Academic literature on the topic 'Acetaminophen'

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Journal articles on the topic "Acetaminophen"

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Myers, Wade C., Terrance A. Otto, Elaine Harris, Daniel Diaco, and Anthony Moreno. "ACETAMINOPHEN OVERDOSE AS A SUICIDAL GESTURE: A SURVEY OF ADOLESCENTS' KNOWLEDGE OF ITS POTENTIAL FOR TOXICITY." Pediatrics 93, no. 6 (June 1, 1994): A36. http://dx.doi.org/10.1542/peds.93.6.a36.

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Acetaminophen is a popular nonprescription analgesic that is often taken in overdose by adolescents during suicidal gestures. The authors hypothesized that most adolescents are naive about the toxic and lethal potential of acetaminophen in overdose. A one-page, 12-item questionnaire was administered to 169 high school students to evaluate their perceptions and knowledge in this area. Whereas only 22% of the sample underestimated the dose of acetaminophen necessary to cause harm, 40.5% underestimated the potential lethality of acetaminophen in overdose. Moreover, 17% of the sample did not believe one could ingest enough acetaminophen to cause death. The lack of knowledge about acetaminophen's potential dangerousness, its widespread availability, and an absence of early symptoms of hepatotoxicity make this medication highly dangerous to those adolescents who take it in overdose during parasuicidal behavior.
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Thibault, Céline, Élaine Pelletier, Christina Nguyen, Evelyne D. Trottier, Marie-Joëlle Doré-Bergeron, Kathryn DeKoven, Anne-Marie Roy, et al. "The Three W's of Acetaminophen In Children: Who, Why, and Which Administration Mode?" Journal of Pediatric Pharmacology and Therapeutics 28, no. 1 (January 1, 2023): 20–28. http://dx.doi.org/10.5863/1551-6776-28.1.20.

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Acetaminophen is one of the oldest medications commonly administered in children. Its efficacy in treating fever and pain is well accepted among clinicians. However, the available evidence supporting the use of acetaminophen's different modes of administration remains relatively scarce and poorly known. This short report summarizes the available evidence and provides a framework to guide clinicians regarding a rational use of acetaminophen in children.
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Keaveney, Alexis, Ellen Peters, and Baldwin Way. "Effects of acetaminophen on risk taking." Social Cognitive and Affective Neuroscience 15, no. 7 (July 2020): 725–32. http://dx.doi.org/10.1093/scan/nsaa108.

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Abstract Acetaminophen, an analgesic and antipyretic available over-the-counter and used in over 600 medicines, is one of the most consumed drugs in the USA. Recent research has suggested that acetaminophen’s effects extend to the blunting of negative as well as positive affect. Because affect is a determinant of risk perception and risk taking, we tested the hypothesis that acute acetaminophen consumption (1000 mg) could influence these important judgments and decisions. In three double-blind, placebo-controlled studies, healthy young adults completed a laboratory measure of risk taking (Balloon Analog Risk Task) and in Studies 1 and 2 completed self-report measures of risk perception. Across all studies (total n = 545), acetaminophen increased risk-taking behavior. On the more affectively stimulating risk perception measure used in Study 2, acetaminophen reduced self-reported perceived risk and this reduction statistically mediated increased risk-taking behavior. These results indicate that acetaminophen can increase risk taking, which may be due to reductions in risk perceptions, particularly those that are highly affect laden.
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Iqbal, Sohail, Rao Salman Aziz, Liaquat Ali, Shoaib Ahmed, Maheen Rana, Hassan Mahmood Makhdoom, Amal Shukat, Amna Batool, Muhammad Sajjad Hassan, and Farah Naz Akbar. "ACETAMINOPHEN." Professional Medical Journal 25, no. 12 (December 8, 2018): 1923–27. http://dx.doi.org/10.29309/tpmj/18.4807.

