Relevant bibliographies by topics / Acetaminophen toxicity

Academic literature on the topic 'Acetaminophen toxicity'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Acetaminophen toxicity"

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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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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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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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Roach, Janey A., and Brett Stacey. "Acetaminophen Toxicity." Orthopaedic Nursing 16, no. 3 (May 1997): 49???55. http://dx.doi.org/10.1097/00006416-199705000-00013.

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Bartlett, Dana. "Acetaminophen Toxicity." Journal of Emergency Nursing 30, no. 3 (June 2004): 281–83. http://dx.doi.org/10.1016/j.jen.2004.01.023.

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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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Roberge, Raymond. "Chronic acetaminophen toxicity." Journal of Emergency Medicine 25, no. 4 (November 2003): 474. http://dx.doi.org/10.1016/j.jemermed.2003.08.006.

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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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Poolsawat, S. S., C. A. Huerta, G. A. Miranda, and L. T. Nguyen. "Acetaminophen: fatty enhanced toxicity." Proceedings, annual meeting, Electron Microscopy Society of America 44 (August 1986): 332–33. http://dx.doi.org/10.1017/s0424820100143286.

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Drug toxicity accounts for 10%-30% of all medical in-patients admissions; some of the drug induced illnesses often occur following hospitalization. 5%-6% of medical in-patients deaths are initiated or induced by drug intake (1-4); about one-third of these cases are caused by non-prescription drugs. Acetaminophen, considered among the safest of all over-the-counter analgesics, has been reported to induce fatal hepatic necrosis both in man and animals (5-8). Frequently, adverse drug reactions arise from hypersensitivity to a drug and its side effects, or to drug interactions with food and food additives. This study is undertaken to observe the effect of acetaminophen on the liver when a fatty diet is simultaneously administered.Swiss Webster mice were individually gavaged with a 286 mg/Kg dosis of acetaminophen for 4 days; control animals received saline alone. Both groups received rat feed plus 20% fat and were euthanized on the 5th day. Liver tissues were either fixed in 2% gluteraldehyde; post-fixed in 1% osmnium tetroxide in 0.1M sodium cacodylate buffer and embedded in Araldite 502 for TEM; or processed for alkaline phosphatase activity (9).Hepatocyte derived from mice exposed to acetaminophen (Fig. 1) showed increased Golgi Apparatus (GA) and secretory granules (SG) activity. These phenomena appear to be responsible for the elevated alkaline phosphatase activity (Fig. 2) in response to acetaminophen detoxification exerted by the hepatocyte. However, when a fatty diet is incorporated into the study: the hepatocyte exhibited generalized cytoplasmic lysis and increased lipid droplets (Fig. 3), localized coagulative necrosis of the hepatocyte normally found in the caudal and right lobes of the liver (Fig. 4) and increased pynotic hepatocytes (Fig. 5) are noted
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Dissertations / Theses on the topic "Acetaminophen toxicity"

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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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Ward, Jeanine. "MicroRNA Markers of Acetaminophen Toxicity: A Master's Thesis." eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/625.

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Background To investigate plasma microRNA (miRNA) profiles indicative of hepatotoxicity in the setting of lethal acetaminophen (APAP) toxicity in mice. Methods Using plasma from APAP poisoned mice, either lethally (500 mg/kg) or sublethally (150 mg/kg) dosed, we screened commercially available murine microRNA libraries (SABiosciences, Qiagen Sciences, MD) to evaluate for unique miRNA profiles between these two dosing parameters. Results We distinguished numerous, unique plasma miRNAs both up- and down-regulated in lethally compared to sublethally dosed mice. Of note, many of the greatest up- and down-regulated miRNAs, included, but were not limited to, 574-5p, 466g, 466f-3p, 375, 29c, and 148a. There was a statistically significant increase in alanine aminotransferase levels in the lethal compared to sublethal APAP dosing groups at the 12 h time point ( P < 0.001). There was 90% mortality in the lethally compared to sublethally dosed mice at the 48 h time point ( P = 0.011). Conclusion We identified unique plasma miRNAs both up- and down-regulated in lethally dosed APAP poisoned mice.
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Anoopkumar-Dukie, Shailendra. "Serotonin-melatonin interactions in acetaminophen and N,N-dimethylformamide toxicity." Thesis, Rhodes University, 2000. http://hdl.handle.net/10962/d1003957.

