Zolafren Olanzapin tablets 10mg №30

Zolafren Olanzapin tablets 10mg №30

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Composition active ingredient: 1 tablet contains 5mg or 10mg of olanzapine; auxiliary substances: lactose, microcrystalline cellulose, starch sodium (type A), magnesium stearate shell: hypromellose (hydroxypropyl methylcellulose), polyethylene glycol (Macrogol) 400, dye Yellow no.6 Al-Lake (e 110), titanium dioxide (E 171), iron oxide yellow (E172), lactose. Dosage form Tablets, film-coated. Basic physical and chemical properties : tablets of 5 mg tablets are beige, film-coated, lenticular, with a notch on one side, diameter 7 mm; tablets 10 mg tablets are beige, film-coated, biconvex with a diameter of 7 mm. Pharmacological group Antipsychotic agents. ATC code N05A H03. Pharmacological properties Pharmacodynamics. Olanzapine is an antipsychotic, antimaniac drug and a mood-stabilizing drug with a wide range of pharmacological effects, due to the influence on various receptors. The identified binding to serotonin receptors 5 HT 2A/2C , 3 5 NT , 5 NT 6 , dopaminovykh receptors D 1 , D 2 , D 3 , D 4 , D 5 , the muscarinic receptors M 1-M 5 , a 1 adrenergic and histamine H 1 receptor. During studies of the behavior of animals, which were injected olanzapine identified as the antagonism of olanzapine to serotonin receptors 5НТ and dopamine and cholinergic. Olanzapine has a high level of binding to the receptors of serotonin 5NT 2, than with dopamine receptors D 2 , and in models of both in vitro and in vivo . Electrophysiological studies demonstrated that olanzapine selectively reduces the excitability of the mesolimbic (a10) dopaminergic neurons, showing a negligible impact on the striate (A9), associated with motor function. Olanzapine inhibits the conditioned reflex of avoidance, which indicates its antipsychotic activity when taken in doses that are lower than the doses that cause catalepsy, which is a symptom of motor side effects. Unlike some other antipsychotic drugs, olanzapine enhances the reaction to stimuli during the anksioliticheskogo test. With a single dose of 10 mg of olanzapine during positron emission tomography (PET) with the participation of volunteers found that olanzapine had a higher level of binding to receptors 5 NT 2A than dopamine receptors D 2 . In addition, the analysis of images obtained during studies of patients with schizophrenia, the method of single photon emission computed tomography (SPECT), revealed that olanzapine-responsive patients showed a lower level of striate binding to D 2 receptors than other antipsychotic - and respiridone patients compared to clasamentului patients. Clinical efficacy. During two of the two placebo-controlled and two of the three comparatively-controlled studies involving more than 2900 patients with schizophrenia with positive and negative symptoms, olanzapine showed statistically significant improvement data for both negative and positive symptoms. In international double-blind comparative studies involving 1,484 patients with schizophrenia, schizoafectivity and associated disorders with varying degrees of disorders associated with depressive symptoms (16.6 points on the Montgomery-Asberg scale for the assessment of depression), a prospective secondary study from the beginning to the end of the assessment of mood changes found a statistically significant improvement (p = 0.001) after olanzapine treatment (-6.0) compared with that in the treatment of haloperidol (-3.1). In patients with manic or mixed episodes in bipolar disorder, olanzapine demonstrated a high efficacy in reducing manic symptoms over 3 weeks compared with placebo and divalproex. Olanzapine also demonstrated comparable efficacy results to haloperidol in terms of the proportion of patients with symptomatic remission, ranging from mania and depression at 6 and 12 weeks of treatment. During the study, during concomitant treatment with lithium or valproate for 2 weeks with the addition of olanzapine at a dose of 10 mg, a significant decrease in the symptoms of mania was found in comparison with those in monotherapy with lithium or valproate after 6 weeks. During the 12-month study of prophylaxis of relapses of manic episodes in patients who have reached remission with olanzapine and were randomized into groups receiving olanzapine or placebo, olanzapine demonstrated a statistically significant advantage over placebo in the endpoint of the evaluation criteria of