Escitalopram Oxalate Oral: Uses, Side Effects, Interactions, Pictures, Warnings & Dosing

Before taking escitalopram, tell your doctor or pharmacist if you are allergic to it; or to citalopram; or if you have any other allergies. This product may contain inactive ingredients, which can cause allergic reactions or other problems. Talk to your pharmacist for more details.

Before using this medication, tell your doctor or pharmacist your medical history, especially of: personal or family history of bipolar/manic-depressive disorder, personal or family history of suicide attempts, liver disease, seizures, intestinal ulcers/bleeding (peptic ulcer disease) or bleeding problems, low sodium in the blood (hyponatremia), personal or family history of glaucoma (angle-closure type).

Escitalopram may cause a condition that affects the heart rhythm (QT prolongation). QT prolongation can rarely cause serious (rarely fatal) fast/irregular heartbeat and other symptoms (such as severe dizziness, fainting) that need medical attention right away.

The risk of QT prolongation may be increased if you have certain medical conditions or are taking other drugs that may cause QT prolongation. Before using escitalopram, tell your doctor or pharmacist of all the drugs you take and if you have any of the following conditions: certain heart problems (heart failure, slow heartbeat, recent heart attack, QT prolongation in the EKG), family history of certain heart problems (QT prolongation in the EKG, sudden cardiac death).

Low levels of potassium or magnesium in the blood may also increase your risk of QT prolongation. This risk may increase if you use certain drugs (such as diuretics/”water pills”) or if you have conditions such as severe sweating, diarrhea, or vomiting. Talk to your doctor about using escitalopram safely.

This drug may make you dizzy or drowsy. Alcohol or marijuana (cannabis) can make you more dizzy or drowsy. Do not drive, use machinery, or do anything that needs alertness until you can do it safely. Avoid alcoholic beverages. Talk to your doctor if you are using marijuana (cannabis).

The liquid form of this medication may contain sugar and/or aspartame. Caution is advised if you have diabetes, phenylketonuria (PKU), or any other condition that requires you to limit/avoid these substances in your diet. Ask your doctor or pharmacist about using this medication safely.

Before having surgery, tell your doctor or dentist about all the products you use (including prescription drugs, nonprescription drugs, and herbal products).

Older adults may be more sensitive to the side effects of this drug, such as QT prolongation (see above), loss of coordination, or bleeding. They may also be more likely to lose too much salt (hyponatremia), especially if they are also taking “water pills” (diuretics) with this medication. Loss of coordination can increase the risk of falling.

Children may be more sensitive to the side effects of this drug, especially loss of appetite and weight loss. Monitor weight and height in children who are taking this drug.

During pregnancy, this medication should be used only when clearly needed. It may harm an unborn baby. Also, babies born to mothers who have used this drug during the last 3 months of pregnancy may rarely develop withdrawal symptoms such as feeding/breathing difficulties, seizures, muscle stiffness, or constant crying. If you notice any of these symptoms in your newborn, tell the doctor promptly.

Since untreated mental/mood problems (such as depression, anxiety, obsessive-compulsive disorder, panic disorder) can be a serious condition, do not stop using this medication unless directed by your doctor. If you are planning pregnancy, become pregnant, or think you may be pregnant, immediately discuss with your doctor the benefits and risks of using this medication during pregnancy.

This medication passes into breast milk and may have undesirable effects on a nursing infant. Consult your doctor before breast-feeding.

Escitalopram (Oral Route) Description and Brand Names

Description and Brand Names

Drug information provided by: IBM Micromedex

US Brand Name

1. Lexapro

Descriptions

Escitalopram is used to treat depression and generalized anxiety disorder (GAD). It is an antidepressant that belongs to a group of medicines known as selective serotonin reuptake inhibitors (SSRIs). These medicines work by increasing the activity of the chemical serotonin in the brain.

This medicine is available only with your doctor’s prescription.

This product is available in the following dosage forms:

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Portions of this document last updated: Nov. 01, 2021

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Lexapro (escitalopram) dosing, indications, interactions, adverse effects, and more

Escitalopram: Uses, Interactions, Mechanism of Action

Escitalopram 10mg tablets – Summary of Product Characteristics (SmPC)

This information is intended for use by health professionals

Escitalopram 10 mg film-coated tablets

Each film-coated tablet contains 10 mg escitalopram (as oxalate).

For a full list of excipients, see section 6.1.

Film-coated tablet.

Escitalopram 10 mg: White to off – white colored, oval shaped, film-coated, biconvex tablets debossed with ‘F’ on one side and ’54’ on the other side with a deep scoreline between ‘5’ and ‘4’. The size is 8.1 mm X 5.6 mm.

The tablets can be divided into equal doses.

Treatment of major depressive episodes.

Treatment of panic disorder with or without agoraphobia.

Treatment of social anxiety disorder (social phobia).

Treatment of generalised anxiety disorder.

Treatment of obsessive-compulsive disorder.

Posology

Safety of daily doses above 20 mg has not been demonstrated.

Major depressive episodes

Usual dosage is 10 mg once daily. Depending on individual patient response, the dose may be increased to a maximum of 20 mg daily.

Usually 2-4 weeks are necessary to obtain antidepressant response. After the symptoms resolve, treatment for at least 6 months is required for consolidation of the response.

Panic disorder with or without agoraphobia

An initial dose of 5 mg is recommended for the first week before increasing the dose to 10 mg daily. The dose may be further increased, up to a maximum of 20 mg daily, dependent on individual patient response.

Maximum effectiveness is reached after about 3 months. The treatment lasts several months.

Social anxiety disorder

Usual dosage is 10 mg once daily. Usually 2-4 weeks are necessary to obtain symptom relief. The dose may subsequently, depending on individual patient response, be decreased to 5 mg or increased to a maximum of 20 mg daily.

Social anxiety disorder is a disease with a chronic course, and treatment for 12 weeks is recommended to consolidate response. Long-term treatment of responders has been studied for 6 months and can be considered on an individual basis to prevent relapse; treatment benefits should be re-evaluated at regular intervals.

Social anxiety disorder is a well-defined diagnostic terminology of a specific disorder, which should not be confounded with excessive shyness. Pharmacotherapy is only indicated if the disorder interferes significantly with professional and social activities.

The place of this treatment compared to cognitive behavioural therapy has not been assessed. Pharmacotherapy is part of an overall therapeutic strategy.

Generalised anxiety disorder

Initial dosage is 10 mg once daily. Depending on the individual patient response, the dose may be increased to a maximum of 20 mg daily.

Long term treatment of responders has been studied for at least 6 months in patients receiving 20 mg/day. Treatment benefits and dose should be re-evaluated at regular intervals (see section 5.1).

Obsessive-Compulsive Disorder

Initial dosage is 10 mg once daily. Depending on the individual patient response, the dose may be increased to a maximum of 20 mg daily.

As OCD is a chronic disease, patients should be treated for a sufficient period to ensure that they are symptom free.

Treatment benefits and dose should be re-evaluated at regular intervals (see section 5.1).

Elderly patients (> 65 years of age)

Initial dosage is 5 mg once daily. Depending on individual patient response the dose may be increased to 10 mg daily (see section 5.2).

The efficacy of Escitalopram in social anxiety disorder has not been studied in elderly patients.

Paediatric population

Escitalopram should not be used in the treatment of children and adolescents under the age of 18 years (see section 4.4).

Reduced renal function

Dosage adjustment is not necessary in patients with mild or moderate renal impairment. Caution is advised in patients with severely reduced renal function (CL_CR less than 30 ml/min) (see section 5.2).

Reduced hepatic function

An initial dose of 5 mg daily for the first two weeks of treatment is recommended in patients with mild or moderate hepatic impairment. Depending on individual patient response, the dose may be increased to 10 mg daily. Caution and extra careful dose titration is advised in patients with severely reduced hepatic function (see section 5.2).

Poor metabolisers of CYP2C19

For patients who are known to be poor metabolisers with respect to CYP2C19, an initial dose of 5 mg daily during the first two weeks of treatment is recommended. Depending on individual patient response, the dose may be increased to 10 mg daily (see section 5.2).

Discontinuation symptoms seen when stopping treatment

Abrupt discontinuation should be avoided. When stopping treatment with escitalopram the dose should be gradually reduced over a period of at least one to two weeks in order to reduce the risk of discontinuation symptoms (see section 4.4 and 4.8). If intolerable symptoms occur following a decrease in the dose or upon discontinuation of treatment, then resuming the previously prescribed dose may be considered. Subsequently, the physician may continue decreasing the dose, but at a more gradual rate.

Method of administration

Escitalopram is administered as a single daily dose and may be taken with or without food.

Hypersensitivity to escitalopram or to any of the excipients.

Concomitant treatment with non-selective, irreversible monoamine oxidase inhibitors (MAO-inhibitors) is contraindicated due to the risk of serotonin syndrome with agitation, tremor, hyperthermia etc. (see section 4.5).

The combination of escitalopram with reversible MAO-A inhibitors (e.g. moclobemide) or the reversible non-selectiveMAO-inhibitor linezolid is contraindicated due to the risk of onset of a serotonin syndrome (see section 4.5).

Escitalopram is contraindicated in patients with known QT interval prolongation or congenital long QT syndrome.

Escitalopram is contraindicated together with medicinal products that are known to prolong the QT interval (see section 4.5).

The following special warnings and precautions apply to the therapeutic class of SSRIs (Selective Serotonin Re-uptake Inhibitors).

Paediatric population

Escitalopram should not be used in the treatment of paediatric population.Suicide related behaviours (suicide attempt and suicidal thoughts), and hostility (predominately aggression, oppositional behaviour and anger) were more frequently observed in clinical trials among paediatric populationtreated with antidepressants compared to those treated with placebo. If, based on clinical need, a decision to treat is nevertheless taken, the patient should be carefully monitored for the appearance of suicidal symptoms. In addition, long-term safety data in the paediatric population concerning growth, maturation and cognitive and behavioural development are lacking.

Paradoxical anxiety

Some patients with panic disorder may experience increased anxiety symptoms at the beginning of treatment with antidepressants. This paradoxical reaction usually subsides within two weeks during continued treatment. A low starting dose is advised to reduce the likelihood of an anxiogenic effect (see section 4.2).

Seizures

Escitalopram should be discontinued if a patient develops seizures for the first time, or if there is an increase in seizure frequency (in patients with a previous diagnosis of epilepsy). SSRIs should be avoided in patients with unstable epilepsy and patients with controlled epilepsy should be closely monitored.

Mania

SSRIs should be used with caution in patients with a history of mania/hypomania. SSRIs should be discontinued in any patient entering a manic phase.

Diabetes

In patients with diabetes, treatment with an SSRI may alter glycaemic control (hypoglycaemia or hyperglycaemia). Insulin and/or oral hypoglycaemic dosage may need to be adjusted.

Suicide/suicidal thoughts or clinical worsening

Depression is associated with an increased risk of suicidal thoughts, self harm and suicide (suicide-related events). This risk persists until significant remission occurs. As improvement may not occur during the first few weeks or more of treatment, patients should be closely monitored until such improvement occurs. It is general clinical experience that the risk of suicide may increase in the early stages of recovery.

Other psychiatric conditions for which Escitalopram is prescribed can also be associated with an increased risk of suicide-related events. In addition, these conditions may be co-morbid with major depressive disorder. The same precautions observed when treating patients with major depressive disorder should therefore be observed when treating patients with other psychiatric disorders.

Patients with a history of suicide-related events, or those exhibiting a significant degree of suicidal ideation prior to commencement of treatment, are known to be at greater risk of suicidal thoughts or suicide attempts and should receive careful monitoring during treatment. A meta analysis of placebo controlled clinical trials of antidepressant drugs in adult patients with psychiatric disorders showed an increased risk of suicidal behaviour with antidepressants compared to placebo in patients less than 25 years old. Close supervision of patients and in particular those at high risk should accompany drug therapy especially in early treatment and following dose changes.

Patients (and caregivers of patients) should be alerted about the need to monitor for any clinical worsening, suicidal behaviour or thoughts and unusual changes in behaviour and to seek medical advice immediately if these symptoms present.

Akathisia/psychomotor restlessness

The use of SSRIs/SNRIs has been associated with the development of akathisia, characterised by a subjectively unpleasant or distressing restlessness and need to move often accompanied by an inability to sit or stand still. This is most likely to occur within the first few weeks of treatment. In patients who develop these symptoms, increasing the dose may be detrimental.

Hyponatraemia

Hyponatraemia, probably due to inappropriate antidiuretic hormone secretion (SIADH), has been reported rarely with the use of SSRIs and generally resolves on discontinuation of therapy. Caution should be exercised in patients at risk, such as the elderly, or patients with cirrhosis, or if used in combination with other medications which may cause hyponatraemia.

Haemorrhage

There have been reports of cutaneous bleeding abnormalities, such as ecchymoses and purpura, with SSRIs. Caution is advised in patients taking SSRIs, particularly in concomitant use with oral anticoagulants, with medicinal products known to affect platelet function (e.g. atypical antipsychotics and phenothiazines, most tricyclic antidepressants, acetylsalicylic acid and non-steroidal anti-inflammatory medicinal products (NSAIDs), ticlopidine and dipyridamole) and in patients with known bleeding tendencies.

