Journal articles: 'Acetaminophen Toxicology'

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David Josephy, P. "The Molecular Toxicology of Acetaminophen." Drug Metabolism Reviews 37, no. 4 (January 2005): 581–94. http://dx.doi.org/10.1080/03602530500205200.

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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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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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Hodell, M., P. D'Eon, R. Hessler, S. Inbar, A. Leck, U. Patel, and G. Whiteley. "143 TOXICOLOGY PANEL FOR ETHANOL, SALICYLATE, and ACETAMINOPHEN." Therapeutic Drug Monitoring 19, no. 5 (October 1997): 583. http://dx.doi.org/10.1097/00007691-199710000-00153.

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Gussow, Leon. "Toxicology Rounds: A New Development in Acetaminophen Toxicity." Emergency Medicine News 33, no. 4 (April 2011): 10. http://dx.doi.org/10.1097/01.eem.0000396895.17374.a6.

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Mofenson, H. C., T. R. Caraccio, H. Nawaz, and G. Steckler. "Acetaminophen Induced Pancreatitis." Journal of Toxicology: Clinical Toxicology 29, no. 2 (January 1991): 223–30. http://dx.doi.org/10.3109/15563659109038615.

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Karadas, S., M. Aslan, H. Gonullu, C. Kati, L. Duran, S. Olmez, ME Kucukoglu, and H. Demir. "Acetaminophen intoxication is associated with decreased serum paraoxonase and arylesterase activities and increased lipid hydroperoxide levels." Human & Experimental Toxicology 33, no. 11 (February 5, 2014): 1134–40. http://dx.doi.org/10.1177/0960327113511477.

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Background: Acetaminophen is at present one of the most commonly used analgesics and antipyretics. Recent evidence has suggested that oxidative stress is involved in the mechanism of acetaminophen intoxication. Paraoxonase-1 (PON1) plays an important role as an endogenous free-radical scavenging molecule. The aim of this study was to evaluate the influence of serum PON1 activity and oxidative stress in patients with acetaminophen intoxication. Methods: A total of 20 patients with acetaminophen intoxication and 25 healthy controls were enrolled. Serum total antioxidant capacity (TAC), lipid hydroperoxide (LOOH) levels, and paraoxonase and arylesterase activities were measured spectrophotometrically. Results: The serum TAC levels and the paraoxonase and arylesterase activities were significantly lower in patients with acetaminophen intoxication compared with controls (all, p < 0.001), while the serum LOOH levels were significantly higher ( p < 0.001). Conclusions: Our results suggest that decreased PON1 activity seems to be associated with increased oxidative stress in patients with acetaminophen intoxication. Measuring serum PON1 activity may be useful in assessing the development of toxicity risk in acetaminophen toxicity. It would be useful to recommend vitamins with antioxidant effects such as vitamins C and E along with medical treatments.

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Rousar, Tomas, Erika Nydlova, Otto Kucera, Petr Cesla, Martina Vrbova, and Zuzana Cervinkova. "Acetaminophen–glutathione conjugate: A possible role in acetaminophen toxicity." Toxicology Letters 221 (August 2013): S88. http://dx.doi.org/10.1016/j.toxlet.2013.05.109.

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Chandrasekaran, Victor Raj Mohan, Se-Ping Chien, Dur-Zong Hsu, and Ming-Yie Liu. "Anti-hepatotoxic effects of 3,4-methylenedioxyphenol and N-acetylcysteine in acutely acetaminophen-overdosed mice." Human & Experimental Toxicology 30, no. 10 (January 14, 2011): 1609–15. http://dx.doi.org/10.1177/0960327110394226.

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3,4-Methylenedioxyphenol (sesamol) is effective against acetaminophen-induced liver injury in rats. Whether sesamol’s anti-hepatotoxic effect is comparable to that of N-acetylcysteine has never been studied. We investigated the anti-hepatotoxic effects of sesamol and N-acetylcysteine on acetaminophen-induced hepatotoxicity in mice. Equimolar doses (1 mmol/kg) of sesamol and N-acetylcysteine significantly inhibited acetaminophen (300 mg/kg)-increased serum aspartate transaminase and alanine transaminase levels 6 h post-administration. Sesamol and N-acetylcysteine maintained hepatic glutathione levels and inhibited lipid peroxidation. Moreover, the combination of sesamol and N-acetylcysteine antagonistically inhibited sesamol’s protection against acetaminophen-induced liver injury. We conclude that the protective effect of sesamol against acetaminophen-induced liver damage is comparable to that of N-acetylcysteine by maintaining glutathione levels and inhibiting lipid peroxidation in mice.

