Oxcarbazepine

252.27

252.27

249-188-8

VZI5B1W380

758693

DTXSID0045703

C47643

Crystals from ethanol|White to faintly orange crystalline powder

N - Nervous system

29339900

63.4

1.7

white solid

1.329±0.06 g/cm3(Predicted)

215.5 °C

457.2°C at 760 mmHg

2℃

1.661

soluble in DMSO(~9 mg/mL), methanol, water, ethanol and acetone.

Store at RT

7.6X10-9 mm Hg at 25 deg C (est)

13.73None

Henry's Law constant = 6.9X10-13 atm-cu m/mol at 25 °C (est)

13.73|pKa = -0.65 (est)

153.8 Ų [M+H]+ [CCS Type: TW, Method: Major Mix IMS/Tof Calibration Kit (Waters)]|152.7 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine and drug standards]

Hydroxyl radical reaction rate constant = 2.8X10-11 cu cm/molec-sec at 25 °C (est)

UN 1648 3 / PGII

3

22-36-20/21/22-11

16-36/37

HN8445000

Xn,F

P261, P264, P270, P271, P280, P301+P312, P302+P352, P304+P312, P304+P340, P312, P322, P330, P363, P501

H302

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl oxcarbazepine, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

|Warning|H302 (98.97%): Harmful if swallowed [Warning Acute toxicity, oral]|P261, P264, P270, P271, P280, P301+P312, P302+P352, P304+P312, P304+P340, P312, P322, P330, P363, and P501|Aggregated GHS information provided by 100 companies from 7 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

The oral LD50 of oxcarbazepine in mammals is 1240 mg/kg and the oral TDLo in children has been reported to be 73 mg/kg. Isolated cases of oxcarbazepine overdose have been reported - patients who ingested up to 24,000mg recovered with symptomatic treatment. Symptoms may include respiratory and CNS depression, movement-related disorders (e.g. dyskinesia, ataxia), nausea/vomiting, hyponatremia, or QTc prolongation. There is no antidote for oxcarbazepine overdose - management should consist of supportive and symptomatic treatment, and consideration should be given to the use of gastric lavage or activated charcoal.

In prelicensure clinical trials, addition of eslicarbazepine to standard anticonvulsant therapy was reported to be associated with ALT elevations above 3 times the upper limit of normal (ULN) in a small proportion of patients (|Chronic therapy with oxcarbazepine is associated with elevations in serum aminotransferase levels in a small proportion of patients. These elevations are rarely clinically significant and do not usually require dose modification. Clinically apparent hepatotoxicity from oxcarbazepine is uncommon but described, and is less common than occurs with carbamazepine. Oxcarbazepine hepatotoxicity usually arises in the setting of anticonvulsant hypersensitivity syndrome with onset of fever, followed by rash, facial edema, lymphadenopathy, elevations in white count and eosinophilia 2 to 8 weeks after starting therapy. The liver involvement ranges from a mild and transient elevation in serum enzymes to abrupt onset of an acute hepatitis-like syndrome, that can be severe and even fatal. The typical enzyme elevations are usually mixed, but can be either hepatocellular or cholestatic. Liver biopsy shows mixed necroinflammatory-cholestatic injury with prominence of eosinophils and occasionally granulomas.

Oxcarbazepine may induce metabolism of some calcium-channel blocking agents (e.g., felodipine, verapamil), possibly via induction of CYP3A4 and CYP3A5 isoenzymes, resulting in decreased AUC of the calcium-channel blocking agents.|Oxcarbazepine may induce metabolism of oral estrogen-progestin contraceptives, possibly via induction of CYP3A4 and CYP3A5, resulting in decreased area under the plasma concentration-time curve (AUC) and consequent decreased efficacy of the contraceptives.|Oxcarbazepine may inhibit metabolism of other anticonvulsants (e.g., phenobarbital, phenytoin), possibly via inhibition of the cytochrome P-450 (CYP) isoenzyme 2C19, resulting in increased plasma concentrations of these drugs. Oxcarbazepine dosages exceeding 1200 mg daily may increase plasma phenytoin concentrations by 40% and, therefore, when such dosages of oxcarbazepine are used concomitantly with phenytoin, dosage reduction of phenytoin may be required. Potent inducers of CYP isoenzymes (e.g., carbamazepine, phenytoin, phenobarbital) may decrease plasma concentrations of oxcarbazepine and its active 10-monohydroxy metabolite (MHD).|Oxcarbazepine and its 10-monohydroxy metabolite may increase the concentration of phenobarbital by about 14%; at oxcarbazepine doses above 1200 mg a day; phenytoin concentrations may be increased by about 40%.|For more Interactions (Complete) data for OXCARBAZEPINE (6 total), please visit the HSDB record page.