SSRIs/SNRIs may increase the risk of postpartum haemorrhage (see sections 4.6, 4.8).

ECT (electroconvulsive therapy)

There is limited clinical experience of concurrent administration of SSRIs and ECT, therefore caution is advisable.

Serotonin syndrome

Caution is advisable if escitalopram is used concomitantly with medicinal products with serotonergic effects such as sumatriptan or other triptans, tryptophan and opioids (such as buprenorphine and tramadol)…

In rare cases, serotonin syndrome has been reported in patients using SSRIs concomitantly with serotonergic medicinal products. A combination of symptoms, such as agitation, tremor, myoclonus,hyperthermia, mental-status changes, autonomic instability, neuromuscular abnormalities, and/or gastrointestinal symptoms may indicate the development of this condition. If this occurs treatment with the SSRI and the serotonergic medicinal product should be discontinued immediately and symptomatic treatment initiated.

St. John´s Wort

Concomitant use of SSRIs and herbal remedies containing St. John´s Wort (Hypericum perforatum) may result in an increased incidence of adverse reactions (see section 4.5).

Discontinuation symptoms seen when stopping treatment

Discontinuation symptoms when stopping treatment are common, particularly if discontinuation is abrupt (see section 4.8). In clinical trials adverse events seen on treatment discontinuation occurred in approximately 25% of patients treated with escitalopram and 15% of patients taking placebo.

The risk of discontinuation symptoms may be dependent on several factors including the duration and dose of therapy and the rate of dose reduction. Dizziness, sensory disturbances (including paraesthesia and electric shock sensations), sleep disturbances (including insomnia and intense dreams), agitation or anxiety, nausea and/or vomiting, tremor, confusion, sweating, headache, diarrhoea, palpitations, emotional instability, irritability, and visual disturbances are the most commonly reported reactions. Generally these symptoms are mild to moderate, however, in some patients they may be severe in intensity.

They usually occur within the first few days of discontinuing treatment, but there have been very rare reports of such symptoms in patients who have inadvertently missed a dose.

Generally these symptoms are self-limiting and usually resolve within 2 weeks, though in some individuals they may be prolonged (2-3 months or more). It is therefore advised that escitalopram should be gradually tapered when discontinuing treatment over a period of several weeks or months, according to the patient’s needs (see “Discontinuation symptoms seen when stopping treatment”, section 4.2).

Coronary heart disease

Due to limited clinical experience, caution is advised in patients with coronary heart disease (see section 5.3).

QT interval prolongation

Escitalopram has been found to cause a dose-dependent prolongation of the QT interval. Cases of QT interval prolongation and ventricular arrhythmia including Torsade de Pointes have been reported during the post-marketing period, predominantly in patients of female gender, with hypokalaemia, or with pre-existing QT interval prolongation or other cardiac diseases (see sections 4.3, 4.5, 4.8, 4.9 and 5.1).

Caution is advised in patients with significant bradycardia; or in patients with recent acute myocardial infarction or uncompensated heart failure.

Electrolyte disturbances such as hypokalaemia and hypomagnesaemia increase the risk for malignant arrhythmias and should be corrected before treatment with escitalopram is started.

If patients with stable cardiac disease are treated, an ECG review should be considered before treatment is started.

If signs of cardiac arrhythmia occur during treatment with escitalopram, the treatment should be withdrawn and an ECG should be performed.

Angle-Closure Glaucoma

SSRIs including escitalopram may have an effect on pupil size resulting in mydriasis. This mydriatic effect has the potential to narrow the eye angle resulting in increased intraocular pressure and angle-closure glaucoma, especially in patients pre-disposed. Escitalopram should therefore be used with caution in patients with angle-closure glaucoma or history of glaucoma.

Sexual dysfunction

Selective serotonin reuptake inhibitors (SSRIs)/serotonin norepinephrine reuptake inhibitors (SNRIs) may cause symptoms of sexual dysfunction (see section 4.8). There have been reports of long-lasting sexual dysfunction where the symptoms have continued despite discontinuation of SSRIs/SNRI.

Escitalopram contains sodium

This medicinal product contains less than 1 mmol sodium (23 mg) per each tablet, that is to say essentially ‘sodium-free’.

Pharmacodynamic interactions

Contra-indicated combinations:

Irreversible non-selective MAOIs

Cases of serious reactions have been reported in patients receiving an SSRI in combination with a non-selective, irreversible monoamine oxidase inhibitor (MAOI), and in patients who have recently discontinued SSRI treatment and have been started on such MAOI treatment (see section 4.3). In some cases, the patient developed serotonin syndrome (see section 4.8).

Escitalopram is contra-indicated in combination with non-selective, irreversible MAOIs. Escitalopram may be started 14 days after discontinuing treatment with an irreversible MAOI. At least 7 days should elapse after discontinuing escitalopram treatment, before starting a non-selective, irreversible MAOI.

Reversible, selective MAO-A inhibitor (moclobemide)

Due to the risk of serotonin syndrome, the combination of escitalopram with a MAO-A inhibitor such as moclobemide is contraindicated (see section 4.3). If the combination proves necessary, it should be started at the minimum recommended dosage and clinical monitoring should be reinforced.

Reversible, non-selective MAO-inhibitor (linezolid)

The antibiotic linezolid is a reversible non-selective MAO-inhibitor and should not be given to patients treated with escitalopram. If the combination proves necessary, it should be given with minimum dosages and under close clinical monitoring (see section 4.3).

Irreversible, selective MAO-B inhibitor (selegiline)

In combination with selegiline (irreversible MAO-B inhibitor), caution is required due to the risk of developing serotonin syndrome. Selegiline doses up to 10 mg/day have been safely co-administered with racemic citalopram.

QT interval prolongation

Pharmacokinetic and pharmacodynamic studies of escitalopram combined with other medicinal products that prolong the QT interval have not been performed. An additive effect of escitalopram and these medicinal products cannot be excluded. Therefore, co-administration of escitalopram with medicinal products that prolong the QT interval, such as Class IA and III antiarrhythmics, antipsychotics (e.g. phenothiazine derivatives, pimozide, haloperidol), tricyclic antidepressants, certain antimicrobial agents (e.g. sparfloxacin, moxifloxacin, erythromycin IV, pentamidine, anti-malarial treatment particularly halofantrine), certain antihistamines (astemizole, mizolastine), is contraindicated.

Combinations requiring precautions for use:

Serotonergic medicinal products

Co-administration with serotonergic medicinal products (e.g. opioids (such as buprenorphine and tramadol), sumatriptan and other triptans) may lead to serotonin syndrome.

Medicinal products lowering the seizure threshold

SSRIs can lower the seizure threshold. Caution is advised when concomitantly using other medicinal products capable of lowering the seizure threshold (e.g. antidepressants (tricyclics, SSRIs), neuroleptics (phenothiazines, thioxanthenes and butyrophenones), mefloquin, bupropion and tramadol).

Lithium, tryptophan

There have been reports of enhanced effects when SSRIs have been given together with lithium or tryptophan, therefore concomitant use of SSRIs with these medicinal products should be undertaken with caution.

St. John’s Wort

Concomitant use of SSRIs and herbal remedies containing St. John´s Wort (Hypericum perforatum) may result in an increased incidence of adverse reactions (see section 4.4).

Haemorrhage

Altered anti-coagulant effects may occur when escitalopram is combined with oral anticoagulants. Patients receiving oral anticoagulant therapy should receive careful coagulation monitoring when escitalopram is started or stopped (see section 4.4).

Concomitant use of non-steroidal anti-inflammatory drugs (NSAIDs) may increase bleeding-tendency (see section 4.4).

Alcohol

No pharmacodynamic or pharmacokinetic interactions are expected between escitalopram and alcohol. However, as with other psychotropic medicinal products, the combination with alcohol is not advisable.

Medicinal products inducing hypokalaemia/hypomagnesaemia

Caution is warranted for concomitant use of hypokalaemia/hypomagnesaemia inducing medicinal products as these conditions increase the risk of malignant arrhythmias (see section 4.4).

Pharmacokinetic interactions

Influence of other medicinal products on the pharmacokinetics of escitalopram

The metabolism of escitalopram is mainly mediated by CYP2C19. CYP3A4 and CYP2D6 may also contribute to the metabolism although to a smaller extent. The metabolism of the major metabolite S-DCT (demethylated escitalopram) seems to be partly catalysed by CYP2D6.

Co-administration of escitalopram with omeprazole 30 mg once daily (a CYP2C19 inhibitor) resulted in moderate (approximately 50%) increase in the plasma concentrations of escitalopram.

Co-administration of escitalopram with cimetidine 400 mg twice daily (moderately potent general enzyme-inhibitor) resulted in a moderate (approximately 70%) increase in the plasma concentrations of escitalopram. Caution is advised when administering escitalopram in combination with cimetidine.

Dose adjustment may be warranted.

Thus, caution should be exercised when used concomitantly with CYP2C19 inhibitors (e.g. omeprazole, esomeprazole, fluconazole, fluvoxamine, lansoprazole, ticlopidine) or cimetidine. A reduction in the dose of escitalopram may be necessary based on monitoring of side-effects during concomitant treatment (see section 4.4).

Effect of escitalopram on the pharmacokinetics of other medicinal products

Escitalopram is an inhibitor of the enzyme CYP2D6. Caution is recommended when escitalopram is co-administered with medicinal products that are mainly metabolised by this enzyme, and that have a narrow therapeutic index, e.g. flecainide, propafenone and metoprolol (when used in cardiac failure), or some CNS acting medicinal products that are mainly metabolised by CYP2D6, e.g. antidepressants such as desipramine, clomipramine and nortriptyline or antipsychotics like risperidone, thioridazine and haloperidol. Dosage adjustment may be warranted.

Co-administration with desipramine or metoprolol resulted in both cases in a twofold increase in the plasma levels of these two CYP2D6 substrates.

In vitro studies have demonstrated that escitalopram may also cause weak inhibition of CYP2C19. Caution is recommended with concomitant use of medicinal products that are metabolised by CYP2C19.

Fertility

Animal data have shown that citalopram may affect sperm quality (see section 5.3). Human case reports with some SSRIs have shown that an effect on sperm quality is reversible. Impact on human fertility has not been observed so far.

Pregnancy

For escitalopram only limited clinical data are available regarding exposed pregnancies. Animal studies have shown reproductive toxicity (see section 5.3). Escitalopram should not be used during pregnancy unless clearly necessary and only after careful consideration of the risk/benefit.

Neonates should be observed if maternal use of Escitalopram continues into the later stages of pregnancy, particularly in the third trimester. Abrupt discontinuation should be avoided during pregnancy.

The following symptoms may occur in the neonate after maternal SSRI/SNRI use in later stages of pregnancy: respiratory distress, cyanosis, apnoea, seizures, temperature instability, feeding difficulty, vomiting, hypoglycaemia, hypertonia, hypotonia, hyperreflexia, tremor, jitteriness, irritability, lethargy, constant crying, somnolence and difficulty sleeping. These symptoms could be due to either serotonergic effects or discontinuation symptoms. In a majority of instances the complications begin immediately or soon (<24 hours) after delivery.

Epidemiological data have suggested that the use of SSRIs in pregnancy, particularly in late pregnancy, may increase the risk of persistent pulmonary hypertension in the newborn (PPHN). The observed risk was approximately 5 cases per 1000 pregnancies. In the general population 1 to 2 cases of PPHN per 1000 pregnancies occur.

Observational data indicate an increased risk (less than 2-fold) of postpartum haemorrhage following SSRI/SNRI exposure within the month prior to birth (see sections 4.4, 4.8).

Breastfeeding

It is expected that escitalopram will be excreted into human milk.

Consequently, breast-feeding is not recommended during treatment.

Although escitalopram has been shown not to affect intellectual function or psychomotor performance, any psychoactive medicinal product may impair judgement or skills. Patients should be cautioned about the potential risk of an influence on their ability to drive a car and operate machinery.

Adverse reactions are most frequent during the first or second week of treatment and usually decrease in intensity and frequency with continued treatment.

Tabulated list of adverse reactions

Adverse reactions known for SSRIs and also reported for escitalopram in either placebo-controlled clinical studies or as spontaneous post-marketing events are listed below by system organ class and frequency.

Frequencies are taken from clinical studies; they are not placebo-corrected. Frequencies are defined as: very common (≥1/10), common (≥1/100 to <1/10), uncommon (≥1/1,000 to <1/100), rare (≥1/10,000 to <1/1,000), very rare (<1/10,000), or not known (cannot be estimated from the available data).

¹ These events have been reported for the therapeutic class of SSRIs.

² Cases of suicidal ideation and suicidal behaviours have been reported during escitalopram therapy or early after treatment discontinuation (see section 4.4).

³ This event has been reported for the therapeutic class of SSRIs/SNRIs (see sections 4.4, 4.6).

QT interval prolongation

Cases of QT interval prolongation and ventricular arrhythmia including torsade de pointes have been reported during the post-marketing period, predominantly in patients of female gender, with hypokalemia, or with pre-existing QT interval prolongation or other cardiac diseases (see sections 4.3, 4.4, 4.5, 4.9 and 5.1).

