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Biomedical subjects

A M Baciewicz

Publications and source records attributed to A M Baciewicz.

At least 19 recordsLinked to original sources
PubMed1999

Isoniazid drug and food interactions.

Isoniazid inhibits the metabolism of several drugs, resulting in clinically significant interactions in some patients. Clinical trials and case reports have documented that isoniazid can cause increased phenytoin and carbamazepine serum concentrations and toxicity. In relatively high doses, isoniazid can also cause increased effect of theophylline and warfarin. Isoniazid inhibits metabolism of selected benzodiazepines and vitamin D. Inhibition of monoamine oxidase and histaminase by isoniazid can cause significant drug-food interactions. Food greatly decreases isoniazid bioavailability. Although probably best recognized as an inhibitor of drug metabolism, isoniazid has a biphasic effect of inhibition-induction on one cytochrome P450 isozyme, CYP2E1, which partially explains the interaction with acetaminophen and increased risk of hepatotoxicity. Continued investigations will likely result in discovery of new isoniazid interactions.

Antitubercular Agents↗
PubMed1997

Update on rifampin drug interactions, III.

Rifampin is a potent inducer of cytochrome P-450 oxidative enzymes. Examples of well-documented, clinically significant interactions include warfarin, oral contraceptives, cyclosporine, glucocorticoids, ketoconazole, theophylline, quinidine, digitoxin, and verapamil. Recent reports have demonstrated clinically relevant interactions with protease inhibitors, zidovudine, delavirdine, itraconazole, nifedipine, midazolam or triazolam, nortriptyline, and doxycycline. To avoid reduced therapeutic response, therapeutic failure, or toxic reactions when rifampin is added to or discontinued from medication regimens, clinicians need to be cognizant of these interactions. Enhanced knowledge of known interactions will continue to develop, including research on induction of specific cytochrome P-450 isoenzymes. New rifampin interactions will be discovered with further investigations.

Antibiotics, Antitubercular↗
PubMed1994

Quality and productivity assessment of clinical pharmacy interventions.

The goal of our program was to implement an easily maintained system that could document, classify, and determine the economic significance of clinical pharmacy interventions on a medicine division of an 874-bed university teaching hospital. This clinical intervention documentation system, which emphasizing both quality of care issues and pharmacist productivity, can be easily implemented by other institutions.

Cost-Benefit Analysis↗
PubMed1993

Ketoconazole and fluconazole drug interactions.

This article reviews potential drug interactions that exist between ketoconazole or fluconazole and other drugs. English-language data sources included human subjects' computerized databases and published indexes. Case reports and studies demonstrate decreased dosage requirements of cyclosporine sodium, methylprednisolone sodium succinate, and possibly anticoagulants and phenytoin after ketoconazole or fluconazole administration, suggesting hepatic enzyme inhibition. Increased dosage requirements of ketoconazole are necessary after rifampin administration, suggesting rifampin's induction of hepatic microsomal enzymes. Possibly a similar effect may occur with concomitant fluconazole and rifampin. The effect of ketoconazole administration on prednisolone sodium phosphate and theophylline warrants further study. Fluconazole, a more selective agent for fungal P-450, seems to be of less concern regarding the potential for drug interactions than ketoconazole.

Drug Interactions↗
PubMed1992

Update on rifampin drug interactions. II.

Rifampin is a potent inducer of hepatic P450 oxidative enzymes. Clinically important drug interactions have been documented between rifampin and numerous other drugs, such as oral anticoagulants, oral contraceptives, cyclosporine, digitalis, and ketoconazole. New, potentially clinically significant rifampin drug interactions have been reported for haloperidol, several antiarrhythmics, fluconazole, diltiazem, and select benzodiazepines. Further research has been conducted for previously reported drug interactions with rifampin involving such drugs as glucocorticoids, cyclosporine, verapamil, and oral anticoagulants. Proper management of these interactions is essential to avoid therapeutic failures on initiating rifampin therapy and potential toxic reactions after discontinuing rifampin. New rifampin drug interactions will continue to be identified with future investigations.

Drug Interactions↗
PubMed1991

Conversion of intravenous ranitidine to oral therapy.

