Lamotrigine dispersible tablets 100 mg blister No. 30

Instructions for Lamotrigine dispersible tablets 100 mg blister No. 30

Composition

active ingredient: lamotrigine;

1 dispersible tablet contains 25 mg, 50 mg or 100 mg of lamotrigine;

excipients: heavy magnesium carbonate, microcrystalline cellulose, povidone, low-substituted hydroxypropylcellulose, sodium saccharin, crospovidone, microcrystalline cellulose and guar gum, "Blackcurrant" flavoring (Silarom 1218203128), magnesium stearate.

Dosage form

The tablets are dispersed.

Main physicochemical properties:

dispersible tablets, 25 mg: white or almost white, round flat-cylindrical with a bevel, without a shell, marked "25", tablet diameter 5.5 mm;

dispersible tablets, 50 mg: white or almost white, round flat-cylindrical with a bevel, without a shell, marked "50", tablet diameter 7 mm;

dispersible tablets, 100 mg: white or almost white, round flat-cylindrical with a bevel, without a shell, marked "100", tablet diameter 9 mm.

Pharmacotherapeutic group

Antiepileptic drugs. Lamotrigine.

ATX code N03A X09.

Pharmacological properties

Pharmacodynamics.

Lamotrigine is an anticonvulsant drug whose mechanism of action is associated with blocking voltage-gated sodium channels of presynaptic neuronal membranes in the slow inactivation phase and with inhibiting the excessive release of glutamate (an amino acid that plays a significant role in the development of an epileptic seizure).

Pharmacokinetics.

After oral administration, lamotrigine is rapidly and completely absorbed from the gastrointestinal tract. Peak plasma concentrations are reached after approximately 2.5 hours.

Lamotrigine is extensively metabolized, with the major metabolite being the N-glucuronide. The mean elimination half-life in adults is 29 hours. Lamotrigine has a linear pharmacological profile. It is excreted primarily as metabolites, and partly unchanged, primarily in the urine. The elimination half-life is shorter in children than in adults.

Indication

Epilepsy Adults and children aged 13 years and over

Adjunctive therapy or monotherapy for partial and generalized epileptic seizures, including tonic-clonic seizures.

Seizures associated with Lennox-Gastaut syndrome. Lamotrigine® is prescribed as adjunctive therapy, but in Lennox-Gastaut syndrome it may be prescribed as an initial antiepileptic drug (AED).

Children aged 2 to 12 years

Adjunctive therapy for partial and generalized seizures in epilepsy, including tonic-clonic seizures and seizures associated with Lennox-Gastaut syndrome.

Monotherapy of typical absence seizures.

Bipolar disorder

Adults (ages 18 and over)

Prevention of depressive states in patients with bipolar I disorder who predominantly suffer from depressive states.

Lamotrigine® is not indicated for the emergency treatment of manic or depressive episodes.

Contraindication

Lamotrigine® is contraindicated in patients with known hypersensitivity to lamotrigine or any other component of the drug.

Interaction with other medicinal products and other types of interactions

Uridine 5'-diphospho (UDP)-glucuronyl transferase (UGT) has been identified as the enzyme responsible for the metabolism of lamotrigine. Therefore, drugs that induce or inhibit glucuronidation may affect the clearance of lamotrigine. Strong or moderate inducers of the cytochrome P450 3A4 (CYP3A4) enzyme, which are known to induce glucuronyl transferase, may also increase the metabolism of lamotrigine.

There is no evidence that lamotrigine can cause clinically significant stimulation or inhibition of cytochrome P450 oxidative enzymes. Lamotrigine can induce its own metabolism, but this effect is moderate and has no significant clinical consequences.

Those drugs that have been shown to have a clinically significant effect on lamotrigine concentrations are listed in Table 1. Specific dosing recommendations for these drugs are provided in the Dosage and Administration section. In addition, this table lists those drugs that have been shown to have little or no effect on lamotrigine concentrations. In general, concomitant use of such drugs is not expected to have any clinical effect. However, caution should be exercised in patients with epilepsy whose disease state is particularly sensitive to fluctuations in lamotrigine concentrations.

