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7 Interactions found for:

propranolol and Zoloft
Interactions Summary
  • 3 Major
  • 3 Moderate
  • 1 Minor
  • propranolol
  • Zoloft

Drug Interactions

Moderate
Propranolol + Zoloft

The following applies to the ingredients: Propranolol and Sertraline (found in Zoloft)

MONITOR: Limited clinical data suggest that selective serotonin reuptake inhibitors (SSRIs) may potentiate the pharmacologic effects of some beta-blockers. The proposed mechanism is SSRI inhibition (competitive and/or noncompetitive) of CYP450 2D6, the isoenzyme responsible for the metabolic clearance of beta-blockers such as carvedilol, labetalol, metoprolol, nebivolol, propranolol, and timolol. Paroxetine and norfluoxetine (the active metabolite of fluoxetine), in particular, are potent inhibitors of CYP450 2D6 and may be more likely than other SSRIs to cause the interaction. There have been case reports of patients stabilized on beta-blocker therapy who developed bradycardia, hypotension, and complete heart block following the addition of a SSRI, subsequently requiring discontinuation of one or both agents and/or institution of a permanent pacemaker. The interaction is also corroborated by data from in vitro and clinical studies involving paroxetine and metoprolol conducted by one group of investigators. Coadministration of nebivolol 5 mg and paroxetine 20 mg in 23 healthy subjects increased nebivolol Cmax and AUC by 5.7-fold and 6.1-fold, respectively, with no increase in pharmacodynamic effects on heart rate or blood pressure. Likewise, coadministration f nebivolol 10 mg with fluoxetine 20 mg in 10 subjects increased nebivolol Cmax and AUC by 2.3-fold and 6-fold, respectively, without reports of vital sign-related adverse effects. Additionally, coadministration of nebivolol 5 mg with fluvoxamine 100 mg, a mild CYP2D6 inhibitor, resulted in a 1.41-fold and 1.44-fold increase in fluvoxamine's Cmax and AUC, respectively, without enhancing nebivolol's pharmacodynamic effects. Conversely, fluvoxamine is a potent inhibitor of CYP450 1A2 and may significantly interact with propranolol, which is a substrate of both CYP450 2D6 and 1A2.

MANAGEMENT: During concomitant therapy with SSRIs, a lower initial dosage and more cautious titration of the beta-blocker may be appropriate. Cardiac function should be closely monitored and the beta-blocker dosage adjusted accordingly, particularly following initiation, discontinuation or change of dosage of SSRI in patients who are stabilized on their beta-blocker regimen. Due to the long half-life of fluoxetine and its active metabolite, norfluoxetine, the risk of an interaction may exist for an extended period (up to several weeks) after discontinuation of fluoxetine. To avoid the interaction, use of beta-blockers that are primarily eliminated by the kidney such as atenolol, acebutolol, betaxolol, carteolol, and nadolol may be considered.

