Carbamazepine-Alsi tablets 200 mg 40 pcs. in St. Petersburg

Indications

Ministry of Health of Russia

• E23.2 Diabetes insipidus
• F10.3 Withdrawal state
• F30 Manic episode
• F31 Bipolar affective disorder
• G35 Multiple sclerosis
• G40 Epilepsy
• G40.1 Localized (focal) (partial) symptomatic epilepsy and epileptic syndromes with simple partial seizures
• G40.2 Localized (focal) (partial) symptomatic epilepsy and epileptic syndromes with complex partial seizures
• G40.3 Generalized idiopathic epilepsy and epileptic syndromes
• G50.0 Trigeminal neuralgia
• G52.1 Lesions of the glossopharyngeal nerve
• G63.2 Diabetic polyneuropathy (E10-E14+ with common fourth character .4)
• R35 Polyuria
• R52.9 Pain, unspecified
• R63.1 Polydipsia

FDA recommendations

• Partial seizures with complex symptoms
• Generalized tonic-clonic seizures (grand mal)
• Mixed seizures
• Trigeminal neuralgia pain
• Acute episode of mania/mixed mania

UK Medicines and Healthcare Products Regulatory Agency guidelines

• Generalized tonic-clonic and partial seizures
• Trigeminal neuralgia pain
• Prevention of manic-depressive psychosis in patients not responding to lithium treatment

Sensitizing agents

They are used in coding against alcoholism to create a so-called chemical barrier that makes it impossible to drink alcohol, and to develop in the patient a sense of fear of the possible unpleasant consequences of drinking alcohol. The most common sensitizing agent used in the treatment of alcohol dependence is teturam (Antabuse, disulfiram). The previously widely prescribed sensitizing drugs metronidazole, furazolidone, and nicotinic acid are now rarely used. Disulfiram has been used to treat alcohol dependence since the 1940s. It is assumed that the therapeutic effects of Teturam are due to the fear of Teturam Alcohol Reaction (TAR). The mechanism of action of this drug is based on blocking the enzyme acetaldehyde dehydrogenase, as a result of which the oxidation of alcohol is delayed at the acetaldehyde stage. Before treatment with Teturam, the patient is warned about the possible adverse effects of drinking alcohol.

The drug Disulfiram for coding against alcohol dependence, valid for up to 1 year:

Currently, a fairly common method of treatment is intramuscular implantation of the drug Esperal, which is produced in sealed ampoules containing 10 tablets of 0.1 g of teturam. As a rule, this method is used when other therapeutic measures are unsuccessful. The patient and his relatives are explained that the drug implanted into the tissue will be constantly absorbed into the blood, and if the patient drinks even a small amount of alcohol, he will experience serious consequences, including death.

The use of Teturam has many contraindications due to the pronounced toxicity of the drug. Against the background of its use, various side effects often develop in the form of allergic reactions, toxic hepatitis, and teturama psychosis. Disulfiram may worsen symptoms of schizophrenia. A necessary condition for treatment is the patient’s good health, high motivation, and regularity of taking the drug. It should be especially noted that it is inadmissible to prescribe disulfiram without the patient’s knowledge (for example, adding it to food) due to the danger of the consequences of a teturam-alcohol reaction.

Treatment regimen

Dosage and dose selection

• 400-1200 mg/day
• Children under 6 years: 10-20 mg/kg per day

Bipolar disorder, seizures (adults, children over 13): Start with 200 mg twice daily; increase every week by 200 mg/day in several doses; maximum for adults 1200 mg/day; maximum for children 13-15 years old – 1000 mg/day; some patients may require doses up to 1600 mg/day.

Trigeminal neuralgia pain: start with 100 mg twice daily; increase every week by 200 mg/day in divided doses.

• Best taken with food
• Slowly increasing the dose delays the onset of the therapeutic effect, but increases tolerance to sedative side effects
• If other sedatives are being taken, increase the dose slowly
• Over time, after several weeks of treatment, dose adjustment is required

How quickly does it work?

Response to acute mania may occur within a few weeks.

It may take several months for your mood to stabilize.

Cramps should stop after 2 weeks.

Expected Result

Disappearance of symptoms.

Treatment can be continued indefinitely to prevent mania or seizures.

If it doesn't work

(for bipolar disorder)

Increase the dose;

Switch to another drug or add another drug;

Connect psychotherapy;

Determine if there is a comorbid condition

How to stop taking it

Reduce the dose gradually. Abruptly stopping use increases the risk of bipolar disorder relapse. In epilepsy, abrupt cessation can trigger seizures [1].