The pharmacologically active metabolite of oxcarbazepine, MHD, is approximately 40% bound to plasma proteins, predominantly albumin.

Oxcarbazepine's production and use as an anticonvulsive drug(1) may result in its release to the environment through various waste streams(SRC). It is on the list of the 300 most prescribed drugs in the US(2).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 360(SRC), determined from a structure estimation method(2), indicates that oxcarbazepine is expected to have moderate mobility in soil(SRC). Volatilization of oxcarbazepine from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 6.9X10-13 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Oxcarbazepine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 7.6X10-9 mm Hg(SRC), determined from a fragment constant method(4). Biodegradation data were not available(SRC, 2007).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 360(SRC), determined from a structure estimation method(2), indicates that oxcarbazepine is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 6.9X10-13 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of <1(SRC), from an estimated log Kow of 1.11(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data were not available(SRC, 2007).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), oxcarbazepine, which has an estimated vapor pressure of 7.6X10-9 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase oxcarbazepine may be removed from the air by wet or dry deposition(SRC). Oxcarbazepine contains chromophores that absorb at wavelengths >290 nm(3) and therefore may be susceptible to direct photolysis by sunlight(SRC).

Oxcarbazepine is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(1). Oxcarbazepine contains chromophores that absorb at wavelengths >290 nm(1) and therefore may be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of <1 was calculated in fish for oxcarbazepine(SRC), using an estimated log Kow of 1.11(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of oxcarbazepine can be estimated to be 360(SRC). According to a classification scheme(2), this estimated Koc value suggests that oxcarbazepine is expected to have moderate mobility in soil.

The Henry's Law constant for oxcarbazepine is estimated as 6.9X10-13 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that oxcarbazepine is expected to be essentially nonvolatile from water surfaces(2). Oxcarbazepine's Henry's Law constant indicates that volatilization from moist soil surfaces will not occur(SRC). Oxcarbazepine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 7.6X10-9 mm Hg(SRC), determined from a fragment constant method(3).

While data specific to oxcarbazepine were not located(SRC, 2007), the literature suggests that some pharmaceutically active compounds originating from human and veterinary therapy are not eliminated completely in municipal sewage treatment plants and are therefore discharged into receiving waters(1). Wastewater treatment processes often were not designed to remove them from the effluent(2). Selected organic waste compounds may be degrading to new and more persistent compounds that may be released instead of or in addition to the parent compound(2).

Occupational exposure to oxcarbazepine may occur through inhalation and dermal contact with this compound at workplaces where oxcarbazepine is produced or used. Exposure to oxcarbazepine among the general population may be limited to those administered the drug Trileptal, an anticonvulsive. (SRC)

In the United States, oxcarbazepine is indicated as monotherapy in the treatment of partial-onset seizures in patients 4 years of age and older, and as adjunctive therapy in the treatment of partial-onset seizures in patients 2 years of age and older. In Canada, oxcarbazepine is indicated for use as monotherapy or adjunctive therapy in the treatment of partial-onset seizures in patients 6 years of age and older.

Eslicarbazepine is an aromatic anticonvulsant similar to oxcarbazepine that is used in combination with other antiepileptic agents as therapy of partial onset seizures. Eslicarbazepine is associated with a low rate of transient serum enzyme elevations during therapy and has been implicated in rare instances of clinically apparent liver injury.|Oxcarbazepine is a keto analogue of carbamazepine and, like the parent drug, is a potent anticonvulsant used alone or in combination with other agents in the therapy of partial seizures. Oxcarbazepine has been linked to rare instances of clinically apparent acute drug induced liver injury which resembles carbamazepine hepatotoxicity.