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Introduction: Nephrotoxicity is an important side effect of many medicine and chemotherapeutic agents. Active ingredients from natural sources have shown promising results to alleviate these side effects. Objectives: We aimed to investigate the effects of aqueous Date fruit extract in animal model of paracetamol induced nephrotoxicity in rats. Study Design: Experimental. Setting: Sargodha Institute of Health Sciences Sargodha. Period: January 2017-September 2017. Material & Methods: 30 rats were randomly divided into five groups treatment groups. Treatments were given daily for two weeks. Control group (Group I) is the treatment naïve one. Paracetamol (2 g/kg body weight/day) was given to group 2. Group 3 received extract of date fruit prepared in water (600 mg per kg body weight per day) for one week before paracetamol (2g per kg body weight per day) in the next week. Animals of group 4 were given paracetamol for a duration of 7 days and were then administered the extract of date palm in water. 5th group was given paracetamol (2 g per kg per day) and 600 mg extract of date fruit in water solution per kg body weight at the same time. Results: Renal function was recorded to be significantly altered by paracetamol toxicity and these effects were effectively reversed by the date fruit extract. Conclusion: The acetaminophen induced nephrotoxic changes were reversed by ductylifera in rats.
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Anker, Anthony L., and Martin J. Smilkstein. "Acetaminophen." Emergency Medicine Clinics of North America 12, no. 2 (May 1994): 335–49. http://dx.doi.org/10.1016/s0733-8627(20)30431-4.

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Turkoski, Beatrice B. "Acetaminophen." Orthopaedic Nursing 29, no. 1 (January 2010): 41–43. http://dx.doi.org/10.1097/nor.0b013e3181c8cd75.

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&NA;. "Acetaminophen." Orthopaedic Nursing 29, no. 1 (January 2010): 44–45. http://dx.doi.org/10.1097/nor.0b013e3181cd36aa.

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Holubek, William J., and Lewis S. Nelson. "Acetaminophen Protein Adducts: Is Acetaminophen to Blame?" Gastroenterology 131, no. 4 (October 2006): 1360. http://dx.doi.org/10.1053/j.gastro.2006.08.056.

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Bertholf, Roger L., Laura M. Johannsen, Alireza Bazooband, and Vafa Mansouri. "False-Positive Acetaminophen Results in a Hyperbilirubinemic Patient." Clinical Chemistry 49, no. 4 (April 1, 2003): 695–98. http://dx.doi.org/10.1373/49.4.695.

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Abstract Background: Acetaminophen was falsely detected in the plasma of a severely jaundiced patient, and a methodologic interference from bilirubin was suspected. Methods: Acetaminophen was measured by an enzymatic method (GDS Diagnostics). The putative bilirubin interference was investigated in 12 hyperbilirubinemic specimens and in bilirubin linearity calibrators. The analytical method was modified to correct for background absorbance at a second wavelength. Hyperbilirubinemic specimens were fortified with acetaminophen to assess the effect of the interference on acetaminophen measurements. Results: Acetaminophen was detected in 12 specimens from hyperbilirubinemic patients without a history of recent acetaminophen exposure. Dilution of hyperbilirubinemic specimens produced a nonproportional decrease in apparent acetaminophen concentrations, and no acetaminophen was detected when bilirubin was <50 mg/L. Background correction at a second wavelength failed to compensate for the interference. Although erroneous acetaminophen concentrations were detected in all specimens with high bilirubin, acetaminophen measurements in fortified specimens were accurate. Conclusion: The data are consistent with bilirubin interference in the enzymatic and/or chromogenic reactions involved in the acetaminophen method.
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Chan, Thomas YK. "Interactions of Acetaminophen, Opiates, and Their Combinations with Warfarin and other Oral Anticoagulants." Journal of Pharmacy Technology 13, no. 2 (March 1997): 89–92. http://dx.doi.org/10.1177/875512259701300211.

