
In our store you can buy online Venlaxor in the specified variations:
- tabs 37.5mg N30;
- tabs 75mg N30.
Active substance:
Venlafaxine.
Manufacture: Grindex.
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Buy Venlaxor
Depression of various etiologies (treatment and prevention).
Inside, with food.
The recommended initial dose is 75 mg in 2 divided doses (37.5 mg daily). If after several weeks of treatment there is no significant improvement, the daily dose can be increased to 150 mg (75 mg twice a day). If, in the doctor's opinion, a higher dose is required (severe depressive disorder or other conditions requiring in-patient treatment), 150 mg can be immediately given in 2 divided doses (75 mg twice a day). After this, the daily dose can be increased by 75 mg every 2-3 days until the desired therapeutic effect is achieved. The maximum daily dose is 375 mg. After achieving the necessary therapeutic effect, it is possible to gradually reduce the daily dose to a minimum effective level.
Supportive therapy and prevention of relapse: supportive treatment can last 6 months or more. The minimum effective doses used in the treatment of a depressive episode are prescribed.
Renal failure: with mild renal failure (GFR -> 30 mL / min), correction of the dosing regimen is not required. With moderate renal failure (GFR - 10-30 ml / min), the dose should be reduced by 25-50%. In connection with the lengthening of the half-life of venlafaxine and its active metabolite EFA, such patients should take the entire dose 1 time per day. It is not recommended to use venlafaxine in severe kidney failure (GFR <10 ml / min), since there is no reliable data on such therapy. Patients on hemodialysis can receive 50% of the usual daily dose of venlafaxine after completion of hemodialysis.
Hepatic failure: with mild hepatic insufficiency (MI - <14 s), correction of the dosing regimen is not required. With moderate hepatic insufficiency (MI - 14 to 18 s), the dose should be reduced by 50%. It is not recommended to use venlafaxine in severe hepatic insufficiency, since there are no reliable data on such therapy.
Elderly patients: the old age of the patient does not require a dose change, however, as with the prescription of other medications, caution is needed in the treatment of elderly patients, for example, due to the possibility of impaired renal function. The lowest effective dose should be used. When the dose is raised, the patient should be under careful medical supervision.
Discontinuation of Venlaxor®:
At the end of taking VENLAKSOR®, it is recommended to gradually reduce the dosage of the drug for at least a week and monitor the patient's condition in order to minimize the risk associated with withdrawal of the drug (see below).
The period required to completely stop taking the drug depends on its dosage, the length of the course of treatment and the individual characteristics of the patient.
The simultaneous use of MAO inhibitors and venlafaxine is contraindicated. The preparation of Venlaxor® can be started no less than 14 days after the end of therapy with MAO inhibitors. If a reversible MAO inhibitor (moclobemide) was used, this interval may be shorter (24 h). Therapy with MAO inhibitors can begin at least 7 days after the cancellation of VENLAKSOR®.
Venlafaxine does not affect the pharmacokinetics of lithium.
With simultaneous use with imipramine, the pharmacokinetics of venlafaxine and its metabolite EFA does not change.
Haloperidol: the effect of the latter may be enhanced due to an increase in the level of the drug in the blood in a joint application.
With simultaneous use with diazepam, the pharmacokinetics of drugs and their major metabolites do not change significantly. Also, there was no effect on the psychomotor and psychometric effects of diazepam.
With simultaneous use with clozapine, there may be an increase in its level in the blood plasma and the development of side effects (eg epileptic seizures).
With simultaneous use with risperidone (despite an increase in risperidone AUC), the pharmacokinetics of the sum of active components (risperidone and its active metabolite) did not change significantly.
Increases the effect of alcohol on psychomotor reactions.
On the background of taking venlafaxine, special care should be taken with electroconvulsive therapy. experience with venlafaxine in these conditions is absent.
Drugs metabolized by cytochrome P450 isoenzymes: unlike many other antidepressants, the dose of venlafaxine can not be decreased by concomitant administration with CYP2D6 inhibitory drugs or in patients with a genetically determined decrease in CYP2D6 activity (the enzyme CYP2D6 of the cytochrome P450 system converts venlafaxine to an active metabolite EFA), since the total concentration of active substance and metabolite (venlafaxine and EFA) will not change.
The main way to eliminate venlafaxine involves metabolism involving CYP2D6 and CYP3A4; therefore, special care should be taken with the appointment of venlafaxine in combination with drugs that depress both of these enzymes. Such drug interactions have not yet been investigated.
Venlafaxine is a relatively weak inhibitor of CYP2D6 and does not suppress the activity of the isoenzymes CYP1A2, CYP2C9 and CYP3A4; therefore, its interaction with other drugs in the metabolism of which these hepatic enzymes are involved should not be expected.
Cimetidine suppresses the metabolism of the "first passage" of venlafaxine and does not affect the pharmacokinetics of EFA. In most patients, only a slight increase in the overall pharmacological activity of venlafaxine and EFA is expected (more pronounced in elderly patients and in liver failure).
Clinically significant interactions of venlafaxine with antihypertensive (including beta-blockers, ACE inhibitors and diuretics) and antidiabetic drugs have not been detected.
Drugs associated with blood plasma proteins: binding to plasma proteins is 27% for venlafaxine and 30% for EFA, so there is no effect on the concentration in the blood plasma of drugs that have a high degree of binding to proteins.
With the simultaneous administration of warfarin, the anticoagulant effect of the latter can be enhanced.
With simultaneous admission with indinavir, the pharmacokinetics of indinavir changes (with a 28% reduction in AUC and a 36% decrease in Cmax), and the pharmacokinetics of venlafaxine and EFA do not change. However, the clinical significance of this effect is unknown.