Anticonvulsants

Oxcarbazepine is indicated for monotherapeutic or adjunctive therapeutic use in the treatment of partial seizures in adults and children ages 4 to 16 with epilepsy. /Included in US product labeling/|/EXPL THER:/ ... Oxcarbazepine /was compared/ with acamprosate in relapse prevention in recently withdrawn alcohol-dependent patients. /They/ investigated the efficacy and safety of oxcarbazepin (vs acamprosate) by conducting a 24-week randomized, parallel-group, open-label, clinical trial on 30 acutely detoxified alcoholic patients. Survival analyses (Kaplan-Meier) were performed to look for evidence of a longer "survival" of patients receiving oxcarbazepine. ... After withdrawal, time to severe relapse and time to first consumption of any ethanol by oxcarbazepin patients were not longer than for acamprosate patients. Abstinent patients in both study groups showed a significantly lower obsessive compulsive drinking scale-German version (OCDS-G) than relapsed patients. No undesired effects occurred when oxcarbazepin patients consumed alcohol. ... It is noteworthy that oxcarbazepine is well tolerated, even when alcohol is on board. ...|/EXPL THER:/ ... Data related to 150 patients harboring supratentorial brain gliomas with the aim to assess the efficacy of oxcarbazepine in preventing the occurrence or the recurrence of early postoperative seizures and its tolerability when it is rapidly titrated /was analyzed/. Only four patients (2.7%) experienced seizures within the first week after surgery. Patients did not report disturbances during the titration phase. Regarding adverse events in the first week, six patients (4%) showed minor skin rash. Persistent symptomatic hyponatremia never occurred. ... Oxcarbazepine can be a good alternative to traditional antiepileptic agents in the prevention of perioperative seizures being efficacy, ease of use (rapid titration in 3 days, not requiring close plasma concentration monitoring) and good tolerability (no major side effects during titration and during the first postoperative week) the key factors. Moreover, oxcarbazepine can be a valid choice when long-term therapy is required because of the low interaction with other drugs and the low hematological side effects.

Multiorgan hypersensitivity reactions occurring days to weeks or months (range 4-60 days) after initiation of oxcarbazepine therapy have been reported in adults and pediatric patients. Although these reactions have been reported rarely, many of these patients required hospitalization, and some reactions were considered life-threatening. Manifestations may include (but are not limited to) fever, rash, lymphadenopathy, hepatitis, abnormal liver function test results, eosinophilia, thrombocytopenia, neutropenia, pruritus, nephritis, oliguria, hepatorenal syndrome, arthralgia, and asthenia.|While severe hyponatremia is reported to be more frequent in adults treated with oxcarbazepine than with carbamazepine, there is not sufficient data about the incidence of hyponatremia in childhood during treatment with oxcarbazepine. ... Changes in serum electrolyte balance in 75 children with epilepsy before and during treatment with oxcarbazepine and after replacing carbamazepine therapy with oxcarbazepine therapy /were evaluate/. All patients had normal sodium serum levels at the onset of oxcarbazepine. During treatment with oxcarbazepine ... hyponatremia (Na +< 135 mmol/L) without clinical symptoms /were found/ in 26.6 % of the children (n = 20), /and/ sodium levels below 125 mmol/L were observed in 2 children (2.6 %). Clinically relevant hyponatremia occurred in one girl only (1.3 %). In a subgroup of 27 children, in whom carbamazepine was directly replaced with oxcarbazepine, hyponatremia without symptoms was found in one child under carbamazepine (3.7 %) and in six children under oxcarbazepine (22.2 %). Dosage of oxcarbazepine, serum levels of the active metabolite of oxcarbazepine, antiepileptic comedication or patients' age and gender were of no predictive value for the development of hyponatremia. ...|Adverse effects occurring in 5% or more of patients and more frequently than placebo include dizziness, somnolence, diplopia, fatigue, nausea, vomiting, ataxia, abnormal vision, abdominal pain, tremor, dyspepsia, abnormal gait.|Serious dermatologic reactions, including Stevens-Johnson syndrome and toxic epidermal necrolysis, have been reported in adults and children receiving oxcarbazepine; reactions have been life-threatening, have required hospitalization, and rarely have been fatal. The incidence of Stevens-Johnson syndrome and toxic epidermal necrolysis reported in patients receiving oxcarbazepine exceeds the rate in the general population by threefold to tenfold. The median time to onset of these reactions was 19 days. Recurrence of serious dermatologic reactions following rechallenge with oxcarbazepine has occurred.|For more Drug Warnings (Complete) data for OXCARBAZEPINE (11 total), please visit the HSDB record page.

