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The most common reasons cited for changing to ODO in preference to standard tablets were the perception that ODO facilitates controlled intake and is easier to administer to uncooperative patients. The authors noted that the results are consistent with studies which demonstrated SOT to be efficacious in the acute treatment of excitement and psychomotor agitation associated with schizophrenia. However, in contrast to other observational studies described below, there was no evidence that ODO was prescribed more often to more severely ill patients in this study.

This suggests that in a routine inpatient setting, the effectiveness of SOT and ODO formulations of olanzapine are comparable, even though ODO was preferentially prescribed to the more difficult-to-treat nonadherent patient group.

Czekalla et al investigated the effectiveness of ODO compared with SOT in a 2-week prospective observational study of patients predominantly with schizophrenia, schizotypal, or delusional disorder However, as pointed out by Czekalla et al, interpretation of these data should take into consideration the higher proportion of severely ill patients ODO: Significant improvement overall from baseline was also seen in Agitation Calmness Evaluation Scale scores for both groups, but not between groups at any time point up to 6 hours.

However, as discussed in a later section, it is important to bear in mind the nonsignificance of secondary comparisons, which may be underpowered, should be interpreted with caution, and should not necessarily imply equivalence. A posthoc analysis of a prospective open-label study by Arranz et al measured core symptom improvement in never-treated first-episode psychotic patients chronologically assigned to either ODO or SOT for 6 weeks 19 patients in each group.

To date, only two head-to-head studies comparing ODO with another antipsychotic have been conducted. Hatta et al evaluated the efficacy and tolerability of ODO compared with risperidone oral solution in Japanese acutely agitated psychotic patients over a short duration 1 hour. Patients were subsequently followed up in a relatively naturalistic way. No significant differences in patient satisfaction with treatment were observed.

Thus, similar efficacy between the two treatments in the acute setting in this patient population was concluded. In a similar study of agitated psychotic patients at an acute care psychiatric ward in Taiwan, Hsu et al followed 42 patients for 24 hours after random allocation to either ODO, intramuscular olanzapine, risperidone oral solution, or intramuscular haloperidol.

However, they found that ODO and intramuscular olanzapine but not risperidone oral solution were more effective than intramuscular haloperidol in the early phase of treatment up to 90 minutes based on PANSS-EC. Kuramochi et al assessed a cohort of schizophrenia patients from a 6-week Japanese noninterventional study of olanzapine in which patients were stratified by formulation initially prescribed ODO or SOT.

In the only randomized double-blind clinical trial comparing ODO and SOT, Karagianis et al administered ODO sublingually in a double-dummy fashion that is, active standard tablet plus placebo ODT or placebo standard tablet plus active ODT in order to preserve blinding to the active formulation. No statistically significant differences between the treatment groups were observed in any efficacy measures CGI-S, Global Assessment of Functioning scale, and Subjective Wellbeing Under Neuroleptics scale.

However, it must be borne in mind that patients in both groups were clinically stable at baseline and so opportunity for improvement was limited. However, it should be noted that in order to be entered into the study, patients had to be stable and tended to have mild to moderate symptoms CGI-S: ODO 2. They were also significantly more severely ill, irrespective of disease type, and were rated significantly less adherent with medication at baseline than SOT-treated patients.

These factors may explain why patients initiated on ODO were prescribed significantly higher doses of olanzapine on average As may be expected, ODO tended to be prescribed to patients with less insight into their illness, its effects, and need for treatment, suggesting that utilization of the two oral olanzapine formulations is associated with different patient profiles. However, regardless of indication, patients on ODO formulation experienced significantly greater improvements in disease severity, global functioning, and wellbeing though not medication adherence and therapeutic alliance compared with the SOT group.

As both ODO and SOT contain olanzapine as the active ingredient, they were expected to have similar safety and tolerability profiles. Indeed, the tolerability profile seen in clinical studies with ODO has been found to be similar to the more extensively studied SOT formulation. A number of studies of ODO have included measurement of safety and tolerability. However, while quantitatively and qualitatively similar to SOT studies, these single-arm studies did not allow direct comparisons of the adverse event profile of ODO with SOT.

