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Kovalenko Svetlana Olegovna 、薬局による医学的評価、 最終更新日:15.03.2022
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成人、青年、および6歳以上の子供における単剤療法。二次性全身発作の有無にかかわらず部分発作があり、一次全身性強壮性間代発作があります。.
2歳以上の子供、二次性汎化または一次性全身性強直間代発作の有無にかかわらず部分発症発作を起こした青年および成人、およびレノックスガストー症候群に関連する発作の治療のための補助療法。.
トピラメートは、可能な代替治療オプションを注意深く評価した後、片頭痛の予防のために成人に適応されます。. トピラメートは急性治療を目的としていません。.
成人、青年、および6歳以上の子供における単剤療法。二次性全身発作の有無にかかわらず部分発作があり、一次全身性強壮性間代発作があります。.
2歳以上の子供、二次性汎化または一次性全身性強直間代発作の有無にかかわらず部分発症発作を起こした青年および成人、およびレノックスガストー症候群に関連する発作の治療のための補助療法。.
プロトマックスは、可能な代替治療オプションを注意深く評価した後、片頭痛の予防のために成人に適応されます。. プロトマックスは急性治療を目的としていません。.
部分的な発症発作と一次一般化トニッククロニック発作。
QUDEXY XR徐放カプセルは、部分発症または一次全身性強壮クローン発作を伴う2歳以上の患者の初期単剤療法および部分発症または一次全身性強壮クローン発作を伴う2歳以上の患者の補助療法として適応されます。. 他の抗けいれん薬の以前のレジメンから単剤療法に変換された患者の安全性と有効性は、対照試験では確立されていません。.
レノックス・ガストー症候群。
QUDEXY XR徐放カプセルは、レノックスガストー症候群に関連する発作を伴う2歳以上の患者の補助療法として適応されます。.
片頭痛。
QUDEXY XR徐放カプセルは、12歳以上の成人および青年の片頭痛の予防に適応されます。. 片頭痛の急性治療におけるQUDEXY XRの有用性は研究されていません。.
Protomaxは、機械を運転して使用する能力に軽微または中程度の影響を与えます。. トピラメートは中枢神経系に作用し、眠気、めまい、またはその他の関連する症状を引き起こす可能性があります。. また、視覚障害や視力障害を引き起こす可能性があります。. これらの副作用は、特に個々の患者の医薬品に関する経験が確立されるまで、車両を運転している患者や機械を操作している患者では潜在的に危険である可能性があります。.
プロトマックスは中枢神経系に作用し、眠気、めまい、またはその他の関連する症状を引き起こす可能性があります。. また、視覚障害や視力障害を引き起こす可能性があります。. これらの副作用は、特に個々の患者の医薬品に関する経験が確立されるまで、車両を運転している患者や機械を操作している患者では潜在的に危険である可能性があります。.
機械を運転して使用する能力への影響に関する研究は行われていません。.
Signs and symptoms
Overdoses of topiramate have been reported. Signs and symptoms included convulsions, drowsiness, speech disturbances, blurred vision, diplopia, impaired mentation, lethargy, abnormal coordination, stupor, hypotension, abdominal pain, agitation, dizziness and depression. The clinical consequences were not severe in most cases, but deaths have been reported after overdoses with multiple medicinal products including topiramate.
Topiramate overdose can result in severe metabolic acidosis.
Treatment
In acute topiramate overdose, if the ingestion is recent, the stomach should be emptied immediately by lavage or by induction of emesis. Activated charcoal has been shown to adsorb topiramate in vitro. Treatment should be appropriately supportive and the patient should be well hydrated. Haemodialysis has been shown to be an effective means of removing topiramate from the body.
Signs and symptoms
Overdoses of Protomax have been reported. Signs and symptoms included convulsions, drowsiness, speech disturbances, blurred vision, diplopia, impaired mentation, lethargy, abnormal coordination, stupor, hypotension, abdominal pain, agitation, dizziness and depression. The clinical consequences were not severe in most cases, but deaths have been reported after overdoses with multiple medicinal products including Protomax.
Protomax overdose can result in severe metabolic acidosis.
