Interaction between phenytoin and antacids.

Kulshrestha, VK; Thomas, M; Wadsworth, J; Richens, A.

doi:10.1111/j.1365-2125.1978.tb00848.x

Cited by 30 publications

(7 citation statements)

References 12 publications

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“…Mixtures of aluminium hydroxide with magnesium hydroxide or magnesium trisilicate have also been reported to reduce phenytoin bioavailability (Garratt et al, 1979;Kulshrestha et al, 1978); however, this effect has not been found consistently in all studies (Chapron et al, 1979a;Kulshrestha et al, 1978;O'Brien et al, 1978), probably because of differences in experimental design, particularly with respect to duration of treatment, time of administration, dosage, and proprietary formulation of the selected antacid. Since the absorption of barbiturates (Hurwitz, 1977) and benzodiazepines (Greenblatt et al, 1976;Shader et al, 1978) may also be reduced by gastric antacids, it seems wise to recommend that antiepileptic drugs be administered at least 2 to 3 hours before ingestion of antacids, and that serum anticonvulsant levels be monitored frequently in patients receiving concomitant therapy.…”

Section: Antacidsmentioning

confidence: 94%

Pharmacokinetic Interactions with Antiepileptic Drugs

Perucca

1982

Clinical Pharmacokinetics

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A large number of pharmacokinetic interactions with antiepileptic drugs have been reported in recent years. Among the interactions affecting the disposition of anticonvulsants, the most important are probably those resulting in inhibition of the metabolism of phenytoin, phenobarbitone and carbamazepine. Drugs which have been shown to inhibit the metabolism of these anticonvulsants and to precipitate clinical signs of intoxication in epileptic patients include sulthiame, valproic acid, chloramphenicol, certain sulphonamides, phenylbutazone, isoniazid and propoxyphene. Interactions affecting the plasma protein binding of antiepileptic drugs are less likely to cause long-lasting alterations in response, but they are important because they change the relationship between serum drug concentrations and clinical effect. Anticonvulsant agents may induce important alterations in the pharmacokinetics of other drugs. Phenytoin and phenobarbitone may decrease the gastrointestinal absorption of frusemide and griseofulvin, respectively. Many of the drugs used in the treatment of the adult epilepsies, including phenytoin, phenobarbitone, primidone and carbamazepine, are potent inducers of the hepatic microsomal enzymes. This results in an increased rate of metabolism and decreased clinical efficacy of a number of drugs, including dicoumarol, steroid oral contraceptives, metyrapone, glucocorticoid agents, doxycycline, quinidine and vitamin D.

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Section: Antacidsmentioning

confidence: 94%

Pharmacokinetic Interactions with Antiepileptic Drugs

Perucca

1982

Clinical Pharmacokinetics

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“…In a recent study, a slight reduction in serum phenytoin concentration was seen after the simultaneous use of phenytoin and an antacid suspension containing magnesium trisilicate and aluminium hydroxide (Kulshrestha et al, 1978). However, neither a suspension of calcium carbonate in multiple dose studies, nor aluminium hydroxide gel (4 % w Iv) or magnesium hydroxide mixture in short term studies altered the bioavailability of phenytoin (Kulshrestha et aI., 1978;O'Brien et aI., 1978).…”

Section: Antacidsmentioning

confidence: 99%

Bioavailability of Phenytoin

Neuvonen

1979

Clinical Pharmacokinetics

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Phenytoin (diphenylhydantoin) is still the most commonly used anticonvulsant drug. It has certain physicochemical characteristics which make it liable to bioavailability problems. Due to the dose dependent metabolism of phenytoin and to its narrow therapeutic range even small changes in the bioavailability can cause major changes in serum phenytoin concentration and have serious clinical consequences. Numerous studies have demonstrated that there are products in general use with considerable differences in their bioavailiability. If the epilepsy is well controlled, a change from one phenytoin product to another should be avoided. Such a change might lead to phenytoin intoxication or to poor control of epilepsy, if the products do not have the same bioavailability. There seems to be no systematic difference in the bioavailability of phenytoin sodium and phenytoin acid, if products of high quality are used. On the other hand, various biopharmaceutical factors, e.g. particle size of phenytoin and the nature of excipients in the product, can have a marked effect on the oral absorption of phenytoin. Gastrointestinal diseases, the concomitant use of other drugs and dietary factors might also modify the bioavailability of phenytoin. The absorption of intramuscularly given phenytoin is rather slow and erratic. The existence of phenytoin products with different bioavailability is a serious practical problem which should be corrected as soon as possible.

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“…The therapeutic range of PT is narrow and the clearance of PT is variable between individuals. Additionally, co-ingestion of PT with an antacid mixture of magnesium trisilicate and aluminum hydroxide reduces serum PT concentrations [ 63 ]. Moreover, some medications, such as Cisplatin and other anti-neoplastic drugs may affect serum PT concentrations [ 64 ].…”

Section: Introductionmentioning

confidence: 99%

The Impact of Anti-Epileptic Drugs on Growth and Bone Metabolism

Fan

Lee

Chang

et al. 2016

IJMS

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Epilepsy is a common neurological disorder worldwide and anti-epileptic drugs (AEDs) are always the first choice for treatment. However, more than 50% of patients with epilepsy who take AEDs have reported bone abnormalities. Cytochrome P450 (CYP450) isoenzymes are induced by AEDs, especially the classical AEDs, such as benzodiazepines (BZDs), carbamazepine (CBZ), phenytoin (PT), phenobarbital (PB), and valproic acid (VPA). The induction of CYP450 isoenzymes may cause vitamin D deficiency, hypocalcemia, increased fracture risks, and altered bone turnover, leading to impaired bone mineral density (BMD). Newer AEDs, such as levetiracetam (LEV), oxcarbazepine (OXC), lamotrigine (LTG), topiramate (TPM), gabapentin (GP), and vigabatrin (VB) have broader spectra, and are safer and better tolerated than the classical AEDs. The effects of AEDs on bone health are controversial. This review focuses on the impact of AEDs on growth and bone metabolism and emphasizes the need for caution and timely withdrawal of these medications to avoid serious disabilities.

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Interaction between phenytoin and antacids.

Cited by 30 publications

References 12 publications

Pharmacokinetic Interactions with Antiepileptic Drugs

Pharmacokinetic Interactions with Antiepileptic Drugs

Bioavailability of Phenytoin

The Impact of Anti-Epileptic Drugs on Growth and Bone Metabolism

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