relapse of bipolar disorder. Olanzapine also showed a statistically significant advantage over placebo in preventing relapse of mania or recurrence of depression. In the course of the subsequent 12-month study of prevention of manic episodes recurrence in patients who achieved remission as a result of concomitant treatment with olanzapine and lithium and were subsequently randomized into olanzapine or lithium intake groups separately, olanzapine did not have a statistically significant advantage over lithium at the end point of the assessment criterion of bipolar disorder recurrence (olanzapine 30%, lithium 38.3%; p = 0.055). In an 18-month study during concomitant treatment for manic or mixed episodes, patients were stabilized with olanzapine as a mood stabilizer with lithium or valproate, prolonged concomitant treatment with lithium or valproate with olanzapine did not establish a statistically significant advantage over monotherapy with lithium or valproate, and deferral of recurrence of bipolar disorders determined in accordance with the syndrome (diagnostic) criterion. Children. Experience of use in children (aged 13 to 17 years) is limited, according to the obtained data on the effectiveness of short-term treatment of schizophrenia (6 weeks) and mania, associated with bipolar disorders (3 weeks), involving less than 200 adolescents. The initial dose of olanzapine was 2.5 mg and reached 20 mg/day. During the treatment with olanzapine body weight in adolescents increased significantly compared to adults. In adolescents there was an increase in levels of total cholesterol, cholesterol of low-density lipoproteins, triglycerides, and prolactin compared to adults. Data on the maintenance of the effect of treatment and long-term studies are limited. Pharmacokinetics. Absorption. The drug is well absorbed after oral administration, C max in plasma is reached after 5-8 hours. On the absorption of olanzapine, food intake is not affected. Bioavailability of oral administration of olanzapine compared with intravenous is not established. Distribution. The level of binding of olanzapine with blood plasma proteins is about 93% for concentrations ranging from 7 ng/ml to 1000 ng/ml of Olanzapine is bound predominantly to albumin and a 1 -kilim glycoprotein. Metabolism. Olanzapine is metabolized in the liver by conjugation and oxidation. The main metabolite circulating is 10-N-glucuronide, which does not penetrate the blood-brain barrier. Cytochromes P450-CYP1A2 and P450-CYP2D6 contribute to the formation of metabolites N-desmethyl and 2-hydroxymethyl, which exhibit significantly less pharmacological activity in vivo than olanzapine , in animal studies. The predominant pharmacological activity is caused by primary olanzapine. Conclusion. After oral administration, the half-life of olanzapine in volunteers varied according to age and sex. At healthy volunteers of advanced age (65 years old) compared to younger volunteers, the elimination half-life was prolonged (up 51.8 versus 33.8 hours), clearance in plasma was lowered (to 17.5 versus 18.2 l/HR). The pharmacokinetic variations observed among volunteers in the elderly, are within the range for younger volunteers. In 44 patients with schizophrenia aged>65 years, the dosage of 5 to 20 mg/day was not associated with any characteristic profile of side effects. In women compared with men, the elimination half-life was prolonged (36,7 32,3 vs hours) and clearance in plasma was reduced (to 18.9 vs. 27.3 l/h). However, olanzapine (5-20 mg) showed a comparable safety profile in both women (N = 467) and men (n = 869). Patients with renal insufficiency. In patients with renal insufficiency (creatinine clearance Patients who smoke. In patients with mild hepatic impairment who smoke, the half-life was long (39.3 hours) and plasma clearance was reduced ( 18.0 l/h) compared with patients without hepatic impairment who do not smoke (48.8 hours and 14.1 l/h, respectively). Compared to smokers (men and women), the average half-life was long (38.6 to 30.4 hours) and the plasma clearance was reduced (18.6 to 27.7 l/h). Olanzapine clearance in plasma is lower in elderly patients compared to young, in women compared to men and in non-smokers compared to smokers. And yet the impact of factors such as age, sex and Smoking can have little effect on the clearance of olanzapine in blood plasma and half-life compared to the General variability between individuals. In the course of studies involving