Ethosuximide

Take the missed dose as soon as you remember it. However, if it is almost time for your next dose, skip the missed dose and continue your regular dosing schedule. Do not take a double dose to make up for a missed one.

Pregnancy Category: C

Lactation: enters breast milk; use with caution (AAP Committee states "compatible with nursing")

Pregnancy Registry: Pregnant women exposed to ethosuximide are encouraged to enroll themselves by calling 1-888-233-2334.

Pregnancy Categories

A:Generally acceptable. Controlled studies in pregnant women show no evidence of fetal risk.

B:May be acceptable. Either animal studies show no risk but human studies not available or animal studies showed minor risks and human studies done and showed no risk.

C:Use with caution if benefits outweigh risks. Animal studies show risk and human studies not available or neither animal nor human studies done.

D:Use in LIFE-THREATENING emergencies when no safer drug available. Positive evidence of human fetal risk.

X:Do not use in pregnancy. Risks involved outweigh potential benefits. Safer alternatives exist.

NA:Information not available.

Body As A Whole: Allergic reaction. Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS).

Gastrointestinal System: Gastrointestinal symptoms occur frequently and include anorexia, vague gastric upset, nausea and vomiting, cramps, epigastric and abdominal pain, weight loss, and diarrhea. There have been reports of gum hypertrophy and swelling of the tongue.

Hemopoietic System: Hemopoietic complications associated with the administration of ethosuximide have included leukopenia, agranulocytosis, pancytopenia, with or without bone marrow suppression, and eosinophilia.

Nervous System: Neurologic and sensory reactions reported during therapy with ethosuximide have included drowsiness, headache, dizziness, euphoria, hiccups, irritability, hyperactivity, lethargy, fatigue, and ataxia. Psychiatric or psychological aberrations associated with ethosuximide administration have included disturbances of sleep, night terrors, inability to concentrate, and aggressiveness. These effects may be noted particularly in patients who have previously exhibited psychological abnormalities. There have been rare reports of paranoid psychosis, increased libido, and increased state of depression with overt suicidal intentions.

Integumentary System: Dermatologic manifestations which have occurred with the administration of ethosuximide have included urticaria, pruritic erythematous rashes, and hirsutism.

Special Senses: Myopia.

Genitourinary System: Vaginal bleeding, microscopic hematuria.

No information provided. Please refer to the WARNINGS and PRECAUTIONS sections.

Ethosuximide is a prescription medication used to treat absence seizures, also known as petit mal seizures. Ethosuximide belongs to a group of drugs called anticonvulsants which work by reducing abnormal activity in the brain.

This medication comes in capsule and liquid (syrup) forms. Ethosuximide is usually taken once or twice daily, with or without food.

Common side effects of ethosuximide include nausea and vomiting, loss of appetite, and diarrhea. 

Ethosuximide is part of the drug class:

• Succinimide derivatives

Medications can interact with certain foods. In some cases, this may be harmful and your doctor may advise you to avoid certain foods. In the case of ethosuximide, there are no specific foods that you must exclude from your diet when receiving this medication.

Usual Adult Dose for Seizures:

Initial dose: 500 mg (10 mL) orally daily
Maintenance dose: Dosage may be increased by small increments, for example 250 mg daily every 4 to 7 days, until optimal seizure control with minimal side effects is achieved. Dosages greater than 1.5 g per day, in divided doses, should be administered only under strict supervision of a physician.

Usual Pediatric Dose for Seizures:

3 to 6 years:
Initial dose: 250 mg (5 mL) orally daily
Maintenance dose: Dosage may be increased by small increments, for example 250 mg daily every 4 to 7 days, until optimal seizure control with minimal side effects is achieved. For most pediatric patients the optimal dose is 20 mg/kg/day in divided doses. Dosages greater than 1.5 g per day, in divided doses, should be administered only under close supervision by a physician.

> 6 to 18 years:
Initial dose: 500 mg (10 mL) orally daily
Maintenance dose: Dosage may be increased by small increments, for example 250 mg daily every 4 to 7 days, until optimal seizure control with minimal side effects is achieved. For most pediatric patients the optimal dose is 20 mg/kg/day in divided doses. Dosages greater than 1.5 g per day, in divided doses, should be administered only under close supervision by a physician.

Succinimide-derivative anticonvulsant; structurally related to other succinimide anticonvulsants (e.g., methsuximide, phensuximide [no longer commercially available in the US]).1 2 3 4 5

In the U.S.