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Objective: To determine whether acetaminophen, opiates, or acetaminophen–opiate combinations potentiate the effect of warfarin. Data Sources: Previous studies or reports of interactions between warfarin and acetaminophen, opiates, or acetaminophen–opiate combinations (MEDLINE search, January 1976 to January 1996). Study Selection: All articles were included in the review. Pertinent information was selected for discussion. Data Synthesis: Studies of the effects of acetaminophen on anticoagulation with warfarin and other oral anticoagulants have yielded conflicting results. In three placebo-controlled studies of patients or healthy men, acetaminophen 2–4 g/d for 2–3 weeks potentiated the anticoagulant effect of warfarin and other related drugs compared with placebo. Similar findings were seen in one uncontrolled study of patients taking acetaminophen 2.6 g/d for 4 weeks, but not in another in which patients took acetaminophen 3.25 g/d for 14 days. Other studies showed that two doses of acetaminophen 650 mg for 1 day did not influence the prothrombin time. There were six reports of adverse interactions between warfarin and acetaminophen–opiate combinations. Of five patients who were given an acetaminophen–propoxyphene combination, the equivalent daily doses of acetaminophen and propoxyphene were specified for four and ranged from 1.95 to 6.5 g and from 195 to 1,000 mg, respectively. The duration of therapy in the five patients ranged from less than 1 day to 10 days. One of these patients also received ibuprofen. Another patient took an unspecified acetaminophen–codeine product equivalent to acetaminophen 1.56 g/d. The exact mechanism underlying such interactions is not clear. Conclusions: During the combined use of warfarin and acetaminophen (in high daily doses for 2–3 wk) or acetaminophen–propoxyphene combinations, patients should be closely monitored for anticoagulant control and bleeding complications.
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Dissertations / Theses on the topic "Acetaminophen"

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Nam, Haemi. "Acetaminophen, Aggression, and Learning: An Investigation of Acetaminophen's Social Side Effects." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1557155429796022.

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Poon, Yuk-king Karen. "The antagonistic effect of paracetamol on ethanol-induced gastric damage in rats /." [Hong Kong] : University of Hong Kong, 1989. http://sunzi.lib.hku.hk/hkuto/record.jsp?B12718592.

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Soliman, Gamal. "A study of acetaminophen analogues' toxicity." Thesis, University of Ottawa (Canada), 1985. http://hdl.handle.net/10393/4926.

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Reddyhoff, Dennis. "Mathematical modelling of acetaminophen induced hepatotoxicity." Thesis, Loughborough University, 2016. https://dspace.lboro.ac.uk/2134/23008.

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Acetaminophen, known as paracetamol in the UK and Tylenol in the United States, is a widespread and commonly used painkiller all over the world. Taken in large enough doses, however, it can cause fatal liver damage. In the U.S., 56000 people are admitted to hospital each year due to acetaminophen overdose and its related effects, at great cost to healthcare services. In this thesis we present a number of different models of acetaminophen metabolism and toxicity. Previously, models of acetaminophen toxicity have been complex and due to this complexity, do not lend themselves well to more advanced mathematical analysis such as the perturbation analysis presented later in this thesis. We begin with a simple model of acetaminophen metabolism, studying a single liver cell and performing numerical and sensitivity analysis to further understand the most important mechanisms and pathways of the model. Through this we identify key parameters that affect the total toxicity in our model. We then proceed to perform singular perturbation analysis, studying the behaviour of the model over different timescales, finding a number of key timescales for the depletion and subsequent recovery of various cofactors as well as critical dose above which we see toxicity occurring. Later in the thesis, this model is used to model metabolism in a spheroid cell culture, examining the difference spatial effects have on metabolism across a 3D cell culture. We then present a more complex model, examining the difference the addition of an adaptive response to acetaminophen overdose from the Nrf2 signalling pathway, has on our results. We aim to reproduce an unexplained result in the experimental data of our colleagues, and so analyse the steady states of our model when subjected to an infused dose, rather than a bolus one. We identify another critical dose which leads to GSH depletion in the infused dose case and find that Nrf2 adaptation decreases toxicity and model sensitivity. This model is then used as part of a whole-body PBPK model, exploring the effects that the distribution of the drug across the bloodstream and different organs has. We explore the affects of that a delay in up-regulation from the Nrf2 pathway has on the model, and find that with rescaled parameters we can qualitatively reproduce the results of our collaborators. Finally, we present the results of in vitro work that we have undertaken, the aim of which was to find new parameters for the model in human hepatocytes, rather than from rodent models, and find a new value for a parameter in our model from human cell lines.
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Mischkowski, Dominik. "The Social Side Effects of Acetaminophen." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1438081282.