Two patients in the ODO arm developed serious adverse events, including one with dizziness requiring hospitalization and one who attempted suicide. As a double-blind trial, this is the most appropriate study design to investigate the comparative effect of treatment on safety and tolerability. Adverse events were also assessed in a prospective comparative cohort study.

Half of the adverse events in both arms were considered mild There were three discontinuations due to adverse events in the ODO arm, caused by allergic reaction, increased creatine kinase, and restlessness. It is important to keep in mind that in this study, both clinicians and patients were aware of which treatment patients were taking. This has the potential to bias the reported rate of adverse events when new treatments are being used. The most common adverse events in the ODO group were weight increase 7.

Both randomized studies have thus shown no difference between ODO and SOT in terms of frequency of TEAEs, 27 , 28 while naturalistic studies, 30 where treatment decisions are made by physicians on the basis of patient characteristics and in the course of normal clinical practice in the knowledge of the treatment being prescribed, have tended to show a higher rate of TEAEs with ODO.

Such patients may, in turn, be prescribed commensurately higher doses of olanzapine or concomitant medications, be more prone to adverse events, and be more closely monitored or more likely to report adverse drug reactions.

On the other hand, randomization, particularly when combined with blinding to treatment, is designed to negate such imbalances between patient characteristics in relation to treatment allocation, allowing for more objective comparison of treatment effects. Therefore, the differences in the rate of adverse events observed with different formulations in open-label naturalistic studies may reflect preexisting differences in characteristics of the patient groups being compared rather than differences in the safety profiles of ODO and SOT.

Treatment-emergent movement disorders, including extrapyramidal symptoms and tardive dyskinesia, are associated with a number of antipsychotic medications and may have a significant impact on treatment nonadherence and discontinuation. In addition, patients showed a reduction in tardive dyskinesia as measured by the Abnormal Involuntary Movement Scale.

However, it should be noted that patients in this study were able to switch to SOT after 1 week of ODO treatment if the treating physician felt that the patient had experienced significant improvement in psychosis and medication adherence, which occurred relatively frequently as noted above, 24 patients switched to SOT while 49 patients remained on ODO.

For this reason, the improvements noted above may not be directly attributable to the ODO formulation. In contrast, Hori et al found no significant change in extrapyramidal symptoms over the course of their 4-week study, although there was a numerical decrease relative to baseline as measured by the Drug-Induced Extrapyramidal Symptoms Scale DIEPSS.

No movement disorders were spontaneously reported by patients. This included 6. The proportion of patients with some degree of suicidal ideation was found to similarly decrease from baseline after 2 weeks of therapy for both treatment groups SOT from No patients with distinct suicidal plans were observed after 2 weeks in either treatment group. Weight gain and changes in metabolic parameters have been reported during treatment with atypical antipsychotics, including olanzapine.

Patients should be monitored at baseline and periodically during treatment. Potential differences in the risk of weight gain and changes in metabolic parameters during treatment with ODO compared to SOT may impact treatment choice and patient adherence.

Studying this potential difference in weight gain, a European research group recently conducted a small randomized crossover study in 12 healthy males to compare the short-term metabolic profiles of ODO and SOT over 8 days.

Thus under such circumstances, in some cases, olanzapine from ODO would be expected to reach the gut and behave in the same way as SOT.

Therefore, validity of the hypothesis of possible weight differences being mediated by gut receptors remains uncertain. Also, in contrast to the small supportive studies mentioned above, recent larger and more rigorous studies, while inconclusive, have not confirmed the hypothesis that ODO has a more favorable weight gain profile than SOT.

In an attempt to resolve the question of whether ODO has a more favorable weight gain profile than SOT, a rigorous double-blind double-dummy study was conducted by Karagianis et al. Moreover, the number of patients experiencing substantial weight gain ODO: However, a significant group difference in adherence was observed whereby ODO patients were more likely to take their medication as indicated, which may have impacted the incidence of weight gain in the ODO group due to greater and more prolonged antipsychotic exposure.