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Sahu, Kamal Kant, Ajay Kumar Mishra, Amos Lal, and Susan V. George. "Acetaminophen induced methemoglobinemia." Clinical Toxicology 58, no. 7 (October 17, 2019): 784–85. http://dx.doi.org/10.1080/15563650.2019.1677909.

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Rianprakaisang, Tony, Adam Blumenberg, and Robert G. Hendrickson. "Acetaminophen-associated methemoglobinemia." Clinical Toxicology 58, no. 7 (November 4, 2019): 785–86. http://dx.doi.org/10.1080/15563650.2019.1682153.

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Huitema, A. DR, M. Soesan, P. L. Meenhorst, C. HW Koks, and J. H. Beijnen. "A dose-dependent delayed hypersensitivity reaction to acetaminophen after repeated acetaminophen intoxications." Human & Experimental Toxicology 17, no. 7 (July 1998): 406–8. http://dx.doi.org/10.1177/096032719801700708.

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We report a case of a 29-year-old woman with a borderline personality disorder who presented with intentional substantial acetaminophen (paracetamol) overdosage on nine occasions during a period of 21 months. In most cases, the patient presented at the hospital within 4 h after ingestion and was treated with gastric lavage, activated charcoal, laxatives and intravenous N-acetylcysteine. During the sixth overdosage the patient developed a rash on her chest and shoulders which was considered an anaphylactoid reaction to N-acetylcysteine. Therefore she was treated with oral methionine subsequently, but developed the rash again. The rash was then ascribed to the repeated high-doses of acetaminophen and treatment with N-acetylcysteine was reinstituted. This case shows that when an anaphylactoid reaction occurs after an acetaminophen overdose and treatment with N-acetylcysteine, acetaminophen must also be taken into account as the cause of the anaphylactoid reaction before effective therapy with N-acetylcysteine is withheld.

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Sebe, Ahmet, Salim Satar, N. Rana Alpay, Mesude Murt, and Birol Güvenç. "Severe acetaminophen poisoning treated with a fractionated plasma separation and absorption system: A case report." Human & Experimental Toxicology 28, no. 11 (October 7, 2009): 729–32. http://dx.doi.org/10.1177/0960327109350800.

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Acetaminophen is an analgesic drug that is frequently used in suicide attempts. In this paper, we report on a 17-year-old girl who was admitted to an emergency department 15 hours after taking acetaminophen pills in a suicide attempt. Her serum acetaminophen level was 73 mg/L on admission; she had elevated liver enzymes suggesting hepatic necrosis. She was started on N-acetyl cystein (NAC), and treated successfully with a fractionated plasma separation and absorption system.

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Kozer, E., and M. McGuigan. "Treatment strategies for early presenting acetaminophen overdose: a survey of medical directors of poison centers in North America and Europe." Human & Experimental Toxicology 21, no. 3 (March 2002): 123–27. http://dx.doi.org/10.1191/0960327102ht235oa.

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Background: Acetaminophen is frequently used in self-poisoning in Western countries. Although treatment withN-acetylcysteine (NAC) reduces liver injury, no consensus exists on the preferred management of acetaminophen toxicity. Objectives: To describe the approach taken by toxicologists in North America and Europe toward the management of acetaminophen toxicity. Methods: Medical directors of poison centers in the US, Canada, and Europe were surveyed by means of a questionnaire presenting two clinical scenarios of acetaminophen overdose: a healthy adolescent with no risk factors who had an acute ingestion of acetaminophen, and an adult with both acute ingestion and possible risk factors. For each case, several questions about the management of these patients were asked. Results: Questionnaires were sent to medical directors of 76 poison centers in North America and 48 in Europe, with response rates of 62% and 44%, respectively. Forty percent of responders suggested using charcoal 4 hours after ingestion of a potential toxic dose of acetaminophen, and 90% recommended treatment with NAC when levels were above 150 μg/mL but below 200 μ g/mL 4 hours after ingestion. Duration of treatment with oral NAC ranged from 24 to 96 hours; 38 responders suggested a duration of 72 hours. Of 49 centers recommending oral NAC, 18 (36.7%) said they might consider treatment for less than 72 hours. Eleven of 29 (37.9%) responders suggested treatment with intravenous NAC for more than 20 hours as their usual protocol or a protocol for specific circumstances. Conclusions: Our study showed large variability in the management of acetaminophen overdose. Variations in treatment protocols should be addressed in clinical trials to optimize the treatment for this common problem.

