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.

1 capsule contains 1.5 mg, 3 mg, 4.5 mg or 6 mg of rivastigmine (as hydrogen tartrate).

Rivastigmine is an inhibitor of acetyl- and butyrylcholinesterase from the group of carbamates, which improves cholinergic neurotransmission, by slowing down the process of acetylcholine decomposition released by functionally functional cholinergic neurons. Thus, rivastigmine may have a positive effect on cognitive deficits related to cognitive processes in patients with dementia associated with Alzheimer's disease and Parkinson's disease. Rivastigmine exerts an inhibitory action against cholinesterases, forming a complex with them by means of a covalent linkage, which causes their inactivation temporarily. Rivastigmine is absorbed quickly and completely, reaching a maximum blood concentration after about 1 hour. Due to the effect of rivastigmine on its target enzyme, the increase in bioavailability is about 1.5 times higher than would result from the increase in dose. The absolute bioavailability at 3 mg is approximately 36% ± 13%. Administration of rivastigmine with food delays the absorption of the drug by 90 minutes, decreases the C value_max and increases the AUC by approximately 30%. Rivastigmine is associated with proteins in approximately 40%. It easily penetrates the blood-brain barrier. It is rapidly and extensively metabolised (T._0,5 in the blood is about 1 hour) mainly in the hydrolysis, by means of cholinesterase, to the decarbamylated metabolite. The resulting metabolite showsin vitro only a small inhibitory activity against acetylcholinesterase (<10%). No unchanged rivastigmine was found in the urine. Excretion of metabolites in urine is the main route of elimination. Fewer than 1% of the administered dose is excreted in the faeces. No accumulation of rivastigmine or its major metabolite was found in patients with Alzheimer's disease.

Hypersensitivity to the active substance, other carbamates or to any of the excipients. Severe liver dysfunction (no studies).

The use of rivastigmine in children is not recommended. Caution should be exercised in patients with sick sinus syndrome or with conduction disorders (sinoatrial block, atrioventricular block), with active gastric or duodenal ulcer disease (and with predisposition to these diseases), with bronchial asthma or obstructive pulmonary disease interview and patients with predisposition to urinary tract obstruction and seizures. Due to the lack of studies, rivastigmine is not recommended for patients with severe dementia in Alzheimer's disease or in the course of Parkinson's disease, other types of dementia or other types of memory impairment (eg age-related cognitive impairment). Like other cholinomimetics, rivastigmine may exacerbate or induce extrapyramidal symptoms (including motor retardation, dyskinesias, gait disturbances, tremor), especially in patients with dementia associated with Parkinson's disease - patients should be monitored for these side effects.

It must not be used during pregnancy unless clearly necessary and should not be used during breastfeeding.

The incidence and severity of side effects increases with increasing dose. Gastrointestinal disorders such as nausea, vomiting and diarrhea are dose related and may occur especially at the beginning of treatment and / or during dose escalation and are more common in women.Patients with Alzheimer's dementia. Very common: dizziness, nausea, vomiting, diarrhea, lack of appetite. Common: agitation, confusion, headache, drowsiness, tremor, abdominal pain and indigestion, increased sweating, fatigue and asthenia, malaise, weight loss.Uncommon: insomnia, depression, fainting, increased value of liver function tests, accidental fall. Rare: convulsions, angina pectoris, peptic ulcer of the stomach and duodenum, rash. Very rare: urinary tract infection, hallucinations, extrapyramidal symptoms (including worsening Parkinson's disease), arrhythmias (eg bradycardia, atrioventricular block, atrial fibrillation, tachycardia), hypertension, gastrointestinal bleeding, pancreatitis. Frequency unknown: cases of severe vomiting associated with esophageal rupture.Patients with dementia associated with Parkinson's disease. Very often: tremor, nausea, vomiting. Common: insomnia, anxiety, anxiety, dizziness, drowsiness, headache, worsening of Parkinson's disease, slowness, dyskinesia, bradycardia, diarrhea, abdominal pain and indigestion, excessive salivation, increased sweating, muscular stiffness, lack of appetite, dehydration, feeling fatigue and asthenia, gait disturbances. Uncommon: dystonia, atrial fibrillation, atrioventricular block.

Orally. Adults. Treatment should be initiated and supervised by a physician experienced in the diagnosis and treatment of Alzheimer's dementia or dementia associated with Parkinson's disease. The starting dose is 1.5 mg 2 times a day. If the dose is well tolerated, it can be increased to 3 mg 2 times a day after at least 2 weeks of treatment. Subsequent titration up to 4.5 mg, and then up to 6 mg twice daily is possible with good tolerability of the current dose and may be considered after at least 2 weeks of treatment with the previous dose. Adverse reactions (eg nausea, vomiting, abdominal pain or loss of appetite), weight loss or exacerbation of extrapyramidal symptoms (eg tremor) in patients with dementia associated with Parkinson's disease, occurring during treatment, may resolve if one or several doses are missed . If side effects persist, the daily dose should be temporarily reduced to the previous well-tolerated dose or treatment should be discontinued. The maintenance dose is 3-6 mg twice daily; for maximum therapeutic effect, patients should continue treatment using 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, the therapeutic effect of the medicine should be regularly reassessed, particularly in patients treated with doses lower than 3 mg twice daily. 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 signs of therapeutic effect. Therapy was not investigated in placebo-controlled clinical trials lasting more than 6 months. If rivastigmine was discontinued for more than a few days, treatment should be resumed at 1.5 mg twice daily. Determination of the optimal dose should then take place as described above. In patients with moderate renal dysfunction and mild to moderate hepatic impairment, the dose should be individually adjusted due to the increased exposure of these patients. The preparation should be taken with a morning and evening meal. Swallow the capsules whole.