'Smoker's paradox' in young patients with acute myocardial infarction

1. Of the patients suffering from acute myocardial infarction (AMI), smokers are younger than non-smokers, which may be a major confounding factor causing 'smoker's paradox'. Therefore, in the present study we evaluated the 'smoker's paradox' in young patients with AMI.2. In all, 1218 young AMI patients (≤ 45 years of age), comprising 990 smokers and 228 non-smokers, were enrolled in the present study. In-hospital and 8 months clinical outcomes were compared between the smokers and non-smokers. 3. Baseline clinical characteristics showed that smokers were more likely to be male (97.9% vs 72.4%; P < 0.001) and had a higher rate of ST-segment elevation myocardial infarction (71.3% vs 59.5%; P = 0.001) than non-smokers. Clinical outcomes showed that smokers had lower rates of in-hospital cardiac death (0.8% vs 3.5%; P = 0.004), total death (0.8% vs 3.5%; P = 0.004) and 8 months cardiac death (1.1% vs 3.9%; P = 0.006) and total death (1.3% vs 4.4%; P = 0.005) than non-smokers. Multivariable logistic analysis showed that current smoking was an independent protective predictor of 8 months cardiac death (odds ratio (OR) 0.25; 95% confidence interval (CI) 0.07-0.92; P = 0.037) and total death (OR 0.26; 95% CI 0.09-0.82; P = 0.021). Subgroup analysis in patients who underwent percutaneous coronary intervention after AMI showed that current smoking was an independent protective predictor of 8 months total major adverse cardiac events (OR 0.47; 95% CI 0.23-0.97; P = 0.041). 4. Current smoking seems to be associated with better clinical outcomes in young patients with AMI, suggesting the existence of the 'smoker's paradox' in this particular subset of patients.     

WHOLE BLOOD AGGREGATION AND PLASMA LYSO-PAF RELATED TO SMOKING AND ATHEROSCLEROSIS

1. Aggregation of diluted whole blood (impedance method) and thromboxane B2 production during aggregation were measured in cigarette smokers and non-smokers, aged 41-68 years, with (n = 14) and without (n = 15) major symptomatic peripheral vascular disease. The plasma level of the lyso derivative of platelet activating factor (lyso-PAF) was also measured using a bioassay with 14C-serotonin labelled rabbit platelets, after extraction and acetylation to active PAF. 2. Aggregation to ADP and collagen was significantly less in non-smokers without vascular disease (n = 8) than in the other three groups (P less than 0.01; ANOVA). Thromboxane B2 production was not significantly different between the groups. There was no significant difference in plasma lyso-PAF between groups. No change was found in any variable after smokers smoked two cigarettes. 3. In these older age subjects, both vascular disease and the smoking habit were associated with greater whole blood aggregation. However, current smoking and the smoking of two cigarettes did not affect aggregation in subjects with vascular disease and plasma lyso-PAF levels were not consistently related to either smoking or vascular disease.     

Does smoking influence the pharmacokinetics and pharmacodynamics of the H2-receptor antagonist famotidine?

Twelve healthy habitual cigarette smokers and eight non-smokers participated in a double-blind placebo controlled study to determine the effect of smoking on the pharmacokinetics and pharmacodynamics of the H2-receptor antagonist famotidine. In smokers, cigarette smoking was standardised and started 1 h before (A), or 2 h after (B) drug administration, or was prohibited (C). Intragastric pH-levels (IGpH) were measured with an ambulatory pH-recorder. Famotidine (40 mg orally) significantly raised median 22 h IGpH in non-smokers and smokers in all study periods. The smoking sequence (A, B, C) did not significantly influence median 22 h IGpH in both placebo-treated and famotidine-treated smokers, and no significant difference in median 22 h IGpH was shown between smokers and non-smokers. Plasma drug concentrations were similar in the various experiments, although famotidine was detected earlier in plasma from non-smokers compared with smokers (P less than 0.05). Smoking did not interfere significantly with the pharmacokinetics and pharmacodynamics of famotidine.     