Class effects

Epidemiological studies, mainly conducted in patients 50 years of age and older, show an increased risk of bone fractures in patients receiving SSRIs and TCAs. The mechanism leading to this risk is unknown.

Discontinuation symptoms seen when stopping treatment

Discontinuation of SSRIs/SNRIs (particularly when abrupt) commonly leads to discontinuation symptoms. Dizziness, sensory disturbances (including paraesthesia and electric shock sensations), sleep disturbances (including insomnia and intense dreams), agitation or anxiety, nausea and/or vomiting, tremor, confusion, sweating, headache, diarrhoea, palpitations, emotional instability, irritability, and visual disturbances are the most commonly reported reactions.

Generally, these events are mild to moderate and are self-limiting, however, in some patients they may be severe and/or prolonged. It is therefore advised that when escitalopram treatment is no longer required, gradual discontinuation by dose tapering should be carried out (see section 4.2 and 4.4).

Reporting of suspected adverse reactions

Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the national reporting system listed in Yellow Card Scheme, Website: www.mhra.gov.uk/yellowcard.

Toxicity

Clinical data on escitalopram overdose are limited and many cases involve concomitant overdoses of other drugs. In the majority of cases mild or no symptoms have been reported. Fatal cases of escitalopram overdose have rarely been reported with escitalopram alone; the majority of cases have involved overdose with concomitant medications. Doses between 400 and 800mg of escitalopram alone have been taken without any severe symptoms.

Symptoms

Symptoms seen in reported overdose of escitalopram include symptoms mainly related to the central nervous system (ranging from dizziness, tremor, and agitation to rare cases of serotonin syndrome, convulsion, and coma), the gastrointestinal system (nausea/vomiting), and the cardiovascular system (hypotension, tachycardia, QT interval prolongation, and arrhythmia) and electrolyte/fluid balance conditions (hypokalaemia, hyponatraemia).

Management

There is no specific antidote. Establish and maintain an airway, ensure adequate oxygenation and respiratory function. Gastric lavage and the use of activated charcoal should be considered. Gastric lavage should be carried out as soon as possible after oral ingestion. Cardiac and vital signs monitoring are recommended along with general symptomatic supportive measures.

ECG monitoring is advised in case of overdose in patients with congestive heart failure/bradyarrhythmias, in patients using concomitant medications that prolong the QT interval, or in patients with altered metabolism, e.g. liver impairment.

Pharmacotherapeutic group: antidepressants, selective serotonin reuptake inhibitors

ATC-code: N 06 AB 10

Mechanism of action

Escitalopram is a selective inhibitor of serotonin (5-HT) re-uptake with high affinity for the primary binding site. It also binds to an allosteric site on the serotonin transporter, with a 1000 fold lower affinity.

Escitalopram has no or low affinity for a number of receptors including 5-HT_1A, 5-HT₂, DA D₁ and D₂ receptors, α₁-, α₂-, β-adrenoceptors, histamine H₁, muscarine cholinergic, benzodiazepine, and opioid receptors.

The inhibition of 5-HT re-uptake is the only likely mechanism of action explaining the pharmacological and clinical effects of escitalopram.

Pharmacodynamic effects

In a double-blind, placebo-controlled ECG study in healthy subjects, the change from baseline in QTc (Fridericia-correction) was 4.3 ms (90% CI: 2.2, 6.4) at the 10 mg/day dose and 10.7 ms (90% CI: 8.6, 12.8) at the supratherapeutic dose 30 mg/day (see section 4.3, 4.4, 4.5, 4.8 and 4.9).

Clinical efficacy

Major Depressive Episodes

Escitalopram has been found to be effective in the acute treatment of major depressive episodes in three out of four double-blind, placebo controlled short-term (8-weeks) studies. In a long-term relapse prevention study, 274 patients who had responded during an initial 8-week open label treatment phase with escitalopram 10 or 20 mg/day, were randomised to continuation with escitalopram at the same dose, or to placebo, for up to 36 weeks. In this study, patients receiving continued escitalopram experienced a significantly longer time to relapse over the subsequent 36 weeks compared to those receiving placebo.

Social Anxiety Disorder

Escitalopram was effective in both three short-term (12- week) studies and in responders in a 6 months relapse prevention study in social anxiety disorder. In a 24-week dose-finding study, efficacy of 5, 10 and 20 mg escitalopram has been demonstrated.

Generalised anxiety disorder

Escitalopram in doses of 10 and 20 mg/day was effective in four out of four placebo-controlled studies.

In pooled data from three studies with similar design comprising 421 escitalopram-treated patients and 419 placebo-treated patients there were 47.5% and 28.9% responders respectively and 37.1% and 20.8% remitters. Sustained effect was seen from week 1.

Maintenance of efficacy of escitalopram 20mg/day was demonstrated in a 24- to 76-week, randomised, maintenance of efficacy study in 373 patients who had responded during the initial 12-week open-label treatment.

Obsessive-compulsive disorder

In a randomized, double-blind, clinical study, 20 mg/day escitalopram separated from placebo on the Y-BOCS total score after 12 weeks. After 24 weeks, both 10 and 20 mg/day escitalopram were superior as compared to placebo.

Prevention of relapse was demonstrated for 10 and 20 mg/day escitalopram in patients who responded to escitalopram in a 16-week open-label period and who entered a 24 week, randomized, double blind, placebo controlled period.

Absorption

Absorption is almost complete and independent of food intake. (Mean time to maximum concentration (mean T_max) is 4 hours after multiple dosing). As with racemic citalopram, the absolute bio-availability of escitalopram is expected to be about 80%.

Distribution

The apparent volume of distribution (V_d,β/F) after oral administration is about 12 to 26 L/kg. The plasma protein binding is below 80% for escitalopram and its main metabolites.

Biotransformation

Escitalopram is metabolised in the liver to the demethylated and didemethylated metabolites. Both of these are pharmacologically active. Alternatively, the nitrogen may be oxidised to form the N-oxide metabolite. Both parent substance and metabolites are partly excreted as glucuronides. After multiple dosing the mean concentrations of the demethyl and didemethyl metabolites are usually 28-31% and <5%, respectively, of the escitalopram concentration. Biotransformation of escitalopram to the demethylated metabolite is mediated primarily by CYP2C19. Some contribution by the enzymes CYP3A4 and CYP2D6 is possible.

Elimination

The elimination half-life (t_{½ β}) after multiple dosing is about 30 hours and the oral plasma clearance (Cl_oral) is about 0.6 L/min. The major metabolites have a significantly longer half-life. Escitalopram and major metabolites are assumed to be eliminated by both the hepatic (metabolic) and the renal routes, with the major part of the dose excreted as metabolites in the urine.

Linearity

There is linear pharmacokinetics. Steady-state plasma levels are achieved in about 1 week. Average steady-state concentrations of 50 nmol/L (range 20 to 125 nmol/L) are achieved at a daily dose of 10 mg.

Elderly patients (> 65 years)

Escitalopram appears to be eliminated more slowly in elderly patients compared to younger patients. Systemic exposure (AUC) is about 50 % higher in elderly compared to young healthy volunteers (see section 4.2).

Reduced hepatic function

In patients with mild or moderate hepatic impairment (Child-Pugh Criteria A and B), the half-life of escitalopram was about twice as long and the exposure was about 60% higher than in subjects with normal liver function (see section 4.2).

Reduced renal function

With racemic citalopram, a longer half-life and a minor increase in exposure have been observed in patients with reduced kidney function (CL_cr 10-53 ml/min). Plasma concentrations of the metabolites have not been studied, but they may be elevated (see section 4.2).

Polymorphism

It has been observed that poor metabolisers with respect to CYP2C19 have twice as high a plasma concentration of escitalopram as extensive metabolisers. No significant change in exposure was observed in poor metabolisers with respect to CYP2D6 (see section 4.2).

No complete conventional battery of preclinical studies was performed with escitalopram since the bridging toxicokinetic and toxicological studies conducted in rats with escitalopram and citalopram showed a similar profile. Therefore, all the citalopram information can be extrapolated to escitalopram.

In comparative toxicological studies in rats, escitalopram and citalopram caused cardiac toxicity, including congestive heart failure, after treatment for some weeks, when using dosages that caused general toxicity. The cardiotoxicity seemed to correlate with peak plasma concentrations rather than to systemic exposures (AUC). Peak plasma concentrations at no-effect-level were in excess (8-fold) of those achieved in clinical use, while AUC for escitalopram was only 3- to 4-fold higher than the exposure achieved in clinical use. For citalopram AUC values for the S-enantiomer were 6- to 7-fold higher than exposure achieved in clinical use. The findings are probably related to an exaggerated influence on biogenic amines i.e. secondary to the primary pharmacological effects, resulting in hemodynamic effects (reduction in coronary flow) and ischemia. However, the exact mechanism of cardiotoxicity in rats is not clear. Clinical experience with citalopram, and the clinical trial experience with escitalopram, do not indicate that these findings have a clinical correlate.

Increased content of phospholipids has been observed in some tissues e.g. lung, epididymides and liver after treatment for longer periods with escitalopram and citalopram in rats. Findings in the epididymides and liver were seen at exposures similar to that in man. The effect is reversible after treatment cessation. Accumulation of phospholipids (phospholipidosis) in animals has been observed in connection with many cationic amphiphilic medicines. It is not known if this phenomenon has any significant relevance for man.

In the developmental toxicity study in the rat embryotoxic effects (reduced foetal weight and reversible delay of ossification) were observed at exposures in terms of AUC in excess of the exposure achieved during clinical use. No increased frequency of malformations was noted. A pre- and postnatal study showed reduced survival during the lactation period at exposures in terms of AUC in excess of the exposure achieved during clinical use.

Animal data have shown that citalopram induces a reduction of fertility index and pregnancy index, reduction in number in implantation and abnormal sperm at exposure well in excess of human exposure. No animal data related to this aspect are available for escitalopram.

Tablet core:

Silicified microcrystalline cellulose

Butylated hydroxyl toluene (E321)

Butylated hydroxyl anisole (E320)

Croscarmellose sodium

Cellulose microcrystalline

Silica, colloidal anhydrous

Talc

Magnesium stearate

Film-coating:

Hypromellose

Macrogol 400

Titanium dioxide (E 171)

This medicinal product does not require any special storage conditions

The tablets are available in PVC/Aclar–Aluminium blisters and white opaque HDPE bottle closed with polypropylene closure.

Pack sizes

PVC/Aclar–Aluminium blister packs: 14, 20, 28, 50, 56, 100 and 500 tablets

HDPE bottle packs: 28, 30, 100, 250 and 500 tablets

Not all pack sizes may be marketed.

Any unused product or waste material should be disposed of in accordance with local requirements.

Milpharm Limited

AresBlock

Odyssey Business Park

West End Road

Ruislip HA4 6QD

United Kingdom

Differences, similarities, and which is better for you

Drug overview & main differences | Conditions treated | Efficacy | Insurance coverage and cost comparison | Side effects | Drug interactions | Warnings | FAQ

There are several medication options available if you have anxiety. Lexapro (escitalopram) and Xanax (alprazolam) are two different prescription drugs that can treat general anxiety as well as anxiety with depression. Lexapro is an SSRI (selective serotonin reuptake inhibitor) drug while Xanax is a benzodiazepine. Both drugs work differently from each other, although they can be used for similar mental health conditions.

What are the main differences between Lexapro vs. Xanax?

Lexapro (Lexapro coupons) is an FDA-approved medication that is also available as a generic. The generic name for Lexapro is escitalopram. It works by blocking the reuptake of serotonin so that there is an increased level in the brain. Serotonin is an important neurotransmitter responsible for mood and well being. Lexapro is usually taken once daily and may take a few weeks to reach maximum therapeutic potential.

Xanax (Xanax coupons) is a brand name medication that is FDA approved to treat anxiety and panic disorders. The generic name for Xanax is alprazolam. It works by increasing the effects of GABA, an inhibitory molecule that can calm nerve activity in the brain. Xanax is usually taken 3 to 4 times per day for anxiety or panic attacks.

RELATED: Lexapro details | Xanax details | Escitalopram details | Alprazolam details

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Conditions treated by Lexapro vs. Xanax

Lexapro and Xanax are two brand name medications that are commonly used for anxiety in adults. They are both indicated to treat anxiety alone or anxiety associated with depression.

Lexapro is also approved to treat major depression in adults and adolescents. Off-label uses for Lexapro include obsessive compulsive disorder, panic disorders, and insomnia.

Xanax is also approved for panic disorder in adults. It may sometimes be used off-label for depression although it’s commonly used for adults with both anxiety and depression. It is also sometimes used off label for insomnia.

Is Lexapro vs. Xanax more effective?

Lexapro and Xanax are both effective for treating anxiety. Although benzodiazepines are not commonly used first for anxiety, some studies show that they may be more effective than SSRIs. However, benzodiazepines are usually only recommended for short-term purposes.

