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Journal articles on the topic 'Paracetamolis'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Lindžiūtė, Ugnė, Eglė Zlatkutė, Tadas Urbonas, Tomas Bukauskas, Donatas Simonaitis, and Andrius Macas. "POOPERACINIO SKAUSMO VALDYMO INTRAVENINIAIS LORNOKSIKAMU IR ACETAMINOFENU PALYGINIMAS PO RADIKALIŲ PROSTATEKTOMIJŲ." Sveikatos mokslai 27, no. 2 (June 12, 2017): 39–43. http://dx.doi.org/10.5200/sm-hs.2017.023.

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Nesteroidiniai vaistai nuo uždegimo yra skirti įvairaus tipo ir lokalizacijos skausmui malšinti. Gera pooperacinio skausmo kontrolė yra svarbi norint išvengti skausmo potencijuojamo paciento būklės pablogėjimo, pvz., tachikardijos, hipertenzijos, miokardo išemijos, alveolių ventiliacijos sumažėjimo, prasto žaizdų gijimo. Šiame tyrime lyginsime acetaminofeno ir lornoksikamo efektyvumą pooperaciniam skausmui malšinti. Darbo tikslas: įvertinti lornoksikamo analgezijos efektyvumo jėgą pooperaciniu laikotarpiu pacientams po radikalių prostatektomijų. Metodai. Įtraukti 35 pacientai, gydyti 2015-2016 metais LSMUL KK Urologijos skyriuje, kuriems atlikta radikali prostatektomija. Gavus raštišką sutikimą, atsitiktiniu būdu pacientams operacijos pabaigoje sušvirkščiami intraveninio lornoksikamo 8 mg arba acetaminofeno 1000mg. Pilvo skausmas vertinamas prieš operaciją, po operacijos praėjus 3, 6, 12 ir 24 valandoms. Rezultatai. Prieš operaciją pilvo skausmą lornoksikamo (L) grupėje jautė 1 (6,25 proc.) pacientas, o acetaminofeno (A) grupėje 1 (5,26 proc.) pacientas jautė rankos skausmą. Po operacijos praėjus 3 valandoms A grupėje 9 (47,37 proc.) pacientai skundėsi vidutinio stiprumo skausmu ir 3 (15,79 proc.) – stipriu skausmu. L grupėje po operacijos praėjus 3 valandoms 3 (18,75 proc.) pacientai jautė stiprų skausmą. Tarp A ir L vaistų po operacijos praėjus 3, 6, 12 ir 24 val. statistiškai reikšmingo skirtumo nebuvo (p=0,329; p=0,917; p=0,4; p=0,903, atitinkamai). Išvados. Intraveninis lornoksikamas ir acetaminofenas efektyviai malšina skausmą po radikalių prostatektomijų. Lornoksikamas i/v nuo skausmo toks pat efektyvus kaip paracetamolis i/v pacientams po radikalių prostatektomijų. Intraveninis lornoksikamas ir paracetamolis yra tinkami vartoti vidutinio stiprumo ir stipriam skausmui malšinti ankstyvuoju pooperaciniu laikotarpiu.

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2

Hinz, Burkhard, and Kay Brune. "Paracetamol and cyclooxygenase inhibition: is there a cause for concern?" Annals of the Rheumatic Diseases 71, no. 1 (October 28, 2011): 20–25. http://dx.doi.org/10.1136/ard.2011.200087.

