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Journal articles on the topic 'Acetaminophen'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 September 2023

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1

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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5

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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6

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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7

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

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8

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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10

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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Jo, Seung Jik, Hyun Young Gang, Si Jin Lee, Gyu Hyun Bae, Eui Jung Lee, Kap Su Han, Su Jin Kim, and Sung Woo Lee. "Continuous Control of Acetaminophen Poisoning after Implementation of Regulation for Ease Access of Acetaminophen: Cohort Study from Emergency Department Based in-depth Injury Surveillance." Journal of The Korean Society of Clinical Toxicology 18, no. 2 (December 31, 2020): 57–65. http://dx.doi.org/10.22537/jksct.2020.18.2.57.

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Purpose: Since 2012, acetaminophen can be accessed easily not only at pharmacies but also at convenience stores. The relationship between the easy access of acetaminophen and the risk of poisoning has been controversial. Several studies also reported different results regarding the risk of acetaminophen poisoning after access to acetaminophen was relaxed. This study examined the long-term effects on the risk of acetaminophen poisoning after easy access to acetaminophen was implemented. Methods: This was a retrospective analysis of an emergency department (ED)-based in-depth Injury Surveillance Cohort by the Korea Center for Disease Control and prevention from 2011 to 2018. Poisoning cases were selected from the Cohort, and the incidence of acetaminophen poisoning and the characteristics of the cases of acetaminophen poisoning were analyzed. The purchase path and the amount of ingestion in acetaminophen poisoning were sub-analyzed from data of six EDs. Results: Of 57,326 poisoning cases, 4.0% (2,272 cases) were acetaminophen poisoning. Of 2,272 cases of acetaminophen poisoning, 42.8% (974 cases) required in-patient care after ED management. Two hundred and sixty-four of these 964 cases required intensive care. The rates of cases that required in-patient treatment and the rates of cases that required intensive care increased from 29.4% in 2011 to 48.1% in 2018, and from 3.1% in 2011 to 15.2% in 2018, respectively (p<0.001, p<0.001). In the poisoning group with in-depth toxic surveillance (n=15,908), the incidence and proportion of acetaminophen (AAP) poisoning increased from 55 cases per year to 187 cases per year and 4.9% to 6.1%, respectively (p=0.009, p<0.001, respectively). The most common age group of acetaminophen poisoning was teenagers, which is different from the most common age group of other pharmaceutical agents: the middle age group of 40-49 years (p<0.001). Of 15,908 in-depth toxic surveillance patients, 693 patients had AAP poisoning, of whom 377 cases (54.2%) purchased acetaminophen from a non-pharmacy. The proportions of the purchase path from non-pharmacy were 41.4% at 2011-12 and 56.4% (2013-18) (p=0.004). The amount of acetaminophen ingestion was 13.5±14.3 g at 2011-12 and 13.9±15.1 g at 2013-18 (p=0.794). Conclusion: Although the incidence of acetaminophen poisoning did not increase remarkably in the short term after the implementation of the new regulation, the incidence of acetaminophen poisoning has increased slightly during the study period of 2017-18. In addition, the proportion of the purchase path from non-pharmacies has increased since the emergence of new regulations for the easy access of acetaminophen in 2012. The incidence of acetaminophen poisoning might have been affected after the increasing accessibility of acetaminophen in convenience stores. Continuous control of acetaminophen poisoning is required. Furthermore, the prevention of acetaminophen poisoning should be focused on teenagers with specialized school education programs.

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Stern, Stephan T., Mary K. Bruno, Gayle E. Hennig, Robert A. Horton, Jeanette C. Roberts, and Steven D. Cohen. "Contribution of acetaminophen-cysteine to acetaminophen nephrotoxicity in CD-1 mice: I. Enhancement of acetaminophen nephrotoxicity by acetaminophen-cysteine." Toxicology and Applied Pharmacology 202, no. 2 (January 2005): 151–59. http://dx.doi.org/10.1016/j.taap.2004.06.030.

