Prednisolone and methylprednisolone kinetics in children receiving anticonvulsant therapy

Bartoszek, Maryanne; Brenner, Anne Manon; Szefler, Stanley J.

doi:10.1038/clpt.1987.173

Cited by 70 publications

(23 citation statements)

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“…Case reports also suggest that valproate, 95,96 carbamazepine, 96 gabapentin, 97 clonazepam, 96,98 and lithium 99,100 may be associated with improvement in psychiatric symptoms in these patients. A caveat with the use of phenytoin or carbamazepine is that these medications with extended use can induce the metabolism of corticosteroids, potentially decreasing their efficacy 101 …”

Section: Risk Factors For Corticosteroid‐induced Psychiatric Symptomsmentioning

confidence: 99%

Effects of Glucocorticoids on Mood, Memory, and the Hippocampus

Brown

2009

Annals of the New York Academy of Sciences

200

119

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Corticosteroids, such as prednisone and dexamethasone, are commonly prescribed medications that suppress the immune system and decrease inflammation. Common side effects of long-term treatment with corticosteroids include weight gain, osteoporosis, and diabetes mellitus. This paper reviews the literature on psychiatric and cognitive changes during corticosteroid therapy and potential treatment options. Hypomania and mania are the most common mood changes during acute corticosteroid therapy, although depression has also been reported. However, depression is reported to be more common than mania during long-term treatment with corticosteroids. A decline in declarative and working memory is also reported during corticosteroid therapy. Corticosteroids are associated with changes in the temporal lobe, detected by structural, functional, and spectroscopic imaging. The mood and cognitive symptoms are dose dependent and frequently occur during the first few weeks of therapy. Other risk factors are not well characterized. Controlled trials suggest that lithium and phenytoin can prevent mood symptoms associated with corticosteroids. Lamotrigine and memantine also have been shown to reverse, at least partially, the declarative memory effects of corticosteroids. Uncontrolled trials suggest that antipsychotics, anti-seizure medications, and perhaps some antidepressants can also be useful for normalizing mood changes associated with corticosteroids. Thus, both the symptoms and treatment response are similar to those of bipolar disorder. Moreover, corticosteroid-induced mood and cognitive alterations have been shown to be reversible with dose reduction or discontinuation of treatment.

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Section: Risk Factors For Corticosteroid‐induced Psychiatric Symptomsmentioning

confidence: 99%

Effects of Glucocorticoids on Mood, Memory, and the Hippocampus

Brown

2009

Annals of the New York Academy of Sciences

200

119

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“…Enzyme-inducing antiepileptic drugs have been reported to stimulate the metabolism of cortisol, prednisone, prednisolone, methylprednisolone, dexamethasone and metyrapone.f3, [192][193][194][195] These interactions are clinically relevant because they may result in a loss of activity when the steroid is used therapeutically or diagnostically in conventional dosages . Discontinuation of the enzymeinducing drugs without an adequate adjustment in steroid dosage has also lead to toxic reactions.…”