European patients, patients of Japanese and Chinese nationalities, no differences in olanzapine pharmacokinetics were found. Children. Olanzapine pharmacokinetics in adolescents and adults alike. In clinical studies, the average olanzapine effect was about 27% higher in adolescents. Demographic differences between the adolescents and adults include a low average body weight and fewer smokers among adolescent patients. Such factors are likely to affect the higher average olanzapine effect observed in adolescents. Indications Olanzapine is indicated for the treatment of schizophrenia. Olanzapine is effective for maintaining the achieved clinical the effect of long-term therapy in patients who have observed a response to initial therapy. Olanzapine is indicated for the treatment of moderate and severe manic episodes. Olanzapine is indicated for the prevention of repeated seizures in patients with bipolar disorders, in which a positive response was received in the treatment of olanzapine mania. Contraindications Hypersensitivity to the active substance or to the auxiliary components of the drug is a known risk of closed-angle glaucoma. Interaction with other medicinal products and other forms of interaction Children. The study of interaction with other drugs was carried out only with the participation of adults. Interactions that have a potential impact on olanzapine . Since olanzapine is metabolized by the isoenzyme CYP1A2, substances that specifically are induced or inhibited by this isoenzyme may affect the pharmacokinetics of olanzapine. Inducers of CYP1A2 . The metabolism of olanzapine can be induced by Smoking and the use of carbamazepine, which leads to a decrease in the concentration of olanzapine. There was a slight or moderate increase in clearance olanzapine. Clinical findings are limited, but clinical monitoring is recommended, and if necessary, an increase in the dose of olanzapine. Inhibitors of CYP1A2. Fluoxamine, a specific inhibitor of CYP1A2 significantly reduces the metabolism of olanzapine. This leads to an average increase from max after taking fluoxamine by 54% in women who do not smoke, and 77% in men who smoke. The average increase in olanzapine AUC is 52% and 108% respectively. For patients who use fluoxamine or any other inhibitors of CYP1A2, for example, ciprofloxacin, it is necessary to appoint reduced doses of olanzapine. It is necessary to consider reducing the dose of olanzapine, if initiated treatment with CYP1A2 inhibitor. The decrease in bioavailability. The purpose of activated charcoal reduced oral bioavailability of taken olanzapine by 50% -60% and should be used within 2:00 before or after 2:00 after taking olanzapine. Fluoxetine (CYP2D6 inhibitor), a single dose of antacids containing aluminum and magnesium or cimetidine, did not significantly affect the pharmacokinetics of olanzapine. Possible effect of olanzapine on other drugs. Olanzapine can be antagonistic to the effects of direct and indirect dopamine agonists. Olanzapine did not suppress the main CYP 450 isoenzymes (e.g. 1A2, 2D6, 2C9, 2C19, 3A4) in vitro. Thus, it is not expected to have any special interactions, which is confirmed by in vivo studies where it was observed the inhibition of metabolism of olanzapine in the administration of such active agents: tricyclic antidepressants (mainly represented by the isoenzyme CYP2D6), warfarin (CYP2C9), theophylline (CYP 1A2) or diazepam (a CYP 2C19 and ZA4). There was no evidence of interaction in the appointment of olanzapine with lithium or biperidenom. Therapeutic monitoring of valproate levels in blood plasma did not reveal the need for correction of valproate dose with simultaneous administration of olanzapine. The total activity in the CNS With caution, olanzapine should be used in patients who take ethanol or medicinal with individuals who may cause Central nervous system depression. The simultaneous use of olanzapine with anti-Parkinsonian drugs in patients with Parkinson's disease and dementia is not recommended. Interval QTс. It should be cautiously prescribed olanzapine with other drugs with a known risk of increasing The Qts interval. Inhibitors of CYP 2D6. Fluoxetine (60 mg per dose or 60 mg daily for 8 days) leads to an average increase in the maximum concentration of olanzapine by 16% and an average decrease in the clearance of olanzapine by 16%. The impact of these factors is small compared to the General variability between individuals, so dose changes are