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Bashir, Shazma. "Mechanism of Paracetamol (acetaminophen) induced hypothermia." Thesis, University of East London, 2018. http://roar.uel.ac.uk/7308/.

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Paracetamol is a potent analgesic and antipyretic with limited side effects compared to the nonsteroidal anti-inflammatory drugs (NSAIDs) and opiates. Worldwide paracetamol is commonly used to treat pain and fever in both children and adults. Although, this drug has been in clinical use for more than a century, the mechanisms of action are not fully understood. Historically some of the actions of paracetamol were attributed to the inhibition of central cyclooxygenase (COX-1 and COX-2) enzymes however given the weak inhibitory effects on COX-1 and COX-2 enzymes, alternative targets have been suggested including a possible novel COX-3. The inhibition of COX-2 is accepted as the mechanism by which paracetamol reduces core temperature (Tc) in febrile animals. However, in non-febrile animals where COX-2 is not induced, paracetamol has also been shown to cause hypothermia by a mechanism that is not fully understood. Both the reduction of pyresis and induction of hypothermia can only occur when peripheral metabolic rate decreases and/or heat loss increases. In terms of antipyresis and hypothermia, the inhibition of lipolysis, fatty acid oxidation and mitochondria function are obvious alternative targets. Studies were undertaken to identify and characterise the putative COX-3 at protein and mRNA level using western blot analysis and reverse transcription polymerase chain reaction (RT-PCR) in mouse brain endothelial cells (b.End3) and whole brain tissues isolated from male C57BL/6 mice. Additional studies were also undertaken to assess if the hypothermic properties of paracetamol could be attributed to direct inhibition of thermogenic pathways in both 3T3-L1 adipocytes and primary brown adipocytes isolated from male Wistar rats. Adipocytes and isolated mitochondria were exposed to paracetamol and lipolysis, fatty acid oxidation (FAO), mitochondrial electron transport chain (ETC), assessed by measuring oxygen consumption rate (OCR). In these studies no expression of the COX-3 protein could be detected in brain endothelial cells and homogenates and no evidence of a COX-3 was detected at mRNA level. However, paracetamol caused a significant decrease (upto 70%; P < 0.01, from control) in both basal and stimulated lipolysis at 1, 3 and 24 hours without affecting cell viability. Paracetamol (10 mM) and its metabolite N-acetyl-p-benzoquinone imine (NAPQI) at 50 μM also significantly (P < 0.01, from control), reduced endogenous and exogenous FAO by 50% and 70% respectively. NAPQI (50 μM) had limited effect on mitochondrial uncoupling. Finally, paracetamol and other antipyretic compounds also significantly reduced ETC activity (upto 90%; P < 0.01, from control). Both the maintenance of normal body temperature (Tb) and the induction of pyresis require increased mitochondrial ETC activity normally initiated centrally and driven peripherally by reduction of substrates such as fatty acids and glucose. The failure to identify the COX-3 protein and the direct inhibition of lipolysis, FAO and ETC activity indicate that antipyretic actions of paracetamol could partly be attributed to it actions on peripheral energy generation systems and provide new drug targets for reducing fever and chemically inducing hypothermia.
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Xu, Zheng. "Developmental Toxicity of Dextromethorphan and Acetaminophen in Zebrafish Embryos/Larvae: Relevance of SULT-mediated Dextromethorphan/Acetaminophen Sulfation." Toledo, Ohio : University of Toledo, 2010. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=toledo1271433014.

