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ALERT: U.S. Boxed Warning
The FDA-approved labeling includes a boxed warning. See Warnings/Precautions section for a concise summary of this information. For verbatim wording of the boxed warning, consult the product labeling or www.fda.gov.
Pronunciation
(trye MI pra meen)
Generic Available (U.S.)
No
Index Terms
Medication Guide
An FDA-approved patient medication guide, which is available with the product information and at http://www.fda.gov/downloads/Drugs/DrugSafety/ucm089832.pdf, must be dispensed with this medication.
U.S. Brand Names
Canadian Brand Names
Pharmacologic Category
Pharmacologic Category Synonyms
Use: Labeled Indications
Treatment of depression
Pregnancy Risk Factor
C
Lactation
Enters breast milk/contraindicated
Contraindications
Hypersensitivity to trimipramine, any component of the formulation, or other dibenzodiazepines; use of MAO inhibitors within 14 days; use in a patient during the acute recovery phase of MI
Warnings/Precautions
Boxed warnings:
• Suicidal thinking/behavior: See “Major psychiatric warnings” below.
Major psychiatric warnings:
• [U.S. Boxed Warning]: Antidepressants increase the risk of suicidal thinking and behavior in children, adolescents, and young adults (18-24 years of age) with major depressive disorder (MDD) and other psychiatric disorders; consider risk prior to prescribing. Short-term studies did not show an increased risk in patients >24 years of age and showed a decreased risk in patients ≥65 years. Closely monitor patients for clinical worsening, suicidality, or unusual changes in behavior, particularly during the initial 1-2 months of therapy or during periods of dosage adjustments (increases or decreases); the patient's family or caregiver should be instructed to closely observe the patient and communicate condition with healthcare provider. A medication guide concerning the use of antidepressants should be dispensed with each prescription. Trimipramine is not FDA approved for use in children.
• The possibility of a suicide attempt is inherent in major depression and may persist until remission occurs. Patients treated with antidepressants should be observed for clinical worsening and suicidality, especially during the initial few months of a course of drug therapy, or at times of dose changes, either increases or decreases. Worsening depression and severe abrupt suicidality that are not part of the presenting symptoms may require discontinuation or modification of drug therapy. Use caution in high-risk patients during initiation of therapy.
• Prescriptions should be written for the smallest quantity consistent with good patient care. The patient's family or caregiver should be alerted to monitor patients for the emergence of suicidality and associated behaviors such as anxiety, agitation, panic attacks, insomnia, irritability, hostility, impulsivity, akathisia, hypomania, and mania; patients should be instructed to notify their healthcare provider if any of these symptoms or worsening depression or psychosis occur.
• May worsen psychosis in some patients or precipitate a shift to mania or hypomania in patients with bipolar disorder. Monotherapy in patients with bipolar disorder should be avoided. Patients presenting with depressive symptoms should be screened for bipolar disorder. Trimipramine is not FDA approved for the treatment of bipolar depression.
Concerns related to adverse effects:
• Anticholinergic effects: May cause anticholinergic effects (constipation, xerostomia, blurred vision, urinary retention); use with caution in patients with decreased gastrointestinal motility, paralytic ileus, urinary retention, BPH, xerostomia, or visual problems. The degree of anticholinergic blockade produced by this agent is very high relative to other antidepressants.
• Orthostatic hypotension: May cause orthostatic hypotension (risk is high relative to other antidepressants); use with caution in patients at risk of this effect or in those who would not tolerate transient hypotensive episodes (cerebrovascular disease, cardiovascular disease, hypovolemia, or concurrent medication use which may predispose to hypotension/bradycardia).
• Sedation: May cause sedation, which may impair physical or mental abilities; patients must be cautioned about performing tasks which require mental alertness (eg, operating machinery or driving). The degree of sedation is very high relative to other antidepressants.
Disease-related concerns:
• Cardiovascular disease: Use with caution in patients with a history of cardiovascular disease (including previous MI, stroke, tachycardia, or conduction abnormalities); the risk conduction abnormalities with this agent is high relative to other antidepressants.
• Diabetes: Use with caution in patients with diabetes mellitus; may alter glucose regulation.
• Hepatic impairment: Use with caution in patients with hepatic impairment.
