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PubMed2003

Motivating and helping smokers to stop smoking.

Smokers try to quit only once every 2 to 3 years and most do not use proven treatments. Repeated, brief, diplomatic advice increases quit rates. Such advice should include a clear request to quit, reinforcing personal risks of smoking and their reversibility, offering solutions to barriers to quitting, and offering treatment. All smokers should be encouraged to use both medications and counseling. Scientifically proven, first-line medications are nicotine gum, inhaler, lozenge, and patch plus the nonnicotine medication bupropion. Proven second-line medications are clonidine, nicotine nasal spray, and nortriptyline. These medications are equally effective and safe and the incidence of dependence is very small. The proven psychosocial therapies are behavioral and supportive therapies. These are as effective as medications and are effective via individual counseling, group, and telephone formats. The writing of this article was supported in part by Senior Scientist Award DA-00450 from the National Institute on Drug Abuse.

Behavior Therapy↗

PubMed1995

Cost considerations in headache treatment. Part 1: Prophylactic migraine treatment.

Effective migraine treatment is clearly the most cost-effective in terms of both direct and indirect costs. Patient education, behavior changes, and prudent medication selection can minimize costs. Low-dose aspirin may reduce headache frequency. Among the antidepressant medications used, amitriptyine 25 mg, 3 qhs ($4.16/month) and doxepin 25 mg, 3 qhs ($10.50/month) remain the standard. Imipramine (25 mg, 3 qhs ($3.75/month) is very inexpensive and should replace nortriptyline 25 mg, 3 qhs ($64.29/month) as a second-line agent. The specific serotonin reuptake inhibitors are expensive and have no proven effect for migraine prevention. Propranolol 80 mg bid ($7.80/month) is inexpensive and frequently a good choice among beta-blockers. Atenolol 100 mg qd ($27.50/month) is less expensive than long-acting propranolol 160 mg ($35.56/month) and nadolol 120 mg qd ($43.68/month) with equivalent effectiveness. It is thus recommended as the long-acting beta-blocker of choice. Sustained-release preparations of verapamil 240 mg qd ($31.98/month) are twice the cost and less well-absorbed than the standard preparation of 120 mg bid ($17.62/month). Better information is needed concerning effectiveness and optimal dosing of some older low-cost medications in the preventive treatment of migraine.

Adrenergic beta-Antagonists↗

PubMed2004

Genetic testing for enzymes of drug metabolism: does it have clinical utility for pain medicine at the present time? A structured review.

STUDY DESIGN: This is a structured review of genomic (genetic) testing for enzymes of drug metabolism. OBJECTIVES: Recently, industry began offering genomic testing for enzymes of drug metabolism. As such, the objective of this review was to determine if genomic testing for enzymes of drug metabolism has any imminent clinical relevance for the practice of pain medicine. METHODS: Relevant references relating to pharmacogenetics, pharmacogenomics, and the metabolizing of drugs used in pain medicine by cytochrome P-450 enzymes were located and reviewed in detail. The P-450 enzymes that metabolize each drug and whether that drug had been identified as being subject to a clinical consequence of a genetic polymorphism of the P-450 enzyme involved in its metabolism were placed into tabular form. RESULTS OF DATA SYNTHESIS: 1) For a large number of drugs, we do not yet know which cytochrome P-450 enzymes are involved in their metabolism; 2) For a large number of drugs, the consequences of a P-450 genetic polymorphism have yet to be determined; 3) Genetic polymorphism can lead to important potential clinical consequences for some opioids, anticonvulsants (phenytoin), benzodiazepines (diazepam), muscle relaxants (succinylcholine), antidepressants (imipramine, nortriptyline, venlafaxine), typical neuroleptics, alcohol, antihypertensives (propranolol, timolol), local anesthetics (procainamide), L-dopa, nicotine, and warfarin. Based on these results, factors for and against using genomic testing were reviewed. CONCLUSIONS/RECOMMENDATIONS: It was concluded that genomic testing for enzymes of drug metabolism has significant potential for improving the efficacy of drug treatment and reducing adverse drug reactions. Recommendations for when such testing would be useful are outlined.

Analgesics↗

PubMed1984

Seizures with antidepressants: an in vitro technique to assess relative risk.