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Paracetamol is recommended as first-line therapy for pain associated with osteoarthrosis and is one of the most widely used over-the-counter analgesic drugs worldwide. Despite its extensive use, its mode of action is still unclear. Although it is commonly stated that paracetamol acts centrally, recent data imply an inhibitory effect on the activity of peripheral prostaglandin-synthesising cyclooxygenase enzymes. In this context paracetamol has been suggested to inhibit both isoforms in tissues with low levels of peroxide by reducing the higher oxidation state of cyclooxygenase enzymes. Two recent studies have also demonstrated a preferential cyclooxygenase 2 (COX-2) inhibition by paracetamol under different clinically relevant conditions. This review attempts to relate data on paracetamol's inhibitory action on peripheral cyclooxygenase enzymes to the published literature on its anti-inflammatory action and its hitherto underestimated side-effects elicited by cyclooxygenase inhibition. As a result, a pronounced COX-2 inhibition by paracetamol is expected to occur in the endothelium, possibly explaining its cardiovascular risk in epidemiological studies. A careful analysis of paracetamol's cardiovascular side-effects in randomised studies is therefore strongly advised. On the basis of epidemiological data showing an increased gastrointestinal risk of paracetamol at high doses or when co-administered with classic cyclooxygenase inhibitors, paracetamol's long-term gastrointestinal impact should be investigated in randomised trials. Finally, paracetamol's fast elimination and consequently short-lived COX-2 inhibition, which requires repetitive dosing, should be definitely considered to avoid overdosage leading to hepatotoxicity.

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Oestmann, Andreas, and Annika Stöppler. "Die saure Patientin." Praxis 108, no. 4 (April 2019): 283–85. http://dx.doi.org/10.1024/1661-8157/a003201.

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Zusammenfassung. Wir berichten über eine 75-jährige Patientin mit einer metabolischen Azidose mit erhöhter Anionenlücke. Die Abklärung ergab eine Pyroglutamatazidose, bedingt durch eine Behandlung mit Paracetamol in therapeutischer Dosierung bei gleichzeitigem Vorliegen weiterer Risikofaktoren wie Mangelernährung, Alkoholkonsum, Niereninsuffizienz, Hepatopathie und weibliches Geschlecht. Nach Sistieren des Paracetamols und Verabreichung von Bicarbonat und N-Acetylcystein wurde eine rasche klinische und laboranalytische Besserung erreicht.

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4

Piluckis, Julius, Martyna Šopauskienė, and Rugilė Dubickaitė. "IŠORINIS OTITAS: RIZIKOS VEIKSNIAI, DIAGNOSTIKA IR GYDYMAS." Health Sciences 31, no. 1 (February 6, 2021): 25–30. http://dx.doi.org/10.35988/sm-hs.2021.005.

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Išorinis otitas, kitaip žinomas kaip „plaukiko ausis“, yra išorinės klausomosios landos uždegimas. Jis gali būti infekcinis ir neinfekcinis. Išorinis otitas dažnai pasitaiko vyresniems nei 2 metų pacientams, 10 proc. populiacijos suserga šia liga nors kartą per gyvenimą. Darbo tikslas – susipažinti su išorinio otito rizikos veiksniais, diagnostika ir gydymu. Pasitelkiant LSMU virtualios bibliotekos šaltinius, buvo apžvelgta mokslinė literatūra nagrinėjamąja tema ir atlikta mokslinių straipsnių analizė. Daugumoje straipsnių buvo paminėti šie rizikos veiksniai: drėgmės susilaikymas ausyse, ausų pH padidėjimas, imunosupresinė būklė, alerginės dermatozės, mechaninis klausomosios landos epitelio pažeidimas. Simptomai skirstomi į specifiškus (ypač jautrus kramslys ir ausies kaušelis) ir nespecifiškus (ausies skausmas, otorėja, niežėjimas, eritema ir klausomosios landos patinimas). Galimas kondukcinis klausos susilpnėjimas. Liga diagnozuojama remiantis klinikiniais požymiais ir klausomosios landos uždegimo simptomais. Svarbu atlikti otoskopiją ar klausomosios landos ir ausies būgnelio (jei vizualizuojasi) otomikroskopinį ištyrimą. Jei ausies būgnelis nesivizualizuoja, reikia atlikti atrankinius klausos testus ar audiologinį ištyrimą. Šie tyrimai atliekami diferencijuojant susirgimą nuo viduriniosios ausies uždegimo. Daugumai pacientų pakanka ambulatorinio gydymo. Kruopštus tualetas, valymas, sausumo palaikymas padeda užtikrinti tinkamą vietinio vartojimo medikamentų patekimą į tolimąją klausomosios landos dalį. Ausų lašai su antibiotikais yra pirmo pasirinkimo gydymas pacientams, sergantiems ūminiu išoriniu otitu. Kombinuota vietine antibiotikų ir gliukokortikosteroidų terapija gydomų pacientų simptomai mažėja viena diena greičiau, nei vien tik vietinio vartojimo antibiotikais gydomų asmenų. Skausmo gydymas yra svarbi gydymo dalis. Lengvo ir vidutinio sunkumo skausmui malšinti tinka paracetamolis ir geriamieji nesteroidiniai vaistai nuo uždegimo. Lašinti analgetikų nerekomenduojama, nes jų efektyvumas nepakankamas, jie galimai maskuoja būklės blogėjimą ar komplikacijų atsiradimą. Sisteminė antibiotikoterapija skiriama tik išskirtiniais atvejais ir tik po gydytojo otorinolaringologo ar gydytojo infektologo konsultacijos. Sunkesnės išorinio otito formos (furunkulas, piktybinis nekrozinis otitas, otomikozė, su dermatozėmis susijęs išorinis otitas) gydomos atsižvelgiant į jį sukėlusią priežastį, bendradarbiaujant su gydytoju otorinolaringologu.