References

  1. Walley T, Pirmohamed M, Proudlove C, Maxwell D "Interaction of metoprolol and fluoxetine." Lancet 341 (1993): 967-8
  2. Otton SV, Wu D, Joffe RT, Cheung SW, Sellers EM "Inhibition by fluoxetine of cytochrome P450 2D6 activity." Clin Pharmacol Ther 53 (1993): 401-9
  3. Brosen K, Skjelbo E, Rasmussen BB, Poulsen HE, Loft S "Fluvoxamine is a potent inhibitor of cytochrome P4501A2." Biochem Pharmacol 45 (1993): 1211-4
  4. Gilman AG, eds., Nies AS, Rall TW, Taylor P "Goodman and Gilman's the Pharmacological Basis of Therapeutics." New York, NY: Pergamon Press Inc. (1990):
  5. Drake WM, Gordon GD "Heart block in a patient on propranolol and fluoxetine." Lancet 343 (1994): 425-6
  6. Perucca E, Gatti G, Spina E "Clinical pharmacokinetics of fluvoxamine." Clin Pharmacokinet 27 (1994): 175-90
  7. Crewe HK, Lennard MS, Tucker GT, Woods FR, Haddock RE "The effect of selective serotonin re-uptake inhibitors on cytochrome P4502D6 (CYP2D6) activity in human liver microsomes." Br J Clin Pharmacol 34 (1992): 262-5
  8. "Product Information. Luvox (fluvoxamine)." Solvay Pharmaceuticals Inc PROD (2001):
  9. Riesenman C "Antidepressant drug interactions and the cytochrome p450 system: a critical appraisal." Pharmacotherapy 15 (1995): s84-99
  10. Nemeroff CB, Devane CL, Pollock BG "Newer antidepressants and the cytochrome p450 system." Am J Psychiatry 153 (1996): 311-20
  11. Ereshefsky L "Treating depression: potential drug-drug interactions: commentary." J Clin Psychopharmacol 16 (suppl (1996): s50-3
  12. Richelson E "Pharmacokinetic interactions of antidepressants." J Clin Psychiatry 59 (1998): 22-6
  13. Kashuba ADM, Nafziger AN, Kearns GL, Leeder JS, Gotschall R, Rocci ML, Kulawy RW, Beck DJ, Bertino JS "Effect of fluvoxamine therapy on the activities of CYP1A2, CYP2D6, and CYP3A as determined by phenotyping." Clin Pharmacol Ther 64 (1998): 257-68
  14. Hemeryck A, Lefebvre RA, DeVriendt C, Belpaire FM "Paroxetine affects metoprolol pharmacokinetics and pharmacodynamics in healthy volunteers." Clin Pharmacol Ther 67 (2000): 283-91
  15. Amchin J, Ereshefsky L, Zarycranski W, Taylor K, Albano D, Klockowski PM "Effect of venlafaxine versus fluoxetine on metabolism of dextromethorphan, a CYP2D6 probe." J Clin Pharmacol 41 (2001): 443-51
  16. Hemeryck A, DeVriendt CA, Belpaire FM "Metoprolol-paroxetine interaction in human liver microsomes: Stereoselective aspects and prediction of the in vivo interaction." Drug Metab Disposition 29 (2001): 656-63
  17. Lindamood C, Ortiz S, shaw a, Rackley R, Gorski JC "Effects of commonly administered agents and genetics on nebivolol pharmacokinetics: drug-drug interaction studies." J Clin Pharmacol 51 (2011): 575-85
  18. Gheldiu AM, Vlase L, Popa A, et al. "Investigation of a potential pharmacokinetic interaction between nebivolol and fluvoxamine in healthy volunteers." J Pharm Pharm Sci 20 (2017): 68-80
  19. Briciu C, Neag M, Muntean D, et al. "A pharmacokinetic drug interaction study between nebivolol and paroxetine in healthy volunteers." J Clin Pharm Ther 39 (2014): 535-40

Drug and Food Interactions

Moderate
Propranolol + Food

The following applies to the ingredients: Propranolol

ADJUST DOSING INTERVAL: The bioavailability of propranolol may be enhanced by food.

MANAGEMENT: Patients may be instructed to take propranolol at the same time each day, preferably with or immediately following meals.

References

  1. Olanoff LS, Walle T, Cowart TD, et al. "Food effects on propranolol systemic and oral clearance: support for a blood flow hypothesis." Clin Pharmacol Ther 40 (1986): 408-14
  2. Byrne AJ, McNeil JJ, Harrison PM, Louis W, Tonkin AM, McLean AJ "Stable oral availability of sustained release propranolol when co-administered with hydralazine or food: evidence implicating substrate delivery rate as a determinant of presystemic drug interactions." Br J Clin Pharmacol 17 (1984): s45-50

The following applies to the ingredients: Propranolol

ADJUST DOSING INTERVAL: Concurrent administration with calcium salts may decrease the oral bioavailability of atenolol and possibly other beta-blockers. The exact mechanism of interaction is unknown. In six healthy subjects, calcium 500 mg (as lactate, carbonate, and gluconate) reduced the mean peak plasma concentration (Cmax) and area under the concentration-time curve (AUC) of atenolol (100 mg) by 51% and 32%, respectively. The elimination half-life increased by 44%. Twelve hours after the combination, beta-blocking activity (as indicated by inhibition of exercise tachycardia) was reduced compared to that with atenolol alone. However, during a 4-week treatment in six hypertensive patients, there was no difference in blood pressure values between treatments. The investigators suggest that prolongation of the elimination half-life induced by calcium coadministration may have led to atenolol cumulation during long-term dosing, which compensated for the reduced bioavailability.

MANAGEMENT: It may help to separate the administration times of beta-blockers and calcium products by at least 2 hours. Patients should be monitored for potentially diminished beta-blocking effects following the addition of calcium therapy.