A two-phase drug program concentrating on inappropriate use of intravenous ranitidine is described at a 612-bed university teaching hospital. Phase 1 of the study was a retrospective audit of 50 randomly selected adult patients receiving i.v. ranitidine. The chart was reviewed for indications for therapy, rationale for i.v. ranitidine, median length of i.v. therapy, and appropriateness of i.v. use. Phase 2 consisted of concurrent monitoring of iv ranitidine solely to assess the appropriateness of the iv dosage form at our hospital. Staff pharmacists reviewed the patient's medication profile from the central pharmacy to determine if the patient had standing orders for any oral or nasogastric medications while concomitantly receiving iv ranitidine. An educational memo was placed in the patient's chart if the patient was concurrently receiving oral or nasogastric medications and i.v. ranitidine. In phase I, i.v. ranitidine was inappropriate either partially or totally in 51 percent of the cases. The median length of inappropriate i.v. therapy was five days. During the second phase, the pharmacy staff reviewed 4301 profiles of patients receiving i.v. ranitidine over eight months. Educational memos were placed in 451 patient charts (11 percent) where conversion from i.v. to oral therapy was feasible; a favorable follow-up occurred in 275 cases (61 percent). This would result in an estimated annual cost savings of $4,685. Based on our ranitidine use review, extrapolating the median length of inappropriate i.v. therapy to five days would result in a yearly cost savings of $23,425. This project demonstrated that staff pharmacists can impact on physician education and cost savings by routinely screening patient's medication profiles from the central pharmacy.

Administration, Oral↗
PubMed1989

Effect of cimetidine and ranitidine on cardiovascular drugs.

A compilation of drug interactions between H2 antagonists and cardiovascular drugs is found in Table I. Cimetidine's potency, lipophilicity, and affinity for binding to the P-450 cytochrome system can probably be attributed to the drug interactions that have been identified with the H2 antagonists. The mechanism for most cimetidine drug interactions is inhibition of hepatic metabolism. There is conflicting evidence regarding significance of altered liver blood flow for both cimetidine and ranitidine and their influence on other agents. Cimetidine may increase propranolol's blood concentrations and potentiate beta blocking effects through inhibition of hepatic microsomal enzymes and possibly through reduction of hepatic blood flow. Ranitidine has no effect on propranolol. Cimetidine, when administered concurrently with metoprolol, could possibly cause an increase in plasma metoprolol concentrations or bioavailability through inhibition of hepatic P-450 metabolizing enzymes. No effect of cimetidine on metoprolol pharmacodynamics was evident. Ranitidine has no effect on metoprolol pharmacokinetics or pharmacodynamics. Neither H2 antagonist altered the kinetics or physiologic effects of atenolol. Atenolol is the drug of choice in patients receiving H2 antagonists, since no interaction has been observed. Metoprolol could probably be used safely in most patients, as no change in pharmacodynamics has been evident. Concurrent administration of cimetidine and nifedipine may result in alterations in heart rate and blood pressure. The mechanism is inhibition of oxidative liver metabolism. Ranitidine has no effect on nifedipine. Studies are needed to investigate the interaction between the H2 antagonists and diltiazem or verapamil. Cimetidine, given concomitantly with lidocaine, may increase lidocaine concentrations and clinical symptoms of lidocaine toxicity. The mechanism involved is probably a reduction in oxidative drug metabolism or liver blood flow. Ranitidine has no significant effects on lidocaine pharmacokinetics. Cimetidine may increase quinidine levels and symptoms of quinidine toxicity. Additionally, enhanced arrhythmic effects may be observed. The interaction probably caused by an inhibition of hepatic drug metabolism of quinidine by cimetidine would be most significant in patients with liver disease and in the elderly. Ranitidine may enhance quinidine's arrhythmic effect. Cimetidine can possibly increase procainamide and NAPA serum concentrations, especially in the elderly and in patients with renal dysfunction, predisposing them to adverse side effects. The interaction is mediated by a reduction of tubular secretion of procainamide and NAPA.

Cardiovascular Agents↗
PubMed1989

Cyclosporine pharmacokinetic drug interactions.

Cyclosporine (CyA) is commonly prescribed as an immunosuppressive to prevent rejection of organ transplants. Numerous pharmacokinetic drug interactions of potential clinical significance exist because other drugs may induce or inhibit the metabolism of CyA. Case reports and studies demonstrate that rifampin, phenytoin, phenobarbital, and carbamazepine may induce the hepatic metabolism of CyA, causing decreased CyA concentrations. Graft rejection through inadequate immunosuppression may be associated with subtherapeutic or decreased CyA levels. Erythromycin, ketoconazole, calcium channel blockers, and sex hormones appear to inhibit CyA metabolism, causing increased CyA concentrations. Signs and symptoms of renal, hepatic, or neurotoxicity may be evident with increased or toxic CyA levels. Mutual inhibition of metabolism occurs between CyA and corticosteroids. Intravenous sulphadimidine and trimethoprim may cause decreased CyA concentrations by an unknown mechanism.

Adrenal Cortex Hormones↗