Treatment
In acute Protomax overdose, if the ingestion is recent, the stomach should be emptied immediately by lavage or by induction of emesis. Activated charcoal has been shown to adsorb Protomax in vitro. Treatment should be appropriately supportive and the patient should be well hydrated. Haemodialysis has been shown to be an effective means of removing Protomax from the body.
Overdoses of topiramate have been reported. Signs and symptoms included convulsions, drowsiness, speech disturbance, blurred vision, diplopia, mentation impaired, lethargy, abnormal coordination, stupor, hypotension, abdominal pain, agitation, dizziness and depression. The clinical consequences were not severe in most cases, but deaths have been reported after polydrug overdoses involving topiramate.
Topiramate overdose has resulted in severe metabolic acidosis.
A patient who ingested a dose between 96 g and 110 g of topiramate was admitted to hospital with coma lasting 20 to 24 hours followed by full recovery after 3 to 4 days.
Similar signs, symptoms, and clinical consequences are expected to occur with overdosage of QUDEXY XR. Therefore, in acute QUDEXY XR overdose, if the ingestion is recent, the stomach should be emptied immediately by lavage or by induction of emesis. Activated charcoal has been shown to adsorb topiramate in vitro. Treatment should be appropriately supportive. Hemodialysis is an effective means of removing topiramate from the body.
Pharmacotherapeutic group: antiepileptics, other antiepileptics, antimigraine preparations, ATC code: N03AX11
Topiramate is classified as a sulfamate-substituted monosaccharide. The precise mechanism by which topiramate exerts its antiseizure and migraine prophylaxis effects are unknown. Electrophysiological and biochemical studies on cultured neurons have identified three properties that may contribute to the antiepileptic efficacy of topiramate.
Action potentials elicited repetitively by a sustained depolarization of the neurons were blocked by topiramate in a time-dependent manner, suggestive of a state-dependent sodium channel blocking action. Topiramate increased the frequency at which γ-aminobutyrate (GABA) activated GABAA receptors, and enhanced the ability of GABA to induce a flux of chloride ions into neurons, suggesting that topiramate potentiates the activity of this inhibitory neurotransmitter.
This effect was not blocked by flumazenil, a benzodiazepine antagonist, nor did topiramate increase the duration of the channel open time, differentiating topiramate from barbiturates that modulate GABAA receptors.
Because the antiepileptic profile of topiramate differs markedly from that of the benzodiazepines, it may modulate a benzodiazepine-insensitive subtype of GABAA receptor. Topiramate antagonized the ability of kainate to activate the kainate/AMPA (α -amino-3-hydroxy-5-methylisoxazole-4-propionic acid) subtype of excitatory amino acid (glutamate) receptor, but had no apparent effect on the activity of N-methyl-D-aspartate (NMDA) at the NMDA receptor subtype. These effects of topiramate were concentration-dependent over a range of 1 µM to 200 µM, with minimum activity observed at 1 µM to 10 µM.
In addition, topiramate inhibits some isoenzymes of carbonic anhydrase. This pharmacologic effect is much weaker than that of acetazolamide, a known carbonic anhydrase inhibitor, and is not thought to be a major component of topiramate's antiepileptic activity.
In animal studies, topiramate exhibits anticonvulsant activity in rat and mouse maximal electroshock seizure (MES) tests and is effective in rodent models of epilepsy, which include tonic and absence-like seizures in the spontaneous epileptic rat (SER) and tonic and clonic seizures induced in rats by kindling of the amygdala or by global ischemia. Topiramate is only weakly effective in blocking clonic seizures induced by the GABAA receptor antagonist, pentylenetetrazole.
Studies in mice receiving concomitant administration of topiramate and carbamazepine or phenobarbital showed synergistic anticonvulsant activity, while combination with phenytoin showed additive anticonvulsant activity. In well-controlled add-on trials, no correlation has been demonstrated between trough plasma concentrations of topiramate and its clinical efficacy. No evidence of tolerance has been demonstrated in man.