• Zarontin

Available Dosage Forms:

• Syrup
• Capsule, Liquid Filled

Therapeutic Class: Anticonvulsant

Chemical Class: Succinimide

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Capsule, Oral:

Zarontin: 250 mg [contains fd&c yellow #10 (quinoline yellow)]

Generic: 250 mg

Solution, Oral:

Zarontin: 250 mg/5 mL (474 mL) [raspberry flavor]

Generic: 250 mg/5 mL (473 mL, 474 mL)

Absence (petit mal) seizures:

Manufacturer’s dosing:

Children 3 to 6 years: Oral: Initial: 250 mg/day. Individualize dose based on patient response by increasing in small increments (eg, ≤250 mg) every 4 to 7 days as needed; usual optimal dose: 20 mg/kg/day; doses >1,500 mg/day, in divided doses, should only be used under the strict supervision of a physician; higher doses may be necessary in some patients.

Children ≥6 years and Adolescents: Oral: Initial: 500 mg/day. Individualize dose based on patient response by increasing in small increments (eg, ≤250 mg) every 4 to 7 days as needed; usual optimal daily dose: 20 mg/kg/day; doses >1,500 mg/day, in divided doses, should only be used under the strict supervision of a physician; higher doses may be necessary in some patients.

Alternate dosing: Children ≥2 years and Adolescents: Oral: Initial: 10 mg/kg/day, titrated to response in 5 to 10 mg/kg/day increments every 7 days as required; usual range: 20 to 30 mg/kg/day in 2 to 3 divided doses (Glauser 2010; Kleigman 2016). Single daily doses have also been shown to be effective and well tolerated (Buchanan 1976; Dooley 1990). Doses reported in literature range from 6.5 to 50 mg/kg/day (Browne 1975; Sato 1982). Maximum daily dose: 60 mg/kg/day or 2,000 mg/day, whichever is less (Glauser 2010).

Alcohol (Ethyl): CNS Depressants may enhance the CNS depressant effect of Alcohol (Ethyl). Monitor therapy

Amphetamines: May diminish the therapeutic effect of Ethosuximide. Amphetamines may decrease the serum concentration of Ethosuximide. Monitor therapy

Analgesics (Opioid): CNS Depressants may enhance the CNS depressant effect of Analgesics (Opioid). Management: Avoid concomitant use of opioid analgesics and benzodiazepines or other CNS depressants when possible. These agents should only be combined if alternative treatment options are inadequate. If combined, limit the dosages and duration of each drug. Consider therapy modification

Aprepitant: May increase the serum concentration of CYP3A4 Substrates. Monitor therapy

Azelastine (Nasal): CNS Depressants may enhance the CNS depressant effect of Azelastine (Nasal). Avoid combination

Blonanserin: CNS Depressants may enhance the CNS depressant effect of Blonanserin. Consider therapy modification

Bosentan: May decrease the serum concentration of CYP3A4 Substrates. Monitor therapy

Brimonidine (Topical): May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Buprenorphine: CNS Depressants may enhance the CNS depressant effect of Buprenorphine. Management: Consider reduced doses of other CNS depressants, and avoiding such drugs in patients at high risk of buprenorphine overuse/self-injection. Initiate buprenorphine patches (Butrans brand) at 5 mcg/hr in adults when used with other CNS depressants. Consider therapy modification

Cannabis: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Chlormethiazole: May enhance the CNS depressant effect of CNS Depressants. Management: Monitor closely for evidence of excessive CNS depression. The chlormethiazole labeling states that an appropriately reduced dose should be used if such a combination must be used. Consider therapy modification

Chlorphenesin Carbamate: May enhance the adverse/toxic effect of CNS Depressants. Monitor therapy

CNS Depressants: May enhance the adverse/toxic effect of other CNS Depressants. Monitor therapy

Cobicistat: May increase the serum concentration of Ethosuximide. Monitor therapy

Conivaptan: May increase the serum concentration of CYP3A4 Substrates. Avoid combination

CYP3A4 Inducers (Moderate): May decrease the serum concentration of CYP3A4 Substrates. Monitor therapy

CYP3A4 Inducers (Strong): May increase the metabolism of CYP3A4 Substrates. Management: Consider an alternative for one of the interacting drugs. Some combinations may be specifically contraindicated. Consult appropriate manufacturer labeling. Consider therapy modification