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Ghannoum, Marc, Sara Kazim, Ami M. Grunbaum, Eric Villeneuve, and Sophie Gosselin. "Massive acetaminophen overdose: effect of hemodialysis on acetaminophen and acetylcysteine kinetics." Clinical Toxicology 54, no. 6 (April 27, 2016): 519–22. http://dx.doi.org/10.1080/15563650.2016.1175006.

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Hassan, Reham. "Acetaminophen induces programmed necrosis." Archives of Toxicology 93, no. 12 (November 14, 2019): 3641–42. http://dx.doi.org/10.1007/s00204-019-02625-0.

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Huitema, A. D. R., M. Soesan, P. L. Meenhorst, C. H. W. Koks, and J. H. Beijnen. "A dose-dependent delayed hypersensitivity reaction to acetaminophen after repeated acetaminophen intoxications." Human & Experimental Toxicology 17, no. 7 (July 1, 1998): 406–8. http://dx.doi.org/10.1191/096032798678908972.

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Yamada, Naoya, Takanori Komada, Nobuhiko Ohno, and Masafumi Takahashi. "Acetaminophen-induced hepatotoxicity: different mechanisms of acetaminophen-induced ferroptosis and mitochondrial damage." Archives of Toxicology 94, no. 6 (March 31, 2020): 2255–57. http://dx.doi.org/10.1007/s00204-020-02722-5.

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Xu, Jinghai J., Bart S. Hendriks, Jie Zhao, and David de Graaf. "Multiple effects of acetaminophen and p38 inhibitors: Towards pathway toxicology." FEBS Letters 582, no. 8 (February 20, 2008): 1276–82. http://dx.doi.org/10.1016/j.febslet.2008.01.063.

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Adekeye, AO, and AA Fafure. "Assessment of the cellular integrity and expression of melatonin receptor (MTNR1A) in the retina assaulted by ethanol and acetaminophen." Human & Experimental Toxicology 41 (January 2022): 096032712211490. http://dx.doi.org/10.1177/09603271221149010.

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Ethanol exposures have been reported to disrupt the development of the retina and optic nerve which can be considered as part of underlying mechanisms of visual pathway impairments. This study aims to investigate the cellular integrity of the retina and the expression of melatonin receptor (MTNR1A) in the retina when assaulted chronically and simultaneously by ethanol and acetaminophen. Animals were randomly grouped into five groups. Control (normal saline), Alcohol group (25% alcohol in 2% sucrose solution), Acetaminophen group, (100 mg/kg BW for 14 days), Acetaminophen + Alcohol group (25% alcohol in 2% sucrose solution + 100 mg/kg BW of paracetamol). Withdrawal group (25% alcohol in 2% sucrose solution + 100 mg/kg BW of paracetamol). The body weight and rectal temperature of the animals were taking every 2 days and a post mortem study was conducted by quantitatively assessing the markers of oxidative stress. Melatonin level was quantified in the retina tissue and Immunohistochemistry was done via MTNR1A to study the expression of melatonin receptor type 1A in the retina. These results demonstrate that alcohol and acetaminophen significantly reduced the activity of retina rat melatonin (MTNR1A) levels, lowers the SOD and MDA activity. Expression of MTNR1A was reduced in the ganglionic cell layer of Alcohol and acetaminophen group as compared to the control and withdrawal group. It can be inferred that chronic simultaneous intake/consumption of alcohol and acetaminophen altered the melatonin level in the retina and this may implicate the circadian clock and melatonin in Wistar rat visual system.

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Lip, Gregory Y. H., and J. Allister Vale. "Does Acetaminophen Damage the Heart?" Journal of Toxicology: Clinical Toxicology 34, no. 2 (January 1996): 145–47. http://dx.doi.org/10.3109/15563659609013761.

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HOIVIK, DEBIE J., JOSÉ E. MANAUTOU, ANN TVEIT, DAYNA C. MANKOWSKI, EDWARD A. KHAIRALLAH, and STEVEN D. COHEN. "Evidence Suggesting the 58-kDa Acetaminophen Binding Protein Is a Preferential Target for Acetaminophen Electrophile." Toxicological Sciences 32, no. 1 (1996): 79–86. http://dx.doi.org/10.1093/toxsci/32.1.79.

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Hoivik, D. "Evidence Suggesting the 58-kDa Acetaminophen Binding Protein Is a Preferential Target for Acetaminophen Electrophile." Fundamental and Applied Toxicology 32, no. 1 (July 1996): 79–86. http://dx.doi.org/10.1006/faat.1996.0109.