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5

Mystakidou, MD, PhD, Kyriaki, Emmanuela Katsouda, MD, PhD, Vassilios Kouloulias, MD, PhD, John Kouvaris, MD, PhD, Marinos Tsiatas, MD, and Lambros Vlahos, MD, PhD. "Comparison of transdermal fentanyl with codeine/paracetamol, in combination with radiotherapy, for the management of metastatic bone pain." Journal of Opioid Management 1, no. 4 (September 1, 2005): 204. http://dx.doi.org/10.5055/jom.2005.0044.

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Radiotherapy (R/T) is frequently used for palliative treatment of painful bone metastases; however, complete alleviation of pain is not always achieved. This study was designed to evaluate pain management outcomes and quality of life (QoL) measures in cancer patients with metastatic bone pain receiving a combination of R/T and either transdermal therapeutic fentanyl (TTS-F) patches or codeine/paracetamol.A total of 460 palliative care patients with bone metastases who received R/T were enrolled in this prospective, open-label study. The patients were randomized to initially receive a total dose of 120 mg codeine/paracetamol per day or TTS-F patches releasing 25 μg fentanyl per hour. Pain measures were assessed on the basis of selected questions from the Greek-Brief Pain Inventory. Overall treatment satisfaction (scale, 1 to 4), QoL, and European Collaborative Oncology Group status were also recorded.Among the 460 patients, 422 were eligible for evaluation. Pain measures in the TTS-F group demonstrated statistically significant improvements during the study that were superior to those in the codeine/paracetamol group (p < 0.05). Likewise, there was a significantly greater increase (p < 0.05) in the mean satisfaction score for patients in TTS-F group at every visit between baseline and month two. The vast majority (95.8 percent) of patients in the codeine/paracetamol group increased their medication dosage until the end of the study, whereas in the TTS-F group the respective percentage was only 6.1. Both treatments were generally well tolerated, with constipation as the most common side effect followed by sleep disturbances and nausea. The overall frequencies of side effects were higher in the codeine/paracetamol group.The results therefore indicate that TTS-F offers more effective pain relief than codeine/paracetamol, in combination with R/T, in patients with metastatic bone pain, obtaining complete treatment satisfaction matched by improvements in their QoL.

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6

Kar, Ayan Kumar, and Banhishikha Kar. "In-Vitro Comparative Dissolution Study of Commercially Available Paracetamol Tablet." Journal of Drug Delivery and Therapeutics 10, no. 1 (January 15, 2020): 18–23. http://dx.doi.org/10.22270/jddt.v10i1.3817.