• Renal impairment: Use with caution in patients with renal impairment.
• Seizure disorder: Use with caution in patients at risk of seizures, including those with a history of seizures, head trauma, brain damage, alcoholism, or concurrent therapy with medications which may lower seizure threshold.
• Thyroid dysfunction: Use with caution in patients with hyperthyroidism or those receiving thyroid supplementation.
Concurrent drug therapy issues:
• Sedatives: Effects may be potentiated when used with other sedative drugs or ethanol.
Special populations:
• Elderly: Use with caution in the elderly.
Other warnings/precautions:
• Discontinuation of therapy: Therapy should not be abruptly discontinued in patients receiving high doses for prolonged periods.
• Electroconvulsive therapy: May increase the risks associated with electroconvulsive therapy; consider discontinuing, when possible, prior to ECT treatment.
Adverse Reactions
Frequency not defined.
Cardiovascular: Arrhythmias, facial edema, flushing, heart block, hyper-/hypotension, MI, palpitation, stroke, tachycardia
Central nervous system: Agitation, anxiety, confusion, delusions, disorientation, dizziness, drowsiness, EEG abnormalities, exacerbation of psychosis, fatigue, hallucinations, headache, hypomania, insomnia, nightmares, restlessness, seizure
Dermatologic: Alopecia, itching, petechiae, photosensitivity, rash, urticaria
Endocrine & metabolic: Breast enlargement, galactorrhea, gynecomastia, hyper-/hypoglycemia, libido (changes in), parotid swelling, syndrome of inappropriate ADH secretion (SIADH)
Gastrointestinal: Abdominal cramps, anorexia, black tongue, constipation, diarrhea, epigastric distress, nausea, paralytic ileus, stomatitis, tongue edema, unpleasant taste, tongue edema, vomiting, weight gain/loss, xerostomia
Genitourinary: Delayed/difficult urination, impotence, polyuria, testicular edema, urinary retention
Hematologic: Agranulocytosis, eosinophilia, purpura, thrombocytopenia
Hepatic: Cholestatic jaundice, liver enzymes increased
Neuromuscular & skeletal: Ataxia, extrapyramidal symptoms, incoordination, numbness, paresthesia, peripheral neuropathy, tingling, tremor, weakness
Ocular: Blurred vision, disturbances in accommodation, mydriasis
Otic: Tinnitus
Miscellaneous: Diaphoresis, withdrawal syndrome
Metabolism/Transport Effects
Substrate (major) of CYP2C19, 2D6, 3A4
Drug Interactions
Abiraterone Acetate: May increase the serum concentration of CYP2D6 Substrates. Management: Avoid concurrent use of abiraterone with CYP2D6 substrates that have a narrow therapeutic index whenever possible. When concurrent use is not avoidable, monitor patients closely for signs/symptoms of toxicity. Risk D: Consider therapy modification
Acetylcholinesterase Inhibitors (Central): Anticholinergics may diminish the therapeutic effect of Acetylcholinesterase Inhibitors (Central). Acetylcholinesterase Inhibitors (Central) may diminish the therapeutic effect of Anticholinergics. If the anticholinergic action is a side effect of the agent, the result may be beneficial. Risk C: Monitor therapy
Alfuzosin: May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk C: Monitor therapy
Alpha-/Beta-Agonists (Direct-Acting): Tricyclic Antidepressants may enhance the vasopressor effect of Alpha-/Beta-Agonists (Direct-Acting). Exceptions: Dipivefrin. Risk D: Consider therapy modification
Alpha1-Agonists: Tricyclic Antidepressants may enhance the vasopressor effect of Alpha1-Agonists. Risk D: Consider therapy modification
Alpha2-Agonists: Tricyclic Antidepressants may diminish the antihypertensive effect of Alpha2-Agonists. Exceptions: Apraclonidine; Brimonidine. Risk D: Consider therapy modification
Altretamine: May enhance the orthostatic hypotensive effect of Tricyclic Antidepressants. Risk C: Monitor therapy
Amphetamines: Tricyclic Antidepressants may enhance the stimulatory effect of Amphetamines. Tricyclic Antidepressants may also potentiate the cardiovascular effects of Amphetamines. Risk C: Monitor therapy
Anticholinergics: May enhance the adverse/toxic effect of other Anticholinergics. Exceptions: Levocabastine (Nasal); Paliperidone. Risk C: Monitor therapy
Artemether: May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk X: Avoid combination