References

  1. Kirch W, Schafer-Korting M, Axthelm T, Kohler H, Mutschler E "Interaction of atenolol with furosemide and calcium and aluminum salts." Clin Pharmacol Ther 30 (1981): 429-35

The following applies to the ingredients: Propranolol

MONITOR: Smoking cessation may lead to elevated plasma concentrations and enhanced pharmacologic effects of drugs that are substrates of CYP450 1A2 (and possibly CYP450 1A1) and/or certain drugs with a narrow therapeutic index (e.g., flecainide, pentazocine). One proposed mechanism is related to the loss of CYP450 1A2 and 1A1 induction by polycyclic aromatic hydrocarbons in tobacco smoke; when smoking cessation agents are initiated and smoking stops, the metabolism of certain drugs may decrease leading to increased plasma concentrations. The mechanism by which smoking cessation affects narrow therapeutic index drugs that are not known substrates of CYP450 1A2 or 1A1 is unknown. The clinical significance of this interaction is unknown as clinical data are lacking.

MANAGEMENT: Until more information is available, caution is advisable if smoking cessation agents are used concomitantly with drugs that are substrates of CYP450 1A2 or 1A1 and/or those with a narrow therapeutic range. Patients receiving smoking cessation agents may require periodic dose adjustments and closer clinical and laboratory monitoring of medications that are substrates of CYP450 1A2 or 1A1.

References

  1. "Product Information. Cytisine (cytisinicline)." Consilient Health Ltd (2024):
  2. jeong sh, Newcombe D, sheridan j, Tingle M "Pharmacokinetics of cytisine, an a4 b2 nicotinic receptor partial agonist, in healthy smokers following a single dose." Drug Test Anal 7 (2015): 475-82
  3. Vaughan DP, Beckett AH, Robbie DS "The influence of smoking on the intersubject variation in pentazocine elimination." Br J Clin Pharmacol 3 (1976): 279-83
  4. Zevin S, Benowitz NL "Drug interactions with tobacco smoking: an update" Clin Pharmacokinet 36 (1999): 425-38

Moderate
Zoloft + Food

The following applies to the ingredients: Sertraline (found in Zoloft)

GENERALLY AVOID: Alcohol may potentiate some of the pharmacologic effects of sertraline. Use in combination may result in additive central nervous system depression and/or impairment of judgment, thinking, and psychomotor skills. In addition, limited clinical data suggest that consumption of grapefruit juice during treatment with sertraline may result in increased plasma concentrations of sertraline. The proposed mechanism is inhibition of CYP450 3A4-mediated metabolism by certain compounds present in grapefruit. An in-vitro study demonstrated that grapefruit juice dose-dependently inhibits the conversion of sertraline to its metabolite, desmethylsertraline. In a study with eight Japanese subjects, mean plasma levels of sertraline increased by approximately 100% and maximum plasma concentrations increased by 66% after the ingestion of three 250 mL glasses of grapefruit juice per day for 5 days and administration of a single dose of sertraline 75 mg on the sixth day. In another small study with 5 patients, mean sertraline trough levels increased by 47% after taking sertraline for at least 6 weeks, then taking sertraline with 240 mL grapefruit juice daily for 1 week. The clinical significance is unknown; however, pharmacokinetic alterations associated with interactions involving grapefruit juice are often subject to a high degree of interpatient variability. The possibility of significant interaction in some patients should be considered.

MANAGEMENT: Patients receiving sertraline should be advised to avoid or limit consumption of alcohol. Ambulatory patients should be counseled to avoid hazardous activities requiring complete mental alertness and motor coordination until they know how sertraline affects them, and to notify their physician if they experience excessive or prolonged CNS effects that interfere with their normal activities. Some authorities recommend that consumption of grapefruit juice should be avoided during sertraline therapy.

References

  1. "Product Information. Zoloft (sertraline)." Roerig Division PROD (2001):
  2. Lee AJ, Chan WK, Harralson AF, Buffum J, Bui BCC "The effects of grapefruit juice on sertraline metabolism: An in vitro and in vivo study." Clin Ther 21 (1999): 1890-9
  3. Cerner Multum, Inc. "UK Summary of Product Characteristics." O 0
  4. Ueda N, Yoshimura R, Umene-Nakano W, et al. "Grapefruit juice alters plasma sertraline levels after single ingestion of sertraline in healthy volunteers." World J Biol Psychiatry 10(4 Pt 3) (2009): 832-5

Drug and Pregnancy Interactions

The following applies to the ingredients: Sertraline (found in Zoloft)

This drug should be used during pregnancy only if the potential benefit outweighs the potential risk to the fetus, taking into account the risks of untreated depression.
-Oral concentrate and solution formulations containing alcohol: Not recommended.