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Quality is the most important issue in the pharmaceutical field due to the presence of a drug which is considered as safe and therapeutically active agent. In-vitro evaluation ensures their quality, bioavailability as well as optimum therapeutic activity. Paracetamol (acetaminophen) which are the active metabolites of phenacetin is commonly used for the relief of headaches and pains, and is a major ingredient in numerous cold and flu remedies. Paracetamols are available in different brands in Indian market. The main objective of the present study was to conduct the comparative in-vitro dissolution studies of various brands collected from the local market to determine whether all the formulations used were equivalent or significantly different. The calibration curve was constructed covering the concentration range of 1 to 10 mcg/ml at 268 nm by UV spectrophotometer (UV 2203 Double beam spectrophotometer, Shimadzu). Five different brands of Paracetamol of 500 mg conventional tablets from different manufacturers were selected in the study and dissolution testing in Phosphate buffer at pH 7.4 was conducted from each brands for 90 mins by using dissolution testing apparatus USP type-II. The dissolution rate was subjected to various mathematical models like zero order, first order, Higuchi and Hixson-Crowell equations to elucidate the kinetic behavior of drug release from the test samples. Different release kinetics model of all the selected brands was assuring the quality standard of manufacturing. Keywords: Paracetamol, Marketed Tablet, In-Vitro dissolution study, Release profile.

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García García, AM, J. Cobos Rodríguez, AJ García Ferreira, and AJ García Cortés. "Acetaminophen acute hepatotoxicity." Revista Andaluza de Patología Digestiva 43, no. 2 (April 30, 2020): 68–75. http://dx.doi.org/10.37352/2020432.1.

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Resumen El paracetamol es el medicamento antipirético y analgésico más utilizado en el mundo. La lesión hepática debida a una sobredosis intencional o no de este fármaco es una situación común que los médicos deben tener en cuenta. La toxicidad que puede producir implica vías metabólicas que tienen lugar en los microsomas de los hepatocitos y puede manifestarse como una hipertransaminasemia asintomática o puede llegar a producir una insuficiencia hepática aguda. La clínica es variada y generalmente ocurre en cuatro fases secuenciales. Para establecer la necesidad de tratamiento con N-acetilcisteína se utiliza el nomograma Rumack-Mathew ya que puede reducir la progresión a un fallo hepático si se administra de manera precoz tras una sobredosis aguda. Sin embargo en algunos pacientes seleccionados puede ser necesario el trasplante hepático.

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8

&NA;. "Paracetamol see Dextropropoxyphene/paracetamol." Reactions Weekly &NA;, no. 350 (May 1991): 10. http://dx.doi.org/10.2165/00128415-199103500-00043.

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&NA;. "Paracetamol see Aspirin + paracetamol." Reactions Weekly &NA;, no. 360 (July 1991): 9. http://dx.doi.org/10.2165/00128415-199103600-00053.

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Aguilar, M. I., S. J. Hart, and I. C. Calder. "Complete separation of urinary metabolites of paracetamol and substituted paracetamols by reversed-phase ion-pair high-performance liquid chromatography." Journal of Chromatography B: Biomedical Sciences and Applications 426 (January 1988): 315–33. http://dx.doi.org/10.1016/s0378-4347(00)81959-3.

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Ortiz, Mario I., Gabriela Murguía-Cánovas, Laura C. Vargas-López, Rodolfo Silva, and Mario González-de la Parra. "Naproxen, paracetamol and pamabrom versus paracetamol, pyrilamine and pamabrom in primary dysmenorrhea: a randomized, double-blind clinical trial." Medwave 16, no. 09 (October 24, 2016): e6587-e6587. http://dx.doi.org/10.5867/medwave.2016.09.6587.

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Tomečková, Vladimíra, Alena Gajová, Beáta Veliká, Lýdia Saxunová, and Zdenka Hertelyová. "Prooxidative and fluorescence properties of paracetamol during interactions with mitochondria." Spectroscopy 25, no. 1 (2011): 45–51. http://dx.doi.org/10.1155/2011/174237.