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Acetaminophen and N,N-dimethylformamide (DMF) are compounds which are extremely toxic to the liver. Acetaminophen is a drug which is well known for its analgesic and antipyretic properties. However, the abuse potential of this agent as a non-narcotic analgesic in alcoholics is well known. It is also the leading cause of overdose in England. DMF toxicity results mainly from occupational exposure. At present there are no known reports of an antidote for DMF poisoning, while N-acetylcysteine, the antidote for acetaminophen poisoning, is known to produce adverse effects. The present study evaluates the potential of melatonin as an antidote for acetaminophen and DMF poisoning. This study also investigates the mechanism underlying acetaminophen addiction and abuse. Initial studies involved in vitro techniques in an attempt to remove the complexities of organ interactions. The photodegradation studies, using ultraviolet (UV) light, revealed that melatonin accelerates the rate of acetaminophen degradation in the presence of air, and reduces the rate of degradation in the presence of nitrogen. This study also revealed that melatonin is rapidly degraded in the presence of air, following UV irradiation. The effect of DMF on hydroxyl radical generation was also determined. DMF was shown to act as a free radical scavenger, rather that a generator of free radicals. The in vitro studies were followed by lipid peroxidation determination. DMF (0.4ml/kg and 0.8ml/kg) did not produce any significant increases in lipid peroxidation in the liver. Three different doses of acetaminophen (30mg/kg, 100mg/kg, and 500mg/kg) were administered to rats for seven days. Acetaminophen (500mg/kg) was shown to significantly increase (p<0.05) lipid peroxidation in the liver. Melatonin (2.5mg/kg) was not able to significantly reduce the damage. The lower doses of acetaminophen (30mg/kg and 100mg/kg) did not increase lipid peroxidation. Electron microscopy studies showed that DMF adversely affects the liver, and in particular, the endoplasmic reticulum. Co administration of melatonin (2.5mg/kg) was able to reduce the damage. Further experiments need to be performed before an accurate assessment can be made on the ability of melatonin as an antidote for DMF and acetaminophen poisoning. Several experiments were done in an attempt to uncover the biochemical mechanism underlying acetaminophen addiction and abuse. The first experiment targeted the liver enzyme tryptophan-2,3-dioxygenase (TDO). This enzyme is the major determinant of tryptophan levels in vivo. Acetaminophen administration (100mg/kg for three hours) was shown to significantly inhibit (p<0.05) the activity of TDO, indicating increased peripheral levels of tryptophan. This experiment was followed up with determination of brain serotonin and pineal melatonin. Brain serotonin was determined using the ELISA technique. Melatonin was estimated using this technique as well as with pineal organ culture. Acetaminophen administration (100mg/kg for three hours) significantly increased (p<0.05) brain serotonin levels. Using organ culture where exogenous (3H) tryptophan is metabolised to (3H) melatonin, acetaminophen (100mg/kg for three hours) was shown to significantly increase (p<0.05) pineal melatonin concentrations. However, the ELISA technique did not reveal any changes in endogenous pineal melatonin levels. The final experiment was the determination of urinary 5-hydroxyindole acetic acid (5- HIAA), the major metabolite of serotonin, following acetaminophen administration (100mg/kg for three hours). Acetaminophen was shown to significantly reduce 5-HIAA levels (p<0.05) suggesting reduced catabolism of serotonin. The findings of this study indicate that acetaminophen mimics the actions of an antidepressant. This compelling finding has important clinical implications, and needs to be examined further.
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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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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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Bruschi, Sam A. "Investigations into mechanisms of paracetamol-induced toxicity using ìn vitro' systems /." Title page, abstract and table of contents only, 1987. http://web4.library.adelaide.edu.au/theses/09PH/09phb192.pdf.

