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Background: Observational studies have suggested an increased risk of nephrotoxicity when piperacillin-tazobactam is added to vancomycin, although the data are confliciting. Objective: To perform a meta-analysis of identified studies to assess if adding piperacillin-tazobactam to vancomycin increases the incidence of nephrotoxicity. Method: A systematic review of PubMed, EMBASE, Cochrane Central, and Google Scholar was conducted to identify studies. Studies selected for meta-analysis were full length reports, retrospective or prospective, and designed specifically to assess if the combining piperacillin-tazobactam with vancomycin increases nephrotoxicity. Results: Six observational trials involving 963 patients were identified and analyzed. Five trials were retrospective and one was prospective. Vancomycin/piperacillin-tazobactam was compared to vancomycin alone in 2 trials, to vancomycin/cefepime in 3 trials, and vancomycin/cefepime or meropenem in one. Meta-analysis showed a statistical increase in the incidence of nephrotoxicity when piperacillin-tazobactam/vancomycin is compared to the control group (2.26 95% CI 1.41-3.63, p= 0.0007). No differences were noted between groups in patients requiring renal replacement. Conclusion: Adding piperacillin-tazobactam to vancomycin increases the risk of nephrotoxicity when compared to vancomycin alone or vancomycin with either cefepime or meropenem.

Background: Salsalate may offer many advantages over other non-steroidal antiinflammatory agents in patients taking warfarin, however a drug-drug interaction may occur which has not been reported in the medical literature or by the manufacturer of salsalate. Objective: To report a case of warfarin potentiation associated with salsalate treatment, which resulted in bleeding. Method: Clinical review of the course of a patient, who was stable on warfarin when salsalate therapy was added for chronic pain. Case Report: A patient taking stable doses of warfarin for over 1 year (with good control) was prescribed salsalate 3 g/day for pain in his knee and lower back. Approximately 1 month later he presents to the anticoagulation clinic with bruising and an International Normalized Ratio (INR) of 6.8. The patient had a good response to his salsalate therapy and wanted to continue it. The warfarin was held for 3 days and dose lowered by 50 %. His bruising then subsided and he had good control of his warfarin therapy with INRs ranging from 1.9 to 2.2 over the next 4 months. The patient was then lost to follow up. Conclusion: This case illustrates a strong association between starting salsalate and subsequent potentiation of warfarin, which heretofore has not been reported in the medical literature.

A retrospective study evaluated the success of dosages of simvastatin lower than the 10–20 mg/day recommended by the manufacturer in patients with hypercholesterolemia. Records of 95 patients enrolled in a pharmacist‐managed lipid clinic receiving stable dosages of simvastatin were reviewed. Data collected were demographics, number of simvastatin refills, dosage distribution, baseline and posttreatment lipid profiles, and proportion of patients with low‐density lipoprotein (LDL) levels below target as recommended by the National Cholesterol and Education Program. Dosages for 62% of patients were less than 20 mg/day. Percentages of patients at goal LDL were 98%, 89%, and 83% for patients taking 2.5, 5, and 10 mg/day, respectively. Patients taking 40 mg/day were least likely to be below the goal. There was an even distribution of patients taking each dosage. No statistical difference in compliance was noted among dosages based on prescription refills. Most patients taking less than the recommended initial dosage of the agent had satisfactory lipid control.

Study Objective. To assess the efficacy of fluvastatin administered every other day versus an equivalent dose given daily in patients with hypercholesterolemia.

Since the introduction of ophthalmic timolol solution in 1978 there have been numerous reports of systemic toxicity associated with its use. The majority of the systemic side effects reported are the same as those associated with oral timolol. Several cases of respiratory distress have been described generally in patients with underlying restrictive airway disease. Cardiovascular effects range from effects on resting pulse rate to the development of overt bradycardia and heart failure. Central nervous system effects reported include fatigue, confusion, depression, and hallucinations. A variety of other systemic effects have also been described. Caution should be used when ophthalmic timolol is administered to elderly patients or those patients with contraindications to systemic β-blockers.

