Index of drugs

Symptomatic treatment of mild to moderately severe Alzheimer's dementia. Symptomatic treatment of mild to moderately severe dementia in patients with idiopathic Parkinson's disease.

One capsule contains 1.5 mg, 3 mg, 4.5 mg or 6 mg of rivastigmine in the form of hydrogen tartrate.

An inhibitor of acetyl- and butyrylcholinesterases from the group of carbamates, improving the cholinergic neurotransmission by slowing the decomposition of acetylcholine, released by functionally functional cholinergic neurons. Rivastigmine may alleviate cognitive deficits associated with the cholinergic system in dementia accompanying Alzheimer's disease and Parkinson's disease. The drug is absorbed very quickly and completely, reaching the maximum plasma concentration after about 1 hour. As a result of the drug's effect on its target enzyme, the increase in bioavailability is about 1.5 times greater than it would result from the increase in the dose. The absolute bioavailability after the 3 mg dose is approximately 36% ± 13%. Taking rivastigmine with food delays absorption by 90 min, decreases the C value_max and increases the AUC by approximately 30%. Rivastigmine binds to proteins in approximately 40%, easily penetrates the blood-brain barrier. It is very rapidly and extensively metabolised (T._0,5 in the plasma is about 1 hour) mainly in the cholinesterase hydrolysis reaction to the decarbamylated metabolite.In vitro this metabolite exhibits only minimal inhibitory activity with respect to acetylcholinesterase (<10%). The main cytochrome P450 isoenzymes play only a minor role in the metabolism of rivastigmine. No unchanged rivastigmine was found in the urine; The main route of elimination is the excretion of metabolites by the kidneys in the urine. Less than 1% of the administered dose is excreted in faeces.

Hypersensitivity to rivastigmine, other carbamate derivatives or to any of the excipients included in the medicine. Severe liver dysfunction (no studies in this group of patients).

Rivastigmine should be used with caution in patients with a sinus node syndrome or with conduction disorders (sinoatrial block, atrioventricular block), in patients with active gastric or duodenal ulcer disease or in patients with predisposition to these diseases. Cholinesterase inhibitors should be used with caution in patients with bronchial asthma or obstructive pulmonary disease. Cholinomimetics may cause or exacerbate urinary tract obstruction and seizures - caution is recommended in the treatment of patients with predisposition to these diseases. Rivastigmine has not been studied in patients with advanced dementia in Alzheimer's disease or Parkinson's disease, other types of dementia or other types of memory impairment (eg age-related cognitive impairment), so it is not advisable to use the medicine in these patient groups. Rivastigmine may exacerbate or precipitate extrapyramidal symptoms - in patients with dementia associated with Parkinson's disease, the severity of the disease (including slowness of movement, dyskinesia, gait abnormalities) and more frequent occurrence and severity of tremor have been observed. These side effects in some cases led to discontinuation of rivastigmine. Clinical control is recommended for these side effects. It is not recommended to use the drug in children.

There is no clinical data on the use of rivastigmine during pregnancy - rivastigmine should not be used during pregnancy unless clearly necessary. It is not known whether rivastigmine is excreted in human breast milk - women taking the drug should not breastfeed.

Very common: dizziness, nausea, vomiting, diarrhea, lack of appetite. Common: agitation, confusion, headache, drowsiness, tremor, abdominal pain, dyspepsia, increased sweating, fatigue, asthenia, malaise, weight loss. Uncommon: insomnia, depression, fainting, increased values ​​of liver function tests, accidental fall.Rare: convulsions, angina, gastric and duodenal ulcer, rash. Very rare: urinary tract infection, hallucinations, extrapyramidal symptoms (including deterioration in patients with Parkinson's disease), arrhythmias (eg bradycardia, atrioventricular block, atrial fibrillation, tachycardia), hypertension, gastrointestinal bleeding, inflammation of the pancreas. Not known: cases of severe vomiting associated with esophageal rupture. Side effects reported in patients with dementia associated with Parkinson's disease: very common: tremors, nausea, vomiting; common: insomnia, anxiety, anxiety, dizziness, drowsiness, headache, worsening Parkinson's disease, slowness, dyskinesia, bradycardia, diarrhea, abdominal pain, indigestion, excessive salivation, increased sweating, muscle stiffness, lack of appetite, dehydration, fatigability and asthenia, gait disturbances; uncommon: dystonia, atrial fibrillation, atrioventricular block.

Orally. Treatment should be initiated and maintained by a physician experienced in the diagnosis and treatment of Alzheimer's dementia or dementia associated with Parkinson's disease. The diagnosis should be made on the basis of current guidelines. Treatment with rivastigmine should only be started when the patient has the care of a person who can control his regular medication. Starting dose: 1.5 mg 2 times a day. Determining the optimal dose: if the initial dose is well tolerated, after at least 2 weeks of treatment, it can be increased to 3 mg 2 times a day. Subsequent titration to 4.5 mg followed by up to 6 mg twice daily must also be conditioned by good tolerability of the previous dose over a period of at least 2 weeks. If patients with dementia associated with Parkinson's disease experience side effects (eg nausea, vomiting, abdominal pain or loss of appetite), weight loss or exacerbation of extrapyramidal symptoms (e.g. tremor), these patients may respond positively to omitting one or more doses. If side effects persist, the daily dose should be temporarily reduced to the previous, well-tolerated dose or treatment should be discontinued. Maintenance dose: the therapeutic dose is 3-6 mg 2 times a day. In order to achieve maximum therapeutic effect, patients should continue treatment taking the highest, well-tolerated dose. The recommended maximum daily dose is 6 mg 2 times a day. Maintenance treatment can be continued as long as the therapeutic effect persists. Therefore, a regular clinical evaluation of the therapeutic effect of rivastigmine is required, especially in patients taking doses lower than 3 mg 2 times a day. If there is no beneficial change in the relief of dementia after 3 months of treatment, treatment should be discontinued. Discontinuation of treatment should also be considered in the absence of therapeutic effects. Individual response to rivastigmine is unpredictable. However, better treatment results were observed in patients with moderate dementia associated with Parkinson's disease. Similarly, a better treatment effect was observed in patients with Parkinson's disease suffering from visual hallucinations. Therapy was not studied in placebo-controlled clinical trials lasting longer than 6 months. If treatment was discontinued for more than a few days, it should be resumed at 1.5 mg 2 times a day and then the optimal dose should be determined. in the manner described above. Due to the increase in exposure in patients with moderate renal impairment and mild to moderate hepatic impairment, the dose should be carefully determined based on individual tolerability.
The preparation should be administered twice a day during the morning and evening meal. The capsules should be swallowed whole.