Treatment combinations

• Lithium
• Valproic acid
• Atypical antipsychotics
• Lamotrigine
• Antidepressants (with caution, as there is a risk of mood destabilization) [1].

Mechanism of action of carbamazepine

According to its chemical structure, carbamazepine belongs to the group of tricyclic antidepressants.
In clinical practice, it is used as a sedative, normothymic and anticonvulsant substance. Pharmaceutical preparations based on it are characterized by low toxicity and low potential for addiction. Unfortunately, the mechanism of action of the substance is still not fully understood. It has been established that its administration makes it possible to stabilize the cell membranes (membranes) of hyperstimulated cells of the nervous system, for example, in epilepsy or acute psychosis with convulsive syndrome. At the same time, it suppresses the development of repeated excitation and inhibits the conduction of neuronal impulses.

Cautions and contraindications

• You need to watch for bleeding, bruising, mouth ulcers, infections, and fever. Taking carbamazepine increases the risk of aplastic anemia and agranulocytosis by 5-8 times.
• Use cautiously with MAOIs.
• May cause exacerbation of angle-closure glaucoma.
• Reduces the effectiveness of hormonal contraceptives.
• Restriction of fluid intake may be necessary due to the risk of interfering with antidiuretic hormone production.
• Cannot be used if the patient has a history of bone marrow suppression.
• Do not use if the patient is allergic to any tricyclic compounds.

CARBAMAZEPINE (tablets)

also applies to the treatment of alcoholism.
Carbamazepine blocks Na channels, which leads to stabilization of the neuronal membrane and a decrease in synaptic conduction of impulses. I didn't quite understand what he was talking about. I paid the doctor 7,300 rubles and we said goodbye. The husband slept until the morning. And when he woke up, he again ran to the store for beer. That is, the drip improved his condition, but did not bring him out of the binge. I bought Carbamazepine and B vitamins for the brain at the pharmacy. First I gave him two Carbamazepine tablets. But the husband did not calm down. I had to close the doors and hide the keys so that I wouldn’t run for beer again. Then she gave him 4 more tablets. Finally the medicine worked and the husband fell asleep. I slept for about three hours. When I woke up, I couldn’t get to my feet, I couldn’t even speak. I realized that his lack of coordination was due to the medication. But it’s better than binge drinking. In the morning he told about the horror he experienced. I thought it was a stroke. I felt absolutely sober, I understood everything, but I could not move or speak. It was an overdose combined with alcohol. By morning, the lack of coordination had almost disappeared. He felt slow and spoke slowly. I realized that he had forgotten to take his medication, and I encouraged him to think that it was the effects of alcohol and possibly a stroke. His desire to drink had passed. The next day, the lethargy and lack of coordination also disappeared.

After 3 months, I saw him drunk in the yard. I took her home. I crushed 4 Carbamazepine tablets in a mortar. Then she poured half a glass of fermented baked milk and added crushed Carbamazepine to it. I gave this to my husband to drink. He quickly fell asleep. Slept all night. In the morning I woke up completely sober. There was no miscoordination. The speech was normal. There was no desire to drink. In general, you need to prevent binge drinking as quickly as possible, use Carbamazepine in small doses so that there is no miscoordination.

Now we sometimes even drink dry wine on holidays. You cannot drink strong alcoholic drinks or beer. They make you want to drink more. I don't keep a tight rein on my husband. I know that prohibitions can provoke breakdowns. And dry or semi-sweet wine does not make him want to drink more and more. Drinks no more than one glass. Life has changed dramatically. No binge drinking. We don’t go to drug addiction specialists anymore. We don't spend a lot of money on them. I got rid of anxiety. Now I always have Carbamazepine in my medicine cabinet. It’s only a pity that not a single narcologist told me about this medicine earlier.

Special patient groups

Patients with kidney problems

The dose needs to be reduced [1].

Patients with liver disease

Use with caution [1].

Patients with heart disease

Use with caution [1].

Elderly patients

In older people, side effects are more pronounced.

Children and teenagers

• Approved for use in epilepsy.
• Children 6-12 years: initial dose 100 mg twice daily; increase every week by 100 mg/day in several doses; maximum dose 1000 mg/day; maintenance dose 400-800 mg/day.
• Children 5 years and younger: initial dose 10-20 mg/kg per day 2-3 times daily; increase every week if there is a need; maximum dose 35 mg/kg/day.