Sometimes SSRI drugs and benzodiazepines are prescribed for anxiety and depression. Because SSRIs may take some time to feel its full effects, a benzodiazepine may help when starting therapy with an SSRI like Lexapro. In a literature review, it was found that benzodiazepines improved control of anxiety and helped with initial anxiety when starting an SSRI.

Other case reports have found that when taken together, benzodiazepines may boost the efficacy of SSRIs. In one report, a patient taking a benzodiazepine and SSRI together experienced mania, or an excitable mood often characterized by increased energy and irrational decision making.

Treatment with Lexapro and/or Xanax is personalized to an individual’s condition and symptoms. It’s important to consult a doctor or mental healthcare professional to explore the different treatment options available.

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Coverage and cost comparison of Lexapro vs. Xanax

Lexapro can be purchased with a prescription and is covered by many Medicare and insurance plans. A 30-day supply of Lexapro tablets can cost around $400. Buying generic escitalopram with a SingleCare discount card can save you money and bring the cost down to $9-$37 depending on which pharmacy you use.

If you’re looking to purchase Xanax from your local pharmacy, most Medicare insurance plans will cover the generic version of it. The average retail price is $400 but you can purchase a bottle of 60 count of 0.5 mg alprazolam generic tablets for around $9-$21.

Try the SingleCare prescription discount card

Common side effects of Lexapro vs. Xanax

Lexapro and Xanax can both affect the central nervous system (CNS). Both medications can cause common CNS side effects such as headache, dizziness, and insomnia. However, drowsiness or sleepiness is a more common side effect of taking Xanax.

Lexapro and Xanax can also cause other side effects such as dry mouth, nausea, vomiting, and constipation. Changes in weight such as weight loss or weight gain are also possible side effects with either drug. Lexapro is more likely to cause gastrointestinal side effects such as indigestion and gas (flatulence).

More serious adverse effects of Lexapro can include serotonin syndrome, a serious medical condition that requires immediate attention. Other adverse effects of Xanax can include memory problems or cognitive dysfunctions when used long term.

This may not be a complete list. Consult your doctor or pharmacist for other side effects.
Source: DailyMed (Lexapro), DailyMed (Xanax)

Drug interactions of Lexapro vs. Xanax

Lexapro and Xanax can interact with some of the same medications such as monoamine oxidase inhibitors (MAOIs), opioids, anticonvulsants, triptans, and serotonergic drugs. Taking these drugs together may affect the level of drug in the body which can increase the risk of adverse effects.

SSRIs like Lexapro can also interact with NSAIDs and other blood thinners like warfarin. Taking these medications together may cause an increased risk of bleeding.

Xanax can also interact with birth control medications. Oral contraceptives may increase the side effects of benzodiazepines.

Because Lexapro and Xanax are processed by certain liver enzymes, they can interact with other drugs that affect these enzymes. Lexapro and Xanax can interact with CYP3A4 enzyme inhibitors and inducers. Consult a doctor or pharmacist to determine which drugs may interact with Lexapro or Xanax.

This may not be a complete list of all possible drug interactions. Consult a doctor with all medications you may be taking.

Warnings of Lexapro vs. Xanax

Taking Lexapro can increase the risk of suicidal thoughts and behavior, especially in children and young adults. Adolescents taking Lexapro for depression may have an increased risk of suicidal ideation. Lexapro should not be used in children younger than 12 years old.

Xanax should not be used with opioids due to the increased risk of respiratory depression, coma, and even death in severe cases. These drugs should only be used together in limited doses and with close monitoring by a healthcare professional.

Treatment with Lexapro or Xanax should not be abruptly stopped. Both medications carry a risk of withdrawal symptoms if they are discontinued. Withdrawal symptoms can include irritability, nausea, vomiting, and headache. Stopping the use of Xanax may also lead to an increased risk of seizures. Instead, these medications should be tapered off slowly with the medical advice of a doctor.

Frequently asked questions about Lexapro vs. Xanax

What is Lexapro?

Lexapro is an SSRI medication that is prescribed for anxiety and depression. Lexapro is available as a generic drug. It may take 1 to 2 weeks to experience the maximum benefits of Lexapro.

What is Xanax?

Xanax is a benzodiazepine that is prescribed for anxiety and panic disorders. It is available as a generic drug, alprazolam. Xanax works quickly with effects experienced within 1 to 2 hours after taking it.

Are Lexapro vs. Xanax the same?

No. Lexapro and Xanax are not the same. Lexapro is an SSRI drug that is taken once daily for depression and anxiety. Xanax is a benzodiazepine that can be taken up to 3 or 4 times per day for anxiety and panic disorders.

Is Lexapro vs. Xanax better?

Xanax is more effective for short-term relief of anxiety. Lexapro is often prescribed for depression and can take a few weeks to fully work. Sometimes Lexapro and Xanax are taken together for anxiety with depression.

Can I use Lexapro vs. Xanax while pregnant?

It is not recommended to take Lexapro while pregnant. Taking Lexapro during the third trimester may cause persistent pulmonary hypertension in the newborn (PPHN). Xanax is not recommended while pregnant.

Can I use Lexapro vs. Xanax with alcohol?

No. Consuming alcohol while on Lexapro or Xanax can increase the risk of CNS side effects such as drowsiness, dizziness, and headache. It is not recommended to drink alcohol while using SSRIs or benzodiazepines.

Does Lexapro reduce anxiety?

Yes. Lexapro can help treat anxiety. It is often prescribed for people with anxiety and depression.

How long does it take for Lexapro to work for anxiety?

As an SSRI, Lexapro may take a few weeks to reach maximum effectiveness for anxiety. Lexapro helps balance neurotransmitters over time to help reduce symptoms of anxiety.

Does Lexapro make you sleepy?

Lexapro can cause fatigue and somnolence in some people. These side effects are most common when first starting the drug. However, most side effects of Lexapro resolve on their own over time.

Can Lexapro help you get off Xanax?

Lexapro may help with anxiety while discontinuing Xanax. Consult a doctor for your best options when getting off Xanax.

Lexapro (Escitalopram) Signs, Symptoms, & Side Effects

Similar to many other antidepressant medications, Lexapro warns of an increased risk of suicide, with a higher risk for adults and teenagers who are younger than 24 years old. Suicidal thoughts may increase when first taking the medication or when there is a change in dosage.

There has also been research that links prenatal exposure to SSRIs with autism or developmental delays, with higher risks among newborns whose mothers were on SSRI medication early in their pregnancy.

Escitalopram has also been associated with weight gain due to large fluid retention and an increased appetite. It is recommended to maintain physical activity to manage weight gain while using Lexapro.

Certain side effects may occur, including:

• Nausea
• Diarrhea
• Constipation
• Changes in sex drive or function
• Drowsiness
• Unusual sweating
• Dizziness
• Heartburn
• Stomach pain
• Extreme tiredness
• Dry mouth
• Greater appetite
• Flu-like symptoms, including sneezing and runny nose

Serious side effects can also occur, such as decreased interest in sex, easy bruising or bleeding, fever, confusion, fast or irregular heartbeat, severe muscle stiffness, extreme restlessness, panic attacks, aggressive behavior, impulsiveness, mania or extreme increase in talking, or worsening depression and anxiety. If you have any of these side effects, seek medical attention immediately.

Due to the increased level of serotonin in the brain, escitalopram and Lexapro can sometimes, although rarely, cause serotonin syndrome/toxicity. This risk increases when taking other medications that also increase serotonin. If symptoms such as hallucinations, loss of coordination, severe dizziness, nausea or diarrhea, twitching muscles, and unusual restlessness occur, seek medical help right away.

It is important to monitor progress while taking escitalopram or Lexapro. At the first sign of adverse side effects, schedule a doctor’s visit to reassess the dosage or to determine if the medication should be stopped altogether.

Active substance ESCITALOPRAM | Compendium – reference book of medicinal products

NLM: 5-isobenzofurancarbonitrile, 1- (3- (dimethylamino) propyl) -1- (4-fluorophenyl) -1,3-dihydro-, (1 S ) -.

M _m = 324.34 Yes.

Release form: p / o tablets, drops for oral administration.

Medicinal preparations containing the active substance ESCITALOPRAM

film-coated tablets 10 mg, blister in a pack, No. 30

Kiev Vitamin Plant

film-coated tablets 20 mg blister in a pack, No. 30

Kiev Vitamin Plant

film-coated tablets 10 mg blister, No. 30

Health for the people

film-coated tablets 20 mg blister, No. 30

Health for the people

film-coated tablets 10 mg blister, No. 30

Medochemie Ltd

film-coated tablets 20 mg blister, No. 30

Medochemie Ltd

film-coated tablets 10 mg, No. 28

Lundbeck Export A / S

film-coated tablets 10 mg, No. 30

Teva Ukraine

film-coated tablets 20 mg, No. 30

Teva Ukraine

coated tablets 10 mg, blister, No. 28

Nobel

coated tablets 20 mg blister, No. 28

Nobel

film-coated tablets 10 mg blister, No. 28

Teva Ukraine

film-coated tablets 20 mg blister, No. 28

Teva Ukraine

film-coated tablets 10 mg blister, No. 30, 60

Acino

film-coated tablets 20 mg blister, No. 30, 60

Acino

film-coated tablets 10 mg blister, No. 30, 60

Acino

film-coated tablets 20 mg blister, No. 30, 60

Acino

escitalopram – antidepressant, selective inhibitor of neuronal serotonin reuptake.It is the S-stereoisomer of racemic citalopram. The mechanism of action is associated with the potentiation of serotonergic activity in the central nervous system, which is due to inhibition of the neuronal reuptake of serotonin (5-HT). The effect on the reverse neuronal uptake of norepinephrine and dopamine is minimal. Escitalopram is at least 100 times more active than the R-enantiomer in inhibiting serotonin reuptake.

Escitalopram has no or very low affinity for 5-HT1 and other receptors, including α- and β-adrenergic, dopaminergic (D ₁ ), histamine (H ₁ ), muscarinic (M ₁ ) and benzodiazepine receptors.Escitalopram also does not bind or has a low degree of binding to various membrane ion channels, including Na ⁺ , K ⁺ , Cl ^– , and Ca ²⁺ channels.

The pharmacokinetics of escitalopram is linear and proportionally dependent on the dose in the range of 10–30 mg / day. After oral administration, C _{max in blood plasma is achieved within 5 hours. The absorption of escitalopram does not depend on the simultaneous intake of food. Bioavailability (for citalopram) is about 80%.The volume of distribution (for citalopram) is 12 l / kg of body weight. About 56% of escitalopram binds to plasma proteins. When taken 1 time per day, an equilibrium state is achieved on average after 1 week. Biotransformation of escitalopram is carried out mainly in the liver. The main metabolites of escitalopram, S-demethylcitalopram and S-didemethylcitalopram, do not have significant pharmacological activity. T1 / 2 ½ is 27–32 hours. Oral clearance is 600 ml / min, renal clearance is 7% of this amount.In the urine, about 8% is excreted in the form of escitalopram and 10% in the form of S-demethylcitalopram.}

major depressive disorder; generalized anxiety disorder.

at the beginning of treatment is prescribed at a dose of 10 mg 1 time per day. If necessary, the dose is increased to 20 mg / day for 1 week. Take 1 time per day (morning or evening), regardless of food. The dose for patients with hepatic insufficiency and elderly patients should not exceed 10 mg / day. No dose adjustment of escitalopram is required for patients with moderate renal impairment.

In major depressive disorder, maintenance therapy at a dose of 10–20 mg / day is carried out for several months (taking into account the clinical situation).

The duration of use for generalized anxiety disorder is usually up to 8 weeks.

Hypersensitivity to escitalopram or citalopram, concomitant use of MAO inhibitors.

most commonly reported nausea, delayed ejaculation, insomnia or drowsiness, increased fatigue, increased sweating.

escitalopram usually does not have a negative effect on psychomotor activity, however, until an individual response to therapy is determined, driving and working with potentially dangerous mechanisms should be avoided.

Prescribing during pregnancy is possible only if the expected therapeutic effect for the mother outweighs the potential risk to the fetus. Racemic citalopram is excreted in breast milk.

does not potentiate the effect of alcohol on the central nervous system, however, alcohol consumption during treatment with escitalopram is not recommended.

Simultaneous use with MAO inhibitors is contraindicated.

With simultaneous use with acetylsalicylic acid, other NSAIDs and other drugs with an antiplatelet effect, the risk of gastrointestinal bleeding increases.

With the simultaneous use of selective serotonin reuptake inhibitors with sumatriptan, isolated cases of weakness, hyperreflexia and discoordination have been described; when prescribing such a combination, the patient should be under medical supervision.

Combined use with ketoconazole can lead to a decrease in the concentration of the latter in the blood plasma.

describe cases of overdose with escitalopram at a dose of up to 600 mg; no symptoms of intoxication were noted. An overdose of racemic citalopram (at a dose of up to 2 g) was not fatal. Death is possible with a more significant overdose, mainly when combined with other psychotropic drugs or alcohol.

In case of an overdose of citalopram, dizziness, increased sweating, nausea, vomiting, tremors, drowsiness, sinus tachycardia, convulsions are most often noted.Less commonly – amnesia, confusion, coma, hyperventilation, cyanosis, rhabdomyolysis, ECG changes (including lengthening of the Q – T interval and ventricular arrhythmias).