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Bentur, Yedidia, Yael Lurie, Ada Tamir, Daniel C. Keyes, and Fuad Basis. "Reliability of history of acetaminophen ingestion in intentional drug overdose patients." Human & Experimental Toxicology 30, no. 1 (March 30, 2010): 44–50. http://dx.doi.org/10.1177/0960327110366784.

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The objective of this study was to determine the reliability of denial of acetaminophen ingestion in intentional drug overdose patients. All intentional drug overdose patients admitted to an emergency department who were able to provide a history were included. A detailed history was obtained on names, timing and number of medications ingested, and serum acetaminophen was assayed. Multidrug ingestion was defined as the reporting of ≥2 medications. Patients were considered ‘reliable’ if they reported acetaminophen ingestion and had detectable acetaminophen levels or the other way around. Validity parameters of acetaminophen history were assessed by sensitivity, specificity and positive and negative predictive values. A total of 154 patients were included. History was significantly more reliable in patients who denied ingestion of acetaminophen (n = 107) compared with patients who reported it (n = 47; 95.3% vs 65.9%, respectively; p < 0.0001, 95% CI of the difference 17.5%—41.2%). No suicidal patient who denied both acetaminophen and multidrug ingestions had a detectable acetaminophen level (negative predictive value 1, 95% CI 0.93—1.0). It is suggested that denial of both acetaminophen and multidrug ingestions by intentional drug overdose patients after a thorough history taking can be considered reliable for acetaminophen history. In facilities with limited resources, these patients may not require routine acetaminophen screening.

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Arun, Oguzhan, Ozgur Canbay, Nalan Celebi, Altan Sahin, Ali Konan, Pergin Atilla, and Ulku Aypar. "The Analgesic Efficacy of Intra-Articular Acetaminophen in an Experimental Model of Carrageenan-Induced Arthritis." Pain Research and Management 18, no. 5 (2013): e63-e67. http://dx.doi.org/10.1155/2013/148392.

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BACKGROUND: Acetaminophen is one of the most common drugs used for the treatment of pain and fever.OBJECTIVES: To examine the effects of intra-articular (IA) acetaminophen on carrageenan-induced arthritic pain-related behaviour and spinal c-Fos expression in rats.METHODS: The present study was performed using 20 Sprague Dawley rats. Forty microlitres of IA 0.9% NaCl was injected in the control group, and 40 μL of IA carrageenan was injected in the carrageenan group. One hour after carrageenan injection, 400 μg of IA acetaminophen was injected in the IA acetaminophen group, and 400 μg of intraperitoneal (IP) acet-aminophen was injected in the IP acetaminophen group. One day before injection, and 4 h and 8 h after injection, diameters of both knee joints, motility of the rat, paw loading and joint mobility were assessed. After the rats were euthanized, L3 and L4 spinal segments were excised for c-Fos assessment.RESULTS: IA acetaminophen decreased both the severity and distribution of c-Fos expression. IP acetaminophen decreased only the distribution of c-Fos expression. IA acetaminophen decreased knee diameter at 8 h. IA and IP acetaminophen increased rat motility and paw loading scores. Joint mobility scores of IP acetaminophen were similar to saline at 8 h.CONCLUSIONS: Results of the present study indicate an analgesic and/or possible anti-inflammatory effect of IA acetaminophen and provide further evidence on the efficacy of systemic acetaminophen injection in reducing arthritic pain.

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Srikanth, Chittur V., Asit K. Chakraborti, and Anand K. Bachhawat. "Acetaminophen toxicity and resistance in the yeast Saccharomyces cerevisiae." Microbiology 151, no. 1 (January 1, 2005): 99–111. http://dx.doi.org/10.1099/mic.0.27374-0.

