Evaluation of online consumer medication information.

BACKGROUND: Millions of Americans search the Internet for health-related information; however, the readability and comprehensiveness of consumer medication information (CMI) on the Internet has not been widely studied. OBJECTIVE: The purpose of this study was to evaluate the readability and comprehensiveness of online CMI. METHODS: The readability and comprehensiveness of consumer drug information found on 3 well-known Web sites (Medline Plus, Yahoo Health, and WebMD) was evaluated; in particular, information related to 10 commonly prescribed medications. Readability was assessed using the Simple Measure of Gobbledygook (SMOG) and Fry Readability Graph (FRG) tools; comprehensiveness of information was evaluated using the Keystone action plan criteria. RESULTS: Using SMOG, the mean reading level of each Web site was 13th grade level or higher. Using the FRG, the mean reading level was 10th grade or higher. Out of the 24 points in the Keystone action plan criteria, information found on each of the Web sites was deemed accurate with mean score of 21, 21, and 19 for Medline Plus, Yahoo Health, and WebMD, respectively. CONCLUSIONS: For the medications reviewed, CMI found on Web sites was accurate when assessed using the Keystone action plan criteria. The readability levels were higher than the recommended sixth grade level.

Interaction between warfarin and nafcillin: case report and review of the literature.

A 39-year-old man with a history of deep vein thrombosis and septic arthritis of the left knee was treated with warfarin and cefazolin. Therapeutic prothrombin times and international normalized ratios (INRs) were maintained with warfarin 32 mg/week for approximately 1 month. When the patient's antibiotic regimen was changed from cefazolin to nafcillin 2 g every 4 hours, his INR declined significantly. His warfarin dosage had to be increased to a maximum of 88 mg/week to achieve a therapeutic INR. After completion of antibiotic therapy with nafcillin, the patient's warfarin requirements slowly declined over several weeks. A maintenance dosage of warfarin 42-48 mg/week was necessary after nafcillin discontinuation. Hepatic cytochrome P450 isoenzyme induction by nafcillin is likely the mechanism of a warfarin-nafcillin interaction. The usual onset of effect is within 1 week after starting nafcillin, and the offset of the effect is usually evident within 4 weeks after nafcillin discontinuation. In patients taking warfarin who are prescribed nafcillin, a 2-4-fold increase in the warfarin dose may be necessary, and clinicians should closely monitor INRs.

Update on the interaction of rifampin and warfarin.

A 79-year-old man with a history of deep vein thrombosis and pulmonary embolism received anticoagulation therapy with warfarin 5 mg daily for 8 months. He was diagnosed with osteomyelitis and underwent partial metatarsal resection of his right foot. After surgery, antibiotics were initiated, including ertapenem sodium 1 g intravenously every 24 hours, vancomycin 1400 mg intravenously every 24 hours, and rifampin 300 mg by mouth twice daily. Achieving a therapeutic level of anticoagulation was difficult despite escalating doses of warfarin, because of the interaction with rifampin. A 5- to 6-fold increase in warfarin dose was prescribed to reach therapeutic international normalized ratios (INRs), but even these increases were insufficient to maintain his INR in the therapeutic range. After rifampin was discontinued, warfarin doses were gradually reduced over the next 2 months. When concurrent warfarin-rifampin therapy is necessary, vigilant monitoring is imperative and significant increases in warfarin doses are likely.

Thrombocytopenia following heparin flush.

A total of 23 patients who developed heparin-induced thrombocytopenia following exposure to heparin solely due to intravascular catheter or filter flush were the subjects of prospective studies of argatroban therapy. Heparin doses were 10-13,000 U, with a mean exposure of 8+/-4 days. Following heparin-induced thrombocytopenia diagnosis and heparin cessation, 13 patients received argatroban (mean dose of 1.8+/-1.1 mg/kg/min for 5.5+/-3.9 days), achieving activated partial thromboplastin times of 63+/-23 seconds, and 10 historical control patients received no direct thrombin inhibitors. Platelet count recovered to a mean of 207+/-153 x 10(9)/L (n=12) after 5.5+/-3.9 days of argatroban therapy and to a mean of 127+/-63 x 10(9)/L (n=8) 5 days after baseline in the control group. A composite end point of death, amputation, or new thrombosis within 37 days occurred in five (38.5%) argatroban-treated patients and four (40%) controls. Death was the most common untoward outcome (approximately 30% of each group). No argatroban-treated patient and two (20%) control patients experienced new thrombosis. Major bleeding was comparable between groups. Heparin-induced thrombocytopenia can occur following minimal heparin exposure, including heparin flushes; in these patients, argatroban provides effective alternative anticoagulation as compared with historical controls.