Pregnant

• In the first trimester, it increases the risk of fetal developmental abnormalities. If treatment continues, tests should be performed to identify pregnancy pathologies. To reduce the risk, you should start taking folic acid (1 mg/day) earlier than usual.
• For bipolar disorder, carbamazepine should be discontinued until pregnancy occurs. During pregnancy, atypical antipsychotics are preferred.

Breast-feeding

• It is recommended that you stop taking carbamazepine or stop breastfeeding.

Carbamazepine

It is effective against all symptoms when withdrawing from binge drinking and can be the drug of choice when interrupting mild to moderate binge drinking. The lack of interaction with alcohol allows the drug to be used even if it is present in the blood. It has been established that Carbamazepine affects the neuronal transmission of GABA, glutamate, norepinephrine, acetylcholine and dopamine. Monotherapy with carbamazepine is effective for mild to moderate withdrawal syndrome; for severe withdrawal, benzodiazepines are recommended. The undoubted advantage of carbamazepine is the absence of a euphoric effect and the risk of dependence on the drug.

Side effects and other risks

Mechanism of side effects

The causes of side effects of carbamazepine are theoretically associated with excessive effects on voltage-gated sodium channels.

Major metabolites may cause side effects.

Side effects

• Sedation, dizziness, confusion, unsteadiness, headache.
• Diarrhea, nausea, vomiting
• Leukopenia
• Rash
• Dangerous side effects: aplastic anemia, agranulocytosis, purpura, Stevens-Johnson syndrome, Parhon syndrome with hyponatremia.
• Weight gain: yes, but infrequently
• Sedation: yes, and may be significant and, for some patients, excessively strong

What to do about side effects

1. Wait;
2. Take in the evening to avoid sedation;
3. To avoid irritation to the stomach, take with food;
4. Switch to another drug [1].

Long term use

Reduces libido;

Monitoring the functioning of the liver, kidneys, and thyroid gland is required, as well as regular general blood tests and sodium level measurements.

addictive

No.

Overdose

May be fatal; nausea, vomiting, involuntary movements, cardiac arrhythmias, difficulty breathing, sedation, coma.

Use for alcoholism

In the treatment of any pathological conditions associated with long-term alcohol abuse, one-size-fits-all medications are never used. The choice of each medicine is approached with the utmost rigor, since in some cases it can only worsen the situation. The patient is thoroughly examined, after which the benefit/risk factor is assessed.

Indications

The main spectrum of action of the drug is the relief of seizures; to a lesser extent, the emotional background is normalized. Carbamazepine is used for alcoholism if the following indications exist:

• The structure of the syndrome of pathological craving for alcohol contains affective (psycho-emotional) disorders.
• Relief of withdrawal symptoms - “withdrawal” during the period of cessation of abuse in fully formed true binge drinking.
• Prevention of the development of convulsive attacks in cases of aggravated medical history.
• The patient is not suitable for other antidepressants or antiepileptic drugs.

Carbamazepine has been shown to be as effective as or superior to barbital, tiapride, clomethiazole, oxazepam, and placebo in open-label and double-blind studies. A double-blind study conducted by Malcolm et al. and repeated by Stuppaeck et al. demonstrated equal effectiveness of carbamazepine and oxazepam in relieving alcohol withdrawal. However, no differences were found in laboratory testing of liver and blood function, although carbamazepine may worsen these indicators. In addition to relieving withdrawal symptoms, carbamazepine, compared to oxazepam, more effectively improves the general condition of the patient, assessed according to the SCL-90-R criteria.”

Portal about medicines Medi Ru

Carbamazepine also enhances the positive effects of other neurotropic drugs that are used during the period of active anti-relapse treatment. In small dosages, it improves the emotional background, eliminates dysphoric symptoms (anxiety, depression, apathy) and reduces convulsive readiness. At the same time, the craving for drinking alcohol is suppressed.

Side effects and contraindications

The dose of the anticonvulsant is selected individually; the drug is usually well tolerated. Carbamazepine is contraindicated in case of clinically significant cardiac rhythm and conduction disturbances, hypersensitivity to tricyclic antidepressants, acute porphyria and a history of myelosuppression. The following side effects are possible:

• disturbance of taste and speech
• headache
• relapse of psychosis
• depression
• appearance of hallucinations
• dizziness
• excessive psychomotor agitation
• nystagmus – multi-frequency involuntary eye movements
• diplopia - double vision
• noise in ears
• conjunctivitis
• peripheral neuropathy
• muscle weakness up to paresis
• atrioventricular block
• worsening heart failure, including due to hemodynamic disorders (hypo- or hypertension)
• kidney damage
• nausea
• vomit
• toxic hepatitis
• thromboembolic complications if there is a predisposition
• electrolyte disorders
• allergic reactions

Choice of valproic acid drugs in the treatment of epilepsy: original drug or generic?