Aspirin: Antidepressants (Tricyclic, Tertiary Amine) may enhance the antiplatelet effect of Aspirin. Risk C: Monitor therapy
Barbiturates: May increase the metabolism of Tricyclic Antidepressants. Risk D: Consider therapy modification
Beta2-Agonists: Tricyclic Antidepressants may enhance the adverse/toxic effect of Beta2-Agonists. Risk C: Monitor therapy
BuPROPion: May decrease the metabolism of Tricyclic Antidepressants. Risk C: Monitor therapy
CarBAMazepine: May increase the metabolism of Tricyclic Antidepressants. Risk C: Monitor therapy
Chloroquine: May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk C: Monitor therapy
Cimetidine: May decrease the metabolism of Tricyclic Antidepressants. Risk C: Monitor therapy
Cinacalcet: May increase the serum concentration of Tricyclic Antidepressants. Risk C: Monitor therapy
Ciprofloxacin: May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk C: Monitor therapy
Ciprofloxacin (Systemic): May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk C: Monitor therapy
Conivaptan: May increase the serum concentration of CYP3A4 Substrates. Management: Upon completion/discontinuation of conivaptan, allow at least 7 days before initiating therapy with drugs that are CYP3A4 substrates. Risk D: Consider therapy modification
CYP2C19 Inducers (Strong): May increase the metabolism of CYP2C19 Substrates. Risk C: Monitor therapy
CYP2C19 Inhibitors (Moderate): May decrease the metabolism of CYP2C19 Substrates. Risk C: Monitor therapy
CYP2C19 Inhibitors (Strong): May decrease the metabolism of CYP2C19 Substrates. Risk D: Consider therapy modification
CYP2D6 Inhibitors (Moderate): May decrease the metabolism of CYP2D6 Substrates. Risk C: Monitor therapy
CYP2D6 Inhibitors (Strong): May decrease the metabolism of CYP2D6 Substrates. Risk D: Consider therapy modification
CYP3A4 Inducers (Strong): May increase the metabolism of CYP3A4 Substrates. Risk C: Monitor therapy
CYP3A4 Inhibitors (Moderate): May decrease the metabolism of CYP3A4 Substrates. Risk C: Monitor therapy
CYP3A4 Inhibitors (Strong): May decrease the metabolism of CYP3A4 Substrates. Risk D: Consider therapy modification
Deferasirox: May decrease the serum concentration of CYP3A4 Substrates. Risk C: Monitor therapy
Desmopressin: Tricyclic Antidepressants may enhance the adverse/toxic effect of Desmopressin. Risk C: Monitor therapy
Dexmethylphenidate: May enhance the adverse/toxic effect of Tricyclic Antidepressants. Dexmethylphenidate may increase the serum concentration of Tricyclic Antidepressants. Risk C: Monitor therapy
Divalproex: May increase the serum concentration of Tricyclic Antidepressants. Risk C: Monitor therapy
Dronedarone: QTc-Prolonging Agents may enhance the QTc-prolonging effect of Dronedarone. Risk X: Avoid combination
DULoxetine: May decrease the metabolism of Tricyclic Antidepressants. Risk C: Monitor therapy
Gadobutrol: May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk D: Consider therapy modification
Iobenguane I 123: Tricyclic Antidepressants may diminish the therapeutic effect of Iobenguane I 123. Risk X: Avoid combination
Lithium: May enhance the neurotoxic effect of Tricyclic Antidepressants. Risk C: Monitor therapy
Lumefantrine: May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk X: Avoid combination
MAO Inhibitors: May enhance the serotonergic effect of Tricyclic Antidepressants. This may cause serotonin syndrome. Risk X: Avoid combination
MAO Inhibitors: May enhance the orthostatic hypotensive effect of Orthostatic Hypotension Producing Agents. Risk C: Monitor therapy
Methylene Blue: Tricyclic Antidepressants may enhance the serotonergic effect of Methylene Blue. This could result in serotonin syndrome. Risk X: Avoid combination
Methylphenidate: May enhance the adverse/toxic effect of Tricyclic Antidepressants. Methylphenidate may increase the serum concentration of Tricyclic Antidepressants. Risk C: Monitor therapy
Metoclopramide: May enhance the adverse/toxic effect of Tricyclic Antidepressants. Management: Seek alternatives to this combination when possible. Monitor patients receiving metoclopramide with tricyclic antidepressants for signs of extrapyramidal symptoms, neuroleptic malignant syndrome, and serotonin syndrome. Risk D: Consider therapy modification