Cigarette smoking enhances the elimination of quinine

The pharmacokinetics of a single dose (600 mg) of quinine sulphate were examined in a group of non-smokers (n = 10) and in heavy cigarette smokers (n = 10). The mean (+/- s.d.) oral clearance of quinine in smokers (0.189 +/- 0.075 1 h(-1) kg(-1)) was significantly greater than in non-smokers (0.107 +/- 0.045 1 h(-1) kg(-1) , P < 0.01). The unbound clearance of quinine which reflects activity of the drug-metabolizing enzyme, was considerably greater (1.5-fold) in the smokers than in the non-smoker subjects. The mean elimination half-life of quinine in smokers was 7.5 +/- 1.4 (s.d.) h, significantly shorter (P < 0.005) than the mean value in non-smokers (12.0 +/- 3.1 h). These results suggest that cigarette smoking enhances the elimination of quinine. The clinical significance of these findings is unknown but they indicate the need for caution in the administration of quinine to patients who are heavy cigarette smokers.     

Vitamin C concentration in plasma and leucocytes of men related to age and smoking habit.

Morning plasma and leucocyte vitamin C concentrations were measured in 178 healthy men aged 17-68 years. In the youngest age group (17-29 years), smokers had significantly lower plasma (P less than 0.01) and leucocyte (P less than 0.001) vitamin C levels than non-smokers. With advancing age plasma and leucocyte vitamin C levels of non-smokers appeared to decline. The lower levels in younger smokers did not significantly alter in the later decades. There was no significant difference between the plasma or leucocyte vitamin C levels of smokers and non-smokers in the decade 60-69 years.     

The effect of variable cigarette consumption on the interaction with clozapine and olanzapine

Objective Cigarette smoking has been shown in several studies to induce the metabolism of the cytochrome P4501A2 (CYP1A2) substrates clozapine and olanzapine. The aim of the present study was to investigate the dose-dependent effect of cigarette smoking on serum concentrations of these drugs in a naturalistic setting.Methods In 73 schizophrenic patients recruited from psychiatric nursing homes, patient characteristics, smoking habits, drug dosing and serum concentrations of clozapine (n=33) and olanzapine (n=40) were registered. Concentration to dose (C/D) ratios of clozapine and olanzapine in non-smokers and subgroups of smokers were compared.Results Fifty-nine patients (80%) were smokers and these were stratified into the following groups according to smoking habits: 1–6 (n=0), 7–12 (n=13), 13–19 (n=18) and ≥20 (n=28) cigarettes daily. While the mean ratio was twice as high in non-smokers compared to smokers for both drugs (p<0.01), the C/D ratios of clozapine and olanzapine were not significantly different between the subgroups of smokers (p >0.15). Absolute serum concentrations were also higher in non-smokers compared to smokers: 50% for clozapine (p=0.058) and 67% for olanzapine (p<0.01).Conclusion A daily consumption of 7–12 cigarettes is probably sufficient for maximum induction of clozapine and olanzapine metabolism. A 50% lower starting dose of both drugs in non-smokers seems rational to avoid side effects.     

Pharmacokinetics of N-desmethyldiazepam after a single oral dose of clorazepate: The effect of smoking

Summary The pharmacokinetics of N-desmethyl-diazepam was evaluated after oral administration of clorazepate 20 mg to 12 healthy male volunteers (6 smokers; 6 non-smokers), aged 23–29 years. Plasma levels of desmethyldiazepam were measured by gas liquid chromatography. The half life of elimination (t_1/2) was significantly longer in the non-smoking volunteers than in the smokers: 54.7±17.7 versus 29.8±9.9 h (p<0.05). Peak plasma concentrations (C_max) were higher in non-smokers than in smokers, 413±106 µg/l and 245±50 µg/l, respectively (p<0.05). The sedative effect of clorazepate was less severe in smokers than in non-smokers.     

Effect of cigarette smoking on salivary epidermal growth factor (EGF) and EGF receptor in human buccal mucosa.

The mouth acts as a primary target for cigarette smoke which is associated with several oral diseases and cancer. The present study investigated the effect of cigarette smoking on salivary EGF and the buccal EGF receptor. Samples of whole saliva and buccal biopsy were obtained from 15 healthy volunteers (10 smokers and 5 non-smokers). The smokers smoked 20 or more cigarettes/day for more than 5 years. Salivary cotinine (a major metabolite of nicotine) was determined by radioimmunoassay (RIA). The salivary cotinine level was consistent with the self-reported smoking status (smokers, 106-530 ng/ml saliva; non-smokers, < 2 ng/ml saliva). As compared to the non-smokers, the salivary EGF concentration (determined by RIA) was 32% lower in those smokers whose salivary cotinine level was 250 ng/ml or higher (non-smokers, 2.21 +/- 0.16; smokers, 1.57 +/- 0.09 ng/ml saliva; mean +/- S.E.M., P < 0.01). There was no significant difference in 125I-labeled EGF binding to the buccal receptor between the two groups. However, EGF stimulated the autophosphorylation of a 170-kDa protein band in the sample of non-smokers, but not in the smokers. The immunoblot analysis using anti-EGF receptor antibody indicated that the smoking-related deficiency in EGF receptor autophosphorylation was due to the functional alteration of the receptor proteins. In conclusion, cigarette smoking reduces the salivary EGF level and impairs the function of buccal EGF receptor, which may be associated with the pathology of smoking-related oral disease.     