Table 1

Effect of drugs on lamotrigine concentrations

For detailed information on dosage, see the section “General dosage recommendations for special patient groups” in the “Method of administration and dosage” section. For dosage instructions for women taking hormonal contraceptives, see the section “Hormonal contraceptives” in the “Special warnings and precautions for use” section.

Interaction with antiepileptic drugs (AEDs) (see section "Method of administration and dosage").

Valproate, which inhibits lamotrigine glucuronidation, reduces lamotrigine metabolism and increases the mean half-life by approximately twofold.

Some AEDs (such as phenytoin, carbamazepine, phenobarbital, and primidone) that induce cytochrome P450 enzymes also induce UGT and accelerate the metabolism of lamotrigine.

Central nervous system adverse events, including dizziness, ataxia, diplopia, blurred vision, and nausea, have been reported in patients receiving carbamazepine concomitantly with lamotrigine. These events usually resolve when the carbamazepine dose is reduced. A similar effect was observed in a study of lamotrigine and oxcarbazepine in healthy adult volunteers, but dose reduction was not studied.

It is known that in the course of studies involving healthy adult volunteers who took a dose of lamotrigine 200 mg and a dose of oxcarbazepine 1200 mg, it was found that oxcarbazepine did not change the metabolism of lamotrigine, and lamotrigine, in turn, did not change the metabolism of oxcarbazepine.

In studies involving healthy volunteers, it was found that the combined use of felbamate at a dose of 1200 mg twice a day and lamotrigine at a dose of 100 mg twice a day for 10 days had no clinically significant effect on the pharmacokinetics of the latter.

A retrospective analysis of plasma levels in patients receiving lamotrigine with or without gabapentin showed that gabapentin did not alter the baseline clearance of lamotrigine.

The potential drug interaction between levetiracetam and lamotrigine was studied by evaluating the serum concentrations of both drugs in placebo-controlled clinical trials. According to these data, the substances do not alter the pharmacokinetics of each other.

Steady-state plasma concentrations of lamotrigine are not altered by co-administration with pregabalin (200 mg 3 times daily). There is no pharmacokinetic interaction between lamotrigine and pregabalin.

Topiramate does not affect the plasma concentration of lamotrigine. The use of lamotrigine increases the concentration of topiramate by 15%.

According to the study, the use of zonisamide (200-400 mg/day) together with lamotrigine (150-500 mg/day) for 35 days for the treatment of epilepsy had no significant effect on the pharmacokinetics of lamotrigine.

Plasma lamotrigine concentrations were not affected by co-administration of lacosamide (200, 400 or 600 mg/day) in placebo-controlled clinical trials in patients with partial-onset seizures. In a pooled analysis of data from three placebo-controlled clinical trials investigating the adjunctive use of perampanel in patients with partial-onset and primary generalized tonic-clonic seizures, the highest dose of perampanel tested (12 mg/day) increased lamotrigine clearance by less than 10%.

Although there have been reports of changes in plasma concentrations of other antiepileptic drugs, controlled studies have shown that lamotrigine does not affect the plasma concentrations of concomitant antiepileptic drugs. In vitro studies have shown that lamotrigine does not displace other antiepileptic drugs from their protein binding.

Interaction with other psychotropic substances (see section "Method of administration and dosage")

When lamotrigine 100 mg/day was coadministered with lithium gluconate 2 g twice daily for 6 days in 20 patients, the pharmacokinetics of lithium were unchanged.

Multiple oral doses of bupropion had no statistically significant effect on the pharmacokinetics of lamotrigine in a study of 12 patients, only resulting in a slight increase in lamotrigine glucuronide levels.

In a study in healthy adult volunteers, 15 mg of olanzapine reduced Cmax and AUC by an average of 24% and 20%, respectively. Lamotrigine 200 mg had no effect on the pharmacokinetics of olanzapine.