As pointed out by Karagianis et al, the analysis was not adjusted for these multiple secondary comparisons. In order to investigate the possible confounding effect that adherence may have had on the original results, Karagianis et al used data from the subset of adherent patients from the PLATYPUS study to investigate factors associated with weight gain during olanzapine treatment.

Also, consistent with previous open-label findings, weight gain was lower in males but not females and patients residing in the US but not in Mexico or Canada treated with ODO, compared with those treated with SOT. Given the posthoc and unpowered nature of these analyses, these exploratory results should be interpreted with caution. The currently available evidence regarding a difference in the potential for weight gain with ODO versus SOT is inconsistent and warrants further study.

However, what does seem apparent is that if a difference exists between formulations in this regard, it is not likely to be a substantial one and may manifest only in certain patient populations.

It should also be borne in mind that equivalence of weight gain during olanzapine treatment should not be an overriding consideration if it comes at the cost of lower adherence and potential relapse. Patient preference is an important factor in long-term treatment adherence and thus treatment outcomes. Patients are more likely to persist with therapies they have had some active involvement in choosing, possibly aided by an enhanced therapeutic alliance as a consequence of improved patient motivation and insight into their illness and its treatment.

One single-arm study provided data on patient acceptance. In other words, while patients preferred the last formulation that they had taken, this preference was not strong enough to overcome the formulation preference in favor of ODO. Common free-text responses by patients as reasons for preference for a specific formulation were ease of use, taste, expectation of better effectiveness, and weight change.

Medication nonadherence is an issue of significant clinical importance in patients with serious mental illnesses such as schizophrenia and bipolar disorder. This is due to the fact that in these populations, the rate of nonadherence is high and is associated with poor outcomes such as low rates of remission and high rates of relapse, including hospitalization. In general, olanzapine studies utilizing SOT formulation have shown it to have an advantage in terms of treatment adherence and persistence over a number of typical and atypical antipsychotics.

The week randomized double-blind double-dummy study by Karagianis et al found a significantly higher proportion Karagianis et al suggested that the difference may be due to ODO possibly having some favorable effect, such as less appetite increase or satiety failure , resulting in patients wanting to take medication more regularly.

They found that overall acceptance was lower for ODO at baseline implying a potentially more noncompliant patient population to begin with , but ODO acceptance improved to a greater degree, almost reaching the same level as in SOT-treated patients, after 2 weeks. This study also found no significant differences between the treatment groups in change in attitude towards treatment, as measured by the Drug Attitude Inventory.

Considering that patients included in this study had to be clinically stable and remained so throughout the study, this lack of significant difference in adherence may result from this being an inherently adherent population of patients to begin with, thus having only minimal opportunity for further improvement in this regard. When study design and differences in patient populations being compared are taken into consideration, overall, the above results suggest ODO is associated with similar, and likely improved, adherence compared with SOT.

Schizophrenia and bipolar disorder impose a significant work burden on nursing staff in inpatient treatment settings where treatment often needs to be administered under difficult circumstances and patients closely monitored on an ongoing basis.

In order to systematically investigate this important aspect of psychiatric treatment and quantify various aspects of nursing resource utilization, Eli Lilly and Company developed the NAMA scale. Results relating to item two compliance were previously noted in the section on adherence.

Kinon et al used the NAMA questionnaire to assess nursing burden of treatment with ODO in acutely ill noncompliant patients with schizophrenia and schizoaffective disorder. Hori et al also used the NAMA questionnaire to assess nursing burden in first-episode schizophrenia.

Consistent with these results, without using NAMA, Van Heeringen et al investigated whether the use of ODO had an impact on nursing workload or the need for intramuscular medication in a retrospective observational study in psychiatric inpatients and outpatients. Thus, there is some evidence to suggest that ODO may not only reduce nursing burden relative to no treatment or other antipsychotics, but also when compared with SOT.