Provide patency of the upper respiratory tract to maintain adequate ventilation and oxygenation, monitor blood pressure, ECG and external respiration. There is no specific antidote; treatment – supportive and symptomatic. Due to the large volume of distribution of escitalopram, forced diuresis, dialysis, hemoperfusion and exchange transfusion are ineffective.

Rapid Toxicology Screening Toolkit for HPLC-MS / MS Version 3

LC / MS / MS Rapid Toxicology Screening System Ver.3 Package of Guidelines for Rapid Toxicology Screening Ver. 3 includes a CD with method files, report files, spectra library, analysis conditions and sample preparation protocol. Excludes columns, guard columns, standards and mobile phases.A set of micro-volume QuEChERS is also purchased additionally.

Library for the determination of 235 compounds significant in toxicology

This package increases the efficiency of the HPLC-MS / MS method, giving the user the opportunity to start analysis without such time-consuming steps as selecting separation conditions and optimizing the parameters of the mass spectrometer. The rapid assay method with chromatographic separation times of less than 15 minutes allows the determination of 235 compounds, including narcotic compounds, psychoactive drugs and sedatives.The package contains optimized data logging conditions for the combined measurement mode used in screening analyzes (includes threshold values ​​of the signal intensity from the MRM to start recording the spectra of daughter ions).

Complete solution including semi-quantitative analysis

For each compound, the method contains calibration curve information based on internal standards, making it possible to quantify after analysis.Using sample preparation based on the QuEChERS method, it is possible to comprehensively extract compounds from biological samples. Qualitative analysis using the spectral library can be carried out at the stage of data processing. In other words, the package of guidelines provides a complete solution covering sample preparation, analysis and data processing.

Sample preparation using QuEChERS microvolume kit

>> More details

Sample Run Analysis Using LabSolutions Insight Library Screening Software

Using LabSolutions Insight Library Screening software, you can check:

• (1) Quantitative results
• (2) Library Search Results
• (3) Mass chromatogram
• (4) MS / MS Spectra
• (5) Structural formula

Warning

1. Requires LabSolutions LCMS Ver.5.97 or later.
2. This system is for research purposes only. Not for use in diagnostic procedures.
3. Depending on the condition and specificity of the equipment used, differences in quantitative results may occur. To obtain accurate quantitative results, it is necessary to construct a calibration curve using the appropriate standard samples. In addition, the convergence rating obtained from a library search shows spectral similarity and is the basis for identifying compounds, but complex information such as retention time and sample information must be used for more accurate identification.

LabSolutions LCMS is a trademark of Shimadzu Corporation

90,000 Depression: A Breakthrough In Understanding The Nature Of Ailment And Its Treatment?

• James Gallagher, Rachel Buchanan and Andrew Luck-Baker,
• BBC

25 August 2016

Photo by Hayley Mason

Caption,

Hayley Mason cannot cope with depression on her own

It is not often reported about a revolution in the understanding and treatment of depression, but this is what doctors call one of the most important discoveries in psychiatry over the past 20 years.

Its essence is that some of us are betrayed by our most important defender – the immune system, which changes our attitude.

This disease affects 350 million people around the world, including Hailey Mason, who lives in the English county of Cambridgeshire.

“My depression drives me to the point where I can’t get out of bed, I can’t leave the bedroom, I can’t go to the living room and talk to my spouse and his children,” Haley says. on all the time, I am annoyed by sounds and lights, I am pursued by suicidal thoughts, I am self-harm, I can’t leave the house, I don’t drive a car.So I sit within four walls all the time, because I cannot cope with the reality around me. “

Antidepressants and psychological assistance, such as cognitive-behavioral therapy, help many people with depression, but there are some who

So now scientists have decided to tackle this problem from a different angle: see if the immune system can cause depression?

“In my opinion, we need to think radically,” says Professor Ed Ballmore Head of the Department of Psychiatry at the University of Cambridge and head of a new direction in the study of depression.

Photo caption,

Professor Ed Ballmore of the University of Cambridge leads a new direction in the study of the nature of depression

Inflammation and mood

“Recent history shows us that if we want to make a breakthrough in treatment in some area that remains extremely important in the sense of causing disability and suffering, then we need to go a new way, “- says the professor.

Therefore, now doctors are studying whether a dysfunctional immune system causes inflammation in the body, which leads to a change in mood.

As Professor Ballmore points out, this applies in a way to each of us – just remember the last time we had the flu or cold.

“Depression and inflammation often go hand in hand. If you have the flu, the immune system reacts to it; you get inflamed, and very often people’s mood changes too. Their behavior changes, they may become less sociable, more sleepy. They may develop negative thoughts that are characteristic of depression, and all this is a consequence of the infection, “says Professor Ballmore.

This is a delicate approach, which at the same time contains a very significant shift in understanding the nature of this disease. It’s not that we feel sorry for ourselves when we’re sick, but that the chemicals that cause inflammation directly affect our mood.

Inflammation is part of our immune system’s response to danger. This is an incredibly complex process that prepares our body to fight against hostile forces.

If the inflammation is insignificant, then the infection can be fought off.If the inflammation is large, then it is harmful, and for some reason, a third of all people with depression have a consistently high level of inflammatory processes in the body. In particular, Hayley: “I have a constantly high level of markers of inflammatory diseases. In my opinion, the normal level is up to 0.7, and I have 40, and this is constantly found in my blood test.”

There is growing evidence that inflammation is not just something that is sometimes found in patients with depression, it is what causes depression; in other words, that the immune system changes how the brain works.

With What is arthritis here?

To learn more about this revolutionary understanding of the nature of depression, we went to the arthritis department at Royal Glasgow Hospital.

It would seem a rather unexpected place, but, as it turned out, it was in such therapeutic departments that doctors first noticed some strange pattern.

Photo author, SPL

Photo caption,

In people with rheumatoid arthritis, the immune system attacks the joints.

Rheumatoid arthritis occurs when the immune system attacks the joints.Doctors have noticed that when such patients are prescribed anti-inflammatory drugs to treat specific problem areas affected by arthritis, their mood also improves.

“When we prescribe these drugs, we see a fairly rapid improvement in the general condition [of the patients], and the mood rises quite significantly, which is even somewhat disproportionate to the degree of inflammation that has affected their joints and skin,” says Professor Ian McKinnes, consultant is a rheumatologist at the Royal Glasgow Hospital.

From this we can conclude that the mood of these patients not only improved from the fact that their joints began to hurt less, but because of some other, deeper processes.

“We scanned the brains of patients with rheumatoid arthritis, then gave them a very specific dose of immunotherapy, and then scanned them again. And what we start to notice when we give these anti-inflammatory drugs are very remarkable changes in the neurochemical structure of the brain,” explains Professor McKinness.“Neural pathways in the brain involved in depression have changed for the better in patients who were given immunotherapy.”

One possible explanation for this phenomenon is that inflammation-inducing chemicals enter the brain and disrupt the production of serotonin, a key neurotransmitter.

What to treat first

To further deepen our understanding of the topic, we visited a laboratory led by Professor of Biological Psychiatry Carmine Pariante at King’s College London.For 20 years now, he has been collecting data on the relationship between depression and inflammation in the body.

“Approximately 30-40% of patients suffering from depression have high levels of inflammation, and this is what, in our opinion, is the cause of their depression in these people. This is also confirmed by the fact that high levels of inflammation are present in those who do not suffers from depression, but is at risk. ” – explains Professor Pariante.

“As a result of our research, we realized that if you have some kind of inflammation today, then you have a higher risk of developing depression in the coming weeks or months, even if today you are okay in this regard,” says the doctor …

His research has shown not only that patients with depression are more likely to have inflammation, but also that people with extremely active immune systems respond less to antidepressants.

This is very important, as one third of depressed patients receive no benefit from medication.

Photo author, Jen Streeting

Caption,

Jennifer Striting has tried many different antidepressants over the years of treating depression. then this does not fit into the usual anamnesis of depressed patients.

Take, for example, future midwife Jennifer Streating from London, who believes her mental health problems began at age 14.

“My grandmother died then, and my mother had breast cancer, so if you ask my therapist, she explains everything with this grief and the fact that no one paid due attention to this then. I think it’s just too much everything fell on me, “says Jennifer.

But Professor Pariante believes that it is these difficult moments in life that alter our immune system, which can further increase the risk of developing depression.

“We believe that the immune system is a key mechanism that, as a result of early [psychological] trauma, can produce a long-term response in later years. We have data that show that adults who experienced early life years of tragedy, even if they do not have a history of depression, they still have an excited immune system, and therefore they are at risk, “he explains.

Now there may be hope that drugs to treat the immune system will have the desired effect on patients who, like Jennifer, have tried everything they can without success.

“I drank sertraline, I drank Prozac, then something else, then I started taking citalopram, then I was prescribed duloxetine, and also mirtazapine. At some point I took three different drugs at once,” says Jennifer.

She is now prescribed a combination of several drugs, which seems to have improved, but it took a very long time.

“This is all achieved by trial and error,” agrees Professor Pariante. “We cannot predict in advance how a patient will react to a particular drug.But we believe that by determining the level of inflammation from a blood test, we will be able to identify those patients who need more comprehensive, intensive treatment with antidepressants, maybe even a combination of antidepressants and anti-inflammatory drugs. “

Photo author, King’s College

Photo caption ,

Professor Carmine Pariante concludes that difficult moments in life change our immune system

In search of a new drug

Most of us have anti-inflammatory drugs like ibuprofen in our home medicine cabinet, but doctors advise against experimenting in this direction on our own. the clinical trials of the new treatment are not yet completed.

The Wellcome Trust, the world’s largest medical research charity, has joined forces with university scientists and the pharmaceutical industry to validate the new theory and quickly develop a new treatment for depression and a test to identify those who need help.

It is the University of Cambridge professor Ed Ballmore who is leading these efforts, but we did not meet with him at the university, but in the laboratory of his other employer, the pharmaceutical giant GlaxoSmithKline.

At the company’s immune-inflammatory laboratories, scientists are developing new molecules that they hope will be effective in treating inflammatory diseases.

Photo author, Science Photo Library

Photo caption,

Depression affects hundreds of millions of people around the world

This process will take more than 10 years, but, according to Professor Ballmore, the required drug may already exist.

“In immunopsychiatry, the good thing is that in other areas of medicine, there are already successfully acting immunological drugs.They may already be licensed or in advanced stages of clinical trials, so the time from the start of this project to the emergence of a drug that could change the lives of many patients could be much shorter, “says the professor.

As we can see, the search The available drugs have already borne fruit: those early data from arthritis sufferers have led to the anti-inflammatory drug sirukumab being tested as a treatment for depression.

Will it all come to the conclusion that immunotherapies will be able to transform the treatment of depression?

“I don’t think they’ll become a panacea. That is, it’s unlikely that every patient with depression symptoms will receive any anti-inflammatory,” says Ed Ballmore. the treatment of mental disorders, when one pill supposedly removes all problems, has already proven its ineffectiveness in the past.We need to look at each case separately, because not everyone with depression suffers from it for the same reason. ”

Blood tests can help determine which patient can benefit from immunotherapy. WALSH

Photo caption,

Professor Pariante believes that depression is a disorder of the whole body

“Pull yourself together”?

Depression is a disease that affects hundreds of millions of people, and if anti-inflammatory drugs can help which a percentage of them, albeit a small one, will already be significant numbers.

And if immunotherapy proves its worth in this matter, then the most important consequence will be that it will change our perception of this ailment: we are unlikely to think about depression sufferers that they “just need to pull themselves together.”

“I hate it when they say that, because if I could, I would,” says Jennifer. “Just like if a person has diabetes and his insulin level is high, and you say: “Oh, come on, stop using drugs.”

Haley echoes her: “If we could prove that depression is a physical problem [of the body], it would change a lot. will become a real disease, and people will be believed. ”

Professor Pariante concludes this thought as follows: “This is a breakthrough because for the first time we show that depression is not only a mental disorder, in fact it is not even a brain disorder, it is a disorder of the whole organism.”

This material was first aired in the program “Inflamed Consciousness” on the BBC Radio-4 channel

what is it, symptoms, how to get rid of a hypochondriac disorder, causes and treatment, can you fight it yourself

Daniil Davydov

medical journalist

Author’s profile

About 6% of Europeans complain of health problems, the origin of which cannot be explained by an illness associated with impaired body function.

For example, they complain to a doctor about unbearable chest pain, which has no explanation.

There are even more such people in hospitals: according to American data, 17% of patients hospitalized with some kind of disease also have physical symptoms that cannot be explained by the underlying disease.

In this article, we will refer to this condition as Hypochondriacal Disorder. But if necessary, we will refer to American textbooks and studies, where this is called either a disorder associated with somatic symptoms or an anxiety disorder.The criteria for these diagnoses overlap and are treated in a very similar manner. Let’s try to understand what hypochondriacal disorder is, where it comes from and how to treat it.