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Acetaminophen (paracetamol), one of the most widely used analgesics, is toxic under conditions of overdose or in certain disease conditions, but the mechanism of acetaminophen toxicity is still not entirely understood. To obtain fresh insights into acetaminophen toxicity, this phenomenon was investigated in yeast. Acetaminophen was found to be toxic to yeast cells, with erg mutants displaying hypersensitivity. Yeast cells grown in the presence of acetaminophen were found to accumulate intracellular acetaminophen, but no metabolic products of acetaminophen could be detected in these extracts. The toxicity response did not lead to an oxidative stress response, although it did involve Yap1p. The cytochrome P450 enzymes of yeast, Erg5p and Erg11p, did not appear to participate in this process, unlike the mammalian systems. Furthermore, we could not establish a central role for glutathione depletion or the cellular glutathione redox status in acetaminophen toxicity, suggesting differences from mammalian systems in the pathways causing toxicity. Investigations of the resistance mechanisms revealed that deletion of the glutathione-conjugate pumps Ycf1p (a target of Yap1p) and Bpt1p, surprisingly, led to acetaminophen resistance, while overexpression of the multidrug resistance pumps Snq2p and Flr1p (also targets of Yap1p) led to acetaminophen resistance. The Yap1p-dependent resistance to acetaminophen required a functional Pdr1p or Pdr3p protein, but not a functional Yrr1p. In contrast, resistance mediated by Pdr1p/Pdr3p did not require a functional Yap1p, and revealed a distinct hierarchy in the resistance to acetaminophen.

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Patel, Anita K., Jiaxiang Gai, Eduardo Trujillo-Rivera, Farhana Faruqe, Dongkyu Kim, James E. Bost, and Murray M. Pollack. "National Intravenous Acetaminophen Use in Pediatric Inpatients From 2011–2016." Journal of Pediatric Pharmacology and Therapeutics 27, no. 4 (April 1, 2022): 358–65. http://dx.doi.org/10.5863/1551-6776-27.4.358.

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OBJECTIVE To 1) determine current intravenous (IV) acetaminophen use in pediatric inpatients; and 2) determine the association between opioid medication duration when used with or without IV acetaminophen. METHODS A retrospective analysis of pediatric inpatients exposed to IV acetaminophen from January 2011 to June 2016, using the national database Health Facts. RESULTS Eighteen thousand one hundred ninety-seven (2.0%) of 893,293 pediatric inpatients received IV acetaminophen for a median of 14 doses per patient (IQR, 8–56). A greater proportion of IV acetaminophen patients were admitted to the intensive care unit (ICU) (14.8% vs 5.1%, p < 0.0001), received positive pressure ventilation (2.0% vs 1.5%, p < 0.0001), had a higher hospital mortality rate (0.9% vs 0.3%, p < 0.0001), and were operative (35.5% vs 12.8%, p < 0.001) than those not receiving IV acetaminophen. The most common operations associated with IV acetaminophen use were musculoskeletal and digestive system operations. Prescription of IV acetaminophen increased over time, both in prescription rates and number of per patient doses. Of the 18,197 patients prescribed IV acetaminophen, 16,241 (89.2%) also were prescribed opioids during their hospitalization. A multivariate analysis revealed patients prescribed both IV acetaminophen and opioids had a 54.8% increase in opioid duration as compared with patients who received opioids alone. CONCLUSIONS This is the first study to assess IV acetaminophen prescription practices for pediatric inpatients. Intravenous acetaminophen prescription was greater in the non-operative pediatric inpatient population than operative patients. Intravenous acetaminophen prescription was associated with an increase in opioid duration as compared with patients who received opioids alone, suggesting that it is commonly used to supplement opioids for pain relief.

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Taylor, Brock M., Shawn R. Chakraborty, Aaron A. Harthan, Sandeep Tripathi, Huaping Wang, and Anil Kumar Swayampakula. "Effect of IV Acetaminophen Usage on Opioid Requirements, Outcomes and Costs of Care for Postoperative Children in a Pediatric Intensive Care Unit." Journal of Pediatric Pharmacology and Therapeutics 25, no. 6 (August 1, 2020): 514–20. http://dx.doi.org/10.5863/1551-6776-25.6.514.