usually not recommended. Olanzapine's potential ability to interact with other drugs. Antihypertensive agents . Olanzapine due to the potential ability to lower blood pressure can enhance the effects of certain antihypertensive drugs. Levodopa and dopamine agonists . Olanzapine can be antagonistic to the effects of levodopa and dopamine agonists. Imipramine. Single doses of olanzapine do not affect the pharmacokinetics of imipramine or its active metabolite desipramine. Application features During treatment with antipsychotics, improving the clinical condition of the patient can take from several days to several weeks. During this period, careful patient monitoring is needed. Psychosis associated with dementia and/or behavioural disorders. Olanzapine is not intended for the treatment of psychoses associated with dementia and/or behavioural disorders, and is not recommended for use in these patients due to increased mortality and risk of cerebrovascular cases. In placebo-controlled clinical trials (6-12 weeks) involving elderly patients (average age 78 years) suffering from psychoses associated with dementia and/or behavioural disorders, the number of fatal cases was 2 times higher in patients taking olanzapine compared with placebo (3.5% versus 1.5%, respectively). High mortality was not associated with the magnitude of the applied doses of olanzapine (mean daily dose 4.4 mg) or duration of treatment. Risk factors that can lead to increased mortality include age 65 years, dysphagia, sedation, malnutrition and dehydration, pulmonary conditions (pneumonia with or without aspiration), the simultaneous use of benzodiazepines. However, cases of mortality were higher in therapy with olanzapine than in placebo, regardless of risk factors. In the course of clinical studies, there were cases of cerebrovascular adverse reactions (stroke, transient ischemic stroke), including fatal ones. The number of cerebrovascular adverse reactions was 3 times higher in patients taking olanzapine, compared with placebo (1.3% vs. 0.4%, respectively). All patients who took olanzapine or placebo and which had a cerebrovascular adverse reactions had risk factors. The age of 75 years and vascular/mixed type dementia were identified as risk factors for cerebrovascular adverse reactions in the treatment olanzapina. The effectiveness of olanzapine is not established in these studies. Parkinson. The use of olanzapine in the treatment of psychoses associated with dopamine agonists is not recommended. Simultaneous use of olanzapine and antiparkinsonic drugs in patients with Parkinson's disease and dementia is not recommended. In clinical studies, very often there was a deterioration in symptoms of Parkinson's disease and hallucinations, more often than when taking placebo; in the treatment of psychotic symptoms, olanzapine therapy was not more effective than using placebo. From the very beginning of these studies, patients were required to constantly use the lowest effective dose of antiparkinsonic drugs (dopamine agonists), as well as the use of the same antiparkinsonic drugs and doses throughout the study. Olanzapine therapy was started with a dose of 2.5 mg/day, increased by titration to a maximum of 15 mg/day. The neuroleptic malignant syndrome . Neuroleptic malignant syndrome (NSS) is a potentially lethal symptom complex described in connection with antipsychotic drugs. Rare cases have been reported in CIP associated with the use of olanzapine. Clinical manifestations of NSAs are hyperpyrexia, muscle rigidity, loss of consciousness and symptoms of cardiac instability (irregular pulse or change in blood pressure, tachycardia, increased sweating and cardiac arrhythmia). Additional signs may include elevated levels of CPK, myoglobinuria (rhabdomyolysis) and acute renal failure. Clinical manifestation of NZS or the presence of hyperthermia without clinical manifestations of NZS requires immediate cancellation of all antipsychotic agents, including olanzapin. Hyperglycemia and diabetes mellitus. Hyperglycemia and/or development of diabetes mellitus or deterioration of the current ketoacidosis or diabetic coma associated with ketoacidosis, as well as lethal cases, have been reported infrequently. Sometimes the previous increase in body weight was reported to be a risk factor. It is recommended to conduct appropriate clinical monitoring of patients with diabetes mellitus and patients with risk factors for diabetes mellitus, in particular to