Multiple oral doses of lamotrigine 400 mg/day had no clinically significant effect on the pharmacokinetics of risperidone given as a single 2 mg dose in a study of 14 healthy adult volunteers. When risperidone 2 mg was coadministered with lamotrigine, 12 of 14 volunteers reported somnolence compared to 1 of 20 volunteers receiving risperidone alone. No cases of somnolence were reported with lamotrigine alone.

In vitro experiments have shown that the formation of the primary metabolite of lamotrigine, 2-N-glucuronide, is only minimally affected by amitriptyline, bupropion, clonazepam, fluoxetine, haloperidol or lorazepam. Studies of the metabolism of bufuralol in human liver microsomes suggest that lamotrigine does not reduce the clearance of drugs that are primarily metabolised by CYP2D6. In vitro experiments also suggest that lamotrigine clearance is unlikely to be affected by clozapine, phenelzine, risperidone, sertraline or trazodone.

Interaction with hormonal contraceptives

Effect of hormonal contraceptives on the pharmacokinetics of lamotrigine

It is known that in a study involving 16 female volunteers taking a lamotrigine tablet with a combination of ethinylestradiol 30 mcg/levonorgestrel 150 mcg, an increase in lamotrigine excretion by approximately 2-fold was noted, which, in turn, caused a decrease in AUC and Cmax of lamotrigine by an average of 52% and 39%, respectively. With a one-week break in contraceptive use (the so-called contraceptive-free week), the concentration of lamotrigine in serum gradually increased during the week-long break, reaching an average concentration approximately 2-fold higher near the end of the week-long break than with concomitant use of the drugs (see sections “Special instructions for use” and “Method of administration and dosage”).

Effect of lamotrigine on the pharmacokinetics of hormonal contraceptives

In a study of 16 female volunteers, a fixed dose of lamotrigine 300 mg did not affect the pharmacokinetics of ethinylestradiol, a component of a combined oral contraceptive pill. There was a consistent small increase in the clearance of levonorgestrel, which in turn resulted in a mean decrease in AUC and Cmax of levonorgestrel of 19% and 12%, respectively. Measurements of serum follicle-stimulating hormone, luteinizing hormone, and estradiol during the study showed suppression of ovarian hormonal activity in some women, although measurements of serum progesterone revealed no hormonal symptoms of ovulation in any of the 16 women. The effect of changes in serum follicle-stimulating hormone and luteinizing hormone levels and the slight increase in levonorgestrel excretion on ovarian ovulatory activity is unknown (see section “General dosage recommendations for special patient groups” in the “Special warnings and precautions for use” section for dosage in women taking hormonal contraceptives and section “Hormonal contraceptives” in the “Special warnings and precautions for use” section). The effect of lamotrigine at daily doses above 300 mg has not been studied. Studies of other hormonal contraceptives have also not been conducted.

Interaction with other drugs

In a study of 10 male volunteers, rifampicin was shown to increase the clearance and decrease the half-life of lamotrigine due to induction of hepatic enzymes responsible for glucuronidation. Patients receiving concomitant rifampicin therapy should follow the treatment regimen recommended for lamotrigine and appropriate inducers of glucuronidation (see section 4.2).

In studies in healthy volunteers, lopinavir/ritonavir has been shown to reduce lamotrigine plasma concentrations by approximately 2-fold through induction of glucuronidation. Patients already taking lopinavir/ritonavir should follow the regimen recommended for lamotrigine and glucuronidation inducers (see section 4.2).

In studies in healthy volunteers, atazanavir/ritonavir (300 mg/100 mg) decreased the plasma AUC and Cmax of lamotrigine (100 mg) by an average of 32% and 6%, respectively (see section 4.2, General dosing recommendations for special patient populations).

According to studies in healthy volunteers, the use of paracetamol at a dosage of 1 g (four times a day) reduced the AUC and Cmin of lamotrigine in blood plasma by an average of 20% and 25%, respectively.

