Betahistine tablets 8 mg, 30 pcs.

ATX CODE: N07SA01.
PHARMACODINAMICS
The mechanism of action of betahistine is only partially known. There are several possible hypotheses confirmed by preclinical and clinical data:
Effects on the histaminergic system:
Partial H1-histamine antagonist H3-histamine receptor antagonist of the vestibular nuclei of the central nervous system (CNS), has little activity against H2-receptors. Betahistine increases histamine metabolism and release by blocking presynaptic H3 receptors and reducing the number of H3 receptors.
Increased blood flow to the cochlear region as well as the entire brain:
According to preclinical studies, betahistine improves blood flow in the inner ear vasculature by relaxing the irascapillary sphincters of inner ear vessels. Betahistine has also been shown to increase cerebral blood flow in humans.
Facilitation of central vestibular coping
Betahistine accelerates recovery of vestibular function in animals after unilateral vestibular neurectomy by accelerating and facilitating central vestibular coping due to antagonism with H3-histamine receptors.
Recovery time after vestibular neurectomy in humans is also reduced.
Excitation of neurons in vestibular nuclei:
Dose-dependently reduces the generation of action potentials in the lateral and medial vestibular neurons.
Pharmacodynamic properties revealed on animals provide a positive therapeutic effect of betahistine in the vestibular system.
The effectiveness of betahistine has been demonstrated in patients with vestibular vertigo and Meniere’s syndrome, as manifested by a reduction in the severity and frequency of dizziness.
PHARMACOKINETICS
Absorption:
When administered orally, betahistine is rapidly and almost completely absorbed in the gastrointestinal tract (GIT). After absorption, the drug is rapidly and almost completely metabolized to form the metabolite 2-pyridylacetic acid in plasma and urine. The plasma concentration of betahistine is very low. Thus, pharmacokinetic assays are based on measuring the concentration of the metabolite 2-pyridylacetic acid. When the drug is taken with food, the maximum concentration (Cmax) of the drug in blood is lower than when taken on an empty stomach. However, total absorption of betahistine is similar in both cases, indicating that food intake slows absorption of betahistine.
Distribution:
Binding of betahistine to plasma proteins is less than 5%.
Biotransformation:
After absorption, betahistine is rapidly and almost completely metabolized to form the metabolite 2-pyridylacetic acid (which has no pharmacological activity).
Maximum concentration of 2-pyridylacetic acid in blood plasma (or urine) is reached one hour after administration. The elimination half-life is approximately 3.5 hours.
Excretion:
2-pyridylacetic acid is rapidly excreted in the urine. When administered at a dose of 8-48 mg, approximately 85% of the initial dose is detected in the urine. Excretion of betahistine by the kidneys or through the intestine is insignificant.
Linearity:
The excretion rate remains constant with oral administration of 8-48 mg of the drug, indicating linearity in the pharmacokinetics of betahistine and suggesting that the metabolic pathway involved remains unsaturated.

Indications

Active ingredient

Composition

1 tablet(8 mg) contains:

active ingredient: betahistine dihydrochloride – 8 mg

excipients: lactose monohydrate, microcrystalline cellulose, magnesium stearate, colloidal silicon dioxide, corn starch.

How to take, the dosage

Internal, with meals. 1/2-1 tablets 3 times a day.

Emprovement is usually seen at the beginning of therapy. Stable therapeutic effect occurs after two weeks of treatment and may increase during several months of treatment. Treatment is long. The duration of therapy is determined individually.

Interaction

Special Instructions

Contraindications

With caution:

Side effects

Overdose

Symptoms: nausea, vomiting, convulsions.

Treatment: gastric lavage, administration of activated charcoal, symptomatic therapy.

Similarities