AU TGA pregnancy category: C
US FDA pregnancy category: Not assigned.

Risk summary: Malformative risk is unlikely when given during the first trimester. There is inconclusive data on use of this drug in the third trimester to inform of a drug-related risk.

Comments:
-A pregnancy exposure registry is available.
-Neonates exposed to this drug late in the third trimester may require respiratory support, tube feeding, and/or prolonged hospitalization.
-Exposed neonates should be monitored after delivery for direct toxic effects of this drug, drug discontinuation syndrome, and serotonin syndrome (e.g., respiratory distress, cyanosis, apnea, seizures, temperature instability, feeding difficulty, vomiting, hypoglycemia, hypo/hypertonia, hyperreflexia, tremor, jitteriness, irritability, constant crying).

Animal studies have failed to reveal evidence of teratogenicity; however, there was evidence of delayed ossification and effects on reproduction attributed to maternal toxicity. Decreased neonatal survival following maternal administration at exposures similar to or slightly greater than the maximum recommended human dose of 200 mg was also observed; the clinical significance is unknown. There are no controlled data in human pregnancy.

The results of several studies suggest that the use of SSRIs in the first trimester of pregnancy may be associated with an increased risk of cardiovascular and/or other congenital malformations; however, this association has not been clearly established. The association appears to be strongest for another SSRI, paroxetine.

Use of sertraline during pregnancy has been reported to cause symptoms compatible with withdrawal reactions in neonates whose mothers had taken sertraline. Neonates exposed to SSRIs and SNRIs late in the third trimester have uncommonly reported clinical findings including respiratory distress, cyanosis, apnea, seizures, temperature instability, feeding difficulty, vomiting, hypoglycemia, hypotonia, hyperreflexia, tremor, jitteriness, irritability, and constant crying. These effects have mostly occurred either at birth or within a few days of birth. These features are consistent with either a direct toxic effect of SSRIs and SNRIs, or possibly a drug discontinuation syndrome; in some cases, the clinical picture is consistent with serotonin syndrome. The results of a cohort study indicate that 30% of neonates who had prolonged exposure to SSRIs in utero experience symptoms, in a dose-response manner, of a neonatal abstinence syndrome after birth. The authors suggest that infants exposed to SSRIs should be closely monitored for a minimum of 48 hours after birth.

Epidemiological data have suggested that the use of SSRIs, particularly in late pregnancy, may increase the risk of persistent pulmonary hypertension in the newborn. Data are not available for SNRIs.

One study compared 267 women exposed to an SSRI - either fluvoxamine, paroxetine, or sertraline, to 267 controls. Exposure to SSRIs was not associated with either increased risk for major malformations, higher rates of miscarriage, stillbirth, or prematurity. Mean birth weights among SSRI users were similar to controls as were the gestational ages. The study concluded that the SSRIs fluvoxamine, paroxetine, and sertraline did not appear to increase teratogenic risk when used in their recommended doses.

Animal data with sertraline have not shown an effect on fertility. Human case reports from some SSRIs have shown an effect on sperm quality that is reversible. As yet, the impact of this on human fertility has not been observed.

To monitor maternal-fetal outcomes of pregnant women exposed to antidepressant therapy, a National Pregnancy Registry for Antidepressants has been established. Healthcare providers are encouraged to prospectively register patients. For additional information: https://womensmentalhealth.org/clinical-and-research-programs/pregnancyregistry/antidepressants/

AU TGA pregnancy category C: Drugs which, owing to their pharmacological effects, have caused or may be suspected of causing, harmful effects on the human fetus or neonate without causing malformations. These effects may be reversible. Accompanying texts should be consulted for further details.

US FDA pregnancy category Not Assigned: The US FDA has amended the pregnancy labeling rule for prescription drug products to require labeling that includes a summary of risk, a discussion of the data supporting that summary, and relevant information to help health care providers make prescribing decisions and counsel women about the use of drugs during pregnancy. Pregnancy categories A, B, C, D, and X are being phased out.

References

  1. "Product Information. Zoloft (sertraline)." Roerig Division PROD (2001):
  2. Cerner Multum, Inc. "UK Summary of Product Characteristics." O 0
  3. Cerner Multum, Inc. "Australian Product Information." O 0

The following applies to the ingredients: Propranolol

This drug is only recommended for use during pregnancy when there are no alternatives and the benefit outweighs the risk.

AU TGA pregnancy category: C
US FDA pregnancy category: C

Beta blockers may cause decreased placental perfusion, fetal and neonatal bradycardia, and hypoglycemia.