In vitro data from studies of the effects of lamotrigine on organic cation transporter 2 (OCT 2) have shown that lamotrigine, but not the 2-N-glucuronide metabolite, is an inhibitor of OCT 2 at potentially clinically relevant concentrations. These data demonstrate that lamotrigine is an inhibitor of OCT 2, with an IC50 of 53.8 µM (see section 4.4).

Interaction with laboratory tests

Lamotrigine has been reported to interfere with the results of rapid urine drug tests, which may result in false-positive results, particularly for phencyclidine. An alternative, more specific chemical method should be used to confirm positive results.

Application features

Special precautions

Skin rash may occur within the first 8 weeks of starting lamotrigine. In most cases, the rash is mild and resolves without treatment, but severe skin reactions requiring hospitalization and discontinuation of lamotrigine have been reported. These have included potentially life-threatening rashes, including Stevens-Johnson syndrome and toxic epidermal necrolysis, and drug reaction with eosinophilia and systemic symptoms (DRESS) (see Adverse Reactions).

Patients who have developed Stevens-Johnson syndrome or toxic epidermal necrolysis and drug reaction with eosinophilia and systemic symptoms (DRESS) after taking lamotrigine should not be re-administered with lamotrigine.

In adults taking lamotrigine in studies using current dosing recommendations, the incidence of severe skin rashes is approximately 1 in 500 patients with epilepsy. Approximately half of these cases were diagnosed as Stevens-Johnson syndrome (1 in 1000).

The incidence of severe skin rashes in patients with bipolar disorder is 1 in 1,000.

Children are at higher risk of developing serious skin rashes than adults.

According to research, the incidence of rashes leading to hospitalization in children varies from 1 in 300 to 1 in 100 patients.

In children, the first signs of skin rashes may be mistaken for infection. Therefore, physicians should consider the possibility of an adverse drug reaction in children if rash and fever occur during the first 8 weeks of therapy.

The overall risk of skin rashes appears to be closely related to high initial doses of lamotrigine and exceeding the recommended dose escalation schedule for lamotrigine therapy, as well as to concomitant use of valproate (see section 4.2).

Lamotrigine should be used with caution in patients with a history of allergy or rash to other antiepileptic drugs, as the incidence of moderate rash after treatment with lamotrigine in this group of patients was 3 times higher than in the group without such a history.

In the event of a skin rash in all patients (adults and children), the physician should immediately examine and discontinue lamotrigine treatment, except in cases where the development of the rash is not associated with lamotrigine. It is not recommended to resume taking lamotrigine in cases where its previous appointment was canceled due to the development of skin reactions. In such cases, when deciding whether to re-prescribe the drug, the expected benefits of treatment should be weighed against the possible risks.

Skin rashes have also been reported as part of the DRESS syndrome, also known as hypersensitivity syndrome. This condition is accompanied by a variety of systemic symptoms including fever, lymphadenopathy, facial swelling, abnormal blood counts, and hepatic and renal dysfunction and aseptic meningitis (see section 4.8). The syndrome can vary in severity and can occasionally lead to disseminated intravascular coagulation and multiorgan failure. It is important to note that early signs of hypersensitivity (e.g. fever and lymphadenopathy) may occur even in the absence of skin rashes. If such symptoms occur, the patient should be evaluated promptly and, unless otherwise indicated, lamotrigine should be discontinued.

In most cases, aseptic meningitis is reversible after discontinuation of the drug, but occasionally it may recur with re-administration of lamotrigine. Re-administration of lamotrigine causes a rapid return of symptoms, often of a more severe nature. Lamotrigine should not be re-administered to patients who have been discontinued due to aseptic meningitis during previous administration.

