Adulteration of dietary supplements.
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Biomedical subjects
Publications and source records attributed to C W Fetrow.
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OBJECTIVE: To review existing published clinical evidence surrounding the dietary supplement SAMe (S-adenosyl-L-methionine). DATA SOURCES: The majority of information was obtained from primary published literature identified through MEDLINE search (1966-February 2001). Information was also obtained through secondary and tertiary sources when available. STUDY SELECTION AND DATA EXTRACTION: All articles identified from data sources were evaluated and all relevant information included in this review. DATA SYNTHESIS: The majority of clinical trial evidence surrounds the application of SAMe for various depressive disorders, osteoarthrits, and fibromyalgia. Sample sizes of these trials and the dose employed have varied considerably. Several reviews and at least two meta-analyses have examined the available evidence surrounding SAMe in the therapy of depression for trials completed prior to 1994 and concluded that SAMe was superior to placebo in treating depressive disorders and approximately as effective as standard tricyclic antidepressants. Much of this information exists in the form of isolated case reports or solitary clinical trials. SAMe appears to be well tolerated, with the majority of adverse effects presenting as mild to moderate gastrointestinal complaints. However, it is apparent that this agent is not without risk of more significant psychiatric and cardiovascular adverse events. Information documenting drug or food interactions with SAMe is very limited. CONCLUSIONS: Consumers should be instructed to avoid unmonitored consumption of this dietary supplement until sufficient discussion has taken place with their primary healthcare provider. Although there exists significant potential for therapeutic application of SAMe, its uncertain risk profile precludes definitive recommendation at this time. Healthcare providers and consumers should likely temper their enthusiasm for this dietary supplement until sufficient information becomes available.
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Historically, oral or intravenous doses of vitamin K1 for supratherapeutic anticoagulation have ranged from 10 mg to 50 mg. Intravenous administration of vitamin K1 carries a rare but serious risk. No data specifically confirm the use of low-dose subcutaneous vitamin K1 for warfarin induced hypoprothrombinemia. The aim of this study was twofold: 1) to test the general utility of recommendations put forth by the Third Conference of Antithrombotic Therapy, and 2) to test the reliability of the subcutaneous route for this treatment. Six patients with excessive international normalized ratios (INRs) and no intervention were compared with 12 patients with excessive INRs who were given low doses of subcutaneous vitamin K1. The rate of decline of the INR to 3 was statistically significantly greater in favor of the treatment group. The amount of time required to achieve an INR of 3 differed between the two groups by almost 1 complete day (23 hours) in favor of the treatment group. The average dose of subcutaneous vitamin K1 required to return a patient to an INR of 3 or less was 4.9 mg. A few participants required an additional dose of the same magnitude or less to return to an INR within the therapeutic range. This study provides sufficient evidence that subcutaneous vitamin K1 is an effective alternative to intravenous administration of vitamin K1 for warfarin-induced hypoprothrombinemia and permits administration in accordance with the current published recommendations for intravenous vitamin K1 administration in this scenario.
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