Epilepsy is one of the most common diseases of the central nervous system (CNS). The annual increase in the incidence of epilepsy ranges from 40 to 70 people per 100 thousand population, while in approximately 1/3 of patients the disease is lifelong. According to WHO, more than 75% of the 40 million people with epilepsy in the world do not receive adequate treatment. The duration of pharmacotherapy for epilepsy averages from two to five years, but about 40% of patients are forced to receive treatment for life. In Russia, 8.65% of patients with epilepsy are in remission, 48.1% of patients have more than 12 attacks per year. 41.18% of patients receive polytherapy; 18.05% do not receive drug therapy, while the rest are treated with one drug. Continuous population studies in different regions of Russia show that the proportion of patients without seizures from the total number of patients receiving anticonvulsant therapy is 13–28%, while with the correct treatment tactics it should be 50–80% [2].

In recent years, there has been an increase in the number of new antiepileptic drugs (AEDs), many of which are already widely used in practice. AEDs receive a lot of attention from manufacturing companies, given their large share among other drugs on the pharmaceutical market. There are several reasons for this:

• high prevalence of epilepsy;
• the need for long-term use of AEDs for epilepsy;
• expansion of indications for the use of AEDs - treatment of other non-epileptic neurological and psychiatric disorders, that is, the need for AEDs in the pharmaceutical market is increasing [5, 15];
• aging of the population around the world and the increase in the incidence of epilepsy after 65 years (the number of patients with epilepsy in this age group is constantly increasing) [5, 12].

Pharmacoeconomic aspects of epilepsy therapy

Epilepsy is a serious socio-economic problem resulting in significant economic losses in society. The price of a drug is a really important factor in selecting treatment for certain populations. Drug costs and treatment costs are becoming increasingly important factors for primary care physicians when treating epilepsy. An independent study carried out in several European countries determined that the direct and indirect costs of treating individual patients with epilepsy increase in direct proportion to the frequency of their seizures [1].

It is patients with recurrent attacks who bear the majority of direct medical costs. Patients who are refractory to treatment, requiring ongoing therapy, frequent physician visits, and ongoing medical care account for approximately 75% of all direct costs attributable to epilepsy. In a population of patients resistant to treatment, direct costs are even higher in patients suffering from epilepsy and with concomitant diseases, such as mental retardation, cerebral stroke, and depression [1].

The basis for good clinical efficacy is optimal control of epileptic seizures with appropriate AEDs used at a dose that maximizes seizure control without causing side effects. These two characteristics - optimal control of attacks and the absence of side effects - determine the value of the drug and are a criterion for the correctness of treatment. Both characteristics are related to bioavailability, from which bioequivalence and therapeutic equivalence of AEDs follow [5]. This coincides with pharmacoeconomic effectiveness: an increased percentage of remissions allows for additional cost savings due to fewer outpatient visits to specialists and reduced bed days [1].

Epilepsy therapy: original drugs and generics

Currently, the problem of prescribing original and generic drugs in the treatment of epilepsy is widely discussed. When registering generic drugs, deviations in bioavailability of ±20% are allowed, compared to original drugs. However, with regard to AEDs, even a slight change in bioavailability can lead not only to the resumption, but also to an increase in the frequency and severity of attacks [2, 3, 5, 6, 7].

Previous clinical observations indicate that replacing the original drug with a generic drug containing the same drug substance may in some cases lead to the resumption of epileptic seizures or the development of toxic effects of the drug. This occurs due to the fact that the bioavailability and associated bioequivalence of generic drugs differ from the original drugs and/or their assessment is not complete or correct [5, 8, 9, 17].

Currently, valproic acid (VA) drugs are the most widely used drugs worldwide to control convulsive and non-convulsive seizures in children and adults. Valproic acid is used in clinical practice for the correction of both partial and generalized (epileptic) seizures [3, 4]. The effectiveness of valproates is 100% confirmed in the control of absences, myoclonic and tonic-clonic seizures in primary generalized forms of epilepsy, as well as in partial seizures with secondary generalization [4].

