31/10/24, 2:57 Nortriptilina - StatPearls - NCBI Bookshelf

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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

Nortriptilina
Gagindip Merwar ; Jonathan R. Gibbons ; Seyed Alireza Hosseini ; Abdolreza Saadabadi .

Información y afiliaciones del autor

Última actualización: 5 de junio de 2023 .

Actividad de Educación Continua

La nortriptilina está indicada para su uso en el tratamiento de la depresión (aprobada por la
FDA). También se puede utilizar fuera de indicación para afecciones como el dolor crónico, la
neuropatía diabética, el dolor miofascial, el dolor orofacial y la neuralgia posherpética. La
nortriptilina también ha demostrado ser útil en pacientes que intentan dejar de fumar. La
nortriptilina no está aprobada por la FDA para su uso en niños. Esta actividad cubre las
indicaciones de la nortriptilina, el mecanismo de acción, la farmacología, la administración, los
perfiles de eventos adversos, las poblaciones de pacientes elegibles, las contraindicaciones y el
seguimiento, y destaca el papel del equipo interprofesional en el manejo de la depresión y otras
enfermedades con terapia con nortriptilina.

Objetivos:

Describa el mecanismo de acción de la nortriptilina.

Revise las indicaciones de uso de nortriptilina.

Resuma los posibles efectos adversos asociados con la terapia con nortriptilina.

Describir la importancia de mejorar la coordinación de la atención entre el equipo

interprofesional para mejorar la prestación de la atención a los pacientes que pueden
beneficiarse de la terapia con nortriptilina.

Acceda gratuitamente a preguntas de opción múltiple sobre este tema.

Indicaciones
La nortriptilina está indicada para el tratamiento de la depresión (aprobada por la FDA). La
nortriptilina no está aprobada por la FDA para su uso en niños.

La nortriptilina también se puede utilizar para las siguientes indicaciones no autorizadas:

Dolor crónico [1]

Neuropatía diabética [2]

Dolor miofascial persistente [3]

Neuralgia del trigémino [4]

Neuralgia posherpética [5]

Dejar de fumar [6]

Profilaxis de la migraña [7]

Tos neurogénica [8]

Mecanismo de acción

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Nortriptyline is an antidepressant that falls under the pharmacological category of tricyclics

(secondary amine), more commonly known as TCAs.The consensus is that nortriptyline inhibits
the reuptake of serotonin and norepinephrine by the presynaptic neuronal membrane, thereby
increasing the concentration of those neurotransmitters in the synapse. Additionally, nortriptyline
inhibits the activity of histamine, 5-hydroxytryptamine, and acetylcholine.
Nortriptyline increases the pressor effect of norepinephrine but hinders the pressor response of
phenethylamine. However, research has found additional receptor effects, including
desensitization of adenylyl cyclase, down-regulation of beta-adrenergic receptors, and
downregulation of serotonin receptors.

The proposed mechanism of nortryptyline in neuropathic pain is an increase in noradrenaline

levels acting within dorsal root ganglia on β2-adrenoceptors expressed by non-neuronal satellite
cells. This stimulation of β2-adrenoreceptors reduces the neuropathy-induced production of
TNFα, resulting in the relief of neuropathic pain.[9] Nortriptyline's mechanism in smoking
cessation is unclear, but the possible action may involve simulating the noradrenergic actions of
nicotine.[10] A recent study suggests that nortriptyline can be used as a new antimicrobial drug
against multidrug-resistant Candida Albicans infection by inhibiting biofilm and ability to kill
cells in a mature biofilm efficiently; however, more research is needed.[11]

Pharmacokinetics

Absorption: Peak plasma concentrations are 7 to 8.5 hours after oral administration,
although antidepressant action is obtained after a few weeks.[12]

Distribution: Nortriptyline is distributed to the brain, heart, and liver. Nortriptyline and its
metabolite are highly bound to plasma and tissue proteins. Nortriptyline crosses the
placenta, and nortriptyline is present in breast milk.[13]

Metabolism: Nortriptyline, when administered orally, undergoes first-pass metabolism in

the liver by CYP2D6.[14]

Excretion: The primary route of elimination is urinary excretion, approximately one-third

of the dose as metabolites within 24 hours, but it is also excreted in feces via the bile.

Administration
Nortriptyline is usually taken orally as a capsule or an oral solution. Capsule form comes in 10
mg, 25 mg, 50 mg, and 75 mg strengths. The oral solution form is usually of the following
composition 10 mg/5 mL (473 mL). The usual adult dose is 25 mg three or four times daily; it
should begin at a low level and increase as needed. As an alternate regimen, the total daily
dosage can be given once daily. When doses higher than 100 mg daily are administered, plasma
levels of nortriptyline should be monitored. Doses higher than 150 mg daily are not
recommended.

Use in Specific Patient Population

Patients with Hepatic impairment: No information has been provided in the

manufacturer's product labeling. However, caution and dose reduction are advised in
patients with hepatic impairment, given the drug's primary metabolism is by liver
enzymes.[14]

Patients with Renal impairment: No information has been provided in the

manufacturer's product labeling.

