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Kigabeq is a brand name for Vigabatrin. The medicine, its uses, side effects and dosage are the same regardless of brand.
Used for: Kigabeq is indicated in infants and children from 1 month to less than 7 years of age for: - Treatment in monotherapy of infantile spasms (West's syndrome). - Treatment in combination with other antiepileptic medicinal products for patients with resistant partial epilepsy (focal onset seizures) with or without…
Verbatim from this product's EMA label. Tap a section to expand.
Vigabatrin treatment may only be initiated by a specialist in epileptology, neurology or paediatric neurology. Follow-up should be arranged under supervision of a specialist in epileptology, neurology or paediatric neurology. Posology Monotherapy for infantile spasms (West’s Syndrome) The recommended starting dose is 50 mg/kg/day.
Subsequent dosing can be titrated by 25 mg/kg/day increments every 3 days up to the maximum recommended dose of 150 mg/kg/day. Doses of vigabatrin should be given twice daily according to the table below. 5 x 500 mg tablet evening 16 4 x 100 mg tablet morning 4 x 100 mg tablet evening 1 x 500 mg and 1 x 100 mg tablet morning 1 x 500 mg and 1 x 100 mg tablet evening 1 x 500 mg and 3 x 100 mg tablet morning 1 x 500 mg and 3 x 100 mg tablet evening Resistant partial epilepsy (focal onset seizures) The recommended starting dose is 40 mg/kg/day.
5 g/day Doses of vigabatrin should be given twice daily according to the table below. 5 x 100 mg tablet evening 25 1 x 500 mg tablet morning 1 x 500 mg tablet evening 28 1 x 500 mg tablet morning 1 x 500 mg and 1 x 100 mg tablet evening 30 1 x 500 mg and 1 x 100 mg tablet morning 1 x 500 mg and 1 x 100 mg tablet evening Kigabeq is for oral or gastric administration twice daily and may be taken before or after meals.
The maximum recommended dose should not be exceeded. If control of epilepsy is not clinically significantly improved after an adequate treatment course, vigabatrin treatment should be discontinued. Vigabatrin should be gradually withdrawn under close medical supervision.
Special populations Renal impairment Since vigabatrin is eliminated via the kidneys, caution should be exercised when administering the medicinal product to patients with creatinine clearance less than 60 ml/min. Adjustment of dose should be considered.
Such patients may respond to a lower maintenance dose. 8). Hepatic impairment 5 Vigabatrin is not metabolised by hepatic enzymes, hence there is no need of adjustment of dose or frequency of administration. 4). Paediatric population There is no relevant use of Kigabeq in neonates (below 27 days of age) in the indication “infantile spasms” and in children and adolescents above 7 years of age in the indication “resistant partial epilepsy” (focal onset seizures).
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8. The onset is usually after months to years of vigabatrin therapy. The degree of visual field constriction may be severe and this may have practical consequences for the patient. Vigabatrin can cause permanent vision loss. Most of the patients with perimetry-confirmed defects have been asymptomatic.
Hence, this undesirable effect can only be reliably detected by systematic perimetry which is usually possible only in patients with a developmental age of more than 9 years. For younger patients electroretinography should be used (see visual field defects).
Available data suggests that visual field defects are irreversible even after discontinuation of vigabatrin. A deterioration of VFD after the treatment is discontinued cannot be excluded. 6 Therefore, vigabatrin should only be used after careful benefit/ risk assessment compared with alternatives.
Vigabatrin is not recommended for use in patients with any pre-existing clinically significant visual field defect. Patients should undergo systematic screening examination when starting vigabatrin and at regular intervals for detection of visual field defects.
Visual field testing should continue at 6-month intervals for the whole duration of treatment. The assessment must be continued 6 to 12 months after the discontinuation of therapy (see visual field defects). Visual field defects (VFD) Based on available data, the usual pattern is a concentric constriction of the visual field of both eyes, which is generally more marked nasally than temporally.