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Dalhoff, Kim, Per Boye Hansen, Peter Ott, Steffen Loft, and Henrik E. Poulsen. "Acute Ethanol Administration Reduces the Antidote Effect of N-Acetylcysteine after Acetaminophen Overdose in Mice." Human & Experimental Toxicology 10, no. 6 (November 1991): 431–33. http://dx.doi.org/10.1177/096032719101000611.

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1 The combined antidote effect of N-acetylcysteine and ethanol on the toxicity of acetaminophen was investigated. 2 Fed male mice were given acetaminophen i.p. (600 mg kg-1) and after 5 min in addition ethanol i.p. (0.2 ml, 19% v/v), N-acetylcysteine i.p. (1.2 g kg -1, 0.2 ml), N-acetylcysteine + ethanol i.p. (same doses as given individually) or saline i.p. (0.4 ml). Survival rates were determined after 24, 48, 72 and 96 h. 3 In the N-acetylcysteine group the survival rate was 85%. This rate was significantly reduced to 43% in the N-acetylcysteine + ethanol group (P = 0.0001). In the groups given ethanol or saline alone only 7% and 3%, respectively, survived 96 h. 4 The data suggest that the protective effect of N-acetylcysteine on acetaminophen-induced toxicity in fed mice is reduced by concomitant administration of ethanol. This may explain the clinical observation that ingestion of ethanol worsens the prognosis after acetaminophen intoxication.

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O'Brien, P. J., M. R. Slaughter, A. Swain, J. M. Birmingham, R. W. Greenhill, F. Elcock, and P. J. Bugelski. "Repeated acetaminophen dosing in rats: adaptation of hepatic antioxidant system." Human & Experimental Toxicology 19, no. 5 (May 2000): 277–83. http://dx.doi.org/10.1191/096032700678815918.

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Repeated dosing of acetaminophen (paracetamol) to rats is reported to decrease their sensitivity to its hepatotoxic effects, which are associated with oxidative stress and glutathione depletion. We determined if repeated acetaminophen dosing produced adaptive response of key antioxidant system enzymes. Male rats (Sprague-Dawley, 10 weeks) were given 800, 1200, or 1600 mg/kg/day acetaminophen by oral gavage for 4 days. Liver was assayed for oxidative stress and antioxidant markers: malondialdehyde (MDA), thiobar-bituric acid reactive substance (TBARS), total antioxidant status (TAS), glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx), glucose-6-phosphate dehydrogenase (G6PD), catalase (CAT), and superoxide dismutase (SOD), and alanine transaminase (ALT) as a marker of hepatocellular injury. Acetaminophen at 1200/1600 mg/kg decreased GSH 26/47%, GPx 21/26%, CAT 35/28%, SOD 21/12%; and TAS 28/18% (correlated with CAT, r=0.91; SOD, r=0.66; GPx, r = 0.45). Despite antioxidant deficiencies, and no TBARS change, MDA decreased 26%/33%/37% at 800/1200/1600 mg/kg, which correlated with increased GR (61%/62%/76%, r = 0.77) and G6PD (130%/110%/190%, r = 0.78). Both MDA (r = 0.68) and G6PD (r = 0.71) correlated with hepatic ALT, which decreased 27%o/43%/48%, respectively. Resistance to acetaminophen hepatotoxicity produced by repeated exposure is partially attributable to upregulation of hepatic G6PD and GR activity as an adaptive and protective response to oxidative stress and glutathione depletion.

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Mehrpour, Omid, Farhad Saeedi, Ali Hadianfar, Bruno Mégarbane, and Christopher Hoyte. "Prognostic factors of acetaminophen exposure in the United States: An analysis of 39,000 patients." Human & Experimental Toxicology 40, no. 12_suppl (November 12, 2021): S814—S825. http://dx.doi.org/10.1177/09603271211061503.