A literature review of the epidemiology and treatment of acute gout.

BACKGROUND: Gout is the most common cause of inflammatory arthritis in men aged >40 years and is frequently encountered in clinical practice. OBJECTIVE: The goal of this article was to review the published literature on the epidemiology, treatment, and estimated burden of illness of acute gout. METHODS: Articles on gout published in English between 1980 and June 2002 were identified through a MEDLINE search. Relevant clinical studies and review articles were found using the text- and keyword-search term gout alone and in combination with epidemiology, prevalence, incidence, complications, outcome, quality of life, economics, cost, prevention or drug therapy. The reference lists of identified articles, especially review articles, were checked for any additional studies that might have been missed in the original MEDLINE search. RESULTS: The epidemiology of gout in various geographic regions has been well documented. Data suggest that environmental, racial, and hereditary factors may influence the development of gout, and that the prevalence of gout appears to be on the rise worldwide. Evidence from well-designed clinical studies evaluating drug therapies for gout is limited. Therapies for acute gout include corticotropin, corticosteroids, colchicine or, more often, nonsteroidal anti-inflammatory drugs (NSAIDs), which have shown comparable efficacy. A recent study suggests that etoricoxib, a new cyclooxygenase-2-selective inhibitor, may be as effective as and better tolerated than traditional NSAIDs in the treatment of gout. Urate-lowering therapy, prophylactic colchicine, and low-dose NSAIDs are used for the long-term prophylaxis of gout. However, all acute and prophylactic therapies are associated with adverse events. Using an economic model for gout, the annual direct burden of illness for new cases of acute gout can be estimated at 27,378,494 US dollars in the United States. CONCLUSIONS: Gout is an increasingly prevalent condition worldwide and creates a heavy economic burden. Available treatments are generally effective; however, they are not devoid of adverse events. Well-designed, long-term, controlled clinical trials evaluating the comparative efficacy and tolerability of treatments for gout are needed.

Fenofibrate potentiates warfarin effects.

OBJECTIVE: To describe 2 patients in whom the initiation of fenofibrate potentiated warfarin's anticoagulant effects. CASE SUMMARY: A 71-year-old white woman and an 80-year-old white woman with multiple medical conditions were both stabilized on long-term warfarin therapy. During the course of anticoagulation, both patients were prescribed fenofibrate and experienced threefold and twofold increases in international normalized ratio (INR), respectively, requiring total weekly warfarin dosage reductions of 30-40%. Before starting fenofibrate therapy, both patients' coagulation values were within the therapeutic range. When interviewed, patients and caregivers denied bleeding, bruising, changes in diet, alcohol ingestion, nonadherence with therapy, or changes in drug regimen except for the addition of fenofibrate. Upon chart review, evaluation of potentially contributory parameters, such as other changes in drug therapy, thyroid function, liver function, and drug-disease interactions, showed that these parameters remained stable and were ruled noncontributory. DISCUSSION: The addition of fenofibrate in 2 patients on stable and therapeutic doses of warfarin increased the anticoagulant response to warfarin. A clear temporal relationship with the addition of fenofibrate and the appearance of the interaction was seen. Fenofibrate is highly protein bound, with the potential to displace warfarin from its binding protein, leading to an enhanced hypoprothrombinemic effect. Fenofibrate is also a mild to moderate inhibitor of CYP2C9, the enzyme responsible for warfarin metabolism. The combination of these effects--displacement of warfarin by fenofibrate coupled with decreased metabolism of warfarin--may increase the anticoagulant response to warfarin. Using the Naranjo probability scale, these interactions were designated as probable. CONCLUSIONS: We suggest serial monitoring of INR and consider an empiric 20% reduction in warfarin dosage when fenofibrate is initiated, with the possibility for a greater warfarin dosage reduction based on INR results.