measure blood glucose levels at the beginning of treatment, after 12 weeks, and annually thereafter. Patients receiving treatment with antipsychotics, including olanzapine, should be monitored for signs and symptoms of hyperglycemia (such as polydipsia, polyuria, polyphagia and weakness). Patients with diabetes mellitus and patients with diabetes risk factors should be regularly monitored regarding the deterioration of glucose control. You should regularly monitor body weight, for example at the beginning of treatment, after 4 weeks, after 8 weeks and after 12 weeks, and once a quarter in the future. Anticholinergic activity . In the course of clinical studies revealed a low frequency of anticholinergic phenomena. However, due to the limitations of clinical experience in the use of olanzapine patients with concomitant diseases should be careful when prescribing the drug to patients with prostate hypertrophy, paralytic intestinal obstruction or similar conditions. Indicators of liver function. When using olanzapine often observed transient asymptomatic increase in liver transaminases ALT and AST, especially at the beginning of treatment. Patients with elevated ALT and/or ALT, signs and symptoms of disorders of the liver, a conditions associated with liver failure, as well as patients who take potentially hepatotoxic drugs, olanzapine should be prescribed with caution. If hepatitis (including hepatocellular, cholestatic or mixed liver damage) is detected, olanzapine should be abolished. Neutropenia. Olanzapine should be used with caution at low levels of leukocytes and/or neutrophils from any cause in patients who are receiving treatment with drugs that can cause neutropenia, patients with a history of drug suppression/toxic damage of bone marrow to patients with bone marrow depression caused by concomitant illness, radiation or chemotherapy, and patients with hypereosinophilia and MYELOPROLIFERATIVE disease. Neutropenia is a frequent side effect in the joint application of valproate and olanzapine. The cessation of therapy. With a sharp discontinuation of therapy, acute symptoms, such as excessive sweating, insomnia, tremor, irritability, nausea or vomiting, were rarely reported (? 0.01% and 0.1%). Qt-interval . In clinical trials, olanzapine did not cause a long prolongation of the absolute QT intervals and QTс. However, as in the treatment of other antipsychotics, prescribe olanzapine in combination with drugs that can cause prolongation of The Qts interval, should be careful, especially in elderly patients with congenital prolongation syndrome Qt interval, congestive heart failure, heart hypertrophy, hypokalemia or hypomagnesemia. Thromboembolism. Temporary links between olanzapine treatment and venous thromboembolism have been reported infrequently(? 0,1% - <1%). The causal relationship between the treatment of olanzapine and the development of venous thromboembolism is not established. However, taking into account the fact that patients with schizophrenia often develop a tendency to thromboembolism, it is necessary to take into account all possible risk factors, such as immobilization of the patient, and take all necessary preventive measures. The total effect on the Central nervous system. Given the predominant effect of olanzapine on the Central nervous system, it is necessary to take additional precautions when taking olanzapine with other drugs of Central action, including alcohol. Epileptic seizure. Olanzapine should be used with caution in patients with a history of epileptic seizures or patients sensitive to factors that reduce the threshold of attacks. Cases of epileptic seizures in the treatment with olanzapine have been reported infrequently. In most of these cases, patients had a history of epileptic seizures or the risk of their occurrence was increased. Tardive dyskinesia. In clinical studies lasting 1 year or less while taking olanzapine, there was a statistically significantly lower incidence of dyskinesia caused by the treatment. Due to the growing risk of late dyskinesia with prolonged use of antipsychotic drugs, a consistent dose reduction or complete withdrawal of the drug when the patient has signs or symptoms of late dyskinesia is necessary. Over time these symptoms can worsen or even arise after discontinuation of treatment. Orthostatic hypotension. Cases of orthostatic hypotension were rarely reported in elderly patients during clinical trials. As with the treatment of other antipsychotics, the