What conclusions of clinical relevance can then be drawn from the existing data? The studies reviewed above included a broad range of patient populations representative of those seen in usual practice settings, including those with first-episode schizophrenia, 36 patients already stabilized on treatment, 22 , 28 patients with diagnoses of schizophrenia, schizoaffective, schizophreniform disorder, and bipolar disorder, 27 , 38 and patients who are known to be nonadherent with treatment.

Data from open-label naturalistic studies, where physicians were free to prescribe according to their usual practice, also indicates that when given the choice of ODO or SOT, they often with some exceptions selected ODO for the treatment of more severely symptomatic patients. In regards to the important consideration of risk of weight gain during treatment with olanzapine, ODO may not have a significant advantage over SOT in all patients but at least does not appear to increase the risk of weight gain over SOT.

However, the choice of ODO over SOT would seem particularly prudent when there is a change in treatment setting which may impact adherence, such as moving from a more controlled environment to a less controlled one, eg, discharge from an inpatient facility or change in caregiver or accommodation. Although there are a number of atypical antipsychotics in orally disintegrating formulations eg, clozapine, risperidone, aripiprazole , very little information is available for those medications.

On the other hand, limited as it is relative to SOT, more substantive data from across patient populations, world geographies, study types, and study measures is available from ODO studies. However, a number of limitations, as well as strengths, of the existing data need to be acknowledged and taken into consideration. Each study design has its advantages and disadvantages which need to be considered in the interpretation of these results.

In the case of randomized trials, this often involves the inclusion of only certain types of patients who meet strict selection criteria and who are willing to consent to a rigid study protocol. Moreover, study conditions may not reflect real life practice conditions and, consequently, it may not be appropriate to generalize the results of such studies to the broader population with the disease state under investigation.

This may be the case with the preference study of Bitter et al, 28 where patients needed to be stabilized on medication prior to entering the study. While naturalistic observational studies have few inclusion criteria and are conducted under usual practice conditions, they are more representative of the types of outcomes that are to be expected in typical clinical practice. However, as patients tend to be allocated to medication the investigator believes is best suited to them, this inevitably leads to imbalance in various characteristics associated with treatment decisions some of which may be unmeasured or unobserved , and may impact the final outcomes.

Thus, in some ODO studies, patients with more severe symptoms who were considered less likely to be adherent with medication tended to be prescribed ODO.

In such cases, comparing potential treatment effects in disparate patient groups may be misleading, even though some attempt may be made to adjust for this baseline imbalance using statistical methods.

This difficulty is further complicated by the generally unrestricted use of concomitant medications and switching of treatments in naturalistic studies which makes linking outcomes with particular treatments more tenuous. The latter provides important insights into how the treatment actually performs and interacts with various patient characteristics, comorbidities, and concomitant medications which are not necessarily present in clinical trials, yet is the environment in which the treatment will ultimately be used.

This distinction is particularly important when considering the actual use and patient population which ODO could benefit ie, those that would typically not be represented in RCTs.

There would also be little value replicating the efficacy of ODO in highly controlled clinical trials when efficacy has already been established with SOT, as the active ingredient, olanzapine, is the same.

The main purpose of the ODO formulation has not been to alter the active ingredient but rather to enhance its palatability, ease of ingestion, convenience, and acceptability in patients, particularly those difficult-to-treat patients with swallowing problems or adherence issues. It is thus entirely understandable and to be expected that, with the exception of the PLATYPUS study which aimed to answer a very specific question, the focus of ODO research has not been the use of randomized clinical trials and replicating efficacy findings, but rather in the conduct of observational research to gain a better understanding of the benefits and limitations of the formulation in the actual target population under realistic conditions.

Another feature of the reviewed studies that complicates interpretation of the results is the tendency to conduct a multitude of secondary analyses, most of which were not sufficiently powered to assess the question at hand. Thus, nonsignificant results of the secondary analyses may arise from type II false negative error, whereas differences deemed significant on this basis may be consequence of type I false positive error.