Burden of mental disorders in Europe – Journal of European Neuropsychopharmacology

See your doctor

Our articles are written with a passion for evidence-based medicine. We refer to reputable sources and go for comments from reputable doctors. But remember: the responsibility for your health lies with you and your doctor.We do not write prescriptions, we make recommendations. It is up to you to rely on our point of view or not.

Some of the sites we link to in the article are not accessible from Russian IP addresses. We hope you know what to do.

What is hypochondriacal disorder

People who suffer from hypochondriacal disorder do not invent symptoms or pretend to be sick. This is a mental illness that is treated by doctors: psychiatrists or psychotherapists. A person with such a diagnosis has the right to receive sick leave for the entire duration of treatment.But usually patients refuse, because they are afraid of the wrong reaction of colleagues and superiors.

Hypochondriacal disorder is a diagnosis from the International Classification of Diseases of the 10th revision, or ICD-10. All Russian doctors are required to use this classifier. ICD-10 classifies hypochondriacal disorder as a somatoform disorder.

ICD-10 – WHO classifier of the 10th revision

Mental and behavioral disorders according to ICD-10, 1998 – Bulletin of the Ministry of Health PDF, 2.1 MB

In somatoform disorders, the patient complains of symptoms resembling somatic, that is, bodily illness.But neither analyzes nor examinations either reveal organic changes that could be attributed to a disease known in medicine, or physical disorders do not explain the origin of these symptoms.

There are seven somatoform disorders in total. They differ from each other mainly in the duration, variety and persistence of physical symptoms.

Hypochondriacal disorder is a disease in which the patient is very afraid of getting sick or thinks that he is already sick with one or more dangerous diseases. Sometimes at a doctor’s appointment, such people can name the alleged illness – but, having received the results of another study, they may decide that they have something else. A person may not have any medically unexplained complaints, but there is always a very strong anxiety and fear of a latent disease.

There is no diagnosis of “hypochondriacal disorder” in this reference book, because American psychiatrists and psychotherapists decided that all somatoform disorders are very similar.They grouped them into one category – a disorder associated with somatic symptoms. The criteria by which patients are diagnosed are very similar to those from ICD-10. But there is one exception.

According to American criteria, physical symptoms are not required to be medically unexplained. It is enough that they disturb this patient much more than other people with the same disease.

After changing the diagnostic criteria, all American patients diagnosed with hypochondriacal disorder were divided into two groups.

Approximately 75% of patients received a new diagnosis for a disorder associated with somatic symptoms. It was received by people who complained of one or more difficult-to-explain bodily symptoms.

People with a somatic symptom disorder have unexplained symptoms from childhood, such as persistent, severe muscle pain. At the same time, examinations do not reveal problems, and the results of laboratory tests are within normal limits. However, these patients usually try to get treatment.Sometimes they even go to surgery, which does not bring relief, but can cause complications.

Approximately 25% of patients were classified as a health-related anxiety disorder. This diagnosis was received by people who were very afraid of getting sick or thought that they were already sick, but they either did not have unexplained bodily symptoms, or they often changed.

These patients are generally fine, but worried that they may be seriously ill, such as cancer.This can last from several months to several years. If during the examinations no dangerous diseases are found, patients can calm down for a while. But then the fear of illness returns: people begin to suspect that they have not been thoroughly examined. Then they go to the doctor again, and everything starts all over again.

According to the ICD, all conditions associated with complaints of unexplained symptoms are called hypochondriacal disorder. The DSM-V includes two diagnoses in this category: Somatic Symptom Disorder and Health Anxiety Disorder

Why Hypochondriacal Disorder Occurs

Nobody fully understands this.At the same time, American experts suggest that the reasons for the development of a disorder associated with somatic symptoms are different from the reasons for an anxiety disorder associated with health concerns.

Researchers suggest that the disorder associated with physical symptoms has genetic causes, which are the same as other similar disorders, such as an eating disorder. But judging by the data that we have, the main role in the development of the disease is still played not by heredity, but by other factors.

Somatic Symptom Disorder – Medscape

Epidemiology of Somatic Symptom Disorder – Uptodate

Most often, the disorder associated with somatic symptoms affects people without higher education and with a low level of income, those who either themselves were ill for a long time in childhood, or their parents were ill. The risk of developing the disorder is higher in women, in those who have experienced violence in the past, in people who tend to pay increased attention to their health, and in those who cannot express their emotions in words.

One can try to explain the influence of these factors.

Perhaps, looking at sick parents, children learn to be vigilant about their own well-being. And for people who have been deprived of parental care since childhood, or for those who were cared for only when they were sick, going to the doctor can be the only chance to get the attention they need so much.

Physical abuse. Abused adults and children are three times more likely to suffer from the disorder than non-abused adults.Perhaps a terrible experience prompts you to pay more attention to your health.

Female There are 10 women for every man with a somatic symptom disorder. Perhaps this is because women are more attentive to their health. But the large number of victims of violence among the victims of the disorder suggests that this is not only the case.

According to the WHO, every third woman experiences violence during her lifetime.This means that women are about two to three times more likely than men to face a factor that increases the risk of developing the disease, that is, violence.

Heightened perception of physical sensations. This problem may be encountered by people whose pain sensitivity has increased due to the experience of violence. When a person is susceptible to pain, even normal bodily sensations can seem overly intense. And if a particularly sensitive person is also affected by unfavorable factors – for example, constant stress associated with poverty, unpleasant sensations can intensify.As a result, the disorder may develop.

Difficulty expressing emotions. The situation when a person does not have enough words to express emotions is called alexithymia. Some experts believe that due to the stress associated with alexithymia, some people may also develop physical symptoms.

In turn, health anxiety disorder resembles other anxiety disorders and depression because they are caused by similar brain disturbances.

Based on the available data, there is no particular genetic predisposition for health anxiety, and men and women suffer with approximately the same frequency. The risk of getting sick, as with somatic symptom disorder, is higher in people with no college education, those with low income, and those with a lot of sickness or abuse during childhood.

What is the danger of hypochondriacal disorder

Although there is no physical problem with hypochondriacal disorder, it causes many problems for patients.

Poor health and problems with family and friends. Fear for one’s health and unpleasant symptoms poison a person’s life. Because of the disorder, some people do not get enough sleep, they begin to have problems at work and with study. Due to the fact that all the thoughts of the patient are absorbed by the disease, he may have problems in relations with others – for example, many people break up their marriage. This can increase the anxiety, so that it becomes unbearable – even to the point of thinking about suicide.

Unreasonable spending on unnecessary research. Medical care is expensive, and procedures, examinations and treatments take time. If a person suffers from hypochondriacal disorder for many years, he risks spending a fortune and several years of his life on treatment.

Iatrogenic diseases. This is the name given to diseases that are triggered by medication, or that have arisen as a result of medical procedures. If a person with a hypochondriacal disorder underwent unnecessary abdominal surgery, due to which adhesions appeared on his internal organs, causing pain during movement, it will be an iatrogenic disease.

What happens if hypochondriacal disorder is not treated

Approximately half of patients recover within a year even without treatment. However, in people who complain of several symptoms at once, and in those who have added anxiety or depression to their hypochondriacal disorder, the problems can last for years. And for those who seem to have recovered, the disease may return over time.

Is it possible to drive a car with hypochondriacal disorder

Sergey Divisenko

psychotherapist

Somatoform disorders, including hypochondria, are included in the list of medical contraindications for driving.After the person is cured, this limitation can be removed. To do this, you will have to go through a medical commission.

If a person is already driving a car, no one will take away his license. But with the next change of rights, when a person comes to a neuropsychiatric dispensary for a certificate, due to the fact that he was registered there, difficulties may arise. To avoid this, it makes sense to seek treatment not in a state neuropsychiatric dispensary, but in a private clinic. Doctors in private clinics do not send the data of patients with whom they work to the PND, so there will be no problems when changing rights.

How is hypochondriacal disorder diagnosed

As a rule, patients with hypochondriacal disorder see a doctor who treats ordinary, rather than mental illnesses – for example, a general practitioner or cardiologist. After examining a patient, experienced doctors usually quickly realize that they are dealing with a patient with a hypochondriacal disorder.

To suspect a hypochondriacal disorder, it is important that the patient has two signs of the disorder at the same time:

1. The patient believes that he has a serious illness for at least six months.To support this idea, he describes the symptoms of his diseases, but research does not reveal any physical causes that could provoke them.
2. The patient does not believe doctors who try to convince him that he does not have a physical illness, even after receiving the test results and medical examinations.

Mental and behavioral disorders according to ICD-10, 1998 – Bulletin of the Ministry of Health PDF, 2.1 MB

To confirm your guess, the doctor may suggest taking a psychological test that will help determine the level of depression or anxiety.Most often it is the Hospital Anxiety and Depression Scale – the HADS test. If the patient scores high on the scale of anxiety or depression and still meets the criteria for hypochondriacal disorder, the doctor’s doubts disappear. The cost of an appointment with a therapist in Moscow is an average of 2500 R.

2500 R

on average it costs an appointment with a therapist in Moscow

However, a non-psychiatric doctor may not diagnose a patient with a psychiatric diagnosis. This can only be done by a psychiatrist or psychotherapist.However, people with hypochondriacal disorder usually do not want to contact them, and if they are offered to do this, they can simply go to another specialist. So there might be a problem at this point.

You can pass the HADS test on your own. To see the results, you can go to the website for medical students Studfile

How patients with hypochondriacal disorder are referred to psychiatrists or psychotherapists

Sergey Divisenko

Psychotherapist

The doctor can use a workaround.Some experts say that they have not yet found problems in their profile, but during the examination they found that the patient suffers from insomnia, anxiety or depression. Therefore, while the examination is underway, it makes sense for the patient to visit a psychotherapist who will help with these problems. When asked this way, patients often agree.

The same tactic can be used if you suspect that your loved one has the disease. Do not deny that the person has, for example, cancer.You still won’t convince him, but you risk ruining the relationship. Try asking him to see a therapist – not to cure cancer, but to deal with anxiety about it.

When a person comes to an appointment with a psychiatrist or a psychotherapist, tests are often no longer needed to confirm the diagnosis – an ordinary conversation is enough. By asking the patient a few questions, the doctor understands whether he can rule out mental health conditions that are not related to a hypochondriacal disorder, such as delusional disorder, obsessive-compulsive disorder, or psychosis.This is important because such diseases are treated differently.

If the diagnosis is confirmed, the doctor is obliged to inform the patient about it. Typically, doctors delicately explain that medication that cures anxiety and insomnia also relieves disturbing bodily symptoms. Pain is one of the most common physical symptoms in hypochondriacal disorder, and antidepressants are the accepted treatment for chronic pain disorders.

If the patient agrees to the therapy, the doctor will suggest the first treatment option at the same appointment.But the first time, the optimal therapy usually does not work out, because different people respond to treatment in different ways. Therefore, it is desirable to have a communication channel with the attending physician. To discuss the efficacy and tolerability of medications, communication can be made by phone, text message or email.

Whether the treatment is working is clear about two weeks after starting. If the patient does not get better, therapy needs to be adjusted. This can be done either by phoning the doctor or at a follow-up appointment.The price for one appointment with a psychotherapist is on average 4615 R. The cost of one appointment with a psychiatrist on average costs 4538 R.

How is hypochondriacal disorder treated?

Psychotherapy. In hypochondriacal disorder, the patient suffers not only from physical symptoms but also from an uncontrollable fear of the illness. Evidence suggests that cognitive behavioral therapy (CBT) therapy can help overcome anxiety. The goal of this approach is to teach the patient to control the emotions associated with the illness.When a person learns to deal with anxiety, they usually feel better.

If a person has few symptoms and has been ill for a little more than six months, then in order to learn how to control his condition, it usually takes 10-15 sessions of cognitive-behavioral therapy. But if the patient has been suffering from the disorder for many years or has many symptoms, a long cycle of psychotherapy may be required – several months or even years.

Classes in cognitive-behavioral therapy are conducted by psychiatrists, psychotherapists, and clinical psychologists.The price for one appointment with a psychologist in Moscow is on average 4304 R.

Pharmacotherapy with drugs. Two types of drugs are most commonly used to treat hypochondriacal disorder: antidepressants and tranquilizers. Modern antidepressants belong to the SSRI groups, that is, selective serotonin reuptake inhibitors, and SNRIs, that is, serotonin and norepinephrine reuptake inhibitors. Two antidepressants from the SSRI group are considered to be among the most effective and safe: sertraline and escitalopram.

Long-term monitoring of the effectiveness of treatment of hypochondria with SSRIs – Journal of Clinical Psychopharmacology

A tranquilizer is needed to relieve anxiety in the first two to three weeks, before the antidepressant begins to work. A good tranquilizer – stresam, trade name “Etifoxin”. It is usually prescribed one capsule twice a day for the first two to four weeks.

With the right therapy, if you take the pills every day, the effect becomes noticeable after about two weeks.On average, patients feel better if they take antidepressants for two and a half months.