Absence seizures
Two small one arm studies were carried out with children aged 4-11 years old (CAPSS-326 and TOPAMAT-ABS-001). One included 5 children and the other included 12 children before it was terminated early due to lack of therapeutic response. The doses used in these studies were up to approximately 12 mg/kg in study TOPAMAT-ABS-001 and a maximum of the lesser of 9 mg/kg/day or 400 mg/day in study CAPSS-326. These studies do not provide sufficient evidence to reach conclusion regarding efficacy or safety in the paediatric population.
Pharmacotherapeutic group: antiepileptics, other antiepileptics, antimigraine preparations, ATC code: N03AX11
Protomax is classified as a sulfamate-substituted monosaccharide. The precise mechanism by which Protomax exerts its antiseizure and migraine prophylaxis effects are unknown. Electrophysiological and biochemical studies on cultured neurons have identified three properties that may contribute to the antiepileptic efficacy of Protomax.
Action potentials elicited repetitively by a sustained depolarization of the neurons were blocked by Protomax in a time-dependent manner, suggestive of a state-dependent sodium channel blocking action. Protomax increased the frequency at which γ-aminobutyrate (GABA) activated GABAA receptors, and enhanced the ability of GABA to induce a flux of chloride ions into neurons, suggesting that Protomax potentiates the activity of this inhibitory neurotransmitter.
This effect was not blocked by flumazenil, a benzodiazepine antagonist, nor did Protomax increase the duration of the channel open time, differentiating Protomax from barbiturates that modulate GABAA receptors.
Because the antiepileptic profile of Protomax differs markedly from that of the benzodiazepines, it may modulate a benzodiazepine-insensitive subtype of GABAA receptor. Protomax antagonized the ability of kainate to activate the kainate/AMPA (α -amino-3-hydroxy-5 methylisoxazole-4-propionic acid) subtype of excitatory amino acid (glutamate) receptor, but had no apparent effect on the activity of N-methyl-Daspartate (NMDA) at the NMDA receptor subtype. These effects of Protomax were concentration dependent over a range of 1 μM to 200 μM, with minimum activity observed at 1 μM to 10 μM.
In addition, Protomax inhibits some isoenzymes of carbonic anhydrase. This pharmacologic effect is much weaker than that of acetazolamide, a known carbonic anhydrase inhibitor, and is not thought to be a major component of Protomax's antiepileptic activity.
In animal studies, Protomax exhibits anticonvulsant activity in rat and mouse maximal electroshock seizure (MES) tests and is effective in rodent models of epilepsy, which include tonic and absence-like seizures in the spontaneous epileptic rat (SER) and tonic and clonic seizures induced in rats by kindling of the amygdala or by global ischemia. Protomax is only weakly effective in blocking clonic seizures induced by the GABAA receptor antagonist, pentylenetetrazole.
Studies in mice receiving concomitant administration of Protomax and carbamazepine or Phenobarbital showed synergistic anticonvulsant activity, while combination with phenytoin showed additive anticonvulsant activity. In well-controlled add-on trials, no correlation has been demonstrated between trough plasma concentrations of Protomax and its clinical efficacy. No evidence of tolerance has been demonstrated in man.
Absence seizures
The results of two studies (CAPSS-326 and TOPMAT-ABS-001) on absences showed that Protomax treatment did not reduce the frequency of absence seizures.
Topiramate has anticonvulsant activity in rat and mouse maximal electroshock seizure (MES) tests. Topiramate is only weakly effective in blocking clonic seizures induced by the GABA-A receptor antagonist, pentylenetetrazole. Topiramate is also effective in rodent models of epilepsy, which include tonic and absence-like seizures in the spontaneous epileptic rat (SER) and tonic and clonic seizures induced in rats by kindling of the amygdala or by global ischemia.
Changes (increases and decreases) from baseline in vital signs (systolic blood pressure-SBP, diastolic blood pressure-DBP, pulse) occurred more frequently in pediatric patients (6 to 17 years) treated with various daily doses of topiramate (50 mg, 100 mg, 200 mg, 2 to 3 mg/kg) than in patients treated with placebo in controlled trials for migraine prophylaxis. The most notable changes were SBP < 90 mm Hg, DBP < 50 mm Hg, SBP or DBP increases or decreases ≥ 20 mm Hg, and pulse increases or decreases ≥ 30 beats per minute. These changes were often dose-related, and were most frequently associated with the greatest treatment difference at the 200 mg dose level. When a position was specified for measurement of vital signs in a trial, measurements were made in a sitting position. Systematic collection of orthostatic vital signs has not been conducted. The clinical significance of these various changes in vital signs has not been clearly established.