吸烟对2型糖尿病男性患者血糖控制的影响

目的：探讨吸烟对2型糖尿病男性患者空腹血糖（FBG）,餐后2 h 血糖（2hPBG）,糖化血红蛋白（HbA1 C）的影响。方法选取2型糖尿病男性患者142例,按吸烟情况分为不吸烟组（从不吸烟,n ＝44）,戒烟组（戒烟半年以上,n ＝33）,少量吸烟组（每天≤20支,n ＝33）,大量吸烟组（每天＞20支,n ＝32）,采用现场调查结合病例对照研究的方法,询问患者年龄、糖尿病病程、工作活动强度、吸烟、降糖药的应用等情况,测量血压、身高、体重、腰围、臀围,计算体重指数（BMI）、腰臀比（WHR）等指标,实验室检测葡萄糖（GLU）、2hPBG、HbA1 C,比较各组间血糖、糖化血红蛋白的差异;逐步回归及偏相关分析,了解吸烟对血糖控制影响的显著性及影响程度。结果（1）不吸烟组与大量吸烟组相比 FBG、2hPBG 明显降低（P ＜0．01）,HbA1 C 有所降低但差异无统计学意义（P ＞0．05）;不吸烟组与戒烟组比较2hPBG 有所升高（P ＜0．05或 P ＜0．01）;（2）少量吸烟组与大量吸烟组比较 FBG、2hPBG所降低但差异无统计学意义（P ＞0．05）;吸烟组与戒烟组相比 FBG、2hPBG、HbA1 C 均增高（P ＜0．05或P ＜0．01）;（3）吸烟是 HbA1 C 的独立危险因素（P ＜0．05,β＝－0．216）,FBG、2hPBG、HbA1 C 与日吸烟量、吸烟年限等无明显相关性（P ＞0．05）。结论吸烟是与年龄、BMI、工作活动强度、DM病程、用药情况等影响无关,为2型糖尿病男性患者血糖控制水平差的独立危险因素;吸烟组与戒烟组,戒烟组与不吸烟组之间血糖控制指标（FBG、2hPBG、HbA1 C）等的差异,表明大量吸烟不利于2型糖尿病男性患者血糖的控制,戒烟对2型糖尿病男性患者血糖控制有明显的积极的作用,在餐后血糖的控制上甚至优于从不吸烟患者。     

Effects of Smoking and Smoking Deprivation on the Articulatory Loop of Working Memory

This study examined the effects of smoking and smoking deprivation on the articulatory loop of working memory. Forty subjects (20 smokers and 20 non-smokers) performed tasks involving serial recall of letters on two occasions 1 week apart. In each test one part was conducted with articulatory suppression and the other without it. The smokers completed one test following 12 h of smoking deprivation, and the other after smoking a cigarette. The order of suppression/non-suppression conditions and the order of smoking and smoking deprivation were balanced across subjects. The results showed that deprived smokers performed significantly worse than both smoking smokers and non-smokers in the task without suppression. Although all the subjects performed significantly worse whilst under articulatory suppression, smoking status was not found to influence performance here. These results imply that smoking has the effect of returning the smoker to a comparable level of performance to that seen in non-smokers, and suggest that smoking abstinence has a negative effect when performance involves the articulatory loop. © 1997 John Wiley & Sons, Ltd.     

Disopyramide pharmacokinetics and metabolism: effect of inducers.