The relative potential of various antidepressants to induce seizures while being used at therapeutic doses was studied by examining their action on spike activity in perfused guinea pig hippocampal slices. Within the range of concentration studied, imipramine, amitriptyline, nortriptyline, maprotiline, and desipramine tended to increase spike activity in a descending order of effect. Doxepin and nomifensine increased spike activity at lower concentrations, but reduced it at higher concentrations. Protriptyline and trimipramine reduced spike activity with increasing concentrations, whereas mianserin and viloxazine had little effect at any concentration. These findings are discussed in light of previous clinical and laboratory reports, and the clinical implications of these findings are presented. Finally, results with the antidepressants are compared with those previously observed with neuroleptics. On the basis of this comparison and a review of clinical reports, the assumption that neuroleptics have greater epileptogenic potential than antidepressants is questioned.

Animals↗

PubMed2001

Selected tricyclic antidepressant ingestions involving children 6 years old or less.

OBJECTIVE: According to the annual report of the American Association of Poison Control Centers, tricyclic antidepressant (TCA) ingestions accounted for 15,708 exposures in 1998, of which 70% (all age groups) were treated at health care facilities (HCFs), with an estimated 2,022 children less than 6 years of age exposed. The study objective was to evaluate the manifestations, referral patterns, HCF management, and medical outcomes in pediatric patients 6 years old or less with TCA ingestions reported to a regional poison control center. METHODS: All TCA (amitriptyline, clomipramine, desipramine, doxepin, imipramine, nortriptyline) ingestions from January 1, 1993, to December 31, 1997, involving patients aged 6 years or less managed by the poison control center were evaluated for dose, symptoms, treatments, disposition, and outcome. RESULTS: Forty-four of 48 patients (92%) were asymptomatic. All were single-drug exposures. Forty-three patients (90%) ingested a TCA dose that was less than the normally prescribed pediatric dose (5 mg/kg). Of the five children ingesting >5 mg/kg (range 5-9.4 mg/kg), only one (5.3 mg/kg) was mildly symptomatic (drowsy) prior to admission. Thirty-one of the 48 (65%) were sent to the emergency department (dose range 0.59-9.4 mg/kg). Fourteen of the 31 were admitted for 12-24-hour observation and none subsequently developed symptoms. Twenty-three (74%) received activated charcoal (AC). There was no difference in outcome between the children who did and did not receive AC. CONCLUSIONS: No case of significant toxicity occurred in the children who experienced unintentional TCA ingestions in this study population. None of the children in the study had toxicity at doses <5 mg/kg. Further study is necessary to develop clinical guidelines for the appropriate referral of unintentional ingestions of TCA involving children.

Administration, Oral↗

PubMed2000

Trazodone-induced hepatotoxicity: a case report with comments on drug-induced hepatotoxicity.

Trazodone (Desyrel) is a second-generation, nontricyclic antidepressant that has been in use in North America since the early 1980s. It has the advantage of being more sedating and having less anticholinergic side effects than other secondary amines in the piperazine class, namely, desipramine and nortriptyline. Five previous cases of trazodone hepatotoxicity have been reported in the literature, one describing chronic damage and the others, more acute cellular and cholestatic injury. We describe a case of acute reversible liver injury with the use of trazodone. This case is unique in that injury occurred after protracted (18 months) drug use and while the patient was on corticosteroids. Moreover, the diagnosis was confirmed by an inadvertent challenge with trazodone. This case reports not only a well documented instance of trazodone-induced liver injury, but also serves as a basis for a brief discussion of mechanisms, clinical monitoring, and therapy in drug-induced hepatotoxicity.

Adult↗

PubMed1981

Effect of antidepressants, lithium and electroconvulsive treatment on rat serum prolactin levels.

The ability of antidepressant drugs, electroconvulsive treatment (ECT), or lithium chloride (LiCl), to modify prolactin secretion in the rat was studied. Chlorimipramine, citalopram, fluoxetine, imipramine and zimelidine potentiated the low dose 5-hydroxytryptophan (5-HTP)-induced increase in prolactin secretion, suggesting inhibition of serotonin (5-HT) uptake by these drugs. Amitriptyline, doxepin, iprindole, mianserin and trazadone inhibited the prolactin stimulating effects of high doses of 5-HTP and quipazine, suggesting that these drugs have 5-HT receptor blocking properties. Tandamine inhibited only 5-HTP-induced increase in prolactin secretion. Chronic administration of imipramine, potentiated the effect of low dose 5-HTP significantly more than an acute dose. Amitriptyline, produced similar inhibition of the 5-HTP-induced increase in prolactin secretion after both acute and chronic administration. The ability of bupropion and mazindol to inhibit alpha-methylparatyrosine-induced prolactin secretion, and of nomifensine to inhibit reserpine-induced prolactin secretion, is consistent with other evidence that these agents are indirect dopamine (DA) agonists. Desipramine, acutely, had no effect on any of the above paradigms but after chronic administration, potentiated the effect of low dose 5-HTP on prolactin secretion. Nortriptyline had no effect on prolactin secretion after acute or chronic treatment. ECT for 10 days did not affect the ability of a 5-HT agonist or d-amphetamine to modify prolactin secretion. However, chronic, but not acute, treatment with LiCl markedly enhanced the prolactin response to 5-HT agonists and reserpine while shifting the dose response curve for d-amphetamine and apomorphine to the right. These results are discussed in light of current theories of the role of 5-HT and DA in depression.

