Choi JS, Burm JP, Jhee SS
… +3 more, Chin A, Ulrich RW, Gill MA
Am J Hosp Pharm
· 1994 Sep · PMID 7801988
The stability of piperacillin sodium plus tazobactam sodium and ranitidine hydrochloride in 0.9% sodium chloride injection during simulated Y-site administration was studied. Triplicate test solutions of piperacillin 40...The stability of piperacillin sodium plus tazobactam sodium and ranitidine hydrochloride in 0.9% sodium chloride injection during simulated Y-site administration was studied. Triplicate test solutions of piperacillin 40 mg/mL plus tazobactam 5 mg/mL (as the sodium salts) or piperacillin 80 mg/mL plus tazobactam 10 mg/mL (as the sodium salts) were mixed 1:1 with ranitidine 0.5 and 2.0 mg/mL (as the hydrochloride salt). The solutions were stored at 23 degrees C, and samples were removed at zero, one, two, and four hours for measurement of drug concentration by stability-indicating high-performance liquid chromatography. At the time of sampling and before any dilution, each sample was visually inspected for color and precipitation, and pH was determined. At all sampling times, the concentrations of piperacillin, tazobactam, and ranitidine were > 90% of initial concentrations. There were no substantial changes in pH or color. Tazobactam 5 mg/mL (as the sodium salt) and ranitidine 0.5 and 2 mg/mL (as the hydrochloride salt) in 0.9% sodium chloride injection were stable for up to four hours during simulated Y-site administration. Piperacillin 80 mg/mL plus tazobactam 10 mg/mL (as the sodium salts) and ranitidine 0.5 and 2 mg/mL (as the hydrochloride salt) were stable for up to four hours during simulated Y-site administration.
Pearson TF, Pittman DG, Longley JM
… +3 more, Grapes ZT, Vigliotti DJ, Mullis SR
Am J Hosp Pharm
· 1994 Sep · PMID 7801987
Factors associated with preventable adverse drug reactions (ADRs) in a community hospital patient population were studied. The following data were collected by concurrent review of all ADRs reported from July 1992 throug...Factors associated with preventable adverse drug reactions (ADRs) in a community hospital patient population were studied. The following data were collected by concurrent review of all ADRs reported from July 1992 through January 1993: patient demographics, ADR variables, length of stay, and preventability of ADR. These data were analyzed to determine factors associated with preventable ADRs. Of the 203 ADRs reported, 38 (19%) were identified as preventable. The only significant difference found between preventable and nonpreventable ADRs was in severity (preventable ADRs were more severe). Length of stay (LOS) for patients who experienced ADRs was longer than the national average for patients in the same diagnosis-related group. Most of the preventable ADRs involved (1) a documented allergy to medication ordered or to similar medications, (2) anticoagulants or thrombolytics, (3) that required serum drug concentration monitoring (in the absence of pharmacokinetics service involvement), and (4) renally eliminated drugs for which dosage adjustments were not made in patients with impaired renal function. Strategies for minimizing ADRs were developed based on these factors. An ADR reporting program helped in identifying preventable ADRs, determining factors associated with preventable ADRs, and developing strategies for preventing ADRs in a community hospital patient population.
The replicative cycle of the human immunodeficiency virus (HIV) is reviewed, and currently used and investigational agents directed against the virus are discussed. The first step in the replication of HIV is selective b...The replicative cycle of the human immunodeficiency virus (HIV) is reviewed, and currently used and investigational agents directed against the virus are discussed. The first step in the replication of HIV is selective binding of the envelope glycoprotein to CD4 receptors located on T lymphocytes. The virion is then uncoated within the cytoplasm, yielding viral genomic RNA. Reverse transcriptase uses the viral RNA as a template to form single-stranded DNA, which is duplicated to form proviral DNA through the activity of ribonuclease H. Host RNA polymerases transcribe the integrated proviral DNA into messenger RNA, and there is subsequent translation to viral proteins. After translation, further modification of precursor polyproteins is necessary to produce functional peptides. The assembled virus then buds from the cell surface and invades other cells. Targets of drug intervention in the replicative cycle include (1) binding and entry, (2) reverse transcriptase, (3) transcription and translation, and (4) viral maturation and budding. Inhibitors of binding and entry include recombinant soluble CD4, immunoadhesins, peptide T, and hypericin. Nucleoside reverse-transcriptase inhibitors include zidovudine, didanosine, zalcitabine, and stavudine. Foscarnet, tetrahydroimidazobenzo-diazepinthione compounds, and nevirapine are some nonnucleoside reverse-transcriptase inhibitors. Inhibitors of transcription and translation include antagonists of the tat gene and GLQ223. Castanospermine, N-butyldeoxynojirimycin, and protease inhibitors interfere with viral maturation and budding. Drug combinations that have been or are being investigated include zidovudine plus interferon alfa, zidovudine plus zalcitabine, and zidovudine plus didanosine. Four agents currently have approved labeling for use against HIV infection: zidovudine, didanosine, zalcitabine, and stavudine. Monotherapy with zidovudine remains the treatment of first choice. Although progress has been made in developing drug therapies for HIV infection, more selective and more potent drugs are urgently needed. The best approach at present is to optimize the use of available agents, continue to investigate new therapies, and educate the public about prevention.