[Drug interactions with the cytochrome P-450 system].
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Cytochrome P-450 Enzyme System↗
Biomedical subjects
M Martin-Facklam
Publications and source records attributed to M Martin-Facklam.
[Individualization of drug therapy in renal or liver insufficiency].
Individualisation of drug dosage in patients with renal or hepatic failure may prevent excessive drug accumulation and thus potentially reduce adverse drug reactions and costs. In renal failure, renal function may be estimated by combined evaluation of serum creatinine values and patient characteristics. Then individual elimination capacity of a given drug in the individual patient may be calculated and dosage accordingly adjusted. In severe liver cirrhosis, after peroral administration of drugs with a high extraction ratio each single dose has to be reduced because of increased bioavailability and decreased clearance. After i.v. administration and dosing of drugs with a low extraction ratio maintenance dose should be reduced either by prolonging the dosing interval or by decreasing each single dose.
Algorithms↗
[Clinically relevant adverse drug interactions].
Drug interactions may lead to adverse drug effects or therapeutic failure. Many clinically relevant unwanted interactions are caused by a change in the activity of cytochrome P450 isoenzymes or the activity of active drug transport systems (e.g. p-glycoprotein). Most drug interactions may be anticipated and prevented by dose modification or using alternative drugs.
ATP Binding Cassette Transporter, Subfamily B↗
Unexplained decrease of cyclosporin trough levels in a compliant renal transplant patient.
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Adult↗
[Anticonvulsant hypersensitivity syndrome. 2 case reports and an overview].
Anticonvulsants with aromatic ring structure such as phenytoine, carbamazepine, phenobarbital and lamotrigine can induce a drug hypersensitivity syndrome ("anticonvulsant hypersensitivity syndrome", AHS). Though the incidence of AHS is low, correct and early diagnosis are crucial to stop further progression by immediately withholding the causative drug. AHS usually starts within the first 2-8 weeks after initiation of therapy with fever, followed over the next 1-2 days by a cutaneous reaction and lymphadenopathy. The skin reaction is usually exanthematous but can also manifest itself as Stevens-Johnson or Lyell syndrome. AHS is commonly associated with symptomatic or asymptomatic internal organ involvement usually affecting the liver, although haematologic, renal or pulmonary impairment may also occur. We report two cases illustrating the clinical course and discuss theories about the potential pathogenesis and the treatment of AHS.
Adult↗