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Thesis (M.S.)--University of Toledo, 2010.
Typescript. "Submitted to the Graduate Faculty as a partial fulfillment of the requirement for the Master of Science in Pharmacology and Toxicology." "A thesis entitled"--at head of title. Title from title page of PDF document. Bibliography: p. 68-81.
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Harnagea, Theophilus Eugenia. "Acetaminophen stimulates proliferation of breast cancer cells." Morgantown, W. Va. : [West Virginia University Libraries], 1999. http://etd.wvu.edu/templates/showETD.cfm?recnum=773.

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Thesis (Ph. D.)--West Virginia University, 1999.
Title from document title page. Document formatted into pages; contains ix, 137 p. : ill. Vita. Includes abstract. Includes bibliographical references (p. 115-134).
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Pandey, Rajiv 1967. "Crystal size manipulation of acetaminophen via recrystallization." Thesis, The University of Arizona, 1993. http://hdl.handle.net/10150/278344.

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The crystal size distribution (CSD) of any material determines its end use. Consequently, comminution processes are used to transform material from one size distribution to another. Often, recrystallization from solution is one of the processes used. Recently, a novel recrystallization process named the GAS process was developed to mill compounds that were thermally labile and insoluble in supercritical fluids. CSD could be manipulated using this process. To further illustrate the applicability of this process, size manipulation studies of acetaminophen (a widely available drug) were performed. The aim of this work was to produce crystals in the mass mean size range from 5mum to 50mum, and identify the conditions for producing the desired size distribution. A modified GAS process and a liquid anti-solvent (LAS) process were also investigated. Together with acetaminophen-butanol, other systems studied were aspirin-methanol and benzoic acid-methanol.
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Ito, Yoshiya, Nancy Machen, Edward Abril, and Robert McCuskey. "Effects of acetaminophen on hepatic microcirculation in mice." BioMed Central, 2004. http://hdl.handle.net/10150/610123.

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Books on the topic "Acetaminophen"

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Hankin, Lester. Analysis of products containing acetaminophen. New Haven, Conn: Connecticut Agricultural Experiment Station, 1986.

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Weglicki, Peter S. Free radical reactions of acetaminophen. Salford: University of Salford, 1987.

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Hankin, Lester. Analysis of products containing acetaminophen. New Haven, Conn: Connecticut Agricultural Experiment Station, 1986.

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Paracetamol (acetaminophen): A critical bibliographic review. 2nd ed. London: Taylor & Francis, 2001.

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Paracetamol (acetaminophen): A critical bibliographic review. London, UK: Taylor & Francis, 1996.

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Folkenberg, Judy. Acetaminophen-codeine: How to take your medicine. [Rockville, Md: Dept. of Health and Human Services, Food and Drug Administratrion, 1991.

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Folkenberg, Judy. Acetaminophen-codeine: How to take your medicine. [Rockville, Md: Dept. of Health and Human Services, Food and Drug Administratrion, 1991.

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Folkenberg, Judy. Acetaminophen-codeine: How to take your medicine. [Rockville, Md: Dept. of Health and Human Services, Food and Drug Administratrion, 1991.

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Folkenberg, Judy. Acetaminophen-codeine: How to take your medicine. [Rockville, Md: Dept. of Health and Human Services, Food and Drug Administratrion, 1991.

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Lin, Meng-Chih. Post-consolidation behaviour of acetaminophen crystals. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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Book chapters on the topic "Acetaminophen"

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Slika, Rania. "Acetaminophen." In Textbook of Clinical Pediatrics, 2593–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-02202-9_272.