Photosensitivity reactions have also been reported with lamotrigine (see section 4.8). In a few cases, the reaction occurred with high doses (400 mg or more), after dose increases or rapid titration. If a patient with signs of photosensitivity (e.g. severe sunburn) is suspected of having photosensitivity related to lamotrigine, discontinuation of treatment should be considered. If continued treatment with lamotrigine is considered clinically warranted, the patient should be advised to avoid exposure to sunlight and artificial ultraviolet light and to take protective measures (e.g. use of protective clothing and sunscreen).

Hemophagocytic lymphohistiocytosis (HLH)

GLH has been reported in patients taking lamotrigine (see section 4.8). GLH is characterised by the following signs and symptoms: fever, rash, neurological symptoms, hepatosplenomegaly, lymphadenopathy, cytopenia, increased serum ferritin, hypertriglyceridaemia and abnormal liver function and coagulation. Symptoms usually occur within 4 weeks of starting treatment.

Patients who develop these signs and symptoms should be evaluated promptly and a diagnosis of GLH should be considered. Lamotrigine therapy should be discontinued immediately if another cause for the symptoms cannot be identified.

Suicidal risk

Patients with epilepsy may experience symptoms of depression and/or bipolar disorder. There is evidence that patients with epilepsy and bipolar disorder have an increased risk of suicide.

Between 25% and 50% of patients with bipolar disorder have at least one suicide attempt. They may experience worsening depressive symptoms and/or the emergence of suicidal thoughts and behavior (suicidality) whether or not they have used medications for bipolar disorder, including lamotrigine.

Suicidal ideation and behavior have been reported in patients treated with antiepileptic drugs for a variety of conditions, including epilepsy. A meta-analysis of randomized, placebo-controlled clinical trials of antiepileptic drugs, including lamotrigine, has shown a small increased risk of suicidal ideation and behavior. The mechanism of this risk is unknown, but the available data do not exclude the possibility of an increased risk with lamotrigine. Therefore, patients should be closely monitored for signs of suicidal ideation and behavior. Patients and caregivers should seek medical attention if such signs appear.

Clinical deterioration in bipolar disorder

Patients treated with lamotrigine for bipolar disorder should be observed closely for clinical worsening (including new symptoms) and for suicidality, particularly at the beginning of treatment or at the time of dose changes. Some patients, those with a history of suicidal behaviour or thoughts, the young, and patients who have demonstrated a significant degree of suicidal ideation prior to initiation of treatment, may be at greater risk of suicidal thoughts or suicide attempts, and will require close monitoring during treatment.

Patients and caregivers should be alerted to the need to monitor for any worsening of their condition (including the appearance of new symptoms) and/or the emergence of suicidal thoughts/behavior or self-harm and to seek immediate medical attention if these symptoms develop.

In this case, the situation should be assessed and appropriate changes made to the therapeutic regimen, including possible discontinuation of treatment for patients with clinical worsening (including the appearance of new symptoms) and/or the appearance of suicidal thoughts/behavior, especially if these symptoms are severe, occur suddenly and are not part of a pre-existing symptomatology.

Hormonal contraceptives

Effect of hormonal contraceptives on the efficacy of lamotrigine

The combination of ethinylestradiol 30 mcg/levonorgestrel 150 mcg has been shown to increase the excretion of lamotrigine by approximately 2-fold, which in turn reduces lamotrigine levels (see section 4.5). In most cases, the maintenance dose of lamotrigine should be increased (by titration) to achieve maximum therapeutic effect. In women not already taking inducers of lamotrigine glucuronidation and already taking hormonal contraceptives (with a one-week break between courses), a gradual temporary increase in lamotrigine levels may occur during the one-week break. This increase will be greater if the lamotrigine dose is increased the day before or during the one-week break. For detailed information on dosing, see the section General dosing recommendations for special patient groups in the section 4.2. Therefore, women who start taking oral contraceptives or finish a course of oral contraceptives should be under constant medical supervision and in most cases they need a dose adjustment of lamotrigine.

Other oral contraceptives and hormone replacement drugs have not been studied, but they may similarly affect the pharmacokinetics of lamotrigine.