To determine the tolerability and efficacy of crystalline niacin in reaching target lipid goals, we conducted a retrospective review of medical records of 62 patients treated with the agent over 2 years in a lipid clinic at a nonacademic veterans hospital. Most patients received niacin for hypercholesterolemia. Thirty‐one patients (50%) stopped therapy due to adverse events, principally, intolerable cutaneous reactions. Twenty‐nine withdrew from therapy during the first 6 weeks of treatment. Of those who tolerated niacin, 23 did not achieve target lipid serum concentrations at the maximum tolerated dosage; 8 did achieve target concentrations. Thus crystalline niacin was largely ineffective in treating patients with dyslipidemia.

OBJECTIVE: To review the risks, manifestations, and treatment of cyanide toxicity from nitroprusside therapy.DATA SOURCES: All English case reports identified in Index Medicus(MEDLINE) of cyanide intoxication related to nitroprusside from 1970 to the present were reviewed. In addition, literature regarding the incidence, risks, and treatment of cyanide toxicity from nitroprusside is presented.CONCLUSIONS: Numerous cases of cyanide toxicity associated with nitroprusside have been reported. The overall incidence appears to be infrequent; however, certain patients may be at high risk. Risk factors may include hypoalbuminemia, cardiopulmonary bypass procedures, or the administration of moderate to high doses of nitroprusside. Treatment of cyanide toxicity requires the cessation of nitroprusside and, for severe toxicity, use of the cyanide antidote kit. Cyanide toxicity from nitroprusside may be prevented by concomitant administration of sodium thiosulfate infusions.

BACKGROUND: Fluconazole has been reported to interact with many medications. This study examined the effect of low-dose fluconazole therapy on the hypoprothrombinemic response of warfarin sodium in patients. METHODS: Patients receiving low-intensity anticoagulation therapy with warfarin were recruited. All patients were taking stable doses of warfarin and had two baseline prothrombin times (PTs) within 10% of each other. Each patient received 100 mg of fluconazole daily for 7 days. Prothrombin times were measured on days 2,5, and 8 during fluconazole administration. RESULTS: All patients had a progressive increase in PTs. Mean (±SD) of PTs increased from 15.8±1 seconds before the administration of fluconazole to 18.9±1.9 seconds on day 5 and 21.9±2.2 seconds on day 8. Fluconazole therapy was stopped early in three patients due to high PTs. The largest change in PT was 9.7 seconds. No bleeding was noted during the study.Conclusion: Fluconazole predictably potentiates the hypoprothrombinemic response of warfarin. Prothrombin times must be monitored when fluconazole is administered to patients taking warfarin.(Arch Intern Med. 1993;153:102-104)

The following describes a patient on a stable regimen of warfarin who developed severe hypoprothrombinemia and bleeding 4 weeks after starting gemfibrozil. Despite a warning by the manufacturer, only one report of this interaction has been published in the literature. This interaction may be overlooked by clinicians, which may result in a serious bleeding risk for patients on warfarin.

We appreciate the remarks made by Cantilena and Honig in reference to our comments on antipyrine metabolism.1 In the "Comment" section, we were only speculative in stating that antipyrine metabolism may predict warfarin metabolism. Cantilena and Honig referred to one study that demonstrated little relationship between antipyrine and tolbutamide disposition when effected by known inhibitors of drug metabolism.2 We are unaware of other studies showing a similar relationship (or lack thereof) between antipyrine and warfarin. Clearly, more investigation is needed in this area before firm conclusions can be made.

The purpose of this study was to assess the effect of fluoxetine on the hypoprothrombinemic response of warfarin in patients chronically anticoagulated.Patients receiving low-intensity anticoagulation with warfarin were recruited. All patients were taking stable dosages of warfarin and had two baseline prothrombin times (PTs) within 10% of each other. Each patient received fluoxetine (20 mg daily) for 21 days. PTs were measured on days 2, 5, 8, 12, 15, 19, and 22 of fluoxetine administration. Six patients completed the study. There was no significant difference in mean PTs before and during fluoxetine administration. Fluoxetine at the dosage studied does not predictably effect the hypoprothrombinemic response of warfarin. (J Clin Psychopharmacol 1997;17:110-112).