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Small changes can reduce adverse drug events. Hospitals looking for a quick fix to reduce adverse drug events usually find out it's not that easy. But implementing several minor changes can make a difference. That's what Luther/Midelfort in Eau Claire, WI, did when it revamped more than 10 processes over three years, resulting in fewer medication errors.
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An 11-year effort by LDS Hospital in Salt Lake City to help physicians prescribe antibiotics wisely is paying off. Mortality among hospitalized patients receiving antibiotics declined to a rate of 1.79 per 100 patients in 1998 from 3.65 per 100 patients in 1988. What are the secrets? Epidemiology, human effort, and integrated data systems.
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This case demonstrates that, despite physician disregard of appropriate expert system warnings during computerized physician order entry, the distribution of alert "override" warnings to non-physician members of the clinical team can help avert adverse drug events.
When V79 pur 1, a purine-requiring auxotroph of a Chinese hamster cell line, is deprived of adenine, nucleic acid and protein synthesis decline rapidly. However, on continuous starvation RNA and DNA synthesis recommences to reach approximately 30% of the normal level between 12 to 24 h starvation. This is accompanied by a rise in the intracellular nucleotide pool. Utilizing mengovirus, which gives a productive infection in V79 pur 1 cells even under conditions of starvation, we can show that rRNA is preferentially degraded and provides the nucleotides for RNA synthesis. Thus "purineless" death in mammalian cells is accompanied by turnover of stable RNA.
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We describe an alternative assay to determine genotoxicity. Its main feature is that it combines two measures in a single experiment; the inhibition of replicative DNA synthesis together with the stimulation of DNA repair. We show that, in tests of four different genotoxic agents, the assay gives results that are entirely consistent with what is known about the mode of action of these agents. In addition, we have demonstrated that chemical carcinogens requiring metabolic activation can be examined using a standard procedure of incubation with a microsomal activating fraction. We consider the combined assay for DNA synthesis inhibition and repair synthesis to be a useful way for the rapid prescreening of chemicals suspected of genotoxic activity on the level of mammalian cells.
The author has summarized the history of discovery, the mechanism and the clinical significance of antibody-dependent enhancement (ADE) of HIV infection. ADE has two major forms: (a) complement-mediated antibody-dependent enhancement (C-ADE) and (b) complement-independent Fc receptor-dependent ADE (FcR-ADE). The most important epitope responsible for the development of C-ADE-mediating antibodies is present in the immunodominant region of gp41 while antibodies mediating FcR-ADE react mainly with V3 loop of gp120. There are at least three fundamentally different hypotheses for the explanation of ADE in vitro: (a) increased adhesion of HIV -antibody-(complement) complexes to FcR or complement receptor carrying cells; (b) facilitation of HIV-target cell fusion by complement fragment deposited on the HIV-virions and (c) complement activation products may have a non-specific stimulatory effect on target cells resulting in enhanced virus production. FcR-ADE and C-ADE have been measured in vitro mostly by using FcR-carrying and complement receptor-carrying cell lines, respectively; no efforts have been made to standardize these methods. Several data support the possible clinical significance of FcR-ADE and C-ADE: (a) Cross-sectional and longitudinal studies indicate a correlation between the amounts of FcR-ADE and C-ADE-mediating antibodies and clinical, immunological and virological progression of the HIV-disease; (b) ADE may facilitate maternal-infant HIV-1 transmission; (c) According to experiments in animal models, ADE are present and may modify the course of SIV (simian immunodeficiency) infection as well. The author raises a new hypothesis on the mechanism of the in vivo effect of C-ADE. According to the hypothesis, C-ADE-mediating antibodies exert their effect through enhancement of HIV propagation and consequent facilitation of the progression of HIV disease. Finally, according to observations from animal experiments and human clinical trials it cannot be excluded that ADE-mediating antibodies may develop, diminish the beneficial effect or may be harmful in volunteers vaccinated with HIV-1 candidate vaccines.
BACKGROUND: Adverse drug events (ADEs) are both common and costly. Most hospitals identify ADEs using spontaneous reporting, but this approach lacks sensitivity; chart review identifies more events but is expensive. Computer-based approaches to ADE identification appear promising, but they have not been directly compared with chart review and they are not widely used. OBJECTIVES: To develop a computer-based ADE monitor, and to compare the rate and type of ADEs found with the monitor with those discovered by chart review and by stimulated voluntary report. DESIGN: Prospective cohort study in one tertiary-care hospital. PARTICIPANTS: All patients admitted to nine medical and surgical units in a tertiary-care hospital over an eight-month period. MAIN OUTCOME MEASURE: Adverse drug events identified by the computer-based monitor, by chart review, and by stimulated voluntary report. METHODS: A computer-based monitoring program identified alerts, which were situations suggesting that an ADE might be present (e.g., an order for an antidote such as naloxone). A trained reviewer then examined patients' hospital records to determine whether an ADE had occurred. The results of the computer-based monitoring strategy were compared with two other ADE detection strategies: intensive chart review and stimulated voluntary report by nurses and pharmacists. The monitor and the chart review strategies were independent, and the reviewers were blinded. RESULTS: The computer monitoring strategy identified 2,620 alerts, of which 275 were determined to be ADEs. The chart review found 398 ADEs, whereas voluntary report detected 23. Of the 617 ADEs detected by at least one method, 76 ADEs were detected by both computer monitor and chart review. The computer monitor identified 45 percent; chart review, 65 percent; and voluntary report, 4 percent. The ADEs identified by computer monitor were more likely to be classified as "severe" than were those identified by chart review (51 versus 42 percent, p = .04). The positive predictive value of computer-generated alerts was 16 percent during the first eight weeks of the study; rule modifications increased this to 23 percent in the final eight weeks. The computer strategy required 11 person-hours per week to execute, whereas chart review required 55 person-hours per week and voluntary report strategy required 5. CONCLUSIONS: The computer-based monitor identified fewer ADEs than did chart review but many more ADEs than did stimulated voluntary report. The overlap among the ADEs identified using different methods was small, suggesting that the incidence of ADEs may be higher than previously reported and that different detection methods capture different events. The computer-based monitoring system represents an efficient approach for measuring ADE frequency and gauging the effectiveness of ADE prevention programs.