In the central visual field (within 30 degree of eccentricity), frequently an annular nasal defect is seen. However, the VFDs reported in patients receiving vigabatrin have ranged from mild to severe. Severe cases are potentially disabling and may be characterized by tunnel vision.
Blindness was also reported in severe cases. Most patients with perimetry-confirmed defects had not previously spontaneously noticed any symptoms, even in cases where a severe defect was observed in perimetry. Available evidence suggests that the VFD is irreversible even after discontinuation of vigabatrin.
Visual field defects (VFD) have been reported in patients receiving vigabatrin with a high prevalence (about 1/3 of patients). 8. The onset is usually after months to years of vigabatrin therapy. The degree of visual field constriction may be severe and this may have practical consequences for the patient.
Vigabatrin can cause permanent vision loss. Most of the patients with perimetry-confirmed defects have been asymptomatic. Hence, this undesirable effect can only be reliably detected by systematic perimetry which is usually possible only in patients with a developmental age of more than 9 years.
For younger patients electroretinography should be used (see visual field defects). Available data suggests that visual field defects are irreversible even after discontinuation of vigabatrin. A deterioration of VFD after the treatment is discontinued cannot be excluded.
6 Therefore, vigabatrin should only be used after careful benefit/ risk assessment compared with alternatives. Vigabatrin is not recommended for use in patients with any pre-existing clinically significant visual field defect. Patients should undergo systematic screening examination when starting vigabatrin and at regular intervals for detection of visual field defects.
Visual field testing should continue at 6-month intervals for the whole duration of treatment. The assessment must be continued 6 to 12 months after the discontinuation of therapy (see visual field defects). Visual field defects (VFD) Based on available data, the usual pattern is a concentric constriction of the visual field of both eyes, which is generally more marked nasally than temporally.
In the central visual field (within 30 degree of eccentricity), frequently an annular nasal defect is seen. However, the VFDs reported in patients receiving vigabatrin have ranged from mild to severe. Severe cases are potentially disabling and may be characterized by tunnel vision.
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A deterioration of VFD after the treatment is discontinued cannot be excluded. Pooled data from prevalence surveys suggest that as many as 1/3 of patients receiving vigabatrin therapy have VFDs. Males may be at greater risk than females.
8. A possible association between the risk of visual field defects and the extent of vigabatrin exposure, both in terms of daily dose (from 1 gram to more than 3 grams) and in terms of duration of treatment (maximum during the first three years) has been shown in this study.
All patients should have ophthalmological consultation before or shortly after the initiation of vigabatrin treatment. Perimetry is seldom possible in children less than 9 years of developmental age. The risks of treatment must be very carefully weighed against possible benefit in children.
Currently, there is no established method to diagnose or exclude visual field defects in children in whom a standardised perimetry cannot be performed. Frequency and severity have only been indirectly characterised in this population on the presence of electroretinogram or visual evoked potential anomalies.
Electroretinography is recommended in infants and children who are unable to cooperate with perimetry. Based on the available data the first oscillatory potential and 30 Hz flicker responses of the electroretinogram appear to be correlated with a vigabatrin associated VFD.
These responses are delayed and reduced beyond the normal limits. Such changes have not been seen in vigabatrin treated patients without a VFD. The parents and/or caregivers must be given a thorough description of the frequency and Implications of the development of VFD during vigabatrin treatment.
VFD may not be detected until it is severe and undetected moderate defects may affect child integrity. Therefore, vision assessment is required at baseline (no later than 4 weeks after starting treatment) and at least every 6 months while on therapy.
The assessment must be continued 6 to 12 months after the discontinuation of therapy. Available data suggests that visual field defects are irreversible. If a visual field constriction is observed during follow-up, consideration should be given to gradual discontinuation of vigabatrin.
If the decision to continue treatment is made, consideration should be 7 given to more frequent follow-up (perimetry) in order to detect progression or sight threatening defects. Vigabatrin should not be used concomitantly with other retinotoxic medicinal products.