5-Hydroxytryptophan↗

PubMed1981

Comparison of peripheral anticholinergic effects of antidepressants: dry mouth.

Twenty-one healthy volunteers were given single doses of placebo or antidepressants corresponding to average daily doses of patient medications. Spontaneous whole mouth and parotid salivation was measured two, six, and ten hours after drug administration in session 1; in session 2 after ten hours. The results indicate that a subdivision of antidepressants into four groups can be made according to inhibitory effect on salivation: (a) isocarboxazide and lithium citrate with no effect, (b) zimelidine and nomifensine with slight effect, (c) imipramine oxide and mianserin with moderate effect and (d) maprotiline, nortriptyline, clomipramine, imipramine, and amitriptyline with pronounced effect. Research implications and predictive value for new antidepressants are discussed.

Adult↗

PubMed1983

Effects of zimeldine and other antidepressants on skilled performance: a comprehensive review.

Existing data suggest that amitriptyline, doxepin, mianserin, viloxazine and imipramine impair the performance of skilled psychomotor tasks. The degree of impairment, as well as the degree of interaction with alcohol, is closely related to the sedative potency of the drug. the adverse effects on psychomotor skills are, however, mainly limited to the first 10 days of treatment. In contrast, nortriptyline, clomipramine, desipramine, protriptyline, nomifensine and zimeldine have much less marked effects on skilled performance. Despite its being a relatively new antidepressant, the effects of zimeldine on psychomotor skills have already been extensively investigated. It has been shown to be without stimulant or sedative effects, and there does not appear to be any additive effect between zimeldine and ethanol. The lack of detrimental effects on skills related to such tasks as driving, makes zimeldine suitable for use in out-patient populations.

Antidepressive Agents↗

PubMed1981

A gas chromatographic method for the determination of antidepressant drugs in human serum.

A universal gas chromatographic method for the determination of the most commonly used antidepressant drugs in 1 ml of serum is described. Prior to extraction the samples were washed with hexane at acid pH. After the hexane wash the drugs were extracted into hexane at pH approximately 10, and subsequently reextracted from the hexane into a 1% solution of formic acid in methanol. The methanolic phase was evaporated, the residue dissolved in isopropanol and analysed by gas chromatography with nitrogen detection on a 3% OV-225 column. Recoveries for amitriptyline, nortriptyline, clomipramine, desmethylclomipramine, doxepin, desmethyldoxepin, imipramine, desipramine, maprotiline, protriptyline, trimipramine and desmethyl-trimipramine were found to be 80% or higher. Limits of detection were found to be 5-10 ng/ml for teritary amines and 10-20 ng/ml for secondary amines. Interferences from some common basic drugs were investigated as well as interferences between different antidepressant drugs. Gas chromatographic data are given for 28 drugs and metabolites.

Antidepressive Agents, Tricyclic↗

PubMed1981

Characterization of 5-hydroxytryptamine uptake in sliced rat lung.

Slices of rat lung were incubated with tritiated 5-hydroxytryptamine and the tissue uptake of tritium was studied after separating the free and bound radioactivity by filtration on glass fiber filters. At 37 degrees a rapid uptake occurred during the first 10 min. After that time the uptake was less marked but it was still present after 60 min. The uptake was moderately potentiated by the MAO inhibitor iproniazid (3 micrometers) after 30-60 min. incubation. The 5-hydroxytryptamine uptake was inhibited by some uptake inhibitors, their order of potency beeing: clomipramine greater than imipramine greater than or equal to nortriptyline greater than or equal to cocaine greater than or equal to desipramine greater than maprotiline. At 0 degrees the uptake of 5-hydroxytryptamine was negligible. Non-linear regression analysis of uptake data indicated that 5-hydroxytryptamine was taken up by two different mechanisms. One of the uptake processes was saturated by high concentrations of 5-hydroxytryptamine and showed an apparent Km of 8 X 10(-7) M. The other uptake was linearly related to the 5-hydroxytryptamine concentration and could not be saturated even by concentration up to 5 X 10(-5) M of the amine.