Oxcarbazepine is an anticonvulsant drug that reduces the incidence of seizures in epilepsy by inhibiting abnormal electrical activity in the brain. There have been rare reports of oxcarbazepine resulting in the development of hematologic abnormalities, including agranulocytosis and aplastic anemia. Patients should be undergo frequent laboratory testing and should be monitored closely for signs and symptoms of blood dyscrasias. Oxcarbazepine has also been associated with the development of dermatologic reactions which can progress from a simple rash to potentially fatal reactions such as toxic epidermal necrolysis (TEN) or Stevens-Johnson Syndrome (SJS). Patients with the HLA-A*3101 and/or HLA-B*1502 alleles may be at higher risk of this reaction. Oxcarbazepine should be discontinued at the first sign of a drug-induced skin reaction.

A class of drugs that inhibit the activation of VOLTAGE-GATED SODIUM CHANNELS. (See all compounds classified as Voltage-Gated Sodium Channel Blockers.)|Drugs used to prevent SEIZURES or reduce their severity. (See all compounds classified as Anticonvulsants.)|Drugs and compounds that induce the synthesis of CYTOCHROME P-450 CYP3A. (See all compounds classified as Cytochrome P-450 CYP3A Inducers.)

Oxcarbazepine is completely absorbed following oral administration. A single 600mg dose of oxcarbazepine resulted in an MHD C_max of 34 μmol/L and a median T_max of 4.5 hours. When administered twice daily, steady-state levels of MHD are attained within 2-3 days. The rate and extent of absorption of oxcarbazepine is not affected by food intake.|Following oral administration, more than 95% of the administered dose of oxcarbazepine is found in the urine. Of this, approximately 49% is MHD glucuronide metabolites, 27% is unchanged MHD, 3% is inactive DHD metabolites, 13% is conjugated oxcarbazepine, and less than 1% is unchanged parent drug. Fecal elimination accounts for only 4% of the administered dose.|The apparent volume of distribution of oxcarbazepine is 49 L. The apparent volumes of distribution of (S)- and (R)-MHD were found to be 23.6 L and 31.7 L, respectively.|Plasma clearance of oxcarbazepine has been estimated to be approximately 84.9 L/h, whereas plasma clearance of its active metabolite, MHD, was estimated to be 2.0 L/h. Rapid metabolic clearance appears to be the main pathway for oxcarbazepine, while clearance of its metabolites occurs mainly via renal excretion.|Oxcarbazepine is completely absorbed. Food does not alter the rate and extent of absorption of oxcarbazepine.|Both oxcarbazepine and its active 10-monohydroxy metabolite (MHD) are distributed into milk in humans.|Elimination: Renal: greater than 95%, with more than 99% of the dose excreted in the form of metabolites. Fecal: less than 4%.|Oxcarbazepine is an antiepileptic drug with a chemical structure similar to carbamazepine, but with different metabolism. Oxcarbazepine is rapidly reduced to 10,11-dihydro-10-hydroxy-carbazepine (monohydroxy derivative, MHD), the clinically relevant metabolite of oxcarbazepine. MHD has (S)-(+)- and the (R)-(-)-enantiomer, but the pharmacokinetics of the racemate are usually reported. The bioavailability of the oral formulation of oxcarbazepine is high (>95%). It is rapidly absorbed after oral administration, reaching peak concentrations within about 1-3 hours after a single dose, whereas the peak of MHD occurs within 4-12 hours. At steady state, the peak of MHD occurs about 2-4 hours after drug intake. The plasma protein binding of MHD is about 40%. Cerebrospinal fluid concentrations of MHD are in the same range as unbound plasma concentrations of MHD. Oxcarbazepine can be transferred significantly through the placenta in humans. Oxcarbazepine and MHD exhibit linear pharmaco-kinetics and no autoinduction occurs. ...|For more Absorption, Distribution and Excretion (Complete) data for OXCARBAZEPINE (9 total), please visit the HSDB record page.