use of olanzapine is recommended periodic measurement of blood pressure in patients aged 65 years. Sudden cardiac death. In post-marketing reports have described cases of sudden cardiac death. According to a retrospective observational cohort study, the risk of sudden cardiac death in patients treated with olanzapine was almost doubled compared to patients who did not use antipsychotics. The risk in the application of olanzapine corresponds to that in the application of atypical antipsychotics, which were included in the combined analysis. Lactose. The drug contains lactose, so it can not be prescribed to patients with hereditary lactose intolerance, lactase deficiency (the Lapp lactose deficiency) or glucose-galactose malabsorption syndrome. Dopaminergic antagonism. Olanzapine in vitro is antagonistic to dopamine and can theoretically counteract the effects of levodopa and dopamine agonists, as well as other antipsychotics. Glucose. During clinical trials (up to 52 weeks) olanzapine caused large changes in the level of glucose compared with placebo. The difference in changes in values between olanzapine and placebo was greater in patients with symptoms of glucose dysregulation in the history (including patients with diabetes mellitus or patients with manifestations of hyperglycemia). These patients had a significant increase in HbA1c compared to the placebo group. The percentage ratio of patients who have changed glucose levels from normal to extreme to high, constantly increased. In the analysis of patients who underwent 9-12-month therapy with olanzapine, increased blood glucose levels decreased after 6 months. Changes in the level of lipids . Undesirable changes in lipid levels can be observed in patients treated with olanzapine. Changes in lipid levels should be treated properly in patients with dyslipidemia and in patients with risk factors for lipid metabolism disorders. Patients receiving treatment with antipsychotics, including olanzapine, should regularly monitor blood lipid levels, for example at the beginning of treatment, after 12 weeks, and every 5 years thereafter. In clinical studies that lasted more than 12 weeks in patients taking olanzapine, there was an increase in the level of total cholesterol, low density lipoproteins and triglycerides compared with the placebo group. A significant increase in the level of lipids (total cholesterol, low-density lipoproteins, triglycerides) were observed more often in patients without disorders of lipid metabolism history. There were no statistically confirmed differences in the increase in high density lipoproteins between patients who took olanzapine and patients who took placebo. The proportion of patients who changed the total cholesterol, low-density lipoproteins or triglycerides from normal or extreme level to high or decrease the level of lipoproteins of high density with normal or marginal to low, was greater in long-term studies (at least 48 weeks) as compared to those in short-term studies. In patients who underwent 12-month therapy, the level of total cholesterol did not grow after 4-6 months. Suicide. The possibility of suicide attempts is inherent in both patients with schizophrenia and patients with bipolar disorder type I, and therefore it is necessary to carefully monitor patients who have a high risk of suicide and receive therapy with olanzapine. In order to reduce the possibility of overdose, olanzapine should be prescribed in tablets in small quantities sufficient to ensure proper therapeutic effect. Body weight. Before starting therapy with olanzapine should take into account the potential consequences of increasing the body weight of the patient. Patients receiving treatment with olanzapine should undergo regular monitoring of body weight. Monotherapy olanzapine adults. In the analysis of 13 placebo-controlled clinical studies it was revealed that patients receiving therapy with olanzapine, there was an average increase in body weight by 2.6 kg compared with weight loss on average 0.3 kg in the placebo group at a median of 6 weeks in 22.2% of those receiving therapy with olanzapine, there was increase in body weight not less than 7 mass% at the start of treatment, compared with 3% of patients in the placebo group at a median application 8 weeks in 4.2% of patients experienced weight gain of at least 15% of the mass at the beginning of treatment, compared to 0.3% of patients in the placebo group at a median use of 12 weeks. A