CYP3A4 Inhibitors (Moderate): May decrease the metabolism of CYP3A4 Substrates. Monitor therapy

CYP3A4 Inhibitors (Strong): May decrease the metabolism of CYP3A4 Substrates. Consider therapy modification

Dabrafenib: May decrease the serum concentration of CYP3A4 Substrates. Management: Seek alternatives to the CYP3A4 substrate when possible. If concomitant therapy cannot be avoided, monitor clinical effects of the substrate closely (particularly therapeutic effects). Consider therapy modification

Dasatinib: May increase the serum concentration of CYP3A4 Substrates. Monitor therapy

Deferasirox: May decrease the serum concentration of CYP3A4 Substrates. Monitor therapy

Dimethindene (Topical): May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Doxylamine: May enhance the CNS depressant effect of CNS Depressants. Management: The manufacturer of Diclegis (doxylamine/pyridoxine), intended for use in pregnancy, specifically states that use with other CNS depressants is not recommended. Monitor therapy

Dronabinol: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Droperidol: May enhance the CNS depressant effect of CNS Depressants. Management: Consider dose reductions of droperidol or of other CNS agents (e.g., opioids, barbiturates) with concomitant use. Consider therapy modification

Enzalutamide: May decrease the serum concentration of CYP3A4 Substrates. Management: Concurrent use of enzalutamide with CYP3A4 substrates that have a narrow therapeutic index should be avoided. Use of enzalutamide and any other CYP3A4 substrate should be performed with caution and close monitoring. Consider therapy modification

Flunitrazepam: CNS Depressants may enhance the CNS depressant effect of Flunitrazepam. Consider therapy modification

Fosaprepitant: May increase the serum concentration of CYP3A4 Substrates. Monitor therapy

Fosphenytoin: Ethosuximide may enhance the CNS depressant effect of Fosphenytoin. Fosphenytoin may decrease the serum concentration of Ethosuximide. Ethosuximide may increase the serum concentration of Fosphenytoin. Monitor therapy

Fusidic Acid (Systemic): May increase the serum concentration of CYP3A4 Substrates. Avoid combination

HYDROcodone: CNS Depressants may enhance the CNS depressant effect of HYDROcodone. Management: Avoid concomitant use of hydrocodone and benzodiazepines or other CNS depressants when possible. These agents should only be combined if alternative treatment options are inadequate. If combined, limit the dosages and duration of each drug. Consider therapy modification

HydrOXYzine: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Idelalisib: May increase the serum concentration of CYP3A4 Substrates. Avoid combination

Kava Kava: May enhance the adverse/toxic effect of CNS Depressants. Monitor therapy

Lofexidine: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Magnesium Sulfate: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Mefloquine: May diminish the therapeutic effect of Anticonvulsants. Mefloquine may decrease the serum concentration of Anticonvulsants. Management: Mefloquine is contraindicated for malaria prophylaxis in persons with a history of convulsions. Monitor anticonvulsant concentrations and treatment response closely with concurrent use. Consider therapy modification

Methotrimeprazine: May enhance the CNS depressant effect of CNS Depressants. CNS Depressants may enhance the CNS depressant effect of Methotrimeprazine. Management: Reduce adult dose of CNS depressant agents by 50% with initiation of concomitant methotrimeprazine therapy. Further CNS depressant dosage adjustments should be initiated only after clinically effective methotrimeprazine dose is established. Consider therapy modification

MetyroSINE: CNS Depressants may enhance the sedative effect of MetyroSINE. Monitor therapy

Mianserin: May diminish the therapeutic effect of Anticonvulsants. Monitor therapy

MiFEPRIStone: May increase the serum concentration of CYP3A4 Substrates. Management: Minimize doses of CYP3A4 substrates, and monitor for increased concentrations/toxicity, during and 2 weeks following treatment with mifepristone. Avoid cyclosporine, dihydroergotamine, ergotamine, fentanyl, pimozide, quinidine, sirolimus, and tacrolimus. Consider therapy modification

Minocycline: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Mirtazapine: CNS Depressants may enhance the CNS depressant effect of Mirtazapine. Monitor therapy

Mitotane: May decrease the serum concentration of CYP3A4 Substrates. Management: Doses of CYP3A4 substrates may need to be adjusted substantially when used in patients being treated with mitotane. Consider therapy modification

Nabilone: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Netupitant: May increase the serum concentration of CYP3A4 Substrates. Monitor therapy