3) it is recommended that patients treated with vigabatrin are closely observed for adverse reactions on neurological function. Rare reports of encephalopathic symptoms such as marked sedation, stupor and confusion in association with non-specific slow wave activity on electroencephalogram have been described soon after the initiation of vigabatrin treatment.
Risk factors for the development of these reactions include higher than recommended starting dose, faster dose escalation at higher steps than recommended and renal failure. 8). Abnormal magnetic resonance imaging signals Abnormal magnetic resonance imaging (MRI) signal changes characterised by increased T2 signal and restricted diffusion in a symmetric pattern involving the thalamus, basal ganglia, brain stem, and cerebellum have been observed in some infants treated with vigabatrin for infantile spasms.
In a retrospective epidemiologic study in infants with infantile spasms (N = 205), the prevalence of these changes was 22 % in vigabatrin treated patients versus 4 % in patients treated with other therapies. In the study above, in […]
Blindness was also reported in severe cases. Most patients with perimetry-confirmed defects had not previously spontaneously noticed any symptoms, even in cases where a severe defect was observed in perimetry. Available evidence suggests that the VFD is irreversible even after discontinuation of vigabatrin.
A deterioration of VFD after the treatment is discontinued cannot be excluded. Pooled data from prevalence surveys suggest that as many as 1/3 of patients receiving vigabatrin therapy have VFDs. Males may be at greater risk than females.
8. A possible association between the risk of visual field defects and the extent of vigabatrin exposure, both in terms of daily dose (from 1 gram to more than 3 grams) and in terms of duration of treatment (maximum during the first three years) has been shown in this study.
All patients should have ophthalmological consultation before or shortly after the initiation of vigabatrin treatment. Perimetry is seldom possible in children less than 9 years of developmental age. The risks of treatment must be very carefully weighed against possible benefit in children.
Currently, there is no established method to diagnose or exclude visual field defects in children in whom a standardised perimetry cannot be performed. Frequency and severity have only been indirectly characterised in this population on the presence of electroretinogram or visual evoked potential anomalies.
Electroretinography is recommended in infants and children who are unable to cooperate with perimetry. Based on the available data the first oscillatory potential and 30 Hz flicker responses of the electroretinogram appear to be correlated with a vigabatrin associated VFD.
These responses are delayed and reduced beyond the normal limits. Such changes have not been seen in vigabatrin treated patients without a VFD. The parents and/or caregivers must be given a thorough description of the frequency and Implications of the development of VFD during vigabatrin treatment.
VFD may not be detected until it is severe and undetected moderate defects may affect child integrity. Therefore, vision assessment is required at baseline (no later than 4 weeks after starting treatment) and at least every 6 months while on therapy.
The assessment must be continued 6 to 12 months after the discontinuation of therapy. Available data suggests that visual field defects are irreversible. If a visual field constriction is observed during follow-up, consideration should be given to gradual discontinuation of vigabatrin.
If the decision to continue treatment is made, consideration should be 7 given to more frequent follow-up (perimetry) in order to detect progression or sight threatening defects. Vigabatrin should not be used concomitantly with other retinotoxic medicinal products.
3) it is recommended that patients treated with vigabatrin are closely observed for adverse reactions on neurological function. Rare reports of encephalopathic symptoms such as marked sedation, stupor and confusion in association with non-specific slow wave activity on electroencephalogram have been described soon after the initiation of vigabatrin treatment.
Risk factors for the development of these reactions include higher than recommended starting dose, faster dose escalation at higher steps than recommended and renal failure. 8). Abnormal magnetic resonance imaging signals Abnormal magnetic resonance imaging (MRI) signal changes characterised by increased T2 signal and restricted diffusion in a symmetric pattern involving the thalamus, basal ganglia, brain stem, and cerebellum have been observed in some infants treated with vigabatrin for infantile spasms.
In a retrospective epidemiologic study […]