clinically significant increase in body weight was observed in all categories of patients with a BMI (body mass index). Cessation of therapy due to weight gain was noted in 0.2% of patients treated with olanzapine, compared with 0% of patients from the placebo group. In the course of long-term clinical trials (at least 48 weeks), the average increase in body weight in patients was 5.6 kg (with a median application of 573 days; N = 2021). The number of patients who experienced an increase in body weight by at least 7%, 15% or 25% of the initial mass, with prolonged use of olanzapine was 64%, 32% and 12% respectively. Discontinuation of therapy due to weight gain was noted in 0.4% of patients treated with olanzapine for at least 48 weeks. Dysphagia. Violation of esophageal motility and shortness of breath were associated with the reception of antipsychotics. Aspiration pneumonia was a frequent cause of morbidity and mortality in patients with Alzheimer's disease. Olanzapine is not approved for the treatment of patients with Alzheimer's disease. Regulation of body temperature . An impaired ability of the body to reduce its temperature was observed in connection with antipsychotics. It is recommended to take this into account in the appointment of olanzapine in patients who are in conditions which may lead to increase in body temperature, such as enhanced training, stay in extreme temperatures, simultaneous application of funds with anticholinergic activity, or dehydration. Application to patients who have comorbidities . Clinical experience with olanzapine in patients with certain diseases is limited. Olanzapine enhances in vitro affinity for muscarinic receptors. In the course of premarketing clinical trials of its use of olanzapine was associated with constipation, feeling of dryness in the mouth, tachycardia and other adverse events, possibly related to cholinergic antagonism. Such side effects rarely led to discontinuation of therapy, olanzapina, but must be wary of olanzapine to patients with clinically significant prostatic hypertrophy, narrow-angle glaucoma, paralytic ileus, history, or related conditions caused by cholinergic antagonism, which can worsen in the presence of olanzapine. During the 5 placebo-controlled studies of olanzapine in elderly patients with psychosis associated with dementia (n = 1184), reported such adverse reactions associated with therapy, with an incidence of at least 2% and significantly higher frequency of occurrence compared with patients in the placebo group: falls, somnolence, peripheral edema, gait disturbance, urinary incontinence, lethargy, weight gain, asthenia, pyrexia, pneumonia, dry mouth and visual hallucinations. The level of cessation of therapy due to side effects was higher in the group receiving olanzapine, compared with placebo (13% compared with 7%, respectively). In elderly patients with dementia-related psychosis receiving olanzapine, there is a high rate of deaths compared to the placebo group. Olanzapine is not indicated for the treatment of elderly patients with psychosis associated with dementia. Olanzapine has not been used in a sufficient number of cases in patients with recent myocardial infarction or unstable heart disease. Patients with the above-mentioned diagnoses were excluded from premarketing clinical trials. Olanzapine should be used with caution to treat patients with heart disease due to the risk of orthostatic hypotension. Laboratory research. It is recommended to control glucose on an empty stomach and lipid profile at the beginning of treatment and periodically during treatment. Hyperprolactinemia. As other properties of antagonists of dopamine D 2 receptors , olanzapine increases in blood prolactin levels, and this increase persists during chronic administration. Hyperprolactinemia can suppress the hypothalamic hormone GnRH, resulting in a decrease in the secretion of pituitary gonadotropin. This, in turn, can inhibit reproductive function by disrupting gonadal spermatogenesis in both men and women. Galactorrhea, amenorrhea, gynecomastia and impotence were reported in patients receiving drugs that increase prolactin levels. Long-term hyperprolactinemia, associated with hypogonadism, can lead to a decrease in bone density in both men and women. Additional research/laboratory data . Taking into account that in some studies neutropenia associated with taking other animals was observed

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