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Acetaminophen is a frequently used over-the-counter or prescribed medication in the United States. Exposure to acetaminophen can lead to acute liver cytolysis, acute liver failure, acute kidney injury, encephalopathy, and coagulopathy. This retrospective cohort study (1/1/2012 to 12/31/2017) investigated the clinical outcomes of intentional and unintentional acetaminophen exposure using the National Poison Data System data. The frequency of outcomes, chronicity, gender, route of exposure, the reasons for exposure, and treatments as described. Binary logistic regression was used to estimate the prognostic factors and odds ratios (OR) with 95% confidence intervals (CI) for outcomes. This study included 39,022 patients with acetaminophen exposure. Our study demonstrated that the likelihood of developing severe outcomes increased by aging (OR = 1.12, 95% CI: 1.08–1.015) and was lower in females (OR = 0.88, 95% CI: 0.78–0.99). Drowsiness/lethargy (OR = 1.48, 95% CI: 1.22–1.82), agitation (OR = 1.66, 95% CI: 1.11–2.50), coma (OR = 23.95, 95% CI: 17.05–33.64), bradycardia (OR = 2.29, 95% CI: 1.22–4.32), rhabdomyolysis (OR = 8.84, 95% CI: 3.71–21.03), hypothermia (OR = 4.1, 95% CI: 1.77–9.51), and hyperthermia 2.10 (OR = 2.10, 95% CI: 1.04–4.22) were likely associated with major outcomes or death. Treatments included intravenous N-acetylcysteine (61%), oral N-acetylcysteine (10%), vasopressor (1%), hemodialysis (0.7%), fomepizole (0.1%), hemoperfusion (0.03%), and liver transplant (0.1%). In conclusion, it is important to consider clinical presentations of patients with acetaminophen toxicity that result in major outcomes and mortality to treat them effectively.

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Zyoud, Sa'ed H., Rahmat Awang, Syed Azhar Syed Sulaiman, and Samah W. Al-jabi. "High prevalence of hypokalemia after acute acetaminophen overdose: Impact of psychiatric illness." Human & Experimental Toxicology 29, no. 9 (February 9, 2010): 773–78. http://dx.doi.org/10.1177/0960327110361759.

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Background: Hypokalemia is not an isolated disease but an associated finding in a number of different diseases. It is also a commonly neglected condition among patients with acute acetaminophen overdose. Objectives: This study intended to determine the prevalence of hypokalemia and its clinical correlates in acute psychiatric illness among hypokalemic and normokalemic patients after acetaminophen overdose. Methods: This is a retrospective cohort study of hospital admissions for acute acetaminophen overdose conducted over a period of 5 years from 1 January 2004 to 31 December 2008. Demographic data and different types of psychiatric illness were compared between hypokalemic and normokalemic patients. Hypokalemia was predefined by a serum concentration <3.5 mmol/L. Statistical Package for Social Sciences (SPSS) 15 was used for data analysis. Results: Two hundred and eighty patients out of 305 admissions were studied. Hypokalemia was found in 63.6% of patients with a higher prevalence in the presence of psychiatric illness (67.7%). Hypokalemic patients were significantly associated with the presence of major depression (p = .04), adjustment disorder (p < .001), anxiety (p = .01), and suicidal attempts (p = .04). Conclusion: Hypokalemia was common among patients with psychiatric illness and acute acetaminophen overdose.

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Shan, Shulin, Zhenyu Shen, and Fuyong Song. "Autophagy and acetaminophen-induced hepatotoxicity." Archives of Toxicology 92, no. 7 (June 6, 2018): 2153–61. http://dx.doi.org/10.1007/s00204-018-2237-5.

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Manautou, José E., Edward A. Khairallah, and Steven D. Cohen. "Evidence for common binding of acetaminophen and bromobenzene to the 58‐kda acetaminophen‐binding protein." Journal of Toxicology and Environmental Health 46, no. 3 (November 1995): 263–69. http://dx.doi.org/10.1080/15287399509532034.

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Stern, Stephan T., Mary K. Bruno, Robert A. Horton, Dennis W. Hill, Jeanette C. Roberts, and Steven D. Cohen. "Contribution of acetaminophen-cysteine to acetaminophen nephrotoxicity II. Possible involvement of the γ-glutamyl cycle." Toxicology and Applied Pharmacology 202, no. 2 (January 2005): 160–71. http://dx.doi.org/10.1016/j.taap.2004.06.029.

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Seltzer, Justin A., Irvan Bubic, Garret A. Winkler, Nathan A. Friedman, Jessica Bagby, Christian A. Tomaszewski, Richard F. Clark, Allyson Kreshak, and Daniel R. Lasoff. "Sulfhemoglobinemia and methemoglobinemia following acetaminophen overdose." Toxicology Reports 9 (2022): 1725–27. http://dx.doi.org/10.1016/j.toxrep.2022.08.011.