Orlistat: May decrease the serum concentration of Anticonvulsants. Monitor therapy

Orphenadrine: CNS Depressants may enhance the CNS depressant effect of Orphenadrine. Avoid combination

Oxomemazine: May enhance the CNS depressant effect of CNS Depressants. Avoid combination

OxyCODONE: CNS Depressants may enhance the CNS depressant effect of OxyCODONE. Management: Avoid concomitant use of oxycodone and benzodiazepines or other CNS depressants when possible. These agents should only be combined if alternative treatment options are inadequate. If combined, limit the dosages and duration of each drug. Consider therapy modification

Palbociclib: May increase the serum concentration of CYP3A4 Substrates. Monitor therapy

Paraldehyde: CNS Depressants may enhance the CNS depressant effect of Paraldehyde. Avoid combination

Perampanel: May enhance the CNS depressant effect of CNS Depressants. Management: Patients taking perampanel with any other drug that has CNS depressant activities should avoid complex and high-risk activities, particularly those such as driving that require alertness and coordination, until they have experience using the combination. Consider therapy modification

Phenytoin: Ethosuximide may enhance the CNS depressant effect of Phenytoin. Phenytoin may decrease the serum concentration of Ethosuximide. Ethosuximide may increase the serum concentration of Phenytoin. Monitor therapy

Piribedil: CNS Depressants may enhance the CNS depressant effect of Piribedil. Monitor therapy

Pramipexole: CNS Depressants may enhance the sedative effect of Pramipexole. Monitor therapy

ROPINIRole: CNS Depressants may enhance the sedative effect of ROPINIRole. Monitor therapy

Rotigotine: CNS Depressants may enhance the sedative effect of Rotigotine. Monitor therapy

Rufinamide: May enhance the adverse/toxic effect of CNS Depressants. Specifically, sleepiness and dizziness may be enhanced. Monitor therapy

Sarilumab: May decrease the serum concentration of CYP3A4 Substrates. Monitor therapy

Selective Serotonin Reuptake Inhibitors: CNS Depressants may enhance the adverse/toxic effect of Selective Serotonin Reuptake Inhibitors. Specifically, the risk of psychomotor impairment may be enhanced. Monitor therapy

Siltuximab: May decrease the serum concentration of CYP3A4 Substrates. Monitor therapy

Simeprevir: May increase the serum concentration of CYP3A4 Substrates. Monitor therapy

Sodium Oxybate: May enhance the CNS depressant effect of CNS Depressants. Management: Consider alternatives to combined use. When combined use is needed, consider minimizing doses of one or more drugs. Use of sodium oxybate with alcohol or sedative hypnotics is contraindicated. Consider therapy modification

St John's Wort: May decrease the serum concentration of CYP3A4 Substrates. Management: Consider an alternative for one of the interacting drugs. Some combinations may be specifically contraindicated. Consult appropriate manufacturer labeling. Consider therapy modification

Stiripentol: May increase the serum concentration of CYP3A4 Substrates. Management: Use of stiripentol with CYP3A4 substrates that are considered to have a narrow therapeutic index should be avoided due to the increased risk for adverse effects and toxicity. Any CYP3A4 substrate used with stiripentol requires closer monitoring. Consider therapy modification

Suvorexant: CNS Depressants may enhance the CNS depressant effect of Suvorexant. Management: Dose reduction of suvorexant and/or any other CNS depressant may be necessary. Use of suvorexant with alcohol is not recommended, and the use of suvorexant with any other drug to treat insomnia is not recommended. Consider therapy modification

Tapentadol: May enhance the CNS depressant effect of CNS Depressants. Management: Avoid concomitant use of tapentadol and benzodiazepines or other CNS depressants when possible. These agents should only be combined if alternative treatment options are inadequate. If combined, limit the dosages and duration of each drug. Consider therapy modification

Tetrahydrocannabinol: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Thalidomide: CNS Depressants may enhance the CNS depressant effect of Thalidomide. Avoid combination

Tocilizumab: May decrease the serum concentration of CYP3A4 Substrates. Monitor therapy

Trimeprazine: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Valproate Products: Ethosuximide may decrease the serum concentration of Valproate Products. Valproate Products may increase the serum concentration of Ethosuximide. Monitor therapy