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Navarro-Zornoza, Maria Dolores. "Improved predictive models for pre-clinical drug toxicity studies." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/21682.

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Increasingly, drug-induced liver injury is one of the main reason for drugs to be withdrawn from the market even after passing toxicity studies in pre-clinical and clinical trials because of risks of toxicity and ineffective treatments. Human immortalised hepatocyte cell lines used in drug testing are widely available, inexpensive and easy to culture. However, these cell lines are commonly known to have poor predictive capabilities and improved in vitro hepatic models are required for predicting hepatotoxicity of large numbers of compounds in drug discovery. In this study, the primary goal was to develop an improved in vitro human hepatic model using a combination of the C3A human hepatic cell line and human umbilical vein endothelial cells (HUVECs), for prediction of acetaminophen (APAP) hepatotoxicity. Initial experiments showed that co-culture of HUVEC:C3A in EGM-2, an endothelial medium, was essential to support both cell types, and that co-cultures maintained the initial cell seeding ratio of 1:1 (HUVEC:C3A) after 3 days. Phenotyping of co-cultured cells using platelet endothelial cell adhesion molecule (PECAM-1/CD31) for HUVECs, and hepatic epithelial (EpCAM) markers for C3As demonstrated that at ratio 1:1 (HUVEC:C3A), there is cross-talk between HUVECs and C3As and cells in co-culture showed properties of self-organisation. This interaction resulted in improved hepatic metabolic activity in vitro in respect of albumin synthesis and cytochrome P450 activity. Treatment with low (5 mM), intermediate (10 mM) and high doses (20 mM) of APAP, showed that prediction of hepatotoxicity using specific kits for cell viability and mitochondria function, was significantly improved in C3As in the presence of HUVECs, thus demonstrating an in vitro human hepatic co-culture could be an invaluable model for drug toxicity studies. We observed that the intermediate APAP dose had no effect on cell viability and mitochondrial function in co-cultures, whilst by comparison both lactate levels and oxidative stress were perturbed in mono-cultures. Co-cultures also up-regulated expression of vascular endothelial growth factor receptor-2 (VEGFR-2) in HUVECs following APAP exposure, which may be important in modulating the toxic effect of APAP on C3As. To further improve the in vitro liver-like model, Matrigel™ was incorporated to promote vascular formation by HUVECs and support hepatic organization, migration and function of C3As. In HUVEC mono-cultures, Matrigel™-promoted vascularization, haptotaxis and self-organization and in HUVEC:C3A co-cultures formation of structures reminiscent of liver sinusoids and maintenance of hepatic albumin synthesis and CYP3A4 activity. Time-lapse imaging showed haptotactic migration of hepatocytes towards endothelial cells, with Matrigel™ likely having a chemotactic effect on HUVECs and C3As, resulting in interconnected vascular network. APAP inhibited angiogenesis in HUVEC mono-cultures whereas APAP had no effect in HUVEC:C3A co-cultures. In conclusion, the development of an in vitro human organotypic co-culture model of HUVECs and C3As significantly enhanced hepatic function, demonstrated by significant improvement in hepatic metabolism, evidence of greater resistance to APAP toxicity, and improved cell-cell communication. Co-cultures markedly modulated APAP hepatotoxicity compared with C3A mono-cultures. Furthermore, co-culture of HUVECs and C3As using a complex basement membrane biomatrix (Matrigel™) produced a self-assembling interconnected vascular network, improved hepatocyte function as well as reproducibility of responses to APAP toxicity. The application of the described co-culture models may improve the accuracy, efficacy and predictive power of drug toxicity testing strategies in drug development.
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Haire, Kambria. "Elucidation of the Role of Poly(ADP-Ribose) Polymerase in Drug-Induced Toxicity." Scholar Commons, 2015. http://scholarcommons.usf.edu/etd/5959.