Nilotinib: May enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk X: Avoid combination
NSAID (COX-2 Inhibitor): Antidepressants (Tricyclic, Tertiary Amine) may enhance the antiplatelet effect of NSAID (COX-2 Inhibitor). Risk C: Monitor therapy
NSAID (Nonselective): Antidepressants (Tricyclic, Tertiary Amine) may enhance the antiplatelet effect of NSAID (Nonselective). Risk C: Monitor therapy
Peginterferon Alfa-2b: May decrease the serum concentration of CYP2D6 Substrates. Risk C: Monitor therapy
Pimozide: QTc-Prolonging Agents may enhance the QTc-prolonging effect of Pimozide. Risk X: Avoid combination
Pramlintide: May enhance the anticholinergic effect of Anticholinergics. These effects are specific to the GI tract. Risk D: Consider therapy modification
Propoxyphene: May enhance the CNS depressant effect of Tricyclic Antidepressants. Risk C: Monitor therapy
Protease Inhibitors: May increase the serum concentration of Tricyclic Antidepressants. Risk C: Monitor therapy
QTc-Prolonging Agents: May enhance the adverse/toxic effect of other QTc-Prolonging Agents. Their effects can be additive, causing life-threatening ventricular arrhythmias. Risk D: Consider therapy modification
QuiNIDine: Tricyclic Antidepressants may enhance the QTc-prolonging effect of QuiNIDine. QuiNIDine may increase the serum concentration of Tricyclic Antidepressants. Risk D: Consider therapy modification
QuiNINE: QTc-Prolonging Agents may enhance the QTc-prolonging effect of QuiNINE. QuiNINE may enhance the QTc-prolonging effect of QTc-Prolonging Agents. Risk X: Avoid combination
Selective Serotonin Reuptake Inhibitors: May decrease the metabolism of Tricyclic Antidepressants. Risk D: Consider therapy modification
Serotonin Modulators: May enhance the adverse/toxic effect of other Serotonin Modulators. The development of serotonin syndrome may occur. Risk D: Consider therapy modification
Sibutramine: May enhance the serotonergic effect of Serotonin Modulators. This may cause serotonin syndrome. Risk X: Avoid combination
Sodium Phosphates: Tricyclic Antidepressants may enhance the adverse/toxic effect of Sodium Phosphates. Specifically, the risk of seizure and/or loss of consciousness may be increased in patients with significant sodium phosphate induced fluid/electrolyte abnormalities. Risk C: Monitor therapy
St Johns Wort: May increase the metabolism of Tricyclic Antidepressants. The risk of serotonin syndrome may theoretically be increased. Risk D: Consider therapy modification
Sulfonylureas: Cyclic Antidepressants may enhance the hypoglycemic effect of Sulfonylureas. Risk C: Monitor therapy
Terbinafine: May decrease the metabolism of Tricyclic Antidepressants. Risk D: Consider therapy modification
Terbinafine (Systemic): May decrease the metabolism of Tricyclic Antidepressants. Risk D: Consider therapy modification
Tetrabenazine: QTc-Prolonging Agents may enhance the QTc-prolonging effect of Tetrabenazine. Risk X: Avoid combination
Thioridazine: QTc-Prolonging Agents may enhance the QTc-prolonging effect of Thioridazine. Risk X: Avoid combination
Tocilizumab: May decrease the serum concentration of CYP3A4 Substrates. Risk C: Monitor therapy
Toremifene: QTc-Prolonging Agents may enhance the QTc-prolonging effect of Toremifene. The risk for potentially dangerous arrhythmias may be increased. Risk X: Avoid combination
TraMADol: Tricyclic Antidepressants may enhance the neuroexcitatory and/or seizure-potentiating effect of TraMADol. Risk C: Monitor therapy
Valproic Acid: May increase the serum concentration of Tricyclic Antidepressants. Risk C: Monitor therapy
Vandetanib: QTc-Prolonging Agents may enhance the arrhythmogenic effect of Vandetanib. Risk X: Avoid combination
Vitamin K Antagonists (eg, warfarin): Tricyclic Antidepressants may enhance the anticoagulant effect of Vitamin K Antagonists. Risk C: Monitor therapy
Yohimbine: Tricyclic Antidepressants may increase the serum concentration of Yohimbine. Risk C: Monitor therapy
Ziprasidone: QTc-Prolonging Agents may enhance the QTc-prolonging effect of Ziprasidone. The risk of a severe arrhythmia may be increased. Risk X: Avoid combination
Ethanol/Nutrition/Herb Interactions
Ethanol: May increase CNS depression; monitor for increased effects with coadministration. Caution patients about effects.