Pregnancy Considerations: According to product labeling, preclinical studies during

pregnancy have been inconclusive. Safe use of nortriptyline during pregnancy has not been
established; therefore, when the drug is administered to pregnant patients or women of

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childbearing potential, clinicians must weigh the potential benefits against the possible
hazard.

Breastfeeding Considerations: According to product labeling, the safe use of nortriptyline

during lactation has not been established. However, nortriptyline's concentration in
breastmilk is low. Consequently, amounts ingested by the infant are small. However, the
less active metabolites are often detectable in low levels in infant serum. Many
reviewers consider nortriptyline preferred TCA during breastfeeding; however, drugs that
have a better safety profile during lactation are paroxetine and sertraline.[13]

Pharmacogenomic considerations: Advancement in the field of pharmacogenomics can

be used to deliver effective patient-centered by individualized drug therapy regimens.[15]

In CYP2D6 ultrarapid metabolizer, clinicians should avoid nortriptyline use due to

potential lack of efficacy and consider alternative drugs not metabolized by
CYP2D6.

In patients who are CYP2D6 poor metabolizers avoid nortriptyline use due to the
potential for adverse drug reactions. Clinicians can consider alternative drugs not
metabolized by CYP2D6. Consider a 50% reduction of the recommended starting
dose if a TCA is warranted.[14]

Adverse Effects
Nortriptyline has a black box warning for increased risk of suicide in adolescents, children, and
young adults with major depressive disorder and multiple other psychiatric disorders.[16]

The most common adverse effects of nortriptyline include downiness, xerostomia, dizziness,
constipation, blurred visions, palpitations, tachycardia, impaired coordination, increased appetite,
nausea/vomiting, diaphoresis, weakness, disorientation, confusion, restlessness, insomnia,
anxiety/agitation, urinary retention, urinary frequency, rash, urticaria, pruritus, weight gain,
libido changes, impotence, gynecomastia, galactorrhea, tremor, hypo/hyperglycemia,
paraesthesia, and photosensitivity.[17]

The most serious adverse effects include orthostatic hypotension, HTN, syncope, ventricular
arrhythmias, AV block, MI, stroke, paralytic ileus, glaucoma, increased IOP, agranulocytosis,
leukopenia, thrombocytopenia, hepatitis, angioedema.[18][19]

Neuropsychiatric adverse drug reactions include EPS symptoms, ataxia, tardive dyskinesia,
hallucinations, psychosis exacerbation, hypomania/mania, exacerbation of depression,
suicidality, serotonin syndrome, SIADH, hyperthermia, and seizures.[20][21][22]

Cardiotoxicity is the hallmark adverse drug reaction of tricyclic antidepressants, such as

nortriptyline. In the case of TCA toxicity, fast cardiac sodium channels are inhibited, which can
lead to cardiac arrhythmias. On electrocardiography. A widened QRS complex is often noted.[23]

A patient can also have withdrawal symptoms such as dizziness, gastrointestinal problems such
as nausea and vomiting, anxiety, headaches, and restlessness if the patient discontinues
nortriptyline abruptly. Clinicians can avoid these withdrawal symptoms by gradually decreasing
the dose of nortriptyline over a period.[24]

Drug Interactions

Clinicians should avoid concurrent usage of cimetidine and tricyclic antidepressants such as
nortriptyline as the drug interaction can increase the concentration of TCAs. Using nortriptyline,
along with alcohol, can increase the effects of alcohol on patients. Cytochrome P450 2D6
metabolizes nortriptyline. All pharmacological drugs that inhibit 2D6 can produce an adverse
reaction. Significant drug interactions that can inhibit cytochrome P450 2D6 include quinidine

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and cimetidine. Cimetidine increases bioavailability and decreases the clearance of this drug due
to its inhibition of metabolic pathways of both demethylation and hydroxylation, as well as its
ability to reduce hepatic extraction of nortriptyline. Other drugs are substrates for CYP2D6, such
as other antidepressants, phenothiazines, and type-1C antiarrhythmics such as propafenone and
flecainide.[25][26]

Concurrent usage of nortriptyline with drugs that can inhibit cytochrome CYP2D6 may require
lower doses than usually prescribed for either nortriptyline or the other medication.

Many patients prescribed nortriptyline may already be taking SSRIs such as fluoxetine. If the
benefit of switching from fluoxetine to nortriptyline is higher than the risk, the clinician should
consider that fluoxetine has an active metabolite, norfluoxetine, with a long half-life. The risk of
adverse effects and interactions may be high for several weeks after discontinuing fluoxetine.
Therefore, usage of nortriptyline with SSRIs like fluoxetine can increase the risk for serotonin
syndrome. Fluoxetine should be discontinued for up to six weeks before starting another
medication that inhibits serotonin reuptake. If serotonin syndrome occurs, clinicians should
promptly administer an antidote, i.e., cyproheptadine. Cyproheptadine is a 5-HT1A, 5-HT2A,
and H1 receptor antagonist.[27]

Contraindications
Tricyclic antidepressants use along with a monoamine oxidase (MAO) inhibitor, linezolid, and
IV methylene blue is contraindicated as they can lead to an increased risk of developing
serotonin syndrome. Serotonin syndrome can be life-threatening as it can cause a change in
mental status, autonomic instability, neuromuscular changes, seizures, and gastrointestinal
symptoms. More importantly, concurrent use of both medications can cause convulsions, hyper-
pyretic crises, and death. The patient must discontinue MAO inhibitors for at least 14 days before
starting nortriptyline.[28] If nortriptyline must be used alongside serotonergic drugs such as
triptans, other TCAs, fentanyl, lithium, tramadol, buspirone, tryptophan, and St. John’s Wort, the
benefits must outweigh the risks.