The effect of lamotrigine on the effectiveness of hormonal contraceptives

A clinical interaction study in 16 healthy volunteers showed a small increase in levonorgestrel excretion and changes in serum levels of follicle-stimulating hormone and luteinizing hormone when lamotrigine was administered with a hormonal contraceptive (combination of ethinylestradiol 30 mcg/levonorgestrel 150 mcg) (see section 4.5). The effect of these changes on ovarian ovulation is unknown. However, it cannot be excluded that in some patients taking lamotrigine and hormonal contraceptives, these changes lead to a decrease in the effectiveness of the latter. Therefore, patients should promptly report any changes in their menstrual cycle, such as breakthrough bleeding.

Lamotrigine is an inhibitor of renal tubular secretion via organic cation transporters (see section 4.5). This may result in increased plasma levels of some drugs that are primarily excreted via the above route. Therefore, the use of lamotrigine with OCT 2 substrates with a narrow therapeutic index, such as dofetilide, is not recommended.

Dihydrofolate reductase

Lamotrigine is a weak inhibitor of dihydrofolate reductase, so its effect on folate metabolism is possible with long-term use. However, long-term use of lamotrigine did not produce any significant changes in hemoglobin, mean red blood cell volume, serum and red blood cell folate concentrations over one year, and red blood cell folate concentrations over five years.

Kidney failure

In single-dose studies in patients with end-stage renal disease, plasma lamotrigine concentrations were not significantly altered. However, accumulation of the glucuronide metabolite is possible. Therefore, caution should be exercised when treating patients with renal impairment.

Patients taking other medications containing lamotrigine

Lamotrigine should not be prescribed to patients who are already being treated with any other medicine containing lamotrigine without consulting a doctor.

Child development

There are no data on the effects of lamotrigine on growth, puberty, or the development of cognitive, emotional, and behavioral functions.

Brugada is a type of ECG

Arrhythmogenic ST-T abnormalities and typical Brugada ECGs have been observed in patients taking lamotrigine. The use of lamotrigine in patients with Brugada syndrome should be carefully considered.

Epilepsy

As with other antiepileptic drugs, abrupt discontinuation of lamotrigine may result in an increase in seizure frequency. Unless the patient's condition requires abrupt discontinuation (such as rash), the dose of lamotrigine should be reduced gradually over a period of at least 2 weeks.

According to published data, severe epileptic seizures can cause rhabdomyolysis, multiple organ failure, and disseminated intravascular coagulation syndrome, sometimes with fatal outcome. Similar cases can also occur during treatment with lamotrigine.

There may be a significant clinical worsening in seizure frequency rather than improvement. In patients with more than one seizure type, improvement in control of one seizure type should be carefully weighed against worsening control of another seizure type. Treatment with lamotrigine may exacerbate myoclonic seizures.

There is evidence that the response to combination therapy with enzyme inducers is weaker than to combination therapy with non-enzyme inducing antiepileptic drugs. The reason for this is unknown.

When treating children with typical minor epileptic seizures, the effect is not achieved in all patients.

Bipolar disorders

Children (under 18 years of age)

Antidepressant treatment is associated with an increased risk of suicidal ideation and behavior in children (under 18 years of age) with major depressive disorder and other psychiatric disorders.

Fertility

Animal reproduction studies with lamotrigine have not shown any impairment of fertility. There are no data on the effects of lamotrigine on fertility in humans.

Teratogenicity

Lamotrigine is a weak inhibitor of dihydrofolate reductase. There is a theoretical risk of birth defects in humans if a woman is treated with folate inhibitors during pregnancy. However, animal reproductive toxicology studies with lamotrigine at doses less than the human dose of 400 mg/day [based on body surface area (mg/m2)] have shown developmental toxicity (increased mortality, decreased body weight, increased structural changes, neurobehavioral abnormalities) but have not revealed a teratogenic effect.