Oxcarbazepine is rapidly and extensively metabolized to its primary metabolite, MHD, which is responsible for the bulk of its anti-epileptic activity and exists in much higher concentrations in the plasma than the parent drug. MHD is formed via reduction by several members of the aldo-keto reductase family of cytosolic liver enzymes and exists as a racemate in plasma in an approximate ratio of 80% (S)-MHD to 20% (R)-MHD. MHD is further metabolized to glucuronide conjugate metabolites for excretion, and small amounts are oxidized to 10-,11-dihydro-10,11-dihydroxycarbamazepine (DHD) which is pharmacologically inactive. Only 10% of an administered dose of oxcarbazepine will remain as either the parent drug or glucuronide conjugates of the parent drug.|Oxcarbazepine is rapidly reduced by cytosolic enzymes in the liver to its 10-monohydroxy metabolite, MHD, which is primarily responsible for the pharmacological effect of Trileptal. MHD is metabolized further by conjugation with glucuronic acid. Minor amounts (4% of the dose) are oxidized to the pharmacologically inactive 10,11-dihydroxy metabolite (DHD). Oxcarbazepine is cleared from the body mostly in the form of metabolites which are predominantly excreted by the kidneys. More than 95% of the dose appears in the urine, with less than 1% as unchanged oxcarbazepine. Fecal excretion accounts for less than 4% of the administered dose. Approximately 80% of the dose is excreted in the urine either as glucuronides of MHD (49%) or as unchanged MHD (27%); the inactive DHD accounts for approximately 3% and conjugates of MHD and oxcarbazepine account for 13% of the dose.|The disposition of the new anti-epileptic agent oxcarbazepine (10,11-dihydro-10-oxo-5H-dibenz[b,f]azepine-5-carboxamide) has been studied in two healthy volunteers following an oral 400 mg dose of (14)C-labelled drug. The dose was excreted almost completely in the urine (94.6 and 97.1%) within six days. Fecal excretion amounted to 4.3 and 1.9% of the dose in the two subjects. In the 0-6 days urine samples the biotransformation products have been isolated and identified. 10,11-Dihydro-10-hydroxycarbamazepine (GP 47,779) and its two diastereoisomeric O-glucuronides were found as main metabolites. Taken together, they accounted for 79% of urinary (14)C. Unchanged oxcarbazepine, and its sulfate and glucuronide conjugates were isolated in smaller amounts only (13%). Other minor metabolites were the trans- and cis-isomers of 10,11-dihydro-10,11-dihydroxy-carbamazepine (approximately 4%), and a phenolic derivative of GP 47,779 (less than 1%). The biotransformation of oxcarbazepine proceeds mainly by reduction to GP 47,779, and subsequent conjugation with glucuronic acid. Reduction is stereospecific, favoring the S-configuration of GP 47,779. Direct conjugation of oxcarbazepine, in the enol form, is a minor pathway. Oxidative reactions are unimportant.|... The interaction potential of oxcarbazepine is relatively low. However, enzyme-inducing antiepileptic drugs such as phenytoin, phenobarbital or carbamazepine can reduce slightly the concentrations of 10,11-dihydro-10-hydroxy-carbazepine (monohydroxy derivative, MHD). Verapamil may moderately decrease MHD concentrations, but this effect is probably without clinical relevance. The influence of oxcarbazepine on other antiepileptic drugs is not clinically relevant in most cases. However, oxcarbazepine appears to increase concentrations of phenytoin and to decrease trough concentrations of lamotrigine and topiramate. Oxcarbazepine lowers concentrations of ethinylestradiol and levonorgestrel, and women treated with oxcarbazepine should consider additional contraceptive measures. Due to the absent or lower enzyme-inducing effect of oxcarbazepine, switching from carbamazepine to oxcarbazepine can result in increased serum concentrations of comedication, sometimes associated with adverse effects. ...

The plasma half-life of oxcarbazepine is approximately 2 hours and the plasma half-life of MHD is approximately 9 hours.|Oxcarbazepine: 2 hours. 10-Monohydroxy metabolite: 9 hours. Note: In patients with renal function impairment with a creatinine clearance < 30 mL/minute, the half life of 10 monohydroxy metabolite is prolonged to 10 hours ...|... Elimination half-lives in healthy volunteers are 1-5 hours for oxcarbazepine and 7-20 hours for 10,11-dihydro-10-hydroxy-carbazepine (monohydroxy derivative, MHD). Longer and shorter elimination half-lives have been reported in elderly volunteers and children, respectively. ...