1. The disposition of orally administered disopyramide was studied in a population of smokers (n = 6) and non-smokers (n = 8) before and during phenobarbitone treatment (100 mg daily for 21 days; Cp 21st day = 13.9 +/- 2.0 micrograms ml-1). The comparative inducibility of these populations by phenobarbitone was assessed as was the inductive effect of cigarette smoking, per se. Furthermore, the determinants of the intensity of the inductive effect were examined, as well as the effect of the barbiturate on the binding of disopyramide to alpha 1-acid glycoprotein (AGP). 2. Smokers and non-smokers exhibited similar half-lives (6.48 +/- 1.49 vs 6.66 +/- 1.02 h), apparent total body clearances (0.100 +/- 0.020 vs 0.117 +/- 0.034 l h-1 kg-1), mean renal clearances (0.043 +/- 0.0093 vs 0.057 +/- 0.013 l h-1 kg-1) and apparent intrinsic metabolic clearances (0.057 +/- 0.015 vs 0.060 +/- 0.024 l h-1 kg-1) before phenobarbitone treatment. 3. Both populations responded comparably to barbiturate exposure in that apparent intrinsic metabolic clearance more than doubled. Interestingly, the magnitude of this increase was highly dependent on the observed baseline apparent intrinsic metabolic clearance, (r' = 0.81; P less than 0.001). 4. Phenobarbitone treatment of non-smokers resulted in an increase in the AUC of the active metabolite N-despropyl disopyramide (MND), but not significantly (3.8 +/- 1.6 vs 4.1 +/- 2.3 micrograms ml-1 h). Similar results were observed in smokers (3.5 +/- 1.4 vs 3.9 +/- 2.0 micrograms ml-1 h, respectively). 5. The percent of administered dose recovered in urine as disopyramide in non-smokers was significantly decreased upon phenobarbitone treatment (43 +/- 6% vs 25 +/- 5%), whereas the percent of dose recovered as MND increased significantly in this group (25 +/- 6% vs 31 +/- 5%). The population of smokers responded similarly. 6. At doses typically used to achieve hepatic microsomal enzyme induction in man, phenobarbitone treatment caused no significant change or trend towards a change in serum AGP concentrations as measured using the radial immunodiffusion method in nonsmokers (67.4 +/- 19.9 mg dl-1 vs 68.0 +/- 40.7 mg dl-1) or smokers (64.5 +/- 15.7 vs 67.9 +/- 14.9). Similarly, when AGP concentration was estimated in serum from non-smokers using a nephelometric method no effect attributable to phenobarbitone was observed (47.9 +/- 1.3 vs 47.9 +/- 16.8 mg dl-1). Consistent with this observation, disopyramide free fraction was not affected by barbiturate treatment.     

The influence of age, smoking and hyperthyroidism on plasma propranolol steady state concentration.

1 Plasma propranolol steady state concentration (Css) was determined during chronic dosage (160 mg/day) in 22 hyperthyroid patients (aged 16-75 years, 11 smokers, 11 non-smokers) and again following treatment when euthyroid. 2 There was a positive correlation between plasma propranolol Css and age in patients both when hyperthyroid (r = 0.74, P less than 0.01) and when euthyroid (r = 0.58, P less than 0.05). 3 Plasma propranolol Css in hyperthyroid patients were lower (P less than 0.05) in smokers than in non-smokers. 4 Following correction of hyperthyroidism there was a significant increase (P less than 0.01) in both the plasma propranolol Css and degree of plasma protein binding of propranolol. 5 Hyperthyroidism and smoking are known to increase the rate of drug metabolism and it is suggested that these variables may give rise to or accentuate an age related reduction in propranolol clearance.     

The effect of cigarette smoking on drug metabolism in the liver and placenta: the use of cotinine in verifying smoking status

Placental and hepatic xenobiotic-metabolising activities were studied in smokers and non-smokers, who were classified by anamnestic interview, plasma thiocyanate and plasma cotinine determinations. Plasma thiocyanate assay is inadequate in the classification of smokers and non-smokers. Plasma cotinine levels reflect more accurately the smoking status. The anamnestic smokers remained smokers and several self-declared non-smokers proved to be smokers. On the basis of plasma cotinine determination all real smokers had higher 7-ethoxyresorufin 0-deethylase (ERDE) activities measured either in placental microsomes or liver biopsy homogenates than non-smokers. Classification based on plasma cotinine levels showed a statistically significant (P less than 0.001) difference between smokers and non-smokers in liver homogenate ERDE activity. However, cotinine levels did not correlate with any of the xenobiotic-metabolising activities tested. An objective biochemical marker, such as cotinine determination seems to be necessary when evaluating the effect of smoking on drug metabolism in man.     