Postmarketing reports have shown a possible association between nortriptyline and the
unmasking of Brugada syndrome. For this reason, patients with confirmed or suspected Brugada
syndrome should avoid nortriptyline as it can result in EKG abnormalities, syncope, and even
sudden cardiac death.[29] Nortriptyline can cause pupillary dilation, potentially resulting in an
angle-closure attack in an individual with anatomically narrow angles. Finally, nortriptyline is
contraindicated during the acute recovery period after myocardial infarction. The use of
nortriptyline is also contraindicated in patients with hypersensitivity to nortriptyline or its
components. Cross-sensitivity between nortriptyline hydrochloride and other dibenzazepines is a
possibility.

Monitoring
As an antidepressant, the therapeutic range for nortriptyline is between 50 to 150 ng/mL (190 to
570 nmol/L). According to APA guidelines, patients using nortriptyline need monitoring for
suicidal ideation, especially at the start of therapy and when making dosage changes. Clinicians
should frequently monitor cardiac parameters such as heart rate, EKG, and blood pressure in
adults who already have existing cardiac disease and elderly patients.[28]

Monitor for improvement/worsening of depression using questionnaires such as PHQ-9 (Patient

Health Questionnaire-9), which are patient-reported outcomes[30], and the Montgomery-Asberg
Depression Rating Scale (MADRS), which is based on clinical judgment.[31] Integration of
clinical decision support tools (CDS tools) in EHR can improve the administration of
questionnaires and management of depression.[32]

Toxicity
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Like many other TCAs, the toxicity of nortriptyline can be very harmful to the body. During an
overdose, there is a blockade of the following receptors: sodium channels (fast) in the heart,
muscarinic Ach receptors (central and peripheral), alpha-1 receptors in the periphery, and H1 and
GABA-A in the central nervous system. Therefore, the most crucial initial step when assessing a
patient with toxicity is ensuring the patient can adequately breathe. Intubation is usually
mandatory for airway protection and proper ventilation. In addition, the clinician can administer
IV fluids for hypotension.

Additionally, sodium bicarbonate is the recommended treatment for patients with prolonged QRS
(greater than 100 milliseconds) or ventricular arrhythmia. The sodium bicarbonate dosage
depends on the patient's weight, usually 1 to 2 mEq/kg. Arrhythmias not responding to sodium
bicarbonate therapy may need lidocaine, phenytoin, or bretylium. TCAs can also cause seizures.
These can have treatment with benzodiazepines such as lorazepam 2 mg or diazepam 5 mg,
administered through the intravenous (IV) route. Treatment with activated charcoal for
gastrointestinal decontamination is only indicated in patients who present within 2 hours of
overdose (1 g/kg). Although there is a strong blockage of muscarinic acetylcholine receptors,
physostigmine is contraindicated in the event of TCA toxicity as it can cause adverse cardiac
effects such as cardiac arrest.[28] The principles of management of pediatric overdose are
similar. However, It is recommended that the clinician contact the local poison control center for
specific pediatric treatment.

Enhancing Healthcare Team Outcomes

Interprofessional healthcare team members, including clinicians, psychiatrists, nurse practitioners
and physician assistants, nurses, and pharmacists, should be aware that nortriptyline is no longer
a first-line choice for its indicated conditions. There are many better and safer antidepressants on
the market. The drug has many side effects, which are often not well tolerated.[33]

However, when a patient is taking nortriptyline, all interprofessional team members should
contribute from their individual disciplines to ensure proper dosing, the absence of drug-drug
interactions, and participate in patient monitoring and education, to drive optimal outcomes with
minimal adverse events. Every team member is responsible for monitoring and counseling the
patient and must be alert for signs of therapeutic failure, possible drug interactions, or adverse
events, including toxicity. If they note an issue with the patient, they should report these to the
other team members and document their observations in the patient's medical record. A
randomized controlled trial aimed at the clinical effectiveness of collaborative care in managing
patients with moderate to severe depression showed optimistic results. Coordinated care between
health care providers had continued promising results up to one year after initiation of the
depression treatment and was preferred by patients.[34] [Level 2]

Review Questions

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Divulgación: Gagindip Merwar declara no tener relaciones financieras relevantes con empresas no elegibles.

Divulgación: Jonathan Gibbons declara no tener relaciones financieras relevantes con empresas no elegibles.

Divulgación: Seyed Alireza Hosseini declara no tener relaciones financieras relevantes con empresas no elegibles.

Divulgación: Abdolreza Saadabadi declara no tener relaciones financieras relevantes con empresas no elegibles.

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