A month of treatment for hypochondriacal disorder can cost from 60,000 R 90 150

Psychotherapy, 10 sessions

From 50,000 R

Appointment of a psychiatrist or psychotherapist

Average from 5000 R

Appointment of a therapist

Average 2500 R

Tranquilizer

From 600 R

Antidepressant

From 200 R

Is it possible to save on antidepressants by buying generics

Sergey Divisenko

Psychotherapist

An original drug with sertraline that can be prescribed for the treatment of hypochondriacal disorder is called Zoloft.When generics entered the market, Pfizer cut the price of the originator drug. If the doctor has prescribed this drug, there is no point in saving: the original will cost less than the generic one.

The original drug with escitalopram, prescribed for the same diagnosis, is called Cipralex. Even when generics appeared on the market, the manufacturer did not reduce the price. If your doctor has prescribed escitalopram, it might make sense to consider buying a generic: the original drug still costs three to four times more, and they work about the same.

It should be borne in mind that not all people are helped by the minimum dose of antidepressants. In about half of cases, trough antidepressant doses do not work. For treatment to help, the minimum dose of “Zoloft” sometimes has to be increased four times, and the dose of escitalopram – two times. Accordingly, drug costs will rise.

Remember

1. Hypochondriacal disorder is a mental illness treated by psychiatrists or psychotherapists. A person with this disorder is eligible for sick leave.
2. Hypochondriacal disorder has a different name in the United States. But we can still use American data: although the names are different, the underlying disorder is the same, so the treatment is the same.
3. No one fully understands why people get hypochondriacal disorder. It is believed that the main causes of the disorder are the difficult living conditions in childhood, the experience of violence, increased sensitivity to pain and, in part, heredity.
4. If left untreated, hypochondriacal disorder resolves on its own in about half of patients.But other people may suffer from the disease for several years.
5. The disease is expensive, destroys the patient’s health and close relationships, and unnecessary examinations and unnecessary treatment of non-existent somatic pathology can lead to iatrogenic diseases.
6. Typically, the patient’s healthcare professional is the first person to know about the disorder, usually a medical specialty. But only a psychiatrist or psychotherapist can diagnose and prescribe treatment.
7. There are two methods of treatment: psychotherapy and antidepressants.If the therapy is selected correctly, 50-80% of patients recover.

90 200 90 000 Do antidepressants help smokers trying to quit smoking

Relevance and issues addressed in the survey

Several medications used to treat depression (antidepressants) have been investigated to see if they can help people trying to quit smoking. Two antidepressants – bupropion (Zyban) and nortriptyline – are sometimes prescribed to help you quit smoking.In this review, we set out to investigate whether the use of antidepressants increases the likelihood of successful smoking cessation for six months or more, and to determine the safety of using these drugs to aid smoking cessation.

Characteristics of research

Evidence is current to July 2013. This update includes 24 new studies, for a total of 90 studies. The studies involved both smokers and people who recently quit smoking.65 studies have been conducted with bupropion, which is approved for use as a smoking cessation drug under the trade name Zyban. Ten studies were conducted with nortriptyline, a tricyclic antidepressant drug not licensed for smoking cessation. We included only those studies that reported a long-term outcome (regardless of whether the study participants quit smoking within six months of starting the study or not).

Key results and quality of evidence

Trials using bupropion (Zyban) for smoking cessation have shown high-quality evidence that the drug increases the likelihood of a successful quit attempt for at least six months (44 trials, over 13,000 participants). Side effects of bupropion include insomnia, dry mouth, nausea, and rarely (1: 1000) seizures and possibly various psychiatric problems, however, the latter are not clear.Moderate-quality evidence, limited by the relatively small number of included studies and participants, indicates that use of the antidepressant nortriptyline also increased smoking cessation rates (six trials, 975 participants). Side effects of using this medication include dry mouth, constipation, nausea and sedation, and this medication can be dangerous if overdosed. Antidepressants such as serotonin reuptake inhibitors (such as fluoxetine), MAO inhibitors (such as selegiline) and the antidepressant venlafaxine have not been shown to help people quit smoking, as has herbal medicine with St. John’s wort or S-adenosyl-L-methionine, a dietary supplement. which is believed to have antidepressant properties.

Discussion

The mechanism of action of bupropion and nortriptyline is not entirely clear. Both drugs help to quit smoking, regardless of whether the patients had previous depression or depressive symptoms while quitting smoking. The likelihood of successful smoking cessation with bupropion or nortriptyline was similar to that of nicotine replacement therapy, but lower than with varenicline.

Problems of general anesthesia while taking psychopharmacotherapy (Part I)

6

Nuances of anesthetic benefits

.Narcotic analgesics such as meperi

din, fentanyl, tramadol, pentazocine can have serious

interactions with SSRIs, as a result of which

can develop the so-called “serotonin syndrome” [Hi-

nes KEL, Marschall , 2010; Choudhury M et al., 2011]. Seroto-

Nine syndrome is a potentially life-threatening condition

. It arises as a result of a sharp increase in the

increase in the serotonin content in the synapses of the brain and

of the spinal cord, leading to hyperstimulation of serotonin receptors

, and the greatest importance in the development of this syndrome is hyperstimulation of 5-HT2A / C

and 5-HT3 serotonin receptor subtypes [Attri JP et al.,

2012]. Clinical signs of this syndrome: disorientation

tation, psychomotor agitation, instability of the autonomic nervous system

(hyperthermia, tachycardia, arterial hypo- and hypertension, diarrhea), acute renal

insufficiency, arrhythmias and death. Therefore, while taking SSRIs, it is not recommended to use meperidine, tramadol, pentazocine and dextromethor-

fan as analgesics during anesthesia;

logical aid.Fentanyl or its derivatives may be used with caution. Preferred from this group is the use of morphine

[Attri JP et

al., 2012]. It is believed that patients taking SSRIs,

, should warn the physician before possible surgery

, since these antidepressants can

increase the risk of bleeding [Huyse FJ et al., 2007]. There is

data that long-term use of antidepressants from the

SSRI group (for example, fluoxetine) can prolong

recovery of consciousness after anesthesia even after

2-4 days since the last dose of the drug

[Ding Z, White PF, 2002].There are isolated reports of

postoperative delusions for two days, psycho-

excitement against the background of uncanceled paroxetics

on [Stanford BJ, Stanford SC, 1999]. It is believed that citalo

pram and escitalopram, and possibly other SSRIs, can

lead to postoperative cardiac arrhythmias.

Described, in particular, a case of atrioventricular tachy-

cardia against the background of anesthesia in a 62-year-old woman with diabetes mellitus

type 2 diabetes, but without previous cardiac pathology

ial pathology, who took paroxetine 20 mg / day on

for anxiety disorder.In this case, heart rhythm disorder

arose at the end of anesthesia and

spontaneously changed to sinus rhythm 10 hours later

after surgery [Kopp R et al., 2001].

Monoamine oxidase inhibitors (MAOIs)

This group of blood pressure is used to treat severe or

resistant depressions, as well as atypical depressions

[Bykov YuV et al., 2013]. In addition, MAOIs are also sometimes prescribed

for depression, combined with panic

attacks and severe anxiety, with social phobia

[E.Morgan, 2000]. IMAO are subdivided into selective and non-selective. Selective MAOIs inhibit

mainly any one of the types of monoamino-

sydases (MAO-A or MAO-B), non-selective – both types. Non-

reversible MAOIs (tranylcypromine, selegiline, niala-

mid, isocarboxazid, phenelzine) and reversible MAOIs (mok-

lobemide, pirlindol) inhibit the destruction of monoamines-

nov – dopamine and other seroradonaline, noradonaline in

including the so-called “trace amines”, such as

phenylethylamine (“endogenous amphetamine”), octopamine,

tyramine, due to its ability to inhibit the activity of

MAO.Their ability to increase the content in the central nervous system not only of

only norepinephrine and serotonin, but also of dopamine and

“trace amines” is associated with both their high blood pressure activity and their effectiveness in severe, resistant

or atypically occurring depressions, so and their strong

stimulating properties. However, the ability of irreversible

MAOIs to inhibit the metabolism of tyramine, supplied

with food, leads to the need to adhere to a strict

“tyramine diet”.Otherwise, even a small amount of tyramine ingested with food

can cause severe hypertensive crisis, acute

renal failure, intestinal necrosis against the background of

spasm of visceral vessels, or cardiovascular

catastrophe, such stroke, heart attack. It is this

that limits their clinical use.

Brief pharmacokinetics and pharmacodynamics.

Despite the fact that the preparations of the MAOI group

leave the body quite quickly, when using

irreversible MAOIs, the clinically significant blockade of MAO

persists from 1 to 4 weeks after the cancellation of the “hydrazine”

nialamide or phenelzine), and from 2 to

14 days after discontinuation of tranylcypromine until

a sufficient amount of the new enzyme is synthesized

[Huyse FJ et al., 2007]. Moclobemide has a T1 / 2 of 1 to 3 hours,

pirlindole –4–6 hours, and since the blockade of

MAO they cause is completely reversible and selective with respect to the

MAO-A subtype, their use is safer [By-

cov SE et al., 2013]. All MAOIs are excreted from the body

by hepatic metabolism [Huyse FJ et al., 2006; Mor-

gan GE, 2008; Hines RL, Marschall KE, 2010]. It is important to know that

hydrazine MAOIs, in addition to their ability to block MAO

, also block many other enzymes

of the mixed liver P450 oxidase system, which can lead to an undesirable increase in the concentration of

drugs (for example , benzodiazepines, barbiturates, chi

nidine, procainamide) in the blood and to dangerous drug interactions

[Bykov YV et al., 2013]. Non-

hydrazine MAOIs, both reversible (moclobemide, pyr-

lindole) and irreversible (tranylcypromine, selegi

lin) have a lower potential for drug-drug interactions

[Bykov YuV et al., 2013].

Main side effects. The most important

side effect is severe hypertension, psi –

homotor agitation and vasoconstriction when consuming food products containing

personal monoamines, primarily tyramine [Bykov Yu.B.

et al., 2013]. This leads to the emergence of the so-called “cheese” or tyramine syndrome, which is

, which is the development of a hypertensive crisis with the

consumption of certain food products (cheese,

cream, coffee, beer, etc.). In the limit, tyramine syn-

nucleus can lead to acute cardiovascular

catastrophe (heart attack, stroke), acute cardiac or

renal failure, pulmonary edema or necrosis of the cervical

.However, the anesthesiologist may be faced with

other side effects of MAOIs, for example, with their

tendency to cause orthostatic hypotension

or, on the contrary, arterial hypertension (even with

strict adherence to the tyramine diet), insomnia,

agitation, other.

Nuances of withdrawal before anesthetic treatment

. On the one hand, it is believed that reversible and selective MAOIs (pyrazidol, moclobemide) are very safe from the point of view of anesthesia [Bykov Yu.V. et al.,

2013]. On the other hand, it is known that abrupt withdrawal of

from the intake of irreversible MAOIs can lead to severe

withdrawal syndrome of MAOIs with manifestations of depression, suicidal activity, hallucinations and delusional

disorders [Huyse FJ et al., 2007; Dilsaver SC, 1988;

1994]. Therefore, the issue of canceling MAOI before the planned

surgical intervention today remains the cause of discussions.The rule according to which

it is recommended to stop taking MAOIs 2 weeks before the operation of the radio

sounds rather contradictory [E. Morgan, 2000].

# Drugsonashe What is the difference between domestic and imported drugs: Business climate: Business: Lenta.ru

Russian patients do not trust domestic drugs. It is generally accepted that our medicines “do not work”, they are of poor quality, and in general, “imported” is better. “Lenta.ru” asked experts to tell where the most common misconceptions about Russian medicines come from and how much they correspond to reality.

The top 20 best-selling drug brands in Russia in 2015, compiled by DSM Group, include only six Russian brands. At the same time, of the remaining 14 drugs, 12 have domestic analogues, and their cost is several times different from the originals. However, for a number of reasons, consumers choose exactly what is more expensive. It’s not just aggressive advertising, in which brands are actively investing, experts at pharmaceutical companies say. Russians have developed certain ideas about domestic and imported drugs.

“Imported is simply better”

This statement is one of the most consistent. As a rule, no evidence is given: better – that’s all. Pharmaceutical companies admit that there are some grounds for such a statement, or rather, there were.

Firstly, imported drugs usually mean drugs produced in the European Union or the United States – Chinese or Indian drugs in the minds of the mass consumer do not belong to “good imported” drugs, said one of the interlocutors of Lenta.RU”. And where this idea came from is generally understandable.

The Soviet Union produced substances (starting material) and inexpensive bulk drugs, but by and large it did not have its own pharmaceutical industry, Roman Ivanov, vice president for R&D and international business development at biotechnology company BIOCAD, told Lente.ru. In Soviet times, – most of the pharmaceuticals were supplied from the member countries of the Commonwealth of Mutual Economic Assistance – Hungary, Poland, the states of the former Yugoslavia.When the USSR was gone, the pharmaceutical market was empty – the domestic pharmaceutical industry turned out to be uncompetitive. There were many reasons: a technological backwardness, an outdated assortment and, in general, the state’s orientation towards the development of the raw materials sector, while the light, textile and food industries received attention on a leftover basis. The market was filled with foreigners, primarily pharmaceutical companies from the USA and European countries. “The availability of medicines has dropped dramatically. It was necessary to explain why foreign drugs are so expensive.In my opinion, then the myth was born that real, high-quality medicines can be created only in the EU countries and the United States, and by definition they cannot be cheap, ”Ivanov said.

