Articles: acetaminophen.
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To test, by completion of a simple questionnaire, patient knowledge of whether 15 commonly used over-the-counter and prescription analgesics and cough/cold remedies contained paracetamol and patient knowledge of the 4 g maximum daily dose of paracetamol. ⋯ Patient knowledge of paracetamol-containing products and of the maximum daily dose is currently insufficient to ensure safe use of the drug. Interventions are required to address these knowledge gaps to prevent unintentional repeated supratherapeutic ingestion of paracetamol. These interventions could include targeted public education and/or appropriate and effective medication labelling.
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To determine the relationship between paracetamol administration and skin blood flow (skBF) and blood pressure (BP) in critically ill patients treated for fever. ⋯ Paracetamol induced increases in skBF consistent with its antipyretic action and may be associated with significant falls in BP in the critically ill.
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Comparative Study
Effects of phenazopyridine on rat bladder primary afferent activity, and comparison with lidocaine and acetaminophen.
The clinical indication of phenazopyridine is unclear, it has been used clinically in conditions with increased bladder sensation as in cystitis and bladder pain syndrome/interstitial cystitis. We explored the effect of phenazopyridine on afferent nerve activity by direct measurement of both Aδ- and C-fibers in the rat, and compared the outcome with the effects of lidocaine (a local anesthetic) and of acetaminophen (an analgesic). ⋯ This study shows that phenazopyridine can directly inhibit the mechanosensitive Aδ-fibers in the normal rat bladder. This finding might explain its clinical effect in conditions of bladder hypersensitivity.
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Liver disease is responsible for more than 42,000 deaths yearly. Elevated hepatic iron levels have been shown to play a role in chronic liver diseases including hereditary hemochromatosis, thalassemia, and chronic hepatitis C, whereas acetaminophen (APAP) is the leading cause of acute liver failure. The goal of this study was to determine whether increased hepatic iron affects APAP-induced cytotoxicity, reactive oxygen species (ROS) production, and/or mitochondrial dysfunction in primary mouse hepatocytes (PMHs) that are differentiated and have gap junctional intracellular integrity, properties associated with hepatocytes in vivo and important for conducting toxicant studies. ⋯ In addition, treatment with the iron chelator deferoxamine (DFO) protected from APAP and resulted in a higher threshold dose being needed to induce cell death. We also showed that after TMHF treatment, APAP induced ROS and mitochondrial dysfunction at earlier time points than treatment with APAP alone; treatment with DFO increased the length of time required for APAP to induce ROS and mitochondrial dysfunction; and treatment with DFO, subsequent to TMHF, partially protected against TMHF-potentiated APAP injury. We conclude that iron potentiates the effects of APAP on cytotoxicity, ROS production, and mitochondrial dysfunction in PMHs.