Propranolol has been used safely to treat a variety of conditions during pregnancy, including hypertension and pheochromocytoma in the mother, and tachyarrhythmias in both the mother and fetus. There are a number of abnormalities associated with the use of propranolol during pregnancy, but many of these may be attributable to underlying diseases. These abnormalities include some signs of beta-blockade, such as bradycardia, hypoglycemia, and respiratory depression. Other abnormalities that may be due to propranolol include intrauterine growth retardation, small placentas, polycythemia, thrombocytopenia, and hypocalcemia.

AU TGA pregnancy category C: Drugs which, owing to their pharmacological effects, have caused or may be suspected of causing, harmful effects on the human fetus or neonate without causing malformations. These effects may be reversible. Accompanying texts should be consulted for further details.

US FDA pregnancy category C: Animal reproduction studies have shown an adverse effect on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant.

References

  1. O'Hare MF, Kinney CD, Murnaghan GA, McDevitt DG "Pharmacokinetics of propranolol during pregnancy." Eur J Clin Pharmacol 27 (1984): 583-7
  2. Levitan AA, Manion JC "Propranolol therapy during pregnancy and lactation." Am J Cardiol 32 (1973): 247
  3. Taylor EA, Turner P "Anti-hypertensive therapy with propranolol during pregnancy and lactation." Postgrad Med J 57 (1981): 427-30
  4. "Product Information. Inderal (propranolol)." Wyeth-Ayerst Laboratories PROD (2001):
  5. O'Connor PC, Jick H, Hunter JR, Stergachis A, Madsen S "Propranolol and pregnancy outcome." Lancet 2 (1981): 1168
  6. Caldroney RD "Beta-blockers in pregnancy." N Engl J Med 306 (1982): 810
  7. Livingstone I, Craswell PW, Bevan EB "Propranolol in pregnancy three year prospective study." Clin Exp Hypertens B 2 (1983): 341-50
  8. Eliahou HE, Silverberg DS, Reisin E, Romem I, Mashiach S, Serr DM "Propranolol for the treatment of hypertension in pregnancy." Br J Obstet Gynaecol 85 (1978): 431-6
  9. Redmond GP "Propranolol and fetal growth retardation." Semin Perinatol 6 (1982): 142-7
  10. Frishman WH, Chesner M "Beta-adrenergic blockers in pregnancy." Am Heart J 115 (1988): 147-52
  11. Belpaire FM, Wynant P, Vantrappen P, Dhont M, Verstraete A, Bogaert MG "Protein binding of propranolol and verapamil enantiomers in maternal and foetal serum." Br J Clin Pharmacol 39 (1995): 190-3
  12. Page RL "Treatment of arrhythmias during pregnancy." Am Heart J 130 (1995): 871-6
  13. "Product Information. InnoPran XL (propranolol)." Reliant Pharmaceuticals LLC (2003):
  14. Cerner Multum, Inc. "UK Summary of Product Characteristics." O 0
  15. TGA. Therapeutic Goods Administration. Australian Drug Evaluation Committee "Prescribing medicines in pregnancy: an Australian categorisation of risk of drug use in pregancy. http://www.tga.gov.au/docs/pdf/medpreg.pdf" (2007):
  16. Cerner Multum, Inc. "Australian Product Information." O 0

Drug and Breastfeeding Interactions

The following applies to the ingredients: Propranolol

Use is not recommended.

Excreted into human milk: Yes

Comments: Propranolol levels in breast milk are low and would not be expected to cause any adverse effects in breastfed infants.

Propranolol milk to maternal plasma ratios as high as 1.5 has been reported. While no adverse effects in the nursing infant have been reported, experts advise monitoring the infant for signs and symptoms of beta-blockade and to schedule feedings at least three hours after maternal propranolol administration.

References

  1. Roberts RJ, Blumer JL, Gorman RL, et al. "American Academy of Pediatrics Committee on Drugs: Transfer of drugs and other chemicals into human milk." Pediatrics 84 (1989): 924-36
  2. Levitan AA, Manion JC "Propranolol therapy during pregnancy and lactation." Am J Cardiol 32 (1973): 247
  3. Bauer JH, Pape B, Zajicek J, Groshong T "Propranolol in human plasma and breast milk." Am J Cardiol 43 (1979): 860-2
  4. Taylor EA, Turner P "Anti-hypertensive therapy with propranolol during pregnancy and lactation." Postgrad Med J 57 (1981): 427-30
  5. "Product Information. Inderal (propranolol)." Wyeth-Ayerst Laboratories PROD (2001):
  6. "Product Information. InnoPran XL (propranolol)." Reliant Pharmaceuticals LLC (2003):
  7. Cerner Multum, Inc. "UK Summary of Product Characteristics." O 0
  8. Cerner Multum, Inc. "Australian Product Information." O 0
  9. United States National Library of Medicine "Toxnet. Toxicology Data Network. http://toxnet.nlm.nih.gov/cgi-bin/sis/htmlgen?LACT" (2013):

The following applies to the ingredients: Sertraline (found in Zoloft)

Use is not recommended; benefit to the mother should outweigh risk to the infant.