Reality helped maintain the negative regarding domestic drugs – there was virtually no industry regulation, outright swindlers appeared on the market, says Ivanov. As a result, both doctors and patients could not be sure that the drugs produced in Russia correspond to their foreign counterparts in quality, effectiveness and safety.Partially, the assertion “imported is better” could have had a basis, the expert states, although at that time there were enough foreign drugs on the market, the quality of which was in serious doubt.

Now the situation is radically different, the expert assures. Since the beginning of the 2000s, the state has tightened regulatory standards. In 2010, the Law “On Circulation of Medicines” was adopted, which seriously changed the rules for access of medicines to the Russian market. Mandatory clinical trials were introduced for generic drugs – that is, now a generic (copy of the original drug, the patent protection of which has expired – approx.”Lenta.ru” ) could appear in Russia only after the manufacturer proves its effectiveness and safety. Then other documents appeared that regulate the entry of drugs on the market, and new legislative acts and rules have basically already been harmonized with similar norms in force in the EU countries, says Roman Ivanov.

Photo: Viktor Korotaev / Kommersant

The last important innovation to date is the compliance of production facilities located in Russia with the GMP (Good Manufacturing Practice) standard.“If production is organized in accordance with this standard, the quality of medicines is guaranteed,” emphasizes the top manager. Now the Ministry of Industry and Trade conducts licensing and checks all Russian pharmaceutical industries for GMP compliance. “BIOCAD was licensed by both domestic and foreign experts. Our experience shows that the level of requirements of expert institutions of the Ministry of Industry absolutely corresponds to the level of requirements of foreign regulatory bodies, ”says Roman Ivanov.

The opinion that imported and domestic drugs are now no different is supported by STADA, one of the leading manufacturers of generics in the world. The Russian division of the company – Nizhpharm JSC – produces medicines not only for Russia, but also for foreign countries, including the European Union. Last year, about a third of all domestic pharma exports fell to the share of the Nizhny Novgorod plant. “Medicines are manufactured in accordance with approved regulatory documents, which may slightly differ in terms of local regulatory requirements of a particular country.But there is no need to talk about fundamental differences, the quality of the drug cannot be better or worse in terms of raw materials, equipment used, or any processes. All medicines are produced using a single technology, on one production line, from one raw material, ”says Dmitry Efimov, General Director of Nizhpharm, Senior Vice President of STADA for Russia, the CIS and South-Eastern Europe.

In other words, modern Russian medicines are no worse and no better than imported analogues – they are just the same, experts say.

“Cheap cannot be good”

As Lenta.ru told in previous materials of the cycle, modern drug development is more concentrated in the field of biotechnology. Almost no new drugs are created in the field of “traditional” pharmaceuticals, and almost every original drug has a generic version for a long time. It is always cheaper – already because the company does not need to invest in development. If the generic is produced in Russia, then its price is much lower than the imported original.However, statistics show that Russians still prefer expensive nurofen to ibuprofen, panadol to paracetamol, and aspirin to acetylsalicylic acid.

“Russia is one of the few“ brand-dependent ”markets. Not only in pharmaceuticals, but also in other industries. Brand loyalty in the luxury segment is normal, but in the case of drugs that use the same active ingredient, it is inexplicable, ”said a top manager of one of the pharmaceutical companies. According to him, in the United States, in the very first year when patent protection expires, generics displace the original drug from retail by 85 percent: “There is an instant washout! What difference does it make which ibuprofen is if it is ibuprofen? Only one costs $ 20 and the other is a dollar.The pharmacist will advise you too. ”

Research and production complex BIOCAD. Photo: Alexander Koryakov / Kommersant

In most Western countries, the pharmacist is obliged to offer the buyer a cheaper analogue, if available, explains the source of Lenta.ru. In Russia, there are no such requirements, therefore, most likely, without a request, the pharmacy employee will not recommend any options to you, and may even suggest something more expensive. Pharmacies make money on this, and it is more profitable for them to sell what is more expensive, the expert comments.

It’s not even that the generic drug itself is inexpensive. Russian drugs are cheaper for objective reasons, says Roman Ivanov from BIOCAD: “If domestic drugs were not cheaper, it would be a very big deception of the consumer. First of all, because the cost of labor has decreased due to the devaluation of the ruble, and it makes a significant contribution to the cost of the drug. ”

But mentality still influences the decision to buy a particular product, and this is perfectly illustrated by the story told by Lenta.ru “by a representative of a Russian pharmaceutical company. A well-known foreign manufacturer specializing in generics, all over the world successfully promoted its products with the thesis “the same [as the original], only cheaper.” In Russia, this thesis did not work.

“Our medicines are of poor quality”

This opinion also appeared in the 90s, during the collapse of the industry, and is deeply rooted in society. Experts say that today it has no foundation.

“Quality is a category that the consumer and the manufacturer understand somewhat differently,” says Dmitry Efimov, senior vice president of STADA for Russia, the CIS and South-Eastern Europe.The buyer calls a drug of low quality, which does not bring the expected effect: “Psychosomatic reactions are often included here: cheap means bad, and vice versa, expensive means better help.”

For specialists working in industry, quality is, first of all, compliance with the requirements of the State Pharmacopoeia and the manufacturer’s regulatory documentation, continues Efimov: values ​​”.

The main criteria – efficacy, safety and quality of the drug – are determined even before it is registered by the Ministry of Health and admitted to the market, says Roman Ivanov from BIOCAD. In the course of research, a generic made in Russia is evaluated according to exactly the same criteria by which a generic is assessed when registering in the EU. Moreover, the Russian registration rules, according to market participants, in some cases are even stricter than, for example, American ones. “We have very strict requirements for registration of a drug, both original and reproduced, both domestic and foreign.

The second important element that ensures the quality of the drug is GMP standards. If the plant where the medicine is produced has passed the appropriate certification, then, according to experts, its products can be trusted. Data on the checks carried out and the certificates issued are available on the website of the Ministry of Industry and Trade or on the websites of pharmaceutical companies. Of course, most consumers will not study these sources, admits Roman Ivanov of BIOCAD: “Pharmaceutical companies should better inform the public – both the medical community and patients – about their compliance with modern regulatory requirements.”

Photo: Viktor Korotaev / Kommersant

There is a third element, which is still in its initial stage of development in our country, say the interlocutors of Lenta.ru. “A pharmacovigilance system has been created in Russia. But so far, unfortunately, we are faced with the unwillingness of doctors to be fully involved in it, ”says Ivanov.

The pharmacovigilance system implies informing Roszdravnadzor about any unwanted adverse reactions that may be associated with the use of a particular drug.The information should, first of all, be provided by the doctor. Having learned from the patient about negative phenomena, the doctor fills out a specific form. This can be requested by the patient, or he can fill out and send a notice to the service on his own. On the basis of the incoming messages, Roszdravnadzor draws conclusions about the need to check drugs.

“Roszdravnadzor has a hotline, and manufacturers have hotlines. The main thing is that if you have an understanding that something went wrong, and you associate it with taking a drug, this must be brought to the attention of the regulatory authorities, ”emphasizes Roman Ivanov.“Most of the responsible manufacturers, including BIOCAD, are very active among doctors and patients, so that they report all cases of adverse events or alleged ineffectiveness of drugs to the regulatory authorities. The way it is done all over the world, ”the expert adds.

“Our medicines are made from Chinese substances”

More advanced consumers who have a good understanding of the drug production process often mention that no substances are produced in Russia.Therefore, they argue, Russian manufacturers have to buy them in China, and Chinese in the public mind is always bad.

Until recently, there was some truth in this. But, firstly, modern production facilities appeared in Russia quite a long time ago, organized according to the full cycle – from the creation of a molecule to the packaging of goods. In this case, the substance is produced within the company. This applies to both traditional drugs and biological ones. In the case of the latter, it is simply impossible to do otherwise – it is very expensive to use an imported substance.

Secondly, says the interlocutor of “Lenta.ru”, the production of substances for many reasons by world manufacturers has long been brought to China. There they are bought by both Russia and the entire world “big pharma”. The quality of the work of local factories is checked by the regulatory authorities of different countries, and bad factories are blacklisted. Responsible companies monitor this and turn to trusted suppliers.

Russia has its own manufacturers of substances, working also for export.And they, by the way, have seriously strengthened their positions in the world market amid the devaluation of the ruble. Russia is far from the volume of China in this regard, but it makes no sense to compete with the Celestial Empire in this matter, the expert assures. “The production of a chemical substance abroad is economically justified in most cases. This is not a particularly marginal process. It becomes marginal only if the substance is boiled in tons. And for Russia, cooking tons of substances in most cases is impractical, ”he explains.

Photo: Roman Yarovitsyn / Kommersant

The pharmaceutical quality system is designed in such a way that verification is carried out throughout the entire manufacturing process of the drug. “At the stage of purchasing raw materials, both active substances and excipients, and materials, the manufacturer / supplier is assessed,” notes Dmitry Efimov from STADA. – At the stage of delivery – control of storage conditions during transportation. The receipt of raw materials and materials at the warehouse accompanies the control of storage conditions, incoming control and admission of raw materials and materials to production.Already in the production process, a multi-stage control is carried out from the analysis of an intermediate product to the study of the stability of an already finished product. ”

With this level of control, drug manufacturers assure, responsible companies tend to zero the probability of the penetration of counterfeit or substandard materials.

“Imported works, but ours does not”

Similar statements can be heard from friends, read on specialized forums, doctors encounter them. “I always tell the patient that there are Russian drugs and their foreign counterparts, and that not always an expensive drug has a better effect than its cheaper counterpart.However, I have repeatedly come across the assertion of patients who bought drugs abroad that the drugs “worked”, and when they came home and bought domestic drugs, either they did not work, or they acted worse, “Ivan shared with Lenta.ru Tarasenko, general director of the Medinterkom clinic in Milyutinsky lane.

Pharmaceutical companies call such statements “pure psychosomatics”. “Roszdravnadzor has repeatedly conducted statistical studies on the number of incoming reports of unwanted side effects.They specifically compared domestic and foreign drugs. And they never found a difference. This is all self-persuasion, ”says a top manager of a domestic pharmaceutical company.

“If a drug also enters the bloodstream, it has the same content of active substance, the same content of impurities, and all this is controlled, then it simply cannot be less or more effective by definition,” agrees Roman Ivanov from BIOCAD. “If we exclude some mysticism and the influence of a particle of the soul of a French manufacturer, everything else that is explained by the laws of biology, physics, chemistry will be exactly the same.”

Dmitry Efimov from STADA also refers to data from Roszdravnadzor: according to the agency’s reports, the percentage of deviations detected in Russian drugs when correlated with the number of batches circulating on the market is not higher than that of imported ones. “Moreover, in 2015, the share of Russian drugs among the series withdrawn by the regulator from circulation decreased by 11 percent,” emphasizes the top manager.

Expertise at the registration stage is a guarantee that a drug is entering the market with the same quality, effectiveness and safety as the original.Compliance with GMP rules guarantees the consistency of these indicators during the release of the drug. All this in general is controlled by the already mentioned pharmacovigilance, insists the top manager of BIOCAD. “Emergency inspections by Roszdravnadzor or the Ministry of Industry and Trade are good additional controls. But in order to systematically provide confidence that, in fact, everything is normal at the enterprise, a working pharmacovigilance system is needed, ”Ivanov repeats.

But both patients and doctors still know little about pharmacovigilance.“I didn’t know that if you report a bad or low-quality drug to Roszdravnadzor, then this remark will be recorded and taken into account in the statistics,” admitted Ivan Tarasenko. He noted that in order for doctors to be actively involved in the process, there must be a conveniently built complaints system that would make it possible to do this online, quickly and correctly. “This system should also somehow take into account the veracity of these complaints from both the patient and the doctor, and cut off inadequate or interested parties, such as competitors,” added the doctor.

Photo: Roman Yarovitsyn / Kommersant

Pharmaceutical companies are confident that building a civilized market is a joint work of the state, manufacturers, doctors and end users of drugs. “There is a new Russian pharma and an old Russian pharma. Pharmaceutical companies from the “new” have invested a lot in improving their production capacities, in the development of their product portfolio. They are also export-oriented, value their reputation very much and strive to work according to the strictest standards, ”says the top manager of BIOCAD.These manufacturers are interested in having the industry under maximum control from all sides. If there is confidence in medicines, there will be sales from domestic companies. With regard to the quality of drugs, the interests of manufacturers and consumers coincide.

A question of trust

Experts in pharmaceutical companies say: the standards that are currently used in production in Russia practically coincide with those in the EU and the USA. The control system organized by the state allows only high-quality and effective drugs to be admitted to the market.Factories of many world pharmaceutical giants are located on the territory of Russia – that is, any drug of any brand can be, in fact, Russian-made. Such medicines, according to experts, are now even safer for health to buy than those produced abroad.

“The regulatory authorities always have the opportunity to suddenly come to a plant located in Russia, seize samples of a medicinal product, check their quality, the conditions in which the product is produced.