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OBJECTIVE Children admitted to the ICU are commonly treated with opioids for postoperative pain. We hypothesized that administration of IV acetaminophen in the immediate postoperative period is effective in lowering cumulative opioid use leading to other benefits. METHODS This was a retrospective chart review of patients admitted to the PICU between December 2016 and April 2019. For each patient, data including demographics, cumulative opioid usage per kilogram, oral or rectal acetaminophen, x-ray findings, hospital costs, and surgical procedure were collected. Cumulative opioid usage was determined by converting all opioids to morphine equivalents (MEs) per kg. Standard descriptive and comparative analyses were conducted using SAS 9.4 (SAS Institute, Inc, Cary, NC). RESULTS A total of 200 patients met inclusion and exclusion criteria (N = 92 in IV acetaminophen group and N = 108 in no IV acetaminophen group). There was no significant difference in ME per kilogram between the groups (0.3 ME/kg in IV acetaminophen group, IQR 0.5 ME/kg versus 0.4 ME/kg in no IV acetaminophen group, IQR 0.5 ME/kg, adjusted p = 0.38). Rate of atelectasis was not significant between the groups (47.8% in IV acetaminophen versus 45.4% in no acetaminophen group, p = 0.28). There was a significant difference in median total hospital costs between the groups ($22,456 in IV acetaminophen group, IQR $18,650 versus $18,552 in no IV acetaminophen group, IQR $13,361, adjusted p = 0.04). CONCLUSIONS IV acetaminophen in the immediate postoperative period did not lead to a decrease in cumulative opioid usage or rate of atelectasis. IV acetaminophen usage was associated with increase in overall hospital costs per patient.

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Nabavi, Nima, Mohammad Moshiri, Shahrad Tajoddini, and Bita Dadpour. "A Basis for the Decision to Rule in or out Acetaminophen Toxicity: Assessment of the Serum Level Within 4 Hours Post Overdose." Iranian Journal of Toxicology 15, no. 4 (October 1, 2021): 265–70. http://dx.doi.org/10.32598/ijt.15.4.820.1.

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Background: Acetaminophen is a popular antipyretic and analgesic medication worldwide; however, its therapeutic window is narrow, which may lead to overdose or toxicity. This study was conducted to assess the correlation between the serum acetaminophen levels before and 4 hours after the acute toxicity with this drug. The objective of this study was to test the validity of the serum level to arrive at a clinical decision on the toxicity with acetaminophen. Methods: This cross-sectional study was performed on patients hospitalized and treated with a diagnosis of acute acetaminophen overdose during one year (Sept. 2018 to Sept. 2019) at the Toxicology Department of Imam Reza Hospital, Mashhad, Iran. Patients were analyzed for demographics, time of ingestion, their first and second serum acetaminophen concentrations. Results: A total of 204 patients (106 male & 98 female) were included in this study. The average dose of acetaminophen ingestion by these patients was 14.5±3.50 g and all patients were treated successfully with N-Acetyl-Cysteine (NAC). The variables of age (P=0.293), serum acetaminophen levels at 1-2 h (P=0.679), and at 2-3 h (P=0.126) did not have significant relationships with the serum acetaminophen level on the fourth hour. However, the serum acetaminophen levels tested between 3-4 h and acetaminophen intoxication dosage had significant relationships with the acetaminophen level on the fourth hour. Conclusion: In patients with acute acetaminophen toxicity, the data on the serum levels obtained before a 4-hour timepoint from the ingestion were not useful to decide on the need for the rescue treatment with N-acetyl-cysteine.

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Chiew, Angela L., and Nicholas A. Buckley. "Acetaminophen Poisoning." Critical Care Clinics 37, no. 3 (July 2021): 543–61. http://dx.doi.org/10.1016/j.ccc.2021.03.005.

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Nadler, Ariella, and Daniel M. Fein. "Acetaminophen Poisoning." Pediatrics in Review 39, no. 6 (June 2018): 316–18. http://dx.doi.org/10.1542/pir.2017-0093.

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Mortensen, M. E., and J. L. Cullen. "Acetaminophen Recommendation." PEDIATRICS 110, no. 3 (September 1, 2002): 646. http://dx.doi.org/10.1542/peds.110.3.646.

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Cook, Matthew D., and Richard F. Clark. "Acetaminophen Toxicity." Pediatric Emergency Care 21, no. 10 (October 2005): 703–4. http://dx.doi.org/10.1097/01.pec.0000181412.33859.51.