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This study was carried out to investigate isolated liver mitochondrial functions after paracetamol administration by monitoring of liver mitochondrial fluorescence properties as well as prooxidative properties of paracetamol. Paracetamol was administered to rat (in subtoxic 500 mg·kg−1dose) invivo. The effect of this dose was compared with the subtoxic and toxic dose of paracetamol added to mitochondria invitro(1 and 1.5) mg paracetamol/mg mitochondrial protein. Subtoxic dose of paracetamol invitrodid not change mitochondrial fluorescence, but it significantly decreased mitochondrial fluorescence invivoin comparison with control mitochondrial group. Toxic dose of paracetamol invitrosignificantly decreased mitochondrial fluorescence. The enzymatic activity of superoxide dismutase (SOD) significantly decreased after paracetamol administration invitroand invivo. While both activities of glutathione peroxidase (GPx) and glutathione reductase (GR) significantly increased in dependence upon paracetamol doses. Our experiment showed, that paracetamol participates in formation of free radicals and confirms previous studies, in which paracetamol administration caused elevation of antioxidative enzymes activities in dependence on dose, which is considered therapeutically as subtoxic and toxic.

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&NA;. "Paracetamol see Phenobarbital + paracetamol poisoning." Reactions Weekly &NA;, no. 313 (August 1990): 7. http://dx.doi.org/10.2165/00128415-199003130-00033.

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&NA;. "Paracetamol see Dextropropoxyphene/paracetamol abuse." Reactions Weekly &NA;, no. 366 (August 1991): 8. http://dx.doi.org/10.2165/00128415-199103660-00035.

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Zhu, Yi Zhun, Chew Lan Chong, Shin Chet Chuah, Shan Hong Huang, Huey Shan Nai, How Teng Tong, Matt Whiteman, and Philip K. Moore. "Cardioprotective effects of nitroparacetamol and paracetamol in acute phase of myocardial infarction in experimental rats." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 2 (February 2006): H517—H524. http://dx.doi.org/10.1152/ajpheart.00572.2005.

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We aimed to determine whether nitroparacetamol (NO-paracetamol) and paracetamol exhibit cardioprotective effects. Myocardial infarction (MI) was induced in rats, and drug treatment was started 1 wk before surgery. Mortality rate and infarct size at 2 days after MI were compared. Treatment groups included vehicle (saline), paracetamol (5 mg·kg−1·day−1) and NO-paracetamol (15 mg·kg−1·day−1). Mortality rates for vehicle ( n = 80), paracetamol ( n = 79), and NO-paracetamol ( n = 76) groups were 37.5%, 21.5%, and 26.3%, respectively. Infarct size for the vehicle group was 44.8% (±6.1%) of the left ventricle (LV). For the paracetamol and NO-paracetamol groups, infarct size was 31.3% (±5.6%) and 30.7% (±8.1%) of the LV, respectively. Both paracetamol- and NO-paracetamol-treated groups showed increased activities of catalase and SOD compared with the vehicle group. They could attenuate endothelial, inducible, and neuronal nitric oxide synthase and cyclooxygenase-1 and -2 gene expression after MI. The observation indicates the potential clinical significance of the cardioprotective effects of these drugs.

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Walubo, A., S. Barr, A. M. Abraham, and C. Coetsee. "The role of cytochrome–P450 inhibitors in the prevention of hepatotoxicity after paracetamol overdose in rats." Human & Experimental Toxicology 23, no. 1 (January 2004): 49–54. http://dx.doi.org/10.1191/0960327104ht415oa.