In nonclinical studies of fertility, despite maternal and paternal toxicity as low as 8 mg/kg/day, no effects on fertility were observed, in male or female rats with doses up to 100 mg/kg/day.
In preclinical studies, topiramate has been shown to have teratogenic effects in the species studied (mice, rats and rabbits). In mice, fetal weights and skeletal ossification were reduced at 500 mg/kg/day in conjunction with maternal toxicity. Overall numbers of fetal malformations in mice were increased for all drug-treated groups (20, 100 and 500 mg/kg/day).
In rats, dosage-related maternal and embryo/fetal toxicity (reduced fetal weights and/or skeletal ossification) were observed down to 20 mg/kg/day with teratogenic effects (limb and digit defects) at 400 mg/kg/day and above. In rabbits, dosage-related maternal toxicity was noted down to 10 mg/kg/day with embryo/fetal toxicity (increased lethality) down to 35 mg/kg/day, and teratogenic effects (rib and vertebral malformations) at 120 mg/kg/day.
The teratogenic effects seen in rats and rabbits were similar to those seen with carbonic anhydrase inhibitors, which have not been associated with malformations in humans. Effects on growth were also indicated by lower weights at birth and during lactation for pups from female rats treated with 20 or 100 mg/kg/day during gestation and lactation. In rats, topiramate crosses the placental barrier.
In juvenile rats, daily oral administration of topiramate at doses up to 300 mg/kg/day during the period of development corresponding to infancy, childhood, and adolescence resulted in toxicities similar to those in adult animals (decreased food consumption with decreased body weight gain, centrolobullar hepatocellular hypertrophy). There were no relevant effects on long bone (tibia) growth or bone (femur) mineral density, preweaning and reproductive development, neurological development (including assessments on memory and learning), mating and fertility or hysterotomy parameters.
In a battery of in vitro and in vivo mutagenicity assays, topiramate did not show genotoxic potential.
In nonclinical studies of fertility, despite maternal and paternal toxicity as low as 8 mg/kg/day, no effects on fertility were observed, in male or female rats with doses up to 100 mg/kg/day.
In preclinical studies, Protomax has been shown to have teratogenic effects in the species studied (mice, rats and rabbits). In mice, fetal weights and skeletal ossification were reduced at 500 mg/kg/day in conjunction with maternal toxicity. Overall numbers of fetal malformations in mice were increased for all drug-treated groups (20, 100 and 500 mg/kg/day).
In rats, dosage-related maternal and embryo/fetal toxicity (reduced fetal weights and/or skeletal ossification) were observed down to 20 mg/kg/day with teratogenic effects (limb and digit defects) at 400 mg/kg/day and above. In rabbits, dosage-related maternal toxicity was noted down to 10 mg/kg/day with embryo/fetal toxicity (increased lethality) down to 35 mg/kg/day, and teratogenic effects (rib and vertebral malformations) at 120 mg/kg/day.
The teratogenic effects seen in rats and rabbits were similar to those seen with carbonic anhydrase inhibitors, which have not been associated with malformations in humans. Effects on growth were also indicated by lower weights at birth and during lactation for pups from female rats treated with 20 or 100 mg/kg/day during gestation and lactation. In rats, Protomax crosses the placental barrier.
In juvenile rats, daily oral administration of Protomax at doses up to 300 mg/kg/day during the period of development corresponding to infancy, childhood, and adolescence resulted in toxicities similar to those in adult animals (decreased food consumption with decreased body weight gain, centrolobullar hepatocellular hypertrophy). There were no relevant effects on long bone (tibia) growth or bone (femur) mineral density, preweaning and reproductive development, neurological development (including assessments on memory and learning), mating and fertility or hysterotomy parameters.
In a battery of in vitro and in vivo mutagenicity assays, Protomax did not show genotoxic potential.
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