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Hantson, Philippe, Marie Christiane Vekemans, Pierre François Laterre, Piet Vanormelingen, Paul Mahieu, and Michael Matthias Koerner. "Heart Donation After Fatal Acetaminophen Poisoning." Journal of Toxicology: Clinical Toxicology 35, no. 3 (January 1997): 325–26. http://dx.doi.org/10.3109/15563659709001221.

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Rumack, Barry H. "Acetaminophen Hepatotoxicity: The First 35 Years." Journal of Toxicology: Clinical Toxicology 40, no. 1 (January 2002): 3–20. http://dx.doi.org/10.1081/clt-120002882.

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Tenenbein, Milton. "Acetaminophen: The 150 mg/kg Myth." Journal of Toxicology: Clinical Toxicology 42, no. 2 (January 2004): 145–48. http://dx.doi.org/10.1081/clt-120030939.

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Carreiro, Stephanie, James Marvel-Coen, Rosalind Lee, Brittany Chapman, and Victor Ambros. "Circulating microRNA Profiles in Acetaminophen Toxicity." Journal of Medical Toxicology 16, no. 2 (December 2, 2019): 177–87. http://dx.doi.org/10.1007/s13181-019-00739-6.

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Potter, David W., and Jack A. Hinson. "Acetaminophen Peroxidation Reactions." Drug Metabolism Reviews 20, no. 2-4 (January 1989): 341–58. http://dx.doi.org/10.3109/03602538909103546.

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Regal, Randolph E. "Acetaminophen Chronic Toxicity." Drug Intelligence & Clinical Pharmacy 20, no. 6 (June 1986): 507. http://dx.doi.org/10.1177/106002808602000620.

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Sorodoc, Laurentiu, Catalina Lionte, Cristina Bologa, Ovidiu Petris, Victorita Sorodoc, and Carmen Buga. "Acute pancreatitis after nifedipine and acetaminophen poisoning — case report." Open Medicine 4, no. 4 (December 1, 2009): 527–31. http://dx.doi.org/10.2478/s11536-009-0057-y.

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AbstractThe incidence of drug-induced pancreatitis is rare. There have been several reports of acute pancreatitis as a complication in acute poisoning with drugs or toxins. We present a case of a young woman with acute pancreatitis secondary to an overdose of nifedipine and acetaminophen in a suicide attempt. We excluded other causes of acute pancreatitis by clinical history, serum toxicology, serology, and abdominal imaging. The most likely underlying pathophysiological mechanism was ischemic injury of the pancreas secondary to severe collapse induced by nifedipine and possible acetaminophen-induced direct pancreatotoxicity. The pancreatitis resolved with treatment that included continuous veno-venous haemofiltration in an intensive care unit. Emergency and intensive care units should be aware of this unusual complication of such poisoning. To our knowledge, this is the first reported association between massive nifedipine overdose and acute pancreatitis.

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Bond, G. Randall. "Acetaminophen protein adducts: A review." Clinical Toxicology 47, no. 1 (January 2009): 2–7. http://dx.doi.org/10.1080/15563650801941831.

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Chomchai, Summon, Chulithida Chomchai, and Taweepong Anusornsuwan. "Acetaminophen psi parameter: A useful tool to quantify hepatotoxicity risk in acute acetaminophen overdose." Clinical Toxicology 49, no. 7 (August 2011): 664–67. http://dx.doi.org/10.3109/15563650.2011.597031.

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BARTOLONE, JOHN B., STEVEN D. COHEN, and EDWARD A. KHAIRALLAH. "Immunohistochemical Localization of Acetaminophen-Bound Liver Proteins." Toxicological Sciences 13, no. 4 (1989): 859–62. http://dx.doi.org/10.1093/toxsci/13.4.859.

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BARTOLONE, J. "Immunohistochemical localization of acetaminophen-bound liver proteins." Fundamental and Applied Toxicology 13, no. 4 (November 1989): 859–62. http://dx.doi.org/10.1016/0272-0590(89)90339-4.

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Zyoud, Sa'ed H., Rahmat Awang, Syed Azhar Syed Sulaiman, Waleed M. Sweileh, and Samah W. Al-jabi. "Incidence of adverse drug reactions induced by N-acetylcysteine in patients with acetaminophen overdose." Human & Experimental Toxicology 29, no. 3 (January 13, 2010): 153–60. http://dx.doi.org/10.1177/0960327109359642.