The exact mechanism through which oxcarbazepine and its active metaoblite, MHD, exert their anti-epileptic effects is unclear, but is thought to primarily involve the blockade of voltage-gated sodium channels. The opening and closing of sodium channels allows for the propagation of action potentials along neurons - in epilepsy, these action potentials can occur in excess of that required for normal function, and the repetitive and pathological firing of these action potentials leads to seizure activity. Both oxcarbazepine and MHD are thought to inhibit seizure activity by binding to the inactive state of voltage-gated sodium channels, thus prolonging the period in which the receptor is unavailable for action potential propagation. This helps to stabilize hyperexcited neuronal membranes, inhibit repetitive neuron firing, and prevent the spread of seizure activity within the CNS without affecting normal neuronal transmission. Increased potassium conductance and modulation of voltage-activated calcium channels is also thought to play a role in the anti-seizure activity of oxcarbazepine. Inhibition of glutamatergic activity was thought to contribute to oxcarbazepine's activity, but this effect could not be replicated _in vivo_.|The pharmacological activity of Trileptal (oxcarbazepine) is primarily exerted through the 10-monohydroxy metabolite (MHD) of oxcarbazepine. The precise mechanism by which oxcarbazepine and MHD exert their antiseizure effect is unknown; however, in vitro electrophysiological studies indicate that they produce blockade of voltage-sensitive sodium channels, resulting in stabilization of hyperexcited neural membranes, inhibition of repetitive neuronal firing, and diminution of propagation of synaptic impulses. These actions are thought to be important in the prevention of seizure spread in the intact brain. In addition, increased potassium conductance and modulation of high-voltage activated calcium channels may contribute to the anticonvulsant effects of the drug. No significant interactions of oxcarbazepine or MHD with brain neurotransmitter or modulator receptor sites have been demonstrated.

Emergency and supportive measures. Maintain an open airway and assist ventilation if necessary. Administer supplemental oxygen. Treat seizures, coma, hyperthermia, arrhythmias, hyponatremia, and dystonias if they occur. Asymptomatic patients should be observed for a minimum of 6 hours after ingestion and for at least 12 hours if an extended-release preparation was ingested. ...|Decontamination. Administer activated charcoal orally if conditions are appropriate. Gastric lavage is not necessary after small to moderate ingestions if activated charcoal can be given promptly. ...|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/SIGNS AND SYMPTOMS/ Serious dermatologic reactions, including Stevens-Johnson syndrome and toxic epidermal necrolysis, have been reported in adults and children receiving oxcarbazepine; reactions have been life-threatening, have required hospitalization, and rarely have been fatal. The incidence of Stevens-Johnson syndrome and toxic epidermal necrolysis reported in patients receiving oxcarbazepine exceeds the rate in the general population by threefold to tenfold. The median time to onset of these reactions was 19 days. Recurrence of serious dermatologic reactions following rechallenge with oxcarbazepine has occurred.|/CASE REPORTS/ Hyponatremia is a commonly encountered clinical problem with potentially severe complications. Among the underlying implicated etiologies are medications such as oxcarbazepine, which has been well documented and attributed to the syndrome of inappropriate antidiuretic hormones (SIADH). ... The case of a 28-year-old woman with a diagnosis of secondary antiphospholipid syndrome who presented with asymptomatic hyponatremia secondary to excessive water intake after oxcarbazepine ingestion, suggesting a new mechanism for oxcarbazepine-induced hyponatremia /is reported/.|/CASE REPORTS/ Oxcarbazepine is a analogue of carbamazepine with anticonvulsant and analgesic activity. We report a case of localized penile edema caused by oxcarbazepine. The association between the drug and the adverse reaction was confirmed by rechallenge test. ...|/CASE REPORTS/ A 70-year-old patient treated with oxcarbazepine experienced severe hyponatremia. The patient used oxcarbazepine (600 mg twice a day) concomitantly with diuretics (torasemide 10 mg and indapamide 1.25 mg once per day), perindopril, an angiotensin-converting enzyme inhibitor, and amlodipine, a Ca(2+) channel blocker. The patient complained of a nausea, malaise, diplopia, drowsiness, apathy, decreased diuresis (creatinine clearance - 41.51 ml/min), and exacerbation of epileptic seizures. Sodium concentration in the plasma was 113 mmol/L. The patient was hospitalized. It was suggested that a decrease in plasma sodium concentration was caused by oxcarbazepine used together with diuretics for six months. Oxcarbazepine-induced hyponatremia is reported in 22.2-50% of patients, although symptoms are present only in 5.9% of patients. The most common symptoms of central nervous system injury, experienced by patients, are drowsiness, dizziness, decreased cognitive function, coordination impairment, etc. ...|For more Human Toxicity Excerpts (Complete) data for OXCARBAZEPINE (9 total), please visit the HSDB record page.

10,11-dihydro-10-oxo-5H-dibenz(b,f)azepine-5-carboxamide

Oral: Suspension: 300 mg/5 mL Trileptal (with alcohol and propylene glycol), (Novartis). Tablets, film-coated: 150 mg Trileptal (scored), (Novartis), 300 mg Trileptal (scored), (Novartis), 600 mg Trileptal (scored), (Novartis).

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