Working memory in cigarette smokers: comparison to non-smokers and effects of abstinence

The present study was designed to examine the effect of cigarette smoking and withdrawal on working memory. Participants included 15 smokers and 22 matched non-smokers. For both groups the N-Back Task (of working memory) was administered in two test blocks on each of two days. On one day, smokers were tested after >or=13 h abstinence; on the other day, testing began or=13 h but not 相似文献   

Ethnic variation in CYP2A6 and association of genetically slow nicotine metabolism and smoking in adult Caucasians

Genetically variable CYP2A6 is the primary enzyme that inactivates nicotine to cotinine. Our objective was to investigate allele frequencies among five ethnic groups and to investigate the relationship between genetically slow nicotine metabolic inactivation and smoking status, cigarette consumption, age of first smoking and duration of smoking. Chinese, Japanese, Canadian Native Indian, African-North American and Caucasian DNA samples were assessed for CYP2A6 allelic frequencies (CYP2A6*1B-*12,*1x2). Adult Caucasian non-smokers (n = 224) (1-99 cigarettes/lifetime) and smokers (n = 375) (> or = 100 cigarettes/lifetime) were assessed for demographics, tobacco/drug use history and DSM-IV dependence and genotyped for CYP2A6 alleles associated with decreased nicotine metabolism (CYP2A6*2, CYP2A6*4, CYP2A6*9, CYP2A6*12). CYP2A6 allele frequencies varied substantially among the ethnic groups. The proportion of Caucasian slow nicotine inactivators was significantly lower in current, DSM-IV dependent smokers compared to non-smokers [7.0% and 12.5%, respectively, P = 0.03, odds ratio (OR) = 0.52; 95% confidence interval (CI) 0.29-0.95]; non-dependent smokers showed similar results. Daily cigarette consumption (cigarettes/day) was significantly (P = 0.003) lower for slow (21.3; 95% CI 17.4-25.2) compared to normal inactivators (28.2; 95% CI 26.4-29.9); this was observed only in DSM-IV dependent smokers. Slow inactivators had a significantly (P = 0.03) lower age of first smoking compared to normal inactivators (13.0 years of age; 95% CI 12.1-14.0 versus 14.2; 95% CI 13.8-14.6), and a trend towards smoking for a shorter duration. This study demonstrates that slow nicotine inactivators are less likely to be adult smokers (dependent or non-dependent). Slow inactivators also smoked fewer cigarettes per day and had an earlier age of first smoking (only dependent smokers).     

Effects of cigarette smoking and exposure to cadmium and lead on phenotypic variability of hepatic CYP2A6 and renal function biomarkers in men

Effects of cigarette smoking and exposure to dietary cadmium (Cd) and lead (Pb) on urinary biomarkers of renal function and phenotypic variability of cytochrome P450 2A6 (CYP2A6) were investigated in a group of 96 healthy Thai men with mean age of 36.7 year (19-57 years). In non-smokers, Cd burden increased with age (r = 0.47, P < 0.001). In current smokers, Cd burden increased with both age (r = 0.45, P = 0.01) and number of cigarettes smoked per day (r = 0.32, P = 0.05). Cd-linked renal tubular dysfunction was seen in both smokers and non-smokers, but Pb-linked glomerular dysfunction was seen in smokers only, possibly due to more recent exposure to high levels of Cd and Pb, as reflected by 30-50% higher serum Cd and Pb levels in smokers than non-smokers (P < 0.05). Exposure to dietary Cd and Pb appeared to be associated with mild tubular dysfunction whereas dietary exposure plus cigarette smoking was associated with tubular plus glomerular dysfunction. Hepatic CYP2A6 activity in non-smokers showed a positive association with Cd burden (adjusted beta = 0.38, P = 0.006), but it showed an inverse correlation with Pb (adjusted beta = -0.29, P = 0.003), suggesting opposing effects of Cd and Pb on hepatic CYP2A6 phenotype. In contrast, CYP2A6 activity in current smokers did not correlate with Cd or Pb, but it showed a positive correlation with serum ferritin levels (r = 0.45, P = 0.01). These finding suggest that Pb concentrations in the liver probably were too low to inhibit hepatic synthesis of heme and CYP2A6 and that the concurrent induction of hepatic CYP2A6 and ferritin was probably due to cigarette smoke constituents other than Cd and Pb.     

Effects of smoking on spontaneous and induced sister chromatid exchanges in lymphocytes

Spontaneous and mitomycin C-induced sister chromatid exchanges (SCEs) in lymphocytes were analyzed in 24 non-smokers and 24 sex- and age-matched smokers. Mean spontaneous SCE frequency for non-smokers was 9.8 SCEs/cell, and that for smokers was 11.5 SCEs/cell. The difference was statistically significant (P less than 0.001 by t-test). These results suggest that spontaneous SCE frequency in lymphocytes is useful for evaluation of biological effects of environmental mutagens. However, we could not find any effects of smoking on the sensitivities of lymphocytes to mitomycin C in vitro. The effects of mutagens on humans may be independent of one another.     