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Drug toxicity may cause liver injury, resulting in damage to cells and tissues. This damage can lead to cytotoxic events that may result in an activation of poly (ADP-ribose) polymerase (PARP). A study was conducted to determine if cocaine and acetaminophen toxicity lead to DNA damage and to the activation of the repair protein, PARP in the liver using the hepatotoxicants: cocaine and acetaminophen (APAP). A dose-response analysis for cocaine concluded that a dose as low as 20 mg/kg resulted in elevated ALT levels. A higher dose of 60 mg/kg was tested for analyses but resulted in severe hemorrhaging. The dose-response analyses for APAP resulted in no elevated liver enzyme levels for a 75 mg/kg and 150 mg/kg dose. A dose of 50 mg/kg for cocaine, and a dose of 300 mg/kg for APAP were used to analyze temporal trends for both toxicants. Both cocaine and APAP produced incremental increases in ALT at the 2 hour, 6 hour, 18 hour, and 24 hour time points, respectively. PARP activity analysis for cocaine measured the highest activity at the 2hr and 6hr time points. PARP analysis for acetaminophen measured gradual increases until the 18 hour time point where the highest level of PARP activity was measured. A PARP inhibition analysis was conducted with cocaine and (APAP) to understand the impact of a PARP inhibitor, 1,5-dihydroxyisoquinoline (DIQ), on PARP activity in the liver. A 50 mg/kg dose of cocaine or a 300 mg/kg dose of APAP was administered, followed by a 10 mg/kg dose of DIQ at 1) the time of initial toxicant dose (0 hour), or 2) 1 hour after initial toxicant dose (1hr). The PARP inhibition analysis for cocaine and APAP was conducted at 6 and 18 hours post initial dose, respectively, when the highest levels of PARP were observed. Inhibition analyses determined that ALT declined significantly when DIQ was administered immediately following the initial toxicant dose for both toxicants. DIQ administered 1 hr after initial toxicant dose resulted in slightly higher ALT than the 0 hr time point. Decreases in PARP activity were observed at the 0 hr time point, with slightly higher PARP levels observed at the 1 hr time point. Decreased PARP activity was observed following DIQ treatment with both, a concurrent drug treatment and treatment following drug administration. Cocaine and APAP treatment did not cause DNA fragmentation. A liver glutathione (GSH) analysis conducted for cocaine and APAP did not correlate with DIQ alteration of PARP activity. The mechanism of DIQ effects on drug-induced hepatotoxicity appears to be GSH independent. DIQ was effective in reducing drug-induced hepatotoxicity and preserving organ function.
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Nicholls-Grzemski, Felicity April. "The effect of short-term pretreatment with peroxisome proliferators on the acute toxicity of various toxicants, including paracetamol /." Title page, table of contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phn6158.pdf.

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Woods, Sally. "Comparison of metformin, rosiglitazone, and acetaminophen in the prevention of olanzapine toxicity in mice." University of Cincinnati / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1305892985.

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Books on the topic "Acetaminophen toxicity"

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Levine, Michael. Management of acetaminophen (paracetamol) poisoning. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0318.

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Acetaminophen overdose remains common, and is one of the most frequent reasons for liver transplant in the United States. Toxicity results from the metabolism to a toxic metabolite, N-acetyl-para-benzoquinoneimine. This chapter begins with a brief discussion of the history and epidemiology of acetaminophen overdose, followed by a discussion on the pharmacokinetics and pharmacodynamics. The risk factors, clinical presentation, and treatment strategies presented.
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Sonia Maria Freitas de Morais. UDP-glucuronyl transferase deficiency as a biochemical determinant of acetaminophen metabolism and toxicity. 1989.