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Despite the understanding that some cytochrome P450 isoforms are responsible for activation of paracetamol to the hepatotoxic metabolite, N–acetyl–p–benzoquinineimine (NAPQI), the use of enzyme inhibitors for prevention and/or treatment of paracetamol hepatotoxicity is still not well researched. Here, a mixture of ketoconazole, isoniazid and caffeine (inhibitor solution), known inhibitors of CYP3A, CYP2E1 and CYP1A2, was investigated for prevention of hepatotoxicity after paracetamol over–dose in rats. The appropriate doses of paracetamol (1000 mg/kg/day) and the ‘inhibitor solution’ (ketoconazole 5 mg/kg, isoniazid 5 mg/kg and caffeine 10 mg;kg;KIC–5–50), were selected in preliminary experiments. Thereafter, two groups of 15 male Sprague–Dawley rats each were treated with the toxic dose of paracetamol intraperitoneally to induce severe hepatotoxicity. But one of the two groups was treated with the KIC–5–50 intraperitoneally 5 min after administration of paracetamol. Five rats were killed at 24, 48 and 72 hours after paracetamol administration. Plasma concentrations of paracetamol were determined by the polarization fluorescent immunoassay and a piece of liver was sent for histopathology examination. Liver function tests at 48 hours were higher in the ‘paracetamol only’ treated group than in the ‘KIC–5–50+paracetamol’ treated group’ (P<0.05), i.e., median (range) AST 2025 (530–4329) g/mL for the ‘paracetamol only’ treated group versus 0.17 (0.07–0.33) μg/ml for the ‘KIC–5–50-paracetamol’ treated group. Centrilobular necrosis, the pathogmonomic feature of paracetamol hepatotoxicity, was demonstrated only in the ‘paracetamol only’ treated group. In conclusion, coadministration of paracetamol with inhibitors of cytochrome P450 prevented the development of paracetamol–induced hepatotoxicity in rats, and this calls for research for enzyme inhibitors that may be of therapeutic value.

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Yanuartono, Yanuartono, Alfarisa Nururrozi, Soedarmanto Indarjulianto, Slamet Raharjo, Hary Purnamaningsih, and Nurman Haribowo. "Keracunan Parasetamol Pada Kucing Dan Anjing: Gejala Klinis dan Terapi." Jurnal Ilmu Peternakan dan Veteriner Tropis (Journal of Tropical Animal and Veterinary Science) 10, no. 1 (May 5, 2020): 55. http://dx.doi.org/10.46549/jipvet.v10i1.86.

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Acetaminophen, commonly known as paracetamol, is a non-steroidal anti-inflammatory drug commonly used in human medicine for its antipyretic and analgesic action. As paracetamol became readily available in many over-the-counter and no-prescription products, reports of paracetamol poisoning in dogs and cats became more common. The toxicity of paracetamol is more pronounced in cats when compared to dogs. Clinical signs of paracetamol toxicity include depression, weakness, tachypnea, dyspnea, vomiting, hypothermia, facial or paw edema, hepatic necrosis, and death. The characteristics of severe paracetamol poisoning are methemoglobinemia, cyanosis, anemia, and jaundice. Although there are no specific antidotes, acetylcysteine is the drug of choice for paracetamol poisoning treatment. Symptomatic and supportive therapies play a more definitive role in the management of paracetamol poisoning. This paper aims to briefly review the clinical symptoms, diagnosis, and treatment of paracetamol poisoning in dogs and cats.

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kulkarni, Dr Sameer. "Acute Paracetamol Toxicity - A Case Report." Indian Journal of Applied Research 3, no. 12 (October 1, 2011): 466–68. http://dx.doi.org/10.15373/2249555x/dec2013/142.

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Karmakar, Palash, and Md Golam Kibria. "In-vitro comparative evaluation of quality control parameters between paracetamol and paracetamol/caffeine tablets available in Bangladesh." International Current Pharmaceutical Journal 1, no. 5 (April 7, 2012): 103–9. http://dx.doi.org/10.3329/icpj.v1i5.10282.

