Nicotine Interactions
Adrenergic agonists
Alpha-blockers
Ergot Alkaloids
Insulins
Nicotine Interactions
Nicotine from smoking cessation products can be additive to the nicotine from tobacco; patients should be warned against continued tobacco use while using nicotine replacement products. Pharmacologically, the effects of nicotine on the cardiovascular system mimick those of sympathetic stimulation; agonism of nicotinic receptors on adrenal medullary cells causes the release of epinephrine and norepinephrine. Nicotine raises systolic and diastolic blood pressure and can increase the inotropic and chronotropic actions of the heart. The degree to which these reactions occur is a function of the nicotine blood concentration. Symptoms of excessive nicotine can include nausea/vomiting, abdominal pain, diarrhea, headache, and hypertension.
Nicotine transdermal systems (NTS) have been used concurrently with bupropion for smoking cessation therapy. However, when used together, the combination may induce clinically significant blood pressure elevations in some patients. Close monitoring of blood pressure is recommended if this combination is prescribed.
It is advisable not to ingest acidic food or beverages (e.g., coffee, colas) during or immediately (i.e., within 15 minutes) before the use of nicotine gum, as the absorption of nicotine from nicotine polacrilex relies on mildly alkaline saliva.
Nicotine may interact with insulins since nicotine activates neuroendocrine pathways (e.g., increases in circulating cortisol and catecholamine levels) and may increase plasma glucose. Monitor blood sugar for needed insulin dosage adjustments in insulin-dependent diabetic patients whenever a change in either nicotine intake or smoking status occurs. Tobacco smoking is known to aggravate insulin resistance. The cessation of nicotine therapy or tobacco smoking may result in a decrease in blood glucose or an increase the subcutaneous absorption of insulin, respectively.
Nicotine has been reported to enhance the cardiovascular effects of adenosine; an increase in angina-like chest pains, heart rate or a decrease in blood pressure may be noted. While no special cautions are recommended when adenosine is used therapeutically to treat supraventricular tachycardia, it may be advisable for patients to avoid nicotine products or tobacco prior to electrophysiologic studies or stress testing where adenosine will be administered.
Cimetidine was reported to reduce nicotine clearance by roughly 30% in healthy volunteers; however, this finding was not demonstrated in patients who were heavy smokers. Other H2-antagonists are unlikely to produce clinically significant interactions with nicotine.
Nicotine has neuroendocrine effects, and may increase circulating cortisol and catecholamine levels. Nicotine use may reduce the clinical effects of the alpha-blockers. If significant changes in nicotine intake occur, the dosages of these drugs may need adjustment.
Nicotine has neuroendocrine effects, and may increase circulating cortisol and catecholamine levels. Nicotine use may potentiate the effects of the adrenergic agonists and the ergot alkaloids. If significant changes in nicotine intake occur, the dosages of these drugs may need adjustment.
Changes in drug therapy that may be related to cessation of tobacco smoking (i.e., the following interactions are not due to an interaction with nicotine, but rather due to the cessation of tobacco smoking):
Tobacco smoke contains hydrocarbons that induce hepatic CYP450 microsomal enzymes. Because the effect on hepatic microsomal enzymes is not related to the nicotine component of tobacco, the sudden cessation of tobacco smoking may result in a reduced clearance of theophylline, despite the initiation of nicotine replacement. Following one week of abstinence from chronic tobacco smoking, theophylline clearance may decrease by roughly 40%, leading to an increase in serum theophylline concentrations. Theophylline serum concentrations should be monitored carefully when changes in smoking status occur.
Tobacco smoke contains hydrocarbons that induce hepatic CYP450 microsomal enzymes. Because the effect on hepatic microsomal enzymes is not related to the nicotine component of tobacco, the sudden cessation of tobacco smoking may reduce the clearance and increase the therapeutic effects of warfarin despite the initiation of a nicotine replacement product. However, the decreased warfarin clearance may not always result in a clinically significant change in the PT or INR; monitor the patient’s INR to assess the need for warfarin dosage adjustment when changes in smoking status occur. Smoking certainly has adverse effects in relation to thrombosis, and such actions may be altered with cessation of smoking.
Tobacco smoke contains hydrocarbons that induce hepatic CYP450 microsomal enzymes. Because the effect on hepatic microsomal enzymes is not related to the nicotine component of tobacco, the sudden cessation of tobacco smoking may result in a reduced clearance of many medications, despite the initiation of nicotine replacement. An increased effect of the following medications may be seen in a patient who suddenly stops smoking: acetaminophen, caffeine, clozapine, oxazepam, pentazocine, olanzapine, phenothiazines, propoxyphene, propranolol (and possibly other beta-adrenergic blockers), tricyclic antidepressants (e.g., imipramine), and potentially other drugs that are metabolized by the hepatic P-450 enzyme system. These drugs may require a decrease in dosage at cessation of smoking.
[ Last revised: 11/11/2004 1:33:00 PM ]
Related entries
Syndicate
|