Food: Grapefruit juice may inhibit the metabolism of some TCAs and clinical toxicity may result.
Herb/Nutraceutical: Avoid valerian, St John's wort, SAMe, kava kava (may increase risk of serotonin syndrome and/or excessive sedation).
Storage
Solutions stable at a pH of 4-5. Turns yellowish or reddish on exposure to light. Slight discoloration does not affect potency; marked discoloration is associated with loss of potency. Capsules stable for 3 years following date of manufacture.
Mechanism of Action
Increases the synaptic concentration of serotonin and/or norepinephrine in the central nervous system by inhibition of their reuptake by the presynaptic neuronal membrane
Pharmacodynamics/Kinetics
Distribution: Vd: 17-48 L/kg
Protein binding: 95%; free drug: 3% to 7%
Metabolism: Hepatic; significant first-pass effect
Bioavailability: 18% to 63%
Half-life elimination: 16-40 hours
Excretion: Urine
Dosage
Oral:
Adolescents: Initial: 50 mg/day; gradually increase dose to 100 mg/day; Maintenance: Lowest effective dose at bedtime
Adults:
Outpatients: Initial: 75 mg/day in divided doses; may increase to 150 mg/day; Maintenance: 50-150 mg/day as a single bedtime dose; maximum: 200 mg/day
Inpatients: Initial: 100 mg /day in divided doses; may increase to 200 mg/day; if no improvement after 2-3 weeks, dose may be increased to 250-300 mg/day
Elderly: 50 mg/day; gradually increase dose to 100 mg/day
Monitoring Parameters
Blood pressure and pulse rate prior to and during initial therapy; evaluate mental status, suicide ideation (especially at the beginning of therapy or when doses are increased or decreased); monitor weight; ECG in older adults
Patient Education
It may take 2-3 weeks to achieve desired results. Take at bedtime. Avoid alcohol. Maintain adequate hydration unless instructed to restrict fluid intake. You may experience drowsiness, lightheadedness, dizziness, blurred vision, nausea, altered taste, dry mouth, constipation, diarrhea, increased appetite, postural hypotension, urinary retention, or sexual dysfunction (reversible). Report persistent CNS effects (eg, insomnia, restlessness, fatigue, anxiety, impaired cognitive function, seizures, suicide ideation); muscle cramping or tremors; chest pain, palpitations, rapid heartbeat, swelling of extremities, or severe dizziness; unresolved urinary retention; vision changes or eye pain; yellowing of eyes or skin; pale stools/dark urine; suicide ideation; or worsening of condition.
Geriatric Considerations
Similar to doxepin in its side effect profile; has not been well studied in the elderly; very anticholinergic and, therefore, not considered a drug of first choice in the elderly when selecting an antidepressant. Data from a clinical trial comparing fluoxetine to tricyclics suggest that fluoxetine is significantly less effective than nortriptyline in hospitalized elderly patients with unipolar major affective disorder, especially those with melancholia and concurrent cardiovascular diseases.
Additional Information
May cause alterations in bleeding time.
Dental Health: Effects on Dental Treatment
Key adverse event(s) related to dental treatment: Xerostomia (normal salivary flow resumes upon discontinuation) and unpleasant taste. Long-term treatment with TCAs, such as trimipramine, increases the risk of caries by reducing salivation and salivary buffer capacity.