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Kerstenetzky, Luiza. "Acetaminophen." In Pain, 231–35. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-99124-5_53.

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Bährle-Rapp, Marina. "Acetaminophen." In Springer Lexikon Kosmetik und Körperpflege, 4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71095-0_59.

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Kim, David J., and Srdjan S. Nedeljkovic. "Acetaminophen." In Pain Medicine, 163–64. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-43133-8_41.

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George, David J. "Acetaminophen." In Poisons, 125–29. Boca Raton : CRC Press, [2018]: CRC Press, 2017. http://dx.doi.org/10.1201/9781315371757-17.

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Edwards, David A., and Obi Okwuchukwu. "Acetaminophen." In Hospitalized Chronic Pain Patient, 165–66. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08376-1_30.

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de Groot, Anton C. "Acetaminophen." In Monographs In Contact Allergy, 51–54. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003158004-7.

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Brennan, Kristin, and Henry Liu. "Acetaminophen." In First Aid Perioperative Ultrasound, 107–25. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-21291-8_7.

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Champion, Howard R., Nova L. Panebianco, Jan J. De Waele, Lewis J. Kaplan, Manu L. N. G. Malbrain, Annie L. Slaughter, Walter L. Biffl, et al. "Acetaminophen Overdose." In Encyclopedia of Intensive Care Medicine, 32–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_795.

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Bateman, D. Nicholas. "Acetaminophen (Paracetamol)." In Critical Care Toxicology, 1–25. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20790-2_108-1.

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Conference papers on the topic "Acetaminophen"

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Vemula, Praveen Kumar, Gregory A. Cruikshank, George John, and Jeffrey M. Karp. "Enzyme responsive acetaminophen hydrogels." In 2009 IEEE 35th Annual Northeast Bioengineering Conference. IEEE, 2009. http://dx.doi.org/10.1109/nebc.2009.4967713.

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Kordić, Nikolina Benco, Mila Lovrić, and Arnes Rešić. "194 Late-presenting acetaminophen self-poisoning." In 10th Europaediatrics Congress, Zagreb, Croatia, 7–9 October 2021. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2021. http://dx.doi.org/10.1136/archdischild-2021-europaediatrics.194.

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Munawar, I., S. Singh, and R. Dean. "Why Isn't the Acetaminophen Level Improving?" In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a5203.

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Kordić, Nikolina Benco, and Arnes Rešić. "195 Intravenous acetaminophen overdose – a therapeutic error." In 10th Europaediatrics Congress, Zagreb, Croatia, 7–9 October 2021. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2021. http://dx.doi.org/10.1136/archdischild-2021-europaediatrics.195.

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Elfers, C., KM Schneider, A. Ghallab, E. Galvez, A. Mohs, E. Bennek, L. Candels, et al. "Intestinal dysbiosis amplifies acetaminophen induced acute liver injury." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402103.

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Ghallab, A., R. Hassan, M. Myllys, A. Friebel, L. Brackhagen, U. Hofmann, S. Sezgin, et al. "A so far unrecognized mechanism of acetaminophen hepatotoxicity." In 37. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0040-1721954.

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Malesker, M. A., D. E. Hilleman, and L. E. Morrow. "Systematic Review of Intravenous Acetaminophen After Cardiac Surgery." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3396.

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Chacey, Michael, Michael Crosser, and Elliott Crouser. "Metabolic Acidosis In Acetaminophen Overdose Without Concurrent Liver Toxicity." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3877.

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Shaik, A. S., A. Deb, R. Rashid, S. Agrawal, and A. Smith. "A Rare Case of Samter's Triad Due to Acetaminophen." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a3062.

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Villota, Natalia, Cristian Ferreiro, Jose Ignacio Lombraña, and Luis Miguel Camarero. "Oxidation of acetaminophen by ultrasound waves and H2O2 combined technology." In 14th Mediterranean Congress of Chemical Engineering (MeCCE14). Grupo Pacífico, 2020. http://dx.doi.org/10.48158/mecce-14.dg.09.07.