Zolpidem: CNS Depressants may enhance the CNS depressant effect of Zolpidem. Management: Reduce the Intermezzo brand sublingual zolpidem adult dose to 1.75 mg for men who are also receiving other CNS depressants. No such dose change is recommended for women. Avoid use with other CNS depressants at bedtime; avoid use with alcohol. Consider therapy modification

Seizure frequency; trough serum concentrations, CBC, platelets, liver enzymes (periodic), urinalysis (periodic); signs of rash; suicidality (eg, suicidal thoughts, depression, behavioral changes)

Applies to ethosuximide: oral capsule, oral syrup

Gastrointestinal

Gastrointestinal side effects have frequently included anorexia, vague gastric upset, nausea, vomiting, cramps, epigastric and abdominal pain, weight loss, and diarrhea. Gum hypertrophy and swelling of the tongue have also been reported.[Ref]

Hematologic

Hematologic side effects have included leukopenia, agranulocytosis, pancytopenia (with or without bone marrow suppression), and eosinophilia.[Ref]

Nervous system

Nervous system side effects have included drowsiness, headache, dizziness, euphoria, hiccups, irritability, hyperactivity, lethargy, fatigue, and ataxia.[Ref]

Psychiatric

The manufacturer reports psychiatric side effects associated with ethosuximide therapy may be more frequent in patients who have previously exhibited psychosocial abnormalities.[Ref]

Psychiatric side effects have included sleep disturbances, night terrors, inability to concentrate, and aggressiveness. Paranoid psychosis, increased libido, and increased state of depression with overt suicidal intentions have been reported rarely.[Ref]

Dermatologic

Dermatologic side effects have included urticaria, Stevens-Johnson syndrome (SJS), systemic lupus erythematosus, pruritic erythematous rashes, and hirsutism. SJS symptoms usually manifest within 28 days, but may occur later and can be fatal.[Ref]

Ocular

Ocular side effects have included myopia.[Ref]

Genitourinary

Genitourinary side effects have included vaginal bleeding and microscopic hematuria.[Ref]

Other

Other side effects reported postmarketing have included Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS).

Some side effects of ethosuximide may not be reported. Always consult your doctor or healthcare specialist for medical advice. You may also report side effects to the FDA.

Summary of Use during Lactation

Average ethosuximide dosages of 50 to 60% of the maternal weight-adjusted dosage are excreted in human milk and infant plasma levels of 25 to 30% of maternal levels are common. Although no adverse effects attributable solely to ethosuximide in breastmilk have been reported, monitor the infant for drowsiness, adequate weight gain, and developmental milestones, especially in younger, exclusively breastfed infants and when using combinations of anticonvulsants. Measurement of an infant serum level might help rule out toxicity if there is a concern.

Drug Levels

In published reports of anticonvulsant use during breastfeeding, most women were taking a combination of anticonvulsants. Some other anticonvulsants (e.g., phenytoin, carbamazepine) stimulate the metabolism of other drugs including anticonvulsants, whereas others (e.g., valproic acid) inhibit the metabolism of other drugs. Therefore, the relationship of the maternal dosage to the concentration in breastmilk can be quite variable, making calculation of the weight-adjusted percentage of maternal dosage less meaningful than for other drugs in this database.

Maternal Levels. An epileptic woman was taking primidone 250 mg and ethosuximide 500 mg orally every 12 hours. She did not nurse her infant, but had milk flow maintained to collect milk for study. Breastmilk ethosuximide levels were 55 to 70 mg/L on 4 occasions (times with respect to doses not stated) on days 3 to 5 postpartum.[1]

Four ethosuximide breastmilk levels were measured between days 3 and 32 postpartum at unstated times after the dose in an unstated number of women who were taking ethosuximide and other anticonvulsants in unstated dosages. Ethosuximide milk levels averaged 21.3 mg/L (range 18 to 24 mg/L), while maternal serum levels averaged 29.3 mg/L.[2]

An epileptic woman was taking oral ethosuximide 250 mg daily as a single agent during pregnancy and breastfeeding. Breastmilk samples were measured on several occasions during the first 4 months postpartum. Maternal serum and milk levels increased to higher levels between 1 and 2 months postpartum and then decreased, although the times of collection with respect to the doses were not reported. Milk levels on day 3 postpartum were about 31 mg/L, increased to about 55 mg/L at 1 month postpartum and decreased to about 42 mg/L at 4.5 months postpartum.[3]

Breastmilk ethosuximide levels were measured 1 to 4 times in 5 mothers who were taking ethosuximide alone (1 woman) or with other anticonvulsants (4 women). Ethosuximide milk levels averaged 49.5 mg/L (range 27 to 68.5 mg/L).[4] Using the average of the reported milk levels and maternal doses reported, exclusively breastfed infants would receive an average of 62% (range 32 to 113%) of the maternal weight-adjusted dosage.