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Morais, Sonia Maria Freitas de. UDP - glucuronyl transferase deficiency as a biochemical determinant of acetaminophen metabolism and toxicity. 1990.

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Izzedine, Hassan, and Victor Gueutin. Drug-induced chronic tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0087.

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The chronic form of drug-induced tubulointerstitial nephritis (CTIN) is an insidious disease and most probably represents the common final response pattern of the kidney to a variety of agents (including analgesics, lithium, antineoplastic chemotherapeutic agents, like cisplatin and nitrosoureas, and immunosuppressive drugs, such as ciclosporin and tacrolimus). Drug-induced CTIN is usually asymptomatic, presenting with slowly progressive renal impairment. Because of its insidious nature, CTIN is often diagnosed incidentally on routine laboratory screening or evaluation of CKD. The diagnosis of drug-induced CTIN largely depends on the history of exposure to a nephrotoxic drug. Clinical investigations may show modest elevation in serum creatinine, evidence of tubular dysfunction (e.g. renal tubular acidosis), or Fanconi syndrome (i.e. aminoaciduria, glycosuria, hypophosphataemia, and hypouricaemia). Urinalysis may be normal or show low-grade proteinuria (< 1.5 g/day) and/or pyuria. Diagnosis depends on renal biopsy, which reveals variable cellular infiltration of the interstitium, tubular atrophy, and fibrosis. Analgesic nephropathy is possibly still the most common category of CTIN worldwide. The amount of phenacetin-acetaminophen combination required to cause CTIN has been estimated to be at least 2–3 kg over many years. Lithium-induced CTIN occurs in a small subset of patients receiving long-term lithium therapy, who have had repeated episodes of lithium toxicity, with high serum drug levels. CTIN induced by ciclosporin or tacrolimus is common among patients receiving kidney, heart, liver, and pancreas transplants. The mechanism appears to be dependent largely on the potent vasoconstrictive effects of these drugs. The recognition of a potential association between a patient’s renal disease and exposure to a drug is crucial, because, unlike many other forms of renal disease, drug-induced CTIN can be prevented and even reversed, by avoiding additional drug exposure.
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Book chapters on the topic "Acetaminophen toxicity"

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Davies, D. S., L. B. G. Tee, C. Hampden, and A. R. Boobis. "Acetaminophen Toxicity in Isolated Hepatocytes." In Biological Reactive Intermediates III, 993–1003. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5134-4_96.

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Viña, Juan R., Federico V. Pallardo, Tadayasu Furukawa, and Jose Viña. "Oral glutathione increases hepatic glutathione and prevents acetaminophen toxicity." In Amino Acids, 724–29. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-011-2262-7_87.

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Lee-Barber, Jasmine, Taylor E. English, Jacquelyn F. Britton, Nara Sobreira, Jason Goldstein, David Valle, and Hans Tomas Bjornsson. "Apparent Acetaminophen Toxicity in a Patient with Transaldolase Deficiency." In JIMD Reports, 9–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/8904_2018_116.

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Roberts, Dean W., Robert W. Benson, Neil R. Pumford, David W. Potter, Henrik E. Poulsen, and Jack A. Hinson. "Sensitive Immunochemical Assays for Monitoring Acetaminophen Toxicity in Humans." In ACS Symposium Series, 314–26. Washington, DC: American Chemical Society, 1990. http://dx.doi.org/10.1021/bk-1990-0451.ch029.

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Eryilmaz, Bilgen, Göknur Aktay, and Funda Bingöl. "Antioxidant Activity of Capsicum annuum L. Fruit Extracts on Acetaminophen Toxicity." In Biodiversity, 261–64. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4419-9242-0_27.

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Svendsen, O., H. B. Christensen, J. Rygaard, and P. Juul. "Comparative Study on the Toxicity of Acetaminophen and Mercuric Chloride in Normal and Athymic Mice and Rats." In Archives of Toxicology, 191–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74117-3_28.

