Treatment of Cigarette Smoking

Hall SM, Reus VI, Munoz RF, et al Nortriptyline and cognitive-behavioral therapy in the treatment of cigarette smoking. Arch Gen Psychiatry 55 683-690, 1998 Hall SM, Humfleet GL, Reus VI, et al Psychological intervention and antidepressant treatment in smoking cessation. Arch Gen Psychiatry 59 930-936, 2002 Hayford KE, Patten CA, Rummans TA, et al Efficacy of bupropion for smoking cessation in smokers with a former history of major depression or alcoholism. Br J Psychiatry 174 173-178, 1999... 

Hall, S., Reus, V., Munoz, R. et al. Nortriptyline and cognitive-behavioral therapy in the treatment of cigarette smoking. Arch. Gen. Psychiatry. 55 683, 1998. 

The Necessity of Formal Treatment Treatment Effectiveness Conclusions about the Treatment of Cigarette Smoking Summary... 

We will examine how the determinants of stopping and resuming smoking have influenced the content of formal treatments and their long-term efTectiveness. Before we get to that, there is the question of whether formal treatments of cigarette smoking arc needed. 

Ahmadi J, Ashkani H, Ahmadi M et al. Twenty four week maintenance treatment of cigarette smoking with nicotine gum, clonidine and naltrexone. J Subst Abuse Treat 2003 24 251-255. 

The a-tocopherol, P-carotene (ATBC) Cancer Prevention study was a randomised-controlled trial that tested the effects of daily doses of either 50 mg (50 lU) vitamin E (all-racemic a-tocopherol acetate), or 20 mg of P-carotene, or both with that of a placebo, in a population of more than 29,000 male smokers for 5-8 years. No reduction in lung cancer or major coronary events was observed with any of the treatments. What was more startling was the unexpected increases in risk of death from lung cancer and ischemic heart disease with P-carotene supplementation (ATBC Cancer Prevention Study Group, 1994). Increases in the risk of both lung cancer and cardiovascular disease mortality were also observed in the P-carotene and Retinol Efficacy Trial (CARET), which tested the effects of combined treatment with 30 mg/d P-carotene and retinyl pahnitate (25,000 lU/d) in 18,000 men and women with a history of cigarette smoking or occupational exposure to asbestos (Hennekens et al, 1996). 

Epstein-Barr virus early antigen induction. Methanol extract of the dried leaf, in cell culture at a concentration of 1 pg/mL, was inactive. The assay was designed for tumor-promoting activity . Two diastere-oisomers of 2,7,1 l-cembratriene-4,6-diol (a- and 3-CBT) from the neutral fractions of cigarette smoke condensate, in Raji cells, produced potent inhibitory effects on the induction of Epstein-Barr virus (EBV)-EA by 12-0-tetradecanoylphorbol-13-acetate (TPA). The doses of a- and P-CBT required for 50% inhibition of EBV-EA induction by TPA were 7.7 and 6.7 mg/mL, respectively. Application of a- and P-CBT to mouse skin before treatment with TPA, inhibited TPA-induced ornithine decarboxylase activity in a dose-dependent manner. Application of 16.5 pM/mouse of a- and p-CBT resulted... 

Life Sci 1991 48(12) 1173-1177. Crebelli, R., L. Conti, S. Fuselli, P. Leopardi, A. Zijno, and A. Carere. Put-ther studies on the comutagenic activity of cigarette smoke condensate. Mutat Res 1991 259(1) 29-36. Padma, P. R., A. J. Amonkar, and S. V. Bhide. Effect of long-term treatment of two tobacco-specific N-nitro-samines on the vitamin A status of mice. Nutr Cancer 1991 15(3—4) 217-220. 

The traditional goal of treatments for cigarette smoking is zero tolerance for nicotine, or abstinence from any use of tobacco products. 

Rodgman, A. and L.C. Cook Treatment of 44X fine-cured tobacco with hydrogen cyanide Its effect on hydrogen cyanide in cigarette smoke RDM, 1967, No. 52, September 14 [Paper XLI in the series The analysis of cigarette smoke condensate], see www.ijrtdocs.com 521188989 -8994. 

A number of synthetic compounds, completely unrelated to the structure of natural cannabinoids have been found to act as CB and/or CB2 antagonist/ inverse agonist. The most important member of this class of compounds is rimonabant (29), a diarylpyrazole derivative [57], approved for the treatment of obesity and as an aid in the cessation of cigarette smoking, but later withdrawn from the market because of the severe depression it could induce in sensitive patients. A number of structural motifs significantly different from the p3razole system have been proposed for CB2 selective antagonists, as exemplified by the quinoline derivative 30. 

Obstructive lung disease has been seen in SSc (48). One of the complicating factors in defining this disorder is the frequency of cigarette smoking in most case series. Other diseases that have prominent interstitial components, such as asbestosis, also have described a mild obstmctive lung disease that is presumably from narrowing or tortuosity of some airways early in the fibrotic process (49). Treatment with bronchodilators or corticosteroids rarely produces clinical improvement. 

The development of easy-to-use assays for determining theophylline blood levels afforded a handle on maintenance of effective but nontoxic levels. The relatively good availabihty of such assays in the United States probably contributed to the historical preference for theophylline treatment by U.S. physicians. Careful titration of the dose must be done on a patient-by-patient basis because individual rates of metaboHsm vary widely. Most ( 85%) of an oral dose of theophylline is metabolized by Hver microsomal enzymes. As a result many dmgs, eg, cimetidine [51481-61-9], anticonvulsants, or conditions, eg, fever, cigarette smoking, Hver disease, which affect Hver function alter theophylline blood levels. 

Occurrence. Carbon monoxide is a product of incomplete combustion and is not likely to result where a flame bums in an abundant air supply, yet may result when a flame touches a cooler surface than the ignition temperature of the gas. Gas or coal heaters in the home and gas space heaters in industry have been frequent sources of carbon monoxide poisoning when not provided with effective vents. Gas heaters, though properly adjusted when installed, may become hazardous sources of carbon monoxide if maintained improperly. Automobile exhaust gas is perhaps the most familiar source of carbon monoxide exposure. The manufacture and use of synthesis gas, calcium carbide manufacture, distillation of coal or wood, combustion operations, heat treatment of metals, fire fighting, mining, and cigarette smoking represent additional sources of carbon monoxide exposure (105—107). 

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