Pharmacotherapy quality improvement: use of a clinical rule-based application.

Heritage's drug usage evaluation (DUE) program focuses on analyzing the dynamics of prescribing, dispensing, and medication usage data for insurers, managed care organizations (MCO), and others involved in the management of pharmacotherapy in the ambulatory care setting. The addition of a new clinical rules-based system (Athena) has increased the flexibility, scope, and speed of Heritage quality improvement products. Its integration into benchmarking, profiling, and disease management programs is described.

Pharmacotherapy quality improvement in the managed care setting.

Physician partnering, value-added relationships, and integrated delivery systems with risk/incentive arrangements are emerging in managed care. These arrangements require time-sensitive program information that can be used in continuous quality improvement programs. Components of any clinical intervention program designed to improve the quality of pharmacotherapy are on a continuum, from those that are primarily individual patient focused to those that are disease or system/process focused. Components include case management, patient profile review, brand to generic drug conversion, targeted therapeutic evaluations, provider profiling, and pharmacoeconomic analysis. All health care professionals involved in pharmacotherapy need to be involved in implementation of these quality improvement programs.

Use of computerized databases for drug therapy quality management.

Although this paper has focused primarily on use of hospital-based databases for DUE purposes, the defunct Medicare Catastrophic Coverage Act did have provisions for ongoing prospective screening for drug interactions and adverse reactions among community Medicare prescriptions. The key to the proposed system was a point-of-service system that would have linked all Medicare pharmacies to a centralized database. This database would have been used for claims processing as well as quality management purposes. Many DUE functions at this time involve labor-intensive retrospective reviews that do not directly benefit or protect the particular patient involved. The future direction of DUE activity is concurrent screening that actively protects the patient from inappropriate prescribing. Use of computerized databases to assist in that process is a necessity.

The effect of everyday exercise on steady state digoxin concentrations.

The purpose of this study was to evaluate the effect of 1 hour of everyday exercise (walking at patient's own pace) on serum digoxin concentrations. Nine white male subjects (ages 58-74) who had been taking the same digoxin dose for greater than 1 month participated. There were three continuous phases: 1 hour of rest, 1 hour of exercise, and a final hour of rest. Serum digoxin concentrations were drawn every 20 minutes. During the first rest period, serum digoxin concentrations rose 30% from the first concentration drawn in the study. After 1 hour of exercise, serum digoxin concentrations fell 26.8% from the last concentration of the first rest period. At the end of the second hour of rest, serum digoxin concentrations increased by 36.6% from the last concentration. Repeated measures analysis of variance demonstrated a significant (P less than .01) change in serum digoxin concentrations. Significant (P less than .01) differences were found between sampling times 0 and 60, 60 and 80, 60 and 100, 60 and 120 and 180 minutes using a paired t-test with Bonferroni correction. A weak correlation (r = 0.74, r2 = 0.55) between percent change in concentrations and age during the exercise phase was found, but there was no correlation between the percent change in concentrations and age during the two immobilization phases. Because significant changes in concentrations occurred during each phase of the study, we conclude that the influence of everyday exercise should be taken into account when interpreting serum digoxin concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of cimetidine on quinidine clearance.

Cimetidine has been reported to inhibit the hepatic metabolism of numerous drugs. Theoretically cimetidine could inhibit the metabolism of quinidine. This study was undertaken to determine the effect of cimetidine on quinidine plasma concentrations. Nine healthy volunteers were entered into the matched-pairs study. Baseline quinidine pharmacokinetic parameters were determined after a single oral 400-mg dose. Study parameters were determined after 3 days of cimetidine 300 mg p.o. q.i.d., when 400 mg quinidine was again administered. Cimetidine increased the area under the time-concentration curve (14.5%, p less than 0.01), decreased the total body clearance (24.9%, p less than 0.05), and prolonged the half-life (22.6%, p less than 0.05) of quinidine in this study. There was no change in peak quinidine concentrations or time to peak. These data document an interaction between cimetidine and quinidine. The clinical importance of this interaction should be greatest in patients with impaired liver function, patients with preexisting near-toxic plasma concentrations of quinidine, and the elderly. Patients placed on cimetidine and quinidine should be monitored closely for signs and symptoms of quinidine toxicity.