Overall, while these studies provide a wealth of valuable information, in many cases the findings need to be replicated independently before they can be accepted as conclusive. ODO may also have benefits over SOT in terms of nursing burden and patient preferences, and this should be taken into consideration when making treatment decisions. While other rapidly dissolving generic formulations of olanzapine are available in various countries around the world, given the ostensibly important role of physical characteristics in determining patient preference and adherence, the recent comparative dissolution study of Hobbs et al 26 suggests that the majority of findings other than bioequivalence reviewed here may not necessarily be extrapolated to these other formulations.

Stop taking the medication and get immediate medical attention if you have symptoms of a severe allergic reaction, including fever, swollen glands, yellowing of the skin or eyes, or flu-like symptoms with skin rash or blistering. Liver disease: Olanzapine can affect liver function and cause liver problems. If you have liver problems, discuss with your doctor how this medication may affect your medical condition, how your medical condition may affect the dosing and effectiveness of this medication, and whether any special monitoring is needed.

Your doctor may want to test your liver function regularly with blood tests while you are taking this medication. If you experience symptoms of liver problems such as fatigue, feeling unwell, loss of appetite, nausea, yellowing of the skin or whites of the eyes, dark urine, pale stools, abdominal pain or swelling, and itchy skin, contact your doctor immediately.

Low blood pressure: Olanzapine may cause low blood pressure, especially when moving from a lying or sitting position to a standing position. If you have heart disease, cerebrovascular disease, or conditions that increase the risk of developing low blood pressure e.

Neuroleptic malignant syndrome NMS : Olanzapine, like other antipsychotic medications, can cause a potentially fatal syndrome known as neuroleptic malignant syndrome NMS. If you notice the symptoms of NMS such as high fever, confusion or loss of consciousness, racing or irregular heartbeat, muscle stiffness, or sweating, get immediate medical attention. Phenylketonuria: People with phenylketonuria an inherited disorder where the enzyme needed to break down phenylalanine is lacking should take the regular tablet forms of olanzapine and not the oral dissolving tablets ODT.

The ODT form of olanzapine contains aspartame, which is a source of phenylalanine. Prolonged erection: In rare cases, use of this medication by some men may cause them to develop priapism a prolonged and painful erection.

If you have an erection that lasts for more than 4 hours, contact your doctor. Seizures: Olanzapine may increase the risk of seizures, especially if you have had seizures in the past. If you are at risk of seizures and take this medication, you should be closely monitored by your doctor. Suicidal or self-harm behaviour: People taking this medication may want to hurt themselves or others. These symptoms may occur within several weeks after starting this medication.

If you experience these side effects or notice them in a family member who is taking this medication, contact your doctor immediately. You should be closely monitored by your doctor for emotional and behaviour changes while taking this medication. Tardive dyskinesia TD : TD, a syndrome consisting of potentially irreversible, involuntary, repetitive movements of the face and tongue muscles, may develop in people who take certain antipsychotic medications including olanzapine.

Although TD appears most commonly in seniors, especially women, it is impossible to predict who will develop TD. The risk of developing TD increases with higher doses and long-term treatment. If your experience muscle twitching or abnormal movements of the face or tongue, contact your doctor as soon as possible.

Urinary problems: This medication can cause urinary retention. If you have a history of urinary retention or benign prostatic hypertrophy, or other prostate problems, discuss with your doctor how this medication may affect your medical condition, how your medical condition may affect the dosing and effectiveness of this medication, and whether any special monitoring is needed.

Weight gain: With long-term treatment, weight gain averaging 5. Weight gain tends to level off after 6 to 8 months of treatment. Pregnancy: This medication should not be used during pregnancy unless the benefits outweigh the risks. If you become pregnant while taking this medication, contact your doctor immediately.

Babies born to mothers that took this medication in the last 3 months of pregnancy may experience withdrawal symptoms after they are born, including breathing problems, difficulty feeding, or irritability.