Animals↗

PubMed2000

Neuropathic orofacial pain. Part 2-Diagnostic procedures, treatment guidelines and case reports.

Neuropathic orofacial pain can be difficult to diagnose because of the lack of clinical and radiographic abnormalities. Further difficulties arise if the patient exhibits significant distress and is a poor historian regarding previous diagnostic tests and treatments, such as somatosensory local anaesthetic blockade. Valuable information can be obtained by utilising the McGill Pain Questionnaire that allows the patient to choose words that describe the qualities of his/her pain in a number of important dimensions (sensory and effective). Basal pain intensity should be measured with the visual analogue scale, a simple instrument that can evaluate the efficacy of subsequent treatments. The dentist or endodontist can employ sequential analgesic blockade with topical anaesthetics and perineural administration of plain local anaesthetic to ascertain sites of neuropathology in the PNS. These can be performed in the dental chair and in a patient blinded manner. Other, more specific, tests necessitate referral to a specialist anaesthetist at a multidisciplinary pain clinic. These tests include placebo controlled lignocaine infusions for assessing neuropathic pain, and placebo controlled phentolamine infusions for sympathetically maintained pain. The treatment/management of neuropathic pain is multidisciplinary. Medication rationalisation utilises first-line antineuropathic drugs including tricyclic antidepressants such as amitriptyline and nortriptyline, and possibly an anticonvulsant such as carbamazepine, sodium valproate, or gabapentin if there are sharp, shooting qualities to the pain. Mexiletine, an antiarrhythmic agent and lignocaine analogue, may be considered following a positive patient response to a lignocaine infusion. All drugs need to be titrated to achieve maximum therapeutic effect and minimum side effects. Topical applications of capsaicin to the gingivae and oral mucosa are a simple and effective treatment in two out of three patients suffering from neuropathic orofacial pain. Temporomandibular disorder is present in two thirds of patients and should be assessed and treated with physiotherapy and where appropriate, occlusal splint therapy. Attention to the patient's psychological status is crucial and requires the skill of a clinical psychologist and/or psychiatrist with pain clinic experience. Psychological variables include distress, depression, expectations of treatment, motivation to improve, and background environmental factors. Unnecessary dental treatment to "remove the pain" with dental extractions is contraindicated and aggravates neuropathic orofacial pain.

Adult↗

PubMed1978

Aggregation of antidepressant drugs in aqueous solution.

Light scattering, conductivity and pH methods have been used to examine the aggregation in aqueous solution of a series of antidepressant drugs. The drugs investigated included the hydrochlorides of amitriptyline, butriptyline, protriptyline, nortriptyline, imipramine, desipramine, clomipramine, dothiepin, dibenzepin, opipramol, iprindole, doxepin, mianserin and maprotiline. No significant association of dibenzepin, mianserin or maprotiline hydrochlorides could be detected up to their respective solubility limits. A micellar pattern of association was established for all other compounds. Critical micelle concentrations and micellar properties are reported.

Antidepressive Agents↗

PubMed1978

The use of 13C-nmr spectroscopy for the detection and identification of metabolites of carbon-13 labelled amitriptyline.

The antidepressant drug amitriptyline and two of its metabolites, nortriptyline and desmethylnortriptyline, each containing two 13C atoms, have been used to determine the sensitivity and selectivity of 13C-nmr spectroscopy for the detection of unchanged amitriptyline and N-desmethyl metabolites in the urine of animals dosed orally with the labelled drug. The resonance signals from the 13C atoms detected in the 13C-nmr spectrum of entire extract from a control 12 h rat urine sample to which 1 mg of each labelled compound had been added were easily detected, using an instrument accumulation time of 1 h. The 13C-nmr spectrum of an extract of hydrolysed urine from a dog that had received an oral dose of [13C2]amitriptyline (30mg) exhibited signals that could be assigned to metabolites resulting from N-dealkylation and N-oxidation, as well as those bearing the intact amitriptyline side-chain. These assignments were confirmed by analysis of the same extract by g.c.--ms and h.p.l.c.

Amitriptyline↗

PubMed2006

Fluoxetine and cocaine induce the epigenetic factors MeCP2 and MBD1 in adult rat brain.