Different response patterns of several ligands at the sphingosine-1-phosphate receptor subtype 3 (S1P3)

Background and purpose:

Recently, some ligands targeting the sphingosine-1-phosphate receptor subtype 3 (S1P₃) have become available. The characterization of these compounds was mainly based on one functional read-out system, although S1P₃ receptors are known to activate different signal transduction pathways. Therefore, this study pharmacologically characterizes these compounds using different assays.

Experimental approach:

Using CHO-FlpIn cells expressing the human S1P₃ receptor the potencies and maximal effects of S1P, FTY720-P, VPC23019, VPC23153 and VPC24191 were determined in three different assays [inhibition of cAMP accumulation, elevation of intracellular calcium concentrations ([Ca²⁺]_i) and S1P₃ receptor internalization].

Key results:

All compounds tested inhibited forskolin-induced cAMP accumulation, increased [Ca²⁺]_i and induced S1P₃ receptor internalization but with different potencies and maximal effects. S1P was the most potent compound in all assays followed by FTY720-P. The VPC compounds were generally less potent than S1P and FTY720-P. Regarding the maximal effects, all compounds except VPC23153, behaved as full agonists in the cAMP accumulation assay. In the calcium assay, FTY720-P, VPC23019 and VPC24191 displayed partial and VPC23153 weak partial agonist activity, relative to S1P. Interestingly, treatment with the G_i inactivator Pertussis toxin, did not affect S1P-induced [Ca²⁺]_i elevations but inhibited those in response to the other compounds, by about 50%.

Conclusions and implications:

This study demonstrated differential response patterns at the S1P₃ receptor for a range of ligands. These differences could indicate the presence of functional selectivity at this receptor as FTY720-P and the VPC compounds seemed to signal predominantly via G_i– whereas S1P activated G_i and G_q-coupled pathways.     

Cognitive avoidance and aversive cues related to tobacco in male smokers

BackgroundTreatment using aversive conditioning has been suggested for smoking cessation. The efficacy of this method is thought to be associated with cognitive avoidance. We compare differences in avoidance traits and patterns of associated brain activation in response to cues that induce cravings versus aversion between smokers and non-smokers.MethodsFifteen smokers and fifteen non-smokers completed cue reactivity tasks while undergoing functional magnetic resonance imaging (fMRI) to examine brain responses to craving-inducing cues (Cr) and aversion-inducing cues (Av). Participant avoidant traits were also assessed.ResultsActivation of the left frontal subcallosal gyrus in response to Cr was greater in smokers than in non-smokers. Smokers showed less activation in the right temporal lobe in response to Av than did non-smokers. Brain activation in response to Cr in the left frontal subcallosal gyrus was positively correlated with Fagerstrom Test for Nicotine Dependence (FTND) scores in smokers. Brain activation in response to Av in the right temporal lobe was negatively correlated with the Korean Version of the Cognitive Avoidance Questionnaire (KCAQ) scores in non-smokers.ConclusionsCognitive avoidance in smokers during aversive stimulation might result in sustaining addictive behaviors. On the other hand, non-smokers may be able to emotionally confront the adverse effects of smoking.     

Cetraxate, a mucosal protective agent, combined with omeprazole, amoxycillin, and clarithromycin increases the eradication rate of helicobacter pylori in smokers

BACKGROUND: Our previous study demonstrated that Helicobacter pylori eradication was less effective in smokers than in non-smokers. Cetraxate is an anti-ulcer drug that increases gastric mucosal blood flow. AIM: To evaluate the effect of cetraxate combined with new triple therapy for the eradication of H. pylori in smokers. METHODS: This study had a single-centre, double-blind, randomized non-placebo design. A total of 106 consecutive H. pylori-positive smoking patients were randomly allocated to one of two regimens: one group received omeprazole (20 mg), amoxycillin (1500 mg), and clarithromycin (600 mg) for 7 days (OAC, n=55). The other group recieved OAC plus cetraxate (600 mg) for 7 days (OAC + CET, n=51). The success of H. pylori eradication was evaluated by histology and the 13C-urea breath test at 4 weeks after completion of treatment. RESULTS: By intention-to-treat analysis, the H. pylori eradication rate was 55% in the OAC group and 92% in the OAC + CET group (P<0.01). By per protocol analysis, the H. pylori eradication rate was 58% in the OAC group and 94% in the OAC + CET group (P<0.01). CONCLUSION: Cetraxate combined with new triple therapy increases the eradication of H. pylori in smokers.