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Cada, Dennis J., Terri L. Levien, and Danial E. Baker. "Acetaminophen Intravenous." Hospital Pharmacy 46, no. 4 (April 2011): 273–85. http://dx.doi.org/10.1310/hpj4604-273.

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Ramachandran, Anup, and Hartmut Jaeschke. "Acetaminophen Hepatotoxicity." Seminars in Liver Disease 39, no. 02 (March 8, 2019): 221–34. http://dx.doi.org/10.1055/s-0039-1679919.

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AbstractAcetaminophen (APAP) is one of the most popular and safe pain medications worldwide. However, due to its wide availability, it is frequently implicated in intentional or unintentional overdoses where it can cause severe liver injury and even acute liver failure (ALF). In fact, APAP toxicity is responsible for 46% of all ALF cases in the United States. Early mechanistic studies in mice demonstrated the formation of a reactive metabolite, which is responsible for hepatic glutathione depletion and initiation of the toxicity. This insight led to the rapid introduction of N-acetylcysteine as a clinical antidote. However, more recently, substantial progress was made in further elucidating the detailed mechanisms of APAP-induced cell death. Mitochondrial protein adducts trigger a mitochondrial oxidant stress, which requires amplification through a MAPK cascade that ultimately results in activation of c-jun N-terminal kinase (JNK) in the cytosol and translocation of phospho-JNK to the mitochondria. The enhanced oxidant stress is responsible for the membrane permeability transition pore opening and the membrane potential breakdown. The ensuing matrix swelling causes the release of intermembrane proteins such as endonuclease G, which translocate to the nucleus and induce DNA fragmentation. These pathophysiological signaling mechanisms can be additionally modulated by removing damaged mitochondria by autophagy and replacing them by mitochondrial biogenesis. Importantly, most of the mechanisms have been confirmed in human hepatocytes and indirectly through biomarkers in plasma of APAP overdose patients. The extensive necrosis caused by APAP overdose leads to a sterile inflammatory response. Although recruitment of inflammatory cells is necessary for removal of cell debris in preparation for regeneration, these cells have the potential to aggravate the injury. This review touches on the newest insight into the intracellular mechanisms of APAP-induced cells death and the resulting inflammatory response. Furthermore, it discusses the translation of these findings to humans and the emergence of new therapeutic interventions.

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Zahrowski, James J. "ACETAMINOPHEN USE." Journal of the American Dental Association 142, no. 6 (June 2011): 596. http://dx.doi.org/10.14219/jada.archive.2011.0230.

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HOFFMAN, CONSTANCE, and LYNN GIBEL. "Acetaminophen overdose." Nursing 35, no. 1 (January 2005): 88. http://dx.doi.org/10.1097/00152193-200501000-00062.

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Thurkauf, G. E. "Acetaminophen overdose." Dimensions of Critical Care Nursing 6, no. 4 (July 1987): 255. http://dx.doi.org/10.1097/00003465-198707000-00011.

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Gevirtz, Clifford. "IV Acetaminophen." Topics in Pain Management 27, no. 8 (March 2012): 1–6. http://dx.doi.org/10.1097/01.tpm.0000413088.33674.f5.

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Vale, Allister. "Paracetamol (Acetaminophen)." Medicine 31, no. 10 (October 2003): 67–68. http://dx.doi.org/10.1383/medc.31.10.67.27822.

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McDonough, Joan. "Acetaminophen Overdose." American Journal of Nursing 98, no. 3 (March 1998): 52. http://dx.doi.org/10.1097/00000446-199803000-00042.

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McBride, Patrick V., and Barry H. Rumack. "Acetaminophen Intoxication." Seminars in Dialysis 5, no. 4 (October 1, 2007): 292–98. http://dx.doi.org/10.1111/j.1525-139x.1992.tb00233.x.

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Jahr, Jonathan S., Peter Filocamo, and Sumit Singh. "Intravenous Acetaminophen." American Journal of Therapeutics 20, no. 2 (2013): 189–99. http://dx.doi.org/10.1097/mjt.0b013e31828900cb.