If you have been taking this medication during pregnancy, make sure that everyone involved in caring for you and your baby are aware. Breast-feeding: This medication passes into breast milk. Women taking this medication should not breast-feed.

Children: The safety and effectiveness of using this medication have not been established for children under the age of Seniors: There may be a higher risk of strokes, heart attacks, and deaths associated with the use of olanzapine by seniors with dementia.

Seek medical attention immediately if you notice the signs and symptoms of a stroke e. Olanzapine should not be used in seniors with dementia. If you are taking any of these medications, speak with your doctor or pharmacist. Depending on your specific circumstances, your doctor may want you to:. An interaction between two medications does not always mean that you must stop taking one of them.

Speak to your doctor about how any drug interactions are being managed or should be managed. Medications other than those listed above may interact with this medication.

Further information on clinical trials: In a multinational, double-blind, comparative study of schizophrenia, schizoaffective, and related disorders which included 1, patients with varying degrees of associated depressive symptoms baseline mean of Pharmacokinetics: Olanzapine orodispersible tablet is bioequivalent to olanzapine coated tablets, with a similar rate and extent of absorption. Olanzapine orodispersible tablets may be used as an alternative to olanzapine coated tablets. Absorption: Olanzapine is well absorbed after oral administration, reaching peak plasma concentrations within 5 to 8 hours.

The absorption is not affected by food. Absolute oral bioavailability relative to intravenous administration has not been determined. Biotransformation: Olanzapine is metabolized in the liver by conjugative and oxidative pathways. The major circulating metabolite is the N-glucuronide, which does not pass the blood brain barrier.

Cytochromes P CYP1A2 and PCYP2D6 contribute to the formation of the N-desmethyl and 2-hydroxymethyl metabolites, both exhibited significantly less in vivo pharmacological activity than olanzapine in animal studies. The predominant pharmacologic activity is from the parent olanzapine. Elimination: After oral administration, the mean terminal elimination half-life of olanzapine in healthy subjects varied on the basis of age and gender.

In healthy elderly 65 and over versus non-elderly subjects, the mean elimination half-life was prolonged The pharmacokinetic variability observed in the elderly is within the range for the non-elderly.

In female versus male subjects the mean elimination half life was somewhat prolonged Smokers: In smoking subjects with mild hepatic dysfunction, mean elimination half-life In non-smoking versus smoking subjects males and females the mean elimination half-life was prolonged The plasma clearance of olanzapine is lower in elderly versus young subjects, in females versus males, and in non-smokers versus smokers.

However, the magnitude of the impact of age, gender, or smoking on olanzapine clearance and half-life is small in comparison to the overall variability between individuals.

In a study of Caucasians, Japanese, and Chinese subjects, there were no differences in the pharmacokinetic parameters among the three populations. Paediatric population: Adolescents ages 13 to 17 years : The pharmacokinetics of olanzapine are similar between adolescents and adults.

Demographic differences between the adolescents and adults include a lower average body weight and fewer adolescents were smokers. Such factors possibly contribute to the higher average exposure observed in adolescents. Toxicology: Preclinical safety data: Acute single-dose toxicity: Signs of oral toxicity in rodents were characteristic of potent neuroleptic compounds: hypoactivity, coma, tremors, clonic convulsions, salivation, and depressed weight gain. Clinical signs included sedation, ataxia, tremors, increased heart rate, labored respiration, miosis, and anorexia.

Repeated-dose toxicity: In studies up to 3 months duration in mice and up to 1 year in rats and dogs, the predominant effects were CNS depression, anticholinergic effects, and peripheral haematological disorders. Tolerance developed to the CNS depression. Growth parameters were decreased at high doses.

Reversible effects consistent with elevated prolactin in rats included decreased weights of ovaries and uterus and morphologic changes in vaginal epithelium and in mammary gland. Haematologic toxicity: Effects on haematology parameters were found in each species, including dose-related reductions in circulating leukocytes in mice and non-specific reductions of circulating leukocytes in rats; however, no evidence of bone marrow cytotoxicity was found.