At this time, PVCs are registered in Russia under the following trade names: the original drug Depakin (manufacturer: Sanofi-Winthrop Industrie, France) and its prolonged forms Depakin Chrono and Depakin Chronosphere; generics Convulex (manufactured by Gerot Pharmazeutika GmbH, Austria), Apilepsin (manufactured by KRKA dd, Slovenia), Convulsofin (marketing authorization holder AWD.pharma GmbH & Co.KG, Germany) and a number of generics manufactured in India: Encorat (manufactured by Sun Pharmaceutical Industries Ltd, India) and Valparin XP (manufactured by Torrent Pharmaceuticals Ltd, India).

Research data

We analyzed the available research data from foreign and domestic authors on the problem of replacing PVK in the treatment of epilepsy.

The data of foreign authors turned out to be quite contradictory. On the one hand, in open randomized studies conducted in 64 patients who took the original PVK drug for 4 weeks, and then the generic drug for 4 weeks, there was no difference in the frequency of attacks or plasma drug concentrations when using both drugs [ 5, 18]. On the other hand, FDA studies in 1998 demonstrated differences in the bioavailability of PVC drugs [5]. In studies by Mattson (2002), the generic PVC caused more gastrointestinal side effects compared to the original long-acting drug [5, 16]. Replacing the original PVC drug with a generic caused a decrease in the concentration of the drug in the blood and the appearance of attacks after a 3-year attack-free period [5, 14].

A study by P. N. Vlasov et al. (2007) showed an increase in patient referrals to the district epileptologist after transferring from the original drug PVK (Depakina Chrono) to generics of the drug (Convulex, Valparin XR, Encorat) due to the adverse side effects of generics (urticaria, dyspeptic symptoms, increased frequency of attacks) [2] .

Of interest is the study of the dynamics of paroxysmal syndrome, EEG parameters and pharmacokinetics in patients with epilepsy against the background of replacing extended-release dosage forms from Depakine Chrono to Konvulex retarded form (T. A. Rogacheva, T. S. Melnikova, A. S. Petrukhin et al. .) [6]. The study involved 21 patients with various forms of epilepsy, aged from 18 to 46 years. According to the results of the study, replacing the extended-release dosage forms of sodium valproate Depakine Chrono with Konvulex (retard) causes unfavorable changes in the course of paroxysmal syndrome. At the same time, changes in indicators of bioelectrical activity of the brain were recorded after three days of taking Konvulex in a retarded form and were manifested by an increase in the slow-wave spectrum of the delta, theta and alpha ranges, transformation of slow-wave activity into discharge (by the 14th day of therapy) with a further increase in dysrhythmia and an increase in discharge activity. In all patients, after changing medications, changes in their maximum concentration in the blood serum were detected, which are directly related to changes in EEG indicators. According to the authors, the results of the study confirm significant differences in bioequivalence between the studied drugs, which are manifested by pronounced changes in the EEG in most patients and a worsening of the course of the paroxysmal syndrome. The authors' data indicate a lack of clinical equivalence between the drugs Depakine Chrono and Konvulex (retard), which may have significant clinical significance.

In a study by A.V. Sokolov et al. (2006) convincingly proved significant differences in the pharmacokinetic parameters of various forms of PVC with controlled release of the active substance [7]. According to the data obtained, Depakine Chrono turned out to be the most adequate in terms of pharmacokinetic characteristics, the concentration dynamics and dosage regimen of which fully corresponded to those declared by the manufacturer. The pharmacokinetic parameters of other drugs - Convulex, Valparin XP and Encorat Chrono - were significantly different: they were absorbed faster, the rate of reaching the maximum concentration in the blood plasma (Cmax) was higher, and the drug was eliminated from the body faster. Therapeutic drug monitoring revealed their non-equivalence to Depakin Chrono, and, as a result, recommendations were made to reduce the single/daily dose and take AEDs more frequently. Moreover, for Convulex, a single dose should be 410 mg instead of 500 mg, and the next dose of the drug should be taken after 8.23 ​​hours, and not after 12 hours, as stated in the annotation. The concentrations of various valproates after a single dose are presented in Fig.

Accordingly, in observations, a really increased single dose of the drug and a high level of Cmax led to the development of side effects, and a rapid drop in concentration and elimination of the drug caused the failure of drug remission [2, 7].

A retrospective study by Yu. B. Belousov and A. B. Gekht et al. showed pharmacoeconomic advantages when using Depakine Chrono [1]. The total number of seizures decreased from an average of 48 to 1.5 per year, which was the lowest of all AEDs studied. The authors associate the high effectiveness, first of all, with pharmacoeconomic properties: if the patient forgets to take a pill, when taking Depakine Chrono, its prolonged 12-hour action allows one to avoid a peak decrease in concentration and, accordingly, epileptic seizures, which cannot be achieved from the retarded form of carbamazepines. This allows you to reduce the number of visits to specialists and hospitalizations by at least 2 times, which significantly saves money.