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Reports on the topic "Acetaminophen"

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Savarie, Peter J. Development of Non-prey Baits for Delivery of Acetaminophen to Brown Treesnakes (Boiga irregularis) on Guam. Version 3. Fort Belvoir, VA: Defense Technical Information Center, March 2012. http://dx.doi.org/10.21236/ada581124.

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Chou, Roger, Jesse Wagner, Azrah Y. Ahmed, Ian Blazina, Erika Brodt, David I. Buckley, Tamara P. Cheney, et al. Treatments for Acute Pain: A Systematic Review. Agency for Healthcare Research and Quality (AHRQ), December 2020. http://dx.doi.org/10.23970/ahrqepccer240.

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Objectives. To evaluate the effectiveness and comparative effectiveness of opioid, nonopioid pharmacologic, and nonpharmacologic therapy in patients with specific types of acute pain, including effects on pain, function, quality of life, adverse events, and long-term use of opioids. Data sources. Electronic databases (Ovid® MEDLINE®, PsycINFO®, Embase®, the Cochrane Central Register of Controlled Trials, and the Cochrane Database of Systematic Reviews) to August 2020, reference lists, and a Federal Register notice. Review methods. Using predefined criteria and dual review, we selected randomized controlled trials (RCTs) of outpatient therapies for eight acute pain conditions: low back pain, neck pain, other musculoskeletal pain, neuropathic pain, postoperative pain following discharge, dental pain (surgical or nonsurgical), pain due to kidney stones, and pain due to sickle cell disease. Meta-analyses were conducted on pharmacologic therapy for dental pain and kidney stone pain, and likelihood of repeat or rescue medication use and adverse events. The magnitude of effects was classified as small, moderate, or large using previously defined criteria, and strength of evidence was assessed. Results. One hundred eighty-three RCTs on the comparative effectiveness of therapies for acute pain were included. Opioid therapy was probably less effective than nonsteroidal anti-inflammatory drugs (NSAIDs) for surgical dental pain and kidney stones, and might be similarly effective as NSAIDs for low back pain. Opioids and NSAIDs were more effective than acetaminophen for surgical dental pain, but opioids were less effective than acetaminophen for kidney stone pain. For postoperative pain, opioids were associated with increased likelihood of repeat or rescue analgesic use, but effects on pain intensity were inconsistent. Being prescribed an opioid for acute low back pain or postoperative pain was associated with increased likelihood of use of opioids at long-term followup versus not being prescribed, based on observational studies. Heat therapy was probably effective for acute low back pain, spinal manipulation might be effective for acute back pain with radiculopathy, acupressure might be effective for acute musculoskeletal pain, an opioid might be effective for acute neuropathic pain, massage might be effective for some types of postoperative pain, and a cervical collar or exercise might be effective for acute neck pain with radiculopathy. Most studies had methodological limitations. Effect sizes were primarily small to moderate for pain, the most commonly evaluated outcome. Opioids were associated with increased risk of short-term adverse events versus NSAIDs or acetaminophen, including any adverse event, nausea, dizziness, and somnolence. Serious adverse events were uncommon for all interventions, but studies were not designed to assess risk of overdose, opioid use disorder, or long-term harms. Evidence on how benefits or harms varied in subgroups was lacking. Conclusions. Opioid therapy was associated with decreased or similar effectiveness as an NSAID for some acute pain conditions, but with increased risk of short-term adverse events. Evidence on nonpharmacological therapies was limited, but heat therapy, spinal manipulation, massage, acupuncture, acupressure, a cervical collar, and exercise were effective for specific acute pain conditions. Research is needed to determine the comparative effectiveness of therapies for sickle cell pain, acute neuropathic pain, neck pain, and management of postoperative pain following discharge; effects of therapies for acute pain on non-pain outcomes; effects of therapies on long-term outcomes, including long-term opioid use; and how benefits and harms of therapies vary in subgroups.
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Halker Singh, Rashmi B., Juliana H. VanderPluym, Allison S. Morrow, Meritxell Urtecho, Tarek Nayfeh, Victor D. Torres Roldan, Magdoleen H. Farah, et al. Acute Treatments for Episodic Migraine. Agency for Healthcare Research and Quality (AHRQ), December 2020. http://dx.doi.org/10.23970/ahrqepccer239.

