity.

Tobacco Smoking in Patients with Cardiovascular Disease.

Smoking tobacco is a major risk factor for patients with cardiovascular disease (CVD). Quitting smoking rapidly reduces the risk for cardiovascular events. The majority of patients who smoke express a desire to stop, and cost-effective interventions are available. Behavioral (counseling) and pharmacologic (nicotine replacement and non-nicotine medications) treatments double or triple the rate of long-term cessation and should be offered in combination to all patients with CVD who use tobacco. Behavioral therapy can be effectively delivered by a variety of health care providers and means (in person, telephone, mail). For patients with CVD, more intensive and sustained interventions should be encouraged. Nicotine patches have been studied extensively in patients with stable CVD and are safe. Bupropion (a non-nicotine aid) also may be especially useful for patients with CVD. Special consideration is needed for patients with acute coronary syndromes (ie, myocardial infarction and unstable angina). It is important to create a clinical environment that supports treatment of patients with nicotine addiction. Simple changes in office and hospital routines and procedures (establishing routine screening to identify users of tobacco, prompts to encourage intervention, establishing links to more intensive nicotine-dependence treatment programs) can substantially improve the identification, treatment, and outcomes for patients with CVD who use tobacco.