Excreted into human milk: Yes

Comments:
-This drug has been considered one of the preferred antidepressants during breastfeeding.
-Accumulation of the drug may occur in preterm infants with impaired metabolic activity; effects similar to neonatal abstinence may rarely present in these infants.
-Mothers taking an SSRI during pregnancy and postpartum may have difficulty breastfeeding and may require additional breastfeeding support.

Benign neonatal sleep myoclonus in a 4-month-old infant and agitation in that spontaneously resolved in another infant was reported to the Australian Adverse Drug Reaction Advisory Committee and may be related to the presence of sertraline in breastmilk.

Levels of sertraline in breastmilk are reported to be low; the weakly active metabolite desmethylsertraline may be detectable in low levels. In a study of 26 breastfeeding women who were, on average, 15.8 weeks postpartum and receiving an average of 124 mg sertraline daily for at least 14 days for severe depression, complete sets of milk sample data were available for 15 mothers. Analysis of these samples led the study authors to estimate that an exclusively breastfed infant would receive an average of 0.54% of the maternal weight-adjusted dosage. Pumping and discarding milk 8 to 9 hours after the mother's dose would decrease the infant's daily dosage by 17%.

Amounts of sertraline ingested by breastfed infants are reported to be small. There was an analysis of 30 breastfed infants aged 6 to 13 weeks, of which 19 were exclusively breastfed and 11 breastfed at least half the time. Serum sertraline levels were below 1 mcg/L in 22 infants. The other 8 infants had an average serum sertraline level of 7.9 mcg/L; their mothers were taking a average of 109 mg sertraline daily, with an average serum level of 52.8 mcg/L.

The data from one study on three breast-fed infants suggested that sertraline and/or its almost inactive metabolite norsertraline may be present at very low concentrations in the plasma of breast-fed infants. No adverse effects were noted in the infants.

A pooled analysis of 53 mother-infant pairs from published and unpublished cases found that infants had an average of 2% of the sertraline plasma levels of the mothers'; three of the infants had a plasma level greater than 10% of the mothers'.

A study of fourteen mother-infant pairs reported that while mothers receiving clinical doses of sertraline experienced substantial blockade of the platelet 5-HT transporter, platelet 5-HT uptake in nursing infants of treated mothers was unaltered.

Another study of twelve breast-feeding mothers reported that both sertraline and desmethylsertraline were present in all breast milk samples. Detectable levels of sertraline were reported in three nursing infants and detectable levels of desmethylsertraline were reported in six infants.

A case study of a mother breast-feeding while receiving sertraline therapy has also been reported. The drug was found to be present in the mother's milk. However, no sertraline was detected in the infant's serum and no abnormal occurrences were noted in the development of this infant either.

References

  1. "Product Information. Zoloft (sertraline)." Roerig Division PROD (2001):
  2. Cerner Multum, Inc. "UK Summary of Product Characteristics." O 0
  3. Cerner Multum, Inc. "Australian Product Information." O 0
  4. United States National Library of Medicine "Toxnet. Toxicology Data Network. http://toxnet.nlm.nih.gov/cgi-bin/sis/htmlgen?LACT" (2013):

Therapeutic Duplication Warnings

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Therapeutic duplication warnings are only returned when drugs within the same group exceed the recommended therapeutic duplication maximum.

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Drug Interaction Classification

These classifications are only a guideline. The relevance of a particular drug interaction to a specific individual is difficult to determine. Always consult your healthcare provider before starting or stopping any medication.
Major Highly clinically significant. Avoid combinations; the risk of the interaction outweighs the benefit.
Moderate Moderately clinically significant. Usually avoid combinations; use it only under special circumstances.
Minor Minimally clinically significant. Minimize risk; assess risk and consider an alternative drug, take steps to circumvent the interaction risk and/or institute a monitoring plan.
Unknown No interaction information available.

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