Section: Glucocorticoids and Metyraponementioning

confidence: 99%

Clinically Significant Pharmacokinetic Drug Interactions with Carbamazepine

Spina

Pisani

Perucca

1996

Clinical Pharmacokinetics

298

149

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Carbamazepine is one of the most commonly prescribed antiepileptic drugs and is also used in the treatment of trigeminal neuralgia and psychiatric disorders, particularly bipolar depression. Because of its widespread and long term use, carbamazepine is frequently prescribed in combination with other drugs, leading to the possibility of drug interactions. The most important interactions affecting carbamazepine pharmacokinetics are those resulting in induction or inhibition of its metabolism. Phenytoin, phenobarbital (phenobarbitone) and primidone accelerate the elimination of carbamazepine, probably by stimulating cytochrome P450 (CYP) 3A4, and reduce plasma carbamazepine concentrations to a clinically important extent. Inhibition of carbamazepine metabolism and elevation of plasma carbamazepine to potentially toxic concentrations can be caused by stiripentol, remacemide, acetazolamide, macrolide antibiotics, isoniazid, metronidazole, certain antidepressants, verapamil, diltiazem, cimetidine, danazol and (dextropropoxyphene) propoxyphene. In other cases, toxic symptoms may result from elevated plasma concentrations of the active metabolite carbamazepine-10,11-epoxide, due to the inhibition of epoxide hydrolase by valproic acid (sodium valproate), valpromide, valnoctamide and progabide. Carbamazepine is a potent inducer of CYP3A4 and other oxidative enzyme system in the liver, and it may also increase glucuronyltransferase activity. This results in the acceleration of the metabolism of concurrently prescribed anticonvulsants, particularly valproic acid, clonazepam, ethosuximide, lamotrigine, topiramate, tiagabine and remacemide. The metabolism of many other drugs such as tricyclic antidepressants, antipsychotics, steroid oral contraceptives, glucocorticoids, oral anticoagulants, cyclosporin, theophylline, chemotherapeutic agents and cardiovascular drugs can also be induced, leading to a number of clinically relevant drug interactions. Interactions with carbamazepine can usually be predicted on the basis of the pharmacological properties of the combined drug, particularly with respect to its therapeutic index, site of metabolism and ability to affect specific drug metabolising isoenzymes. Avoidance of unnecessary polypharmacy, selection of alternative agents with lower interaction potential, and careful dosage adjustments based on serum drug concentration monitoring and clinical observation represent the mainstays for the minimisation of risks associated with these interactions.

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“…The levels or effects of corticosteroids may be reduced by antacids, barbiturates, and rifamycin derivatives. [60][61][62] 4. Drug Dosing Table I lists the commonly used immunosuppressant agents, dosing, and therapeutic ranges, or commonly used laboratory tests for adjusting the dose of these agents.…”

Section: Corticosteroidsmentioning

confidence: 99%

Strategies to Prevent Cellular Rejection in Pediatric Heart Transplant Recipients

Denfield

2010

Pediatric Drugs

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Despite more than 40 years' experience in pediatric heart transplantation, cellular rejection remains a significant cause of morbidity and mortality. In this review, strategies and agents to prevent acute cellular rejection are discussed. Strategies to prevent rejection are divided into two phases - induction and maintenance therapies. Currently, the most commonly used induction agents are polyclonal antibodies (rabbit or equine antithymocyte globulin) and interleukin-2 receptor antibodies (daclizumab or basiliximab). Induction therapies have reduced early rejection, are renal sparing, and can reduce corticosteroid exposure, but have not yet been shown to have a longer term survival benefit. Multiple maintenance immunosuppressants are available. Nearly all regimens include a calcineurin inhibitor (either ciclosporin [cyclosporine] or tacrolimus). Most combinations in pediatric heart transplantation include an antiproliferative agent (azathioprine, mycophenolate mofetil or, less commonly, sirolimus). Everolimus has seen increasing use in adult heart transplant patients in Europe but, to date, its use is rare in pediatric heart transplantation. The use of corticosteroids as a third agent is still common, but strategies to avoid or minimize their use are increasing. The 'best' combination of therapies varies between studies. By gaining a better understanding of individuals' genetic and environmental risk factors, we may in the future be able to better predict the course of cardiac allografts and enhance our ability to tailor immunosuppression to individual patient variables with the ultimate goal of inducing a state of immune tolerance.

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Prednisolone and methylprednisolone kinetics in children receiving anticonvulsant therapy

Cited by 70 publications

References 0 publications

Effects of Glucocorticoids on Mood, Memory, and the Hippocampus

Effects of Glucocorticoids on Mood, Memory, and the Hippocampus

Clinically Significant Pharmacokinetic Drug Interactions with Carbamazepine

Strategies to Prevent Cellular Rejection in Pediatric Heart Transplant Recipients

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