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Singla, Neil K., Martin E. Hale, Jeffrey C. Davis, Alex Bekker, Joseph Gimbel, Jonathan Jahr, Mike A. Royal, Robert Y. Ang, and Eugene R. Viscusi. "IV Acetaminophen." American Journal of Therapeutics 22, no. 1 (2015): 2–10. http://dx.doi.org/10.1097/mjt.0000000000000026.

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Golembiewski, Julie. "Intravenous Acetaminophen." Journal of PeriAnesthesia Nursing 32, no. 2 (April 2017): 151–55. http://dx.doi.org/10.1016/j.jopan.2017.01.004.

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Vale, Allister. "Paracetamol (acetaminophen)." Medicine 35, no. 12 (December 2007): 643–45. http://dx.doi.org/10.1016/j.mpmed.2007.09.011.

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Vale, Allister. "Paracetamol (acetaminophen)." Medicine 40, no. 3 (March 2012): 144–46. http://dx.doi.org/10.1016/j.mpmed.2011.12.010.

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Bateman, D. Nicholas, and Allister Vale. "Paracetamol (acetaminophen)." Medicine 44, no. 3 (March 2016): 190–92. http://dx.doi.org/10.1016/j.mpmed.2015.12.014.

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Hawton, K. "Acetaminophen/Dextropropoxyphene." Clin-Alert 41, no. 10 (May 31, 2003): 2. http://dx.doi.org/10.1177/0069477003041010002.

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Twycross, Robert, Victor Pace, Mary Mihalyo, and Andrew Wilcock. "Acetaminophen (Paracetamol)." Journal of Pain and Symptom Management 46, no. 5 (November 2013): 747–55. http://dx.doi.org/10.1016/j.jpainsymman.2013.08.001.

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Mayhew, Maren. "Acetaminophen Toxicity." Journal for Nurse Practitioners 3, no. 3 (March 2007): 186–88. http://dx.doi.org/10.1016/j.nurpra.2007.01.025.

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Augenstein, W. Lynn, Kenneth W. Kulig, and Barry H. Rumack. "Acetaminophen levels." Annals of Emergency Medicine 16, no. 9 (September 1987): 1096. http://dx.doi.org/10.1016/s0196-0644(87)80777-1.

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Bromer, Matthew Q., and Martin Black. "Acetaminophen hepatotoxicity." Clinics in Liver Disease 7, no. 2 (May 2003): 351–67. http://dx.doi.org/10.1016/s1089-3261(03)00025-4.

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Zimmerman, Hyman J. "ACETAMINOPHEN HEPATOTOXICITY." Clinics in Liver Disease 2, no. 3 (August 1998): 523–41. http://dx.doi.org/10.1016/s1089-3261(05)70025-8.

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Mace, Sharon E. "Intravenous Acetaminophen." Current Emergency and Hospital Medicine Reports 5, no. 4 (October 18, 2017): 126–36. http://dx.doi.org/10.1007/s40138-017-0142-5.

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Rowden, Adam K., Jeffrey Norvell, David L. Eldridge, and Mark A. Kirk. "Acetaminophen Poisoning." Clinics in Laboratory Medicine 26, no. 1 (March 2006): 49–65. http://dx.doi.org/10.1016/j.cll.2006.01.004.

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Menges, K. "Paracetamol (Acetaminophen)." Der Schmerz 1, no. 2 (September 1987): 130–34. http://dx.doi.org/10.1007/bf02527742.

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Larson, Anne M. "Acetaminophen Hepatotoxicity." Clinics in Liver Disease 11, no. 3 (August 2007): 525–48. http://dx.doi.org/10.1016/j.cld.2007.06.006.

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Mitchell, Jerry R. "Acetaminophen Toxicity." New England Journal of Medicine 319, no. 24 (December 15, 1988): 1601–2. http://dx.doi.org/10.1056/nejm198812153192409.

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Mirochnitchenko, Oleg, Miriam Weisbrot-Lefkowitz, Kenneth Reuhl, Laishun Chen, Chung Yang, and Masayori Inouye. "Acetaminophen Toxicity." Journal of Biological Chemistry 274, no. 15 (April 9, 1999): 10349–55. http://dx.doi.org/10.1074/jbc.274.15.10349.

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