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Adam Algren, D. "Acetaminophen toxicity." In Toxicology Cases for the Clinical and Forensic Laboratory, 75–77. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-815846-3.00035-1.

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Badal, Sachendra, and Shuvendu Roy. "Acetaminophen Toxicity." In The Acutely Ill Child: A Ready Reckoner, 186. Jaypee Brothers Medical Publishers (P) Ltd., 2013. http://dx.doi.org/10.5005/jp/books/11952_55.

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Johnson, Amberly. "Acetaminophen Toxicity." In PharmacotherapyFirst: A Multimedia Learning Resource. 2215 Constitution Avenue, N.W. Washington, DC 20037-2985: The American Pharmacists Association, 2017. http://dx.doi.org/10.21019/pharmacotherapyfirst.apap-tox_overview.

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"Ibuprofen and Acetaminophen Toxicity." In Clinical Veterinary Advisor, 464–65. Elsevier, 2013. http://dx.doi.org/10.1016/b978-1-4160-3969-3.00214-6.

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Conference papers on the topic "Acetaminophen toxicity"

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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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Malia, R. G., H. J. Kennedy, D. R. Triger, and F. E. Preston. "PROTECTIVE EFFECT OF VITAMIN K AGAINST ACETAMINOPHEN (PARACETAMOL) TOXICITY IN THE HAMSTER." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644341.

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We have previously reported that paracetamol may interfere with the metabolism of vitamin K via the vitamin K 2, 3-epoxide cycle. (Thrombosis and Haemostasis, 54,205,1985). In this study we have examined the effects of large doses of vitamin K on experimentally induced paracetamol hepatic necrosis in a hamster model. Paracetamol (1.2g/Kg) when given by gavage to 24 hamsters (Group I) resulted in 10 deaths (42%) at 24 hours. Simultaneous administration of lmg vitamin K intraperitoneally (Group II) reduced mortality to 3/24 (12%); mortality was 2/24 (8%) if vitamin K was given 4 hours after the paracetamol (Group III). In a further series of experiments (N=18) the prothrombin time in Group I was prolonged by 28 seconds compared with 14 seconds in Group II and 10 seconds in Group III. In samples taken for biochemical and histological analysis there was evidence of severe hepatic necrosis in all groups. When the dose of paracetamol was reduced to 1.0g/Kg (N=18) there was substantially less histological damage in Group II compared with other groups and the prothrombin times were only prolonged by 2 seconds (Group I); 1.5 seconds (Group II) and 3-5 seconds (Group III) respectively. In the final experiment (N=18) when Group II animals were divided into 3 sub-groups and the dose of vitamin K given was altered to 1.0, 0.5 and O.lmg following the paracetamol (1.2g/Kg) the prothrombin times were prolonged by 8 seconds, (1-0mg vitamin K), 21 seconds (0.5mg vitamin K) and 35 seconds (0.1mg vitamin K) respectively, indicating a dose dependant effect. The hypothesis that paracetamol induced hepatic necrosis occurs solely as a consequence of failure of glutathione to conjugate the reactive metabolites of paracetamol is not consistent with the protective effects of vitamin K observed here and the known mode of action of the vitamin. Other mechanisms such as free radical scavenging deserve to be studied.
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Asghar, A., A. Khan, T. Martins, and S. Hodgins. ""Analysis By Dialysis": Hemodialysis as a Salvage Therapy in a Critical Case of Acetaminophen Toxicity and Cerebral Edema." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1576.

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"The Protective Effect of Withania somnifera Root Extract Against Acetaminophen Induced Liver Toxicity in Cyprinus carpio Compared to Silymaryn." In International Conference on Chemical, Environment & Biological Sciences. International Institute of Chemical, Biological & Environmental Engineering, 2014. http://dx.doi.org/10.15242/iicbe.c914122.

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