In cytopenic dogs, there were no adverse effects on progenitor and proliferating cells in the bone marrow. Reproductive toxicity: Olanzapine had no teratogenic effects. Sedation affected mating performance of male rats. Estrous cycles were affected at doses of 1.

In the offspring of rats given olanzapine, delays in foetal development and transient decreases in offspring activity levels were seen. Mutagenicity: Olanzapine was not mutagenic or clastogenic in a full range of standard tests, which included bacterial mutation tests and in vitro and in vivo mammalian tests.

Carcinogenicity: Based on the results of studies in mice and rats, it was concluded that olanzapine is not carcinogenic. Olanzapine is indicated for the treatment of schizophrenia. Olanzapine is effective in maintaining the clinical improvement during continuing therapy in patients who have shown initial treatment response. Olanzapine is indicated for short-term treatment of acute manic episode associated with Bipolar I Disorder.

Olanzapine is indicated for preventing recurrence of manic, mixed or depressive episodes in Bipolar I Disorder. Manic episode: The starting dose is 15 mg as a single daily dose in monotherapy or 10 mg daily in combination therapy See Pharmacology: Pharmacodynamics under Actions. For patients who have been receiving olanzapine for treatment of manic episode, continue therapy for preventing recurrence at the same dose.

If a new manic, mixed, or depressive episode occurs, olanzapine treatment should be continued with dose optimisation as needed , with supplementary therapy to treat mood symptoms, as clinically indicated. An increase to a dose greater than the recommended starting dose is advised only after appropriate clinical reassessment and should generally occur at intervals of not less than 24 hours. Olanzapine can be given without regards for meals as absorption is not affected by food.

Gradual tapering of the dose should be considered when discontinuing olanzapine. Olanzapine orodispersible tablet should be placed in the mouth, where it will rapidly disperse in saliva, so it can be easily swallowed. Removal of the intact orodispersible tablet from the mouth is difficult. Since the orodispersible tablet is fragile, it should be taken immediately on opening the blister. Alternatively, it may be dispersed in a full glass of water or other suitable beverage orange juice, apple juice, milk or coffee immediately before administration.

Olanzapine orodispersible tablet is bioequivalent to olanzapine coated tablets, with a similar rate and extent of absorption. It has the same dosage and frequency of administration as olanzapine coated tablets. In cases of moderate hepatic insufficiency cirrhosis, Child-Pugh Class A or B , the starting dose should be 5 mg and only increased with caution. Smokers: The starting dose and dose range need not be routinely altered for non-smokers relative to smokers. The metabolism of olanzapine may be induced by smoking.

Clinical monitoring is recommended and an increase of olanzapine dose may be considered if necessary see Interactions. When more than one factor is present which might result in slower metabolism female gender, geriatric age, non-smoking status , consideration should be given to decreasing the starting dose. Dose escalation, when indicated, should be conservative in such patients. In cases where dose increments of 2. See Pharmacology: Pharmacokinetics under Actions and Interactions. Paediatric population: Olanzapine is not recommended for use in children and adolescents below 18 years of age due to a lack of data on safety and efficacy.

A greater magnitude of weight gain, lipid and prolactin alterations has been reported in short term studies of adolescent patients than in studies of adult patients see Pharmacology: Pharmacokinetics under Actions, Precautions and Adverse Reactions. Fatal outcomes have been reported for acute overdoses as low as mg but survival has also been reported following acute overdose of approximately 2 g of oral olanzapine.

Treatment: There is no specific antidote for olanzapine. Induction of emesis is not recommended. Standard procedures for management of overdose maybe indicated i. Symptomatic treatment and monitoring of vital organ function should be instituted according to clinical presentation, including treatment of hypotension and circulatory collapse and support of respiratory function.

Do not use epinephrine, dopamine, or other sympathomimetic agents with beta-agonist activity since beta stimulation may worsen hypotension. Cardiovascular monitoring is necessary to detect possible arrhythmias. Close medical supervision and monitoring should continue until the patient recovers.