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Abstract:
Objectives. To evaluate the effectiveness and comparative effectiveness of pharmacologic and nonpharmacologic therapies for the acute treatment of episodic migraine in adults. Data sources. MEDLINE®, Embase®, Cochrane Central Registrar of Controlled Trials, Cochrane Database of Systematic Reviews, PsycINFO®, Scopus, and various grey literature sources from database inception to July 24, 2020. Comparative effectiveness evidence about triptans and nonsteroidal anti-inflammatory drugs (NSAIDs) was extracted from existing systematic reviews. Review methods. We included randomized controlled trials (RCTs) and comparative observational studies that enrolled adults who received an intervention to acutely treat episodic migraine. Pairs of independent reviewers selected and appraised studies. Results. Data on triptans were derived from 186 RCTs summarized in nine systematic reviews (101,276 patients; most studied was sumatriptan, followed by zolmitriptan, eletriptan, naratriptan, almotriptan, rizatriptan, and frovatriptan). Compared with placebo, triptans resolved pain at 2 hours and 1 day, and increased the risk of mild and transient adverse events (high strength of the body of evidence [SOE]). Data on NSAIDs were derived from five systematic reviews (13,214 patients; most studied was ibuprofen, followed by diclofenac and ketorolac). Compared with placebo, NSAIDs probably resolved pain at 2 hours and 1 day, and increased the risk of mild and transient adverse events (moderate SOE). For other interventions, we included 135 RCTs and 6 comparative observational studies (37,653 patients). Compared with placebo, antiemetics (low SOE), dihydroergotamine (moderate to high SOE), ergotamine plus caffeine (moderate SOE), and acetaminophen (moderate SOE) reduced acute pain. Opioids were evaluated in 15 studies (2,208 patients).Butorphanol, meperidine, morphine, hydromorphone, and tramadol in combination with acetaminophen may reduce pain at 2 hours and 1 day, compared with placebo (low SOE). Some opioids may be less effective than some antiemetics or dexamethasone (low SOE). No studies evaluated instruments for predicting risk of opioid misuse, opioid use disorder, or overdose, or evaluated risk mitigation strategies to be used when prescribing opioids for the acute treatment of episodic migraine. Calcitonin gene-related peptide (CGRP) receptor antagonists improved headache relief at 2 hours and increased the likelihood of being headache-free at 2 hours, at 1 day, and at 1 week (low to high SOE). Lasmiditan (the first approved 5-HT1F receptor agonist) restored function at 2 hours and resolved pain at 2 hours, 1 day, and 1 week (moderate to high SOE). Sparse and low SOE suggested possible effectiveness of dexamethasone, dipyrone, magnesium sulfate, and octreotide. Compared with placebo, several nonpharmacologic treatments may improve various measures of pain, including remote electrical neuromodulation (moderate SOE), magnetic stimulation (low SOE), acupuncture (low SOE), chamomile oil (low SOE), external trigeminal nerve stimulation (low SOE), and eye movement desensitization re-processing (low SOE). However, these interventions, including the noninvasive neuromodulation devices, have been evaluated only by single or very few trials. Conclusions. A number of acute treatments for episodic migraine exist with varying degrees of evidence for effectiveness and harms. Use of triptans, NSAIDs, antiemetics, dihydroergotamine, CGRP antagonists, and lasmiditan is associated with improved pain and function. The evidence base for many other interventions for acute treatment, including opioids, remains limited.
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