The product contains 0.65, 1.3 or 2.6 mg of saccharin sodium (depending on the dosage of Lamotrigine® 25 mg, 50 mg or 100 mg). This should be taken into account when calculating the daily sodium intake for patients on a controlled sodium diet.

Use during pregnancy or breastfeeding

General risk associated with the use of antiepileptic drugs

Women of childbearing potential should seek medical advice. Treatment with antiepileptic drugs should be considered when planning pregnancy. In women receiving treatment for epilepsy, abrupt withdrawal of antiepileptic drugs should be avoided as this may lead to recurrence of seizures, which may have serious consequences for the woman and the fetus. In all cases, monotherapy should be preferred, as the use of combination AED therapy may be associated with an increased risk of congenital malformations compared with monotherapy, depending on the AED used.

Risk associated with the use of lamotrigine

Postmarketing data from several prospective registries involving over 8700 women exposed to lamotrigine monotherapy during the first trimester of pregnancy do not indicate a significant increased risk of major congenital malformations, including cleft palate. Animal studies have shown embryofetal toxicity.

If lamotrigine therapy is considered necessary during pregnancy, it is recommended that it be used at the lowest possible therapeutic dose.

Lamotrigine has a weak inhibitory effect on dihydrofolate reductase and therefore could theoretically increase the risk of fetal malformations by reducing folic acid levels (see section 4.4). Therefore, the need for folic acid supplementation should be considered during planning and early pregnancy.

Physiological changes during pregnancy may affect lamotrigine levels and/or its therapeutic effect. There have been reports of decreased lamotrigine plasma concentrations during pregnancy with a potential risk of loss of seizure control. After delivery, lamotrigine levels may increase rapidly with a potential risk of dose-related adverse reactions. Therefore, serum lamotrigine levels should be monitored before, during pregnancy, and after delivery. If necessary, the lamotrigine dose should be modified to maintain lamotrigine serum concentrations at pre-pregnancy levels or adjusted according to the clinical condition. In addition, dose-related adverse reactions should be monitored after delivery.

Breastfeeding period

Lamotrigine has been reported to be excreted in breast milk in variable concentrations. Infant lamotrigine levels may be as high as 50% of the maternal level. Therefore, in some breastfed infants, serum lamotrigine levels may have reached levels at which a pharmacological effect was possible.

The potential benefit of breastfeeding should be weighed against the potential risk of adverse effects in the infant. If a woman receiving lamotrigine treatment decides to breastfeed, the infant should be closely observed for adverse events such as sedation, rash, and poor weight gain.

Fertility.

Animal studies have not shown any effect of lamotrigine on fertility.

The ability to influence the reaction speed when driving or working with other mechanisms

Two studies in volunteers found that the effects of lamotrigine on visual coordination, eye movement, body control, and subjective sedation were no different from those of placebo. Neurological adverse reactions such as dizziness and diplopia have been reported with lamotrigine in clinical trials, and patients should first assess their own response to lamotrigine treatment before driving or operating machinery. Since individual responses to antiepileptic drugs vary, patients should consult their physician regarding the possibility of driving in these cases.

Method of administration and doses

Lamotrigine dispersible tablets may be chewed, dissolved in a small amount of water (enough to cover the entire tablet), or swallowed whole with a small amount of water. If the calculated dose of lamotrigine (e.g., for the treatment of children with epilepsy or patients with impaired liver function) is not a multiple of whole tablets, the dose administered should correspond to the nearest smaller number of whole tablets.

Restarting treatment.

Physicians should consider the need to increase the maintenance dose when resuming lamotrigine in patients who have discontinued lamotrigine for any reason, as the risk of serious rash is associated with high initial doses and exceeding the recommended dose escalation schedule for lamotrigine (see section 4.4). The longer the time interval since the previous dose, the more careful consideration should be given to increasing the maintenance dose. If the interval since discontinuation of lamotrigine exceeds five half-lives, the dose of Lamotrigine should be increased.

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