Three women taking ethosuximide alone and one taking ethosuximide and phenytoin had colostrum levels that were 79 to 103% of maternal plasma levels; at 1.5 to 4.5 months postpartum, the average ratio was 1.[5]

A mother taking ethosuximide 1 gram daily during pregnancy and postpartum had breastmilk levels measured during the first week postpartum. The breastmilk concentration was 36 mg/L which was 92% of the maternal serum concentration.[6]

Two epileptic women who were taking ethosuximide had breastmilk samples measured. One mother who was taking ethosuximide 1 g daily plus carbamazepine 1.2 g daily had a breastmilk ethosuximide level of 33.9 mg/L at 2 weeks postpartum. The other mother taking ethosuximide monotherapy 750 mg daily had a milk level of 52.5 mg/L at 3.5 months postpartum.[7] Their infants would receive 35 and 57% of the maternal weight-adjusted dosage if they were exclusively breastfed.

Infant Levels. An exclusively breastfed infant whose mother was taking ethosuximide 250 mg daily began nursing (extent not stated) on day 2 postpartum and continued through 4.5 months of observation. Infant serum levels increased in parallel to maternal serum and breastmilk concentrations. The infant serum level was 22 mg/L on day 3 and reached a maximum of 29.5 mg/L at 1 month of age before decreasing to about 8.5 mg/L at 4.5 months of age. Intensive sampling of infant serum levels at 4 and 4.5 months of age found little fluctuation during the day and infant plasma levels were 24 to 30% of simultaneous maternal serum levels on the 2 days.[3]

Three fully breastfed infants whose mothers were taking ethosuximide had plasma levels that were 24 to 75% of their mother's average plasma levels. A fourth infant who was mostly formula-fed had undetectable plasma levels.[5]

The breastfed infant of a mother taking ethosuximide monotherapy 750 mg daily had a serum level of 16.9 mg/L which was 32% of the simultaneous maternal plasma level.[7]

Effects in Breastfed Infants

An infant whose mother was taking ethosuximide 250 mg daily began exclusive breastfeeding on day 2 postpartum and continued through 4.5 months of observation. The infant developed normally during this time and had no signs of an adverse reaction.[3]

Sedation, poor sucking and poor weight gain during the first 4 weeks of life occurred in a breastfed newborn whose mother was taking ethosuximide.[4] The reaction was possibly caused by ethosuximide in breastmilk; however, the mother was also taking primidone and valproic acid.

Three fully breastfed infants and a mostly formula-fed whose mothers were taking ethosuximide had no adverse reactions observed during the first 1.5 to 4.5 months of life.[5]

Effects on Lactation and Breastmilk

Relevant published information was not found as of the revision date.

References

1. Koup JR, Rose JQ, Cohen ME. Ethosuximide pharmacokinetics in a pregnant patient and her newborn. Epilepsia. 1978;19:535-9. PMID: 104867

2. Kaneko S, Sato T, Suzuki K. The levels of anticonvulsants in breast milk. Br J Clin Pharmacol. 1979;7:624-7. Letter. PMID: 465285

3. Rane A, Tunell R. Ethosuximide in human milk and in plasma of a mother and her nursed infant. Br J Clin Pharmacol. 1981;12:855-8. PMID: 7340887

4. Kuhnz W, Koch S, Jacob S et al. Ethosuximide in epileptic women during pregnancy and lactation period. Placental transfer, serum concentration in nursed infants. Br J Clin Pharmacol. 1984;18:671-7. PMID: 6508976

5. Soderman P, Rane A. Ethosuximide and nursing. Acta Pharmacol Toxicol (Copenh). 1986;59 (Suppl 5 Pt 2): Abstract 513. PMID: 3766157

6. Meyer FP, Quednow B, Potrafki A, Walther H. [The perinatal pharmacokinetics of anticonvulsant drugs]. Zentralbl Gynakol. 1988;110:1195-205. PMID: 3239295

7. Tomson T, Villen T. Ethosuximide enantiomers in pregnancy and lactation. Ther Drug Monit. 1994;16:621-3. PMID: 7878705