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Background: Intravenous N-acetylcysteine (IV-NAC) is widely recognized as the antidote of choice for acetaminophen overdose. However, its use is not without adverse drug reactions (ADR) that might affect therapeutic outcome or lead to treatment delay. Objective: the aim of this study was to investigate the type and incidence of ADR induced by IV-NAC in patients treated for acetaminophen overdose. Methods: This is a retrospective study of patients admitted to the hospital for acute acetaminophen overdose over a period of 4 years (1 January 2005 to 31 December 2008). The primary outcome of interest in this study was the occurrence of ADR during NAC administration. Pearson chi-square test or Fisher’s exact test, student’s t test, and Mann-Whitney U test were used in univariate analysis. SPSS 15 was used for data analysis. Results: Two hundred and fifty five patients were studied. Different types of ADR were observed in 119 (46.7%) cases. Of those patients, 83 (69.7%) had been treated with IV-NAC versus 36 (30.3%) who had not (p < .001). The following ADR were significantly associated with IV-NAC administration: vomiting (p = .001), flushing (p < .001), rash (p < .001), pruritus (p < .001), chest pain (p = .001), bronchospasm (p = .03), coughing (p = .01), headache (p = .001), dizziness (p < .001), convulsion (p = .03), and hypotension (p = .001). ADR were mild in 54 (43.2%), moderate in 17 (13.6%), and severe in 12 (9.6%) patients. There were no ADR in 42 (33.6%) patients. Comparative results of the characteristics of patients who reacted to IV-NAC and nonreactors showed that patients with ADR had no significant difference in age, gender, ethnicity, amount ingested, latency time, and acetaminophen level than nonreactors. Conclusion: ADR to IV-NAC were common among patients with acetaminophen overdose, but mostly minor and all reported adverse reactions were easily managed.

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Hart, S. G. E., W. P. Beierschmitt, D. S. Wyand, E. A. Khairallah, and S. D. Cohen. "Acetaminophen Nephrotoxicity in CD-1 Mice." Toxicology and Applied Pharmacology 126, no. 2 (June 1994): 267–75. http://dx.doi.org/10.1006/taap.1994.1116.

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Jørgensen, L., P. Thomsen, and H. E. Poulsen. "Disulfiram Prevents Acetaminophen Hepatotoxicity in Rats." Pharmacology & Toxicology 62, no. 5 (May 1988): 267–71. http://dx.doi.org/10.1111/j.1600-0773.1988.tb01885.x.

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Mehrpour, Omid, Shahin Shadnia, and Hossein Sanaei-Zadeh. "Late extensive intravenous administration of N-acetylcysteine can reverse hepatic failure in acetaminophen overdose." Human & Experimental Toxicology 30, no. 1 (March 23, 2010): 51–54. http://dx.doi.org/10.1177/0960327110366182.

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Acetaminophen is a commonly used analgesic and has been shown to be a main cause of drug-induced liver failure. N-acetylcysteine (NAC) should be employed as the antidote in case of acetaminophen poisoning within the first 8-10 hours. Oral administration of NAC is universally recommended and due to the adverse effects, the intravenous administration of the agent is reserved for patients with oral intolerance and severe complications. We here report an 18-year-old man with severe liver failure due to a huge ingestion of acetaminophen, who was taken into the Loghman Hakim Hospital Poison Center 72 hours after attempted suicide. Regarding the poor prognostic clues as his level of consciousness and impaired liver functions, an extensive intravenous regimen of NAC was started. The patient survived the condition with an additional intravenous administration of NAC past the first 72 hours of treatment. We discuss that even in late phases of intoxication; high-dose intravenous NAC can serve a substantial improvement.

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Donkor, Shadrack, Christopher Larbie, Gustav Komlaga, and Benjamin Obukowho Emikpe. "Evaluation of the Acute Hepatoprotective Potential of Hydroethanolic Extract of Duranta erecta L. Parts." Journal of Toxicology 2020 (December 9, 2020): 1–10. http://dx.doi.org/10.1155/2020/8815719.