Thus, data from domestic studies indicate a higher incidence of adverse reactions when transferring from the original PVC to a generic.

Diagnosis: epilepsy. What to prescribe: original drug or generic?

When prescribing treatment for a patient with newly diagnosed epilepsy, a decision must be made: to prescribe the original drug or a generic? In patients with newly diagnosed epilepsy, treatment can begin with the use of an original drug or a generic, selected in accordance with the general principles of adequate seizure control without side effects. In most cases, control of attacks is achieved by using average dosages of the drug [5, 10, 13, 16] and the likelihood of fluctuations in the concentration of AEDs in the blood is not as important as, for example, in the case of the drug concentration in plasma at the level of the upper or lower level. therapeutic. The same is true in the case of long-term epilepsy with good control of seizures using medium dosages of the drug. Considering that the result of treatment is assessed clinically based on the level of drug concentration in the blood, a correctly reproduced generic is a drug whose blood concentration corresponds to the therapeutic level accepted for both patients with newly diagnosed epilepsy and for patients with chronic epilepsy. In such situations, the physician may be guided by economic principles when prescribing the drug, based on the fact that the generic meets all established requirements for registration [5].

However, there are situations when it is undesirable to prescribe a generic, as there is a risk of worsening the clinical picture, for example, when choosing a drug for patients with a high risk of deterioration. These are the following categories of patients:

• patients with intractable epilepsy with optimally controlled seizures without side effects when taking AEDs. When treating these patients, doses of AEDs are prescribed above the level of drug tolerability or close to it [5, 16]. In practice, this means that the concentration in the blood is determined at the level of the upper (or even higher) therapeutic limit. In such patients, even small fluctuations in drug bioavailability can be clinically significant. A drug that is prescribed to a patient instead of one previously taken (a generic instead of the original and vice versa, or one generic instead of another), which has higher bioavailability (which may not go beyond the accepted fluctuations of ±20%), can provoke toxic manifestations, including the development of previously unregistered types of epileptic seizures. Conversely, a drug with lower bioavailability may provoke an increase in epileptic seizures, which until then were well controlled;
• patients with long-term remission of attacks while taking low doses of the drug or during a period of dose reduction. The introduction of another drug may trigger attacks if the AED has lower bioavailability, resulting in a too rapid decrease in the concentration of the active substance in the blood. In this group of patients, if the new drug has higher bioavailability, toxic effects will not develop, since the concentration indicators will not exceed the upper limit of the maximum therapeutic;
• patients with altered pharmacokinetics of AEDs. Problems associated with replacing the original drug with a generic and vice versa become especially relevant for pregnant women, especially in the period before childbirth, as well as for women in labor, elderly patients, newborns and children. In premature infants, newborns and children under one year of age, due to immature metabolic systems, the concentration of AEDs in the blood is significantly higher than in older children and adults. Over the course of several months, metabolic processes gradually become mature and the level of AED concentrations decreases, reaching levels characteristic of children. These figures are usually lower than in adults, in terms of drug dose per body weight. In this regard, the use of generics in newborns and older children may be associated with a higher difference (up to 40%) in drug concentrations than in adults [5, 11].

Conclusion

The results of an analysis of the costs of treating epilepsy indicate that the following relationship exists: the cost of treatment is lower, the better the control of seizures. Therefore, optimal seizure control (with minimal side effects) is the most important element in reducing the cost of therapy. Replacing one drug with another (the original generic and vice versa, or one generic with another) can have dangerous consequences for the course of epilepsy (increased frequency of attacks and/or side effects). These consequences entail unexpected direct costs associated with additional doctor visits, laboratory tests, and hospitalizations.

It is necessary to remember the following categories of patients at risk of worsening the clinical picture when replacing the original AED with a generic. These are patients with intractable epilepsy with optimally controlled seizures without side effects when taking AEDs; patients with long-term remission of attacks while taking low doses of the drug or during a period of dose reduction; patients with altered pharmacokinetics of AEDs [5].

Pharmacists should not replace one drug with another without the doctor's permission, and the doctor, in turn, should inform the patient about the possible consequences of the replacement.

For questions regarding literature, please contact the editor.

D. V. Marushkin , Candidate of Medical Sciences, Associate Professor L. G. Raevskaya VolGMU , Volgograd