acute and chronic psychosis; sluggish schizophrenia; neurotic state; psychosomatic disease; psychoaffective disorders; migraines; behavioral disorders in childhood; as an adjunct to gastric and duodenal ulcer.
Eglonil 200 mg Composition
active substance: sulpiride;
1 capsule contains 50 mg sulpiride;
Eglonil 200 mg excipients: lactose, methylcellulose, talc, magnesium stearate, capsule shell: gelatin, titanium dioxide (E 171).
Eglonil 200 mg Dosage form
Basic physical and chemical properties: opaque white or almost white capsules No. 4, containing a creamy white powder.
Antipsychotic drugs. ATX code N05A L01.
Sulpiride affects dopaminergic nerve transmission in the brain as a dopaminomimetic, due to which it has an activating effect in low doses. At higher doses, sulpiride also reduces productive symptoms.
After oral administration of one capsule of 50 mg, the maximum plasma concentration of sulpiride (0.25 mg / l) is reached after 3-6 hours.
The bioavailability of oral dosage forms is 25-35% with wide individual variations; sulpiride has a linear pharmacokinetic profile after administration in doses ranging from 50 to 300 mg.
Sulpiride is rapidly distributed in body tissues: the apparent volume of distribution at steady state is 0.94 l / kg. Plasma protein binding is 40%.
Sulpiride is found in small amounts in breast milk and can cross the placental barrier.
Sulpiride is practically not metabolized in the human body.
Sulpiride is excreted mainly by the kidneys by glomerular filtration. Its renal clearance is 126 ml / min. The half-life is 7 hours.
Short-term symptomatic treatment of anxiety in adults when conventional therapeutic measures have failed.
Serious behavioral disorders (agitation, self-harm, stereotypy) in children over 6 years of age, especially in patients with autistic syndromes.
Hypersensitivity to sulpiride or any of the excipients of the drug (see Section “Composition”).
Prolactin-dependent tumors (eg prolactin-secreting pituitary adenoma (prolactinoma) and breast cancer).
Known or suspected diagnosis of pheochromocytoma.
Combinations with dopamine receptor agonists not for the treatment of Parkinson’s disease (cabergoline, quinagolide), citalopram and escitalopram, hydroxyzine, domperidone and piperazine (see Section “Interaction with other medicinal products and other forms of interaction”).
Interaction with other medicinal products and other forms of interaction
It should be remembered that many drugs or substances can have an additive inhibitory effect on the central nervous system and lead to a decrease in mental activity. These drugs include morphine derivatives (analgesics, antitussives, and substitution therapy), antipsychotics, barbiturates, benzodiazepines, non-benzodiazepine anxiolytics (such as meprobamate), hypnotics, sedative antidepressants (amitriptyline, doxepin, mianserin-1 , centrally acting antihypertensives, baclofen and thalidomide.
Drugs that can cause the development of paroxysmal ventricular tachycardia (torsades de pointes)
A number of drugs with or without antiarrhythmic activity can lead to this serious disturbance of the heart rhythm. The provoking factors are hypokalemia (see “Potassium-deficient drugs”) and bradycardia (see “Drugs that cause bradycardia”) or the presence of congenital or acquired lengthening of the QT interval.
These drugs include, in particular, class Ia and III antiarrhythmic drugs and some antipsychotics. This effect is also induced by other drugs that do not belong to these classes.