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Liver disease is a major health problem and its treatment is costly in most developing countries with attendant adverse effects. This study aimed at determining the acute hepatoprotective efficacy of Duranta erecta hydroethanolic extracts of leaves, ripe and unripe fruits against CCl4-, and acetaminophen-induced hepatotoxicity in animals. Materials and Methods. CCl4 (1 mL/kg body weight in olive oil) and acetaminophen (500 mg/kg b.wt) were used to induce hepatotoxicity in the animals. Animals were treated with extracts at 250 mg/kg b.wt and standard drug, silymarin (100 mg/kg), for 7 days. Hepatoprotective efficacy was assessed by assaying serum biochemical markers such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (γGT), bilirubin (Bil), antioxidative biomarkers including reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione transferase (GST), superoxide dismutase (SOD), malondialdehyde (MDA), hydrogen peroxidase (H202), and nitric oxide (NO), as well as histological observations. Results. Exposure of the animals to CCl4 and acetaminophen resulted in liver injury as evidenced by elevated ALT, AST, ALP, γGT, Bil, MDA, H2O2, and NO levels with resultant derangement in liver microarchitecture. Pretreatment with hydroethanolic extracts, particularly ripe fruits of Duranta erecta, led to a reduction in these indicators and an increase in GSH, GPx, GST, and SOD levels. Biochemical data were supported by improvement in liver structure. Conclusion. The findings suggest that hydroethanolic Duranta erecta ripe fruits extract possesses hepatoprotective and antioxidative activities against CCl4- and acetaminophen-induced toxicity and could be developed as a potent agent for drug-induced liver diseases.

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Wojdyla, Katarzyna, Krzysztof Wrzesinski, James Williamson, Stephen J. Fey, and Adelina Rogowska-Wrzesinska. "Acetaminophen-induced S-nitrosylation and S-sulfenylation signalling in 3D cultured hepatocarcinoma cell spheroids." Toxicology Research 5, no. 3 (2016): 905–20. http://dx.doi.org/10.1039/c5tx00469a.

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Polyakov, Alexey V., Andrey A. Svistunov, Svetlana N. Kondratenko, Irina V. Kovachevich, Lyudmila G. Repenkova, Marina I. Savelyeva, Evgenia V. Shikh, and Lidiya Y. Badriddinova. "Study of the pharmacokinetics of various drugs under conditions of antiorthostatic hypokinesia and the pharmacokinetics of acetaminophen under long-term spaceflight conditions." Drug Metabolism and Personalized Therapy 37, no. 2 (November 29, 2021): 163–75. http://dx.doi.org/10.1515/dmpt-2021-0159.

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Abstract Objectives To study the pharmacokinetics and relative bioavailability of drugs of different chemical structure and pharmacological action under conditions simulating the effects of some factors of spaceflight, as well as the peculiarities of the pharmacokinetics of acetaminophen under long-term spaceflight conditions. Methods The pharmacokinetics of verapamil (n=8), propranolol (n=8), etacizine (n=9), furosemide (n=6), and acetaminophen (n=7) in healthy volunteers after a single oral administration under normal conditions (background) and under antiorthostatic hypokinesia (ANOH), the pharmacokinetics of acetaminophen in spaceflight members under normal ground conditions (background) (n=8) and under prolonged spaceflight conditions (SF) (n=5) were studied. Results The stay of volunteers under antiorthostatic hypokinesia had different effects on the pharmacokinetics and bioavailability of drugs: Compared to background, there was a decreasing trend in Vz for verapamil (−54 Δ%), furosemide (−20 Δ%), propranolol (−8 Δ%), and acetaminophen (−9 Δ%), but a statistically significant increase in Vz was found for etacizine (+39 Δ%); there was an increasing trend in Clt for propranolol (+13 Δ%) and acetaminophen (+16 Δ%), and a decreasing trend in Clt for etacizine, verapamil, and furosemide (−22, −23 and −9 Δ% respectively) in ANOH. The relative bioavailability of etacizine, verapamil, and furosemide in ANOH increased compared to background (+40, +23 and +13 Δ%, respectively), propranolol and acetaminophen decreased (−5 and −12 Δ% accordingly). The relative rate of absorption of etacizine and furosemide in ANOH decreased (−19 and −20 Δ%, respectively) while that of verapamil, propranolol, and acetaminophen increased (+42, +58 and +26 Δ%, respectively). A statistically significant decrease in AUC0-∞ (−57 Δ%), Cmax (−53 Δ%), relative bioavailability of acetaminophen (−52 Δ%) and a sharp increase in Clt (+147 Δ%), Tmax (+131 Δ%) as well as a trend towards a significant decrease in T1/2 (−53 Δ%), MRT (−36 Δ%) and a moderate increase in Vz (+24 Δ%) were found under control compared to background. Unidirectional changes in AUC0-∞, Clt, T1/2, MRT and relative bioavailability of acetaminophen, which are more pronounced in SF and opposite dynamics for Cmax, Tmax, Vz were found in ANOH and SP compared to background studies. Conclusions The data obtained allow recommending the studied drugs for rational pharmacotherapy in the possible development of cardiovascular disease in manned spaceflight.

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Journal articles on the topic 'Acetaminophen Toxicology'

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