Dental Health: Vasoconstrictor/Local Anesthetic Precautions
Use with caution; epinephrine and levonordefrin have been shown to have an increased pressor response in combination with TCAs. Trimipramine is one of the drugs confirmed to prolong the QT interval and is accepted as having a risk of causing torsade de pointes. The risk of drug-induced torsade de pointes is extremely low when a single QT interval prolonging drug is prescribed. In terms of epinephrine, it is not known what effect vasoconstrictors in the local anesthetic regimen will have in patients with a known history of congenital prolonged QT interval or in patients taking any medication that prolongs the QT interval. Until more information is obtained, it is suggested that the clinician consult with the physician prior to the use of a vasoconstrictor in suspected patients, and that the vasoconstrictor (epinephrine, mepivacaine and levonordefrin [Carbocaine® 2% with Neo-Cobefrin®]) be used with caution.
Dental Comment
Trimipramine is known to prolong the QT interval. The QT interval is measured as the time and distance between the Q point of the QRS complex and the end of the T wave in the ECG tracing. After adjustment for heart rate, the QT interval is defined as prolonged if it is more than 450 msec in men and 460 msec in women. A long QT syndrome was first described in the 1950s and 60s as a congenital syndrome involving QT interval prolongation and syncope and sudden death. Some of the congenital long QT syndromes were characterized by a peculiar electrocardiographic appearance of the QRS complex involving a premature atria beat followed by a pause, then a subsequent sinus beat showing marked QT prolongation and deformity. This type of cardiac arrhythmia was originally termed “torsade de pointes” (translated from the French as “twisting of the points”). Trimipramine is considered as having a risk of causing torsade de pointes. Since it is not known what effect vasoconstrictors in the local anesthetic regimen will have in patients with a known history of congenital prolonged QT interval or in patients taking any medication that prolongs the QT interval, a medical consult is suggested.
Mental Health: Comment
Tricyclic antidepressants may be classified as tertiary (amitriptyline, doxepin, clomipramine, imipramine, trimipramine) or secondary amines (nortriptyline, desipramine, protriptyline). The tertiary amines are not recommended to treat depression in the elderly. If a TCA is used in the elderly, it should be a secondary amine. The tertiary amines are commonly used in low dosages for various conditions associated with pain. Toxicity is generally dose dependent. Relatively small overdoses (1-week supply) can be potentially fatal.
Nursing: Physical Assessment/Monitoring
Monitor for CNS depression, thoughts of suicide. Taper dosage slowly when discontinuing.
Dosage Forms
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Capsule, oral: 25 mg [DSC], 50 mg [DSC]
Surmontil®: 25 mg, 50 mg, 100 mg
Pricing: U.S. (www.drugstore.com)
Capsules (Surmontil)
50 mg (100): $209.98
50 mg (100): $399.97
References
Druid H and Holmgren P, “Fatal Seizures Associated With Trimipramine Overdose,” Forensic Sci Int, 1991, 49(1):75-9.
Mokhlesi B, Leikin JB, Murray P, et al, “Adult Toxicology in Critical Care: Part II: Specific Poisonings,” Chest, 2003, 123(3):897-922.
Nebinger P and Koel M, “Specificity Data of the Tricyclic Antidepressants Assay by Fluorescent Polarization Immunoassay,” J Anal Toxicol, 1990, 14(4):219-21.
Pass SE and Simpson RW, “Discontinuation and Reinstitution of Medications During the Perioperative Period,” Am J Health Syst Pharm, 2004, 61(9):899-912.
Remy AJ, Larrey D, Pageaux GP, et al, “Cross Hepatotoxicity Between Tricyclic Antidepressants and Phenothiazines,” Eur J Gastroenterol Hepatol, 1995, 7(4):373-6.
Roose SP, Glassman AH, Attia E, et al, “Comparative Efficacy of Selective Serotonin Reuptake Inhibitors and Tricyclics in the Treatment of Melancholia,” Am J Psychiatry, 1994, 151(12):1735-9.
International Brand Names
Lexi-Comp.com
Last full review/revision May 2011
Content last modified May 2011
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