Once bound to methylated CpG sites, methyl-CpG-binding protein 2 (MeCP2) is thought to silence transcription of downstream genes by recruiting a histone deacetylase (HDAC). Mutations within the MeCP2 gene have been found to cause Rett syndrome, a disorder of arrested neuronal development. Using immunohistochemistry, we found that Mecp2, as well as the methyl-CpG-binding protein MBD1, were significantly induced in normal adult rat brain after repeated injections of fluoxetine or cocaine for 10 days (one injection per day). Mecp2 was not induced by repeated injections of 1-(2-bis(4-fluorphenyl)-methoxy)-ethyl)-4-(3-phenyl-propyl)piperazine (GBR-12909) or nortriptyline. Together, the data indicate that the serotonergic system is predominantly involved. Using real-time reverse transcription-polymerase chain reaction experiments, MBD1 mRNA and both Mecp2_e1 and Mecp2_e2 transcripts were found to be induced by fluoxetine. Induction of the methylbinding proteins was accompanied with enhanced HDAC2 labeling intensity and mRNA synthesis in response to fluoxetine. In tandem, acetylated forms of histone H3 were found to be decreased. The effect was characterized in three serotonin projection areas, the caudate-putamen, the frontal cortex, and the dentate gyrus subregion of hippocampus. Our data highlight GABAergic neurons as major target cells expressing Mecp2 in response to the serotonin-elevating agents and suggest that serotonin signaling enhances gene silencing in postmitotic neurons.

Animals↗

PubMed1983

Lack of influence of commonly used drugs on bioassay indicator organisms.

Many commonly used pharmaceutical agents have been found to inhibit bacterial growth in vitro. Determinations of antimicrobial concentrations in sera of patients taking nonrecognized antibacterial agents could possibly be altered if bioassay systems are utilized for the determinations. We therefore attempted to determine the in vitro effect of commonly used drugs on bioassay indicator organisms. Fifty-one different agents (antihistamines, anticholinergics, central nervous system agents, cardiovascular agents, analgesics, steroids, muscle blockers, and other miscellaneous agents) were tested for inhibition or enhancement of the growth of Bacillus subtilis, Staphylococcus aureus, Micrococcus luteus, and Klebsiella pneumoniae. None of the agents tested exhibited any effect on standard in vitro bioassay organisms. Nortriptyline hydrochloride inhibited the growth of B. subtilis and M. luteus at a concentration of 500 micrograms/ml (zones of inhibition, 14 and 13 mm, respectively), but no inhibition was observed with concentrations of 50 micrograms/ml or lower.

Bacteria↗

PubMed2007

Non-nicotinic therapies for smoking cessation.

Cigarette smoking is the primary cause of numerous preventable diseases; as such, the goals of smoking cessation are both to reduce health risks and to improve the quality of life. Currently, the first-line smoking cessation therapies include nicotine replacement products and bupropion. The nicotinic receptor partial agonist varenicline has recently been approved by the FDA for smoking cessation. A newer product currently under development and seeking approval by the FDA are nicotine vaccines. Clonidine and nortriptyline have demonstrated some efficacy but side effects may limit their use to second-line therapeutic products. Other therapeutic drugs that are under development include rimonabant, mecamylamine, monoamine oxidase inhibitors, and dopamine receptor D3 antagonists. Inhibitors of nicotine metabolism are also promising candidates for smoking reduction and cessation. In conclusion, promising new therapeutic products are emerging and they will provide smokers additional options to assist in achieving smoking cessation.

Benzazepines↗

PubMed1976

Plasma levels of imipramine in depression. Environmental and genetic factors.

On the basis of tentative evidence obtained with 26 patients with unipolar affective illness, the variability in the response to imipramine is mostly due to interindividual differences in hydroxylating microsomal enzymes which are genetically controlled but whose activities are subject to modification by environmental factors such as overall pharmacological exposure and tobacco smoking. Additional significant pharmacodynamic variability (twofold) was found in the range of the volumes of distribution of imipramine in the patients. Clinical outcome was unequivocally related to plasma level. Unipolar nondelusional patients with levels less than 180 ng/ml had a low probability of recovery, while levels above 180 ng/ml were assoicated with a high probability of recovery. Unlike the findings of investigators working with nortriptyline, our data do not suggest an upper limit on plasma levels beyond which clinical response deteriorates. It appears that, on the basis of family studies, similar genetic characteristics are related to the ones controlling the pharmacodynamics will be the subject of further examination in our continuing studies.

Adult↗