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Paracetamol is a widely used non-prescription analgesic and antipyretic medicine. The study was conducted to assess the comparative in-vitro quality control parameters through the evaluation of weight variation, hardness, friability, disintegration time and dissolution profile between the commercially available tablet brands of paraceta-mol and paracetamol/caffeine combination in Bangladesh. Tablets of five top level manufacturers those have both of the formulations were evaluated in two groups. Both similarities and dissimilarities were found between the groups. All tablets either paracetamol (1.07 to 2.14%) or paracetamol/caffeine (0.98 to 2.09%) showed acceptable weight variation and friability (below 1%). Formulations were somewhat different in their hardness, disintegration time and dissolution profile. All tablets of paracetamol/caffeine were found harder than paracetamol tablets of the same manufacturer. 1 out of 5 for paracetamol and 3 out of 5 for paracetamol/caffeine tablets exceeded the limit of tablet hardness or crushing strength. The disintegration time in 0.1N HCl of paracetamol tablet brands (24 seconds to 4 minutes 52 seconds) were less than the paracetamol/caffeine (6 minutes 33 seconds to 17 minutes 43 seconds) brands. On the other hand in phosphate buffer, pH 7.4, paracetamol/caffeine tablets dissolved quickly and showed better release profile than tablets containing only paracetamol. It can be concluded that standard quality control parameters always should be maintained not only for paracetamol or its combination but also for all kinds of medicine for getting better drug products.DOI: http://dx.doi.org/10.3329/icpj.v1i5.10282International Current Pharmaceutical Journal 2012, 1(5): 103-109

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Radosavljevic, Tatjana, Dusan Mladenovic, Danijela Vucevic, and Rada Jesic-Vukicevic. "The role of oxidative/nitrosative stress in pathogenesis of paracetamol-induced toxic hepatitis." Medical review 63, no. 11-12 (2010): 827–32. http://dx.doi.org/10.2298/mpns1012827r.

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Introduction. Paracetamol is an effective analgesic/antipyretic drug when used at therapeutic doses. However, the overdose of paracetamol can cause severe liver injury and liver necrosis. The mechanism of paracetamol-induced liver injury is still not completely understood. Reactive metabolite formation, depletion of glutathione and alkylation of proteins are the triggers of inhibition of mitochondrial respiration, adenosine triphosphate depletion and mitochondrial oxidant stress leading to hepatocellular necrosis. Role of oxidative stress in paracetamol-induced liver injury. The importance of oxidative stress in paracetamol hepatotoxicity is controversial. Paracetamol induced liver injury cause the formation of reactive oxygen species. The potent sources of reactive oxygen are mitochondria, neutrophils, Kupffer cells and the enzyme xatnine oxidase. Free radicals lead to lipid peroxidation, enzymatic inactivation and protein oxidation. Role of mitochondria in paracetamol-induced oxidative stress. The production of mitochondrial reactive oxygen species is increased, and the glutathione content is decreased in paracetamol overdose. Oxidative stress in mitochondria leads to mito?chondrial dysfunction with adenosine triphosphate depletion, increase mitochondrial permeability transition, deoxyribonu?cleic acid fragmentation which contribute to the development of hepatocellular necrosis in the liver after paracetamol overdose. Role of Kupffer cells in paracetamol-induced liver injury. Paracetamol activates Kupffer cells, which then release numerous cytokines and signalling molecules, including nitric oxide and superoxide. Kupffer cells are important in peroxynitrite formation. On the other hand, the activated Kupffer cells release anti-inflammatory cytokines. Role of neutrophils in paracetamol-induced liver injury. Paracetamol-induced liver injury leads to the accumulation of neutrophils, which release lysosomal enzymes and generate superoxide anion radicals through the enzyme nicotinamide adenine dinucleotide phosphate oxidase. Hydrogen peroxide, which is influenced by the neutrophil-derived enzyme myeloperoxidase, generates hypochlorus acid as a potent oxidant. Role of peroxynitrite in paracetamol-induced oxidative stress. Superoxide can react with nitric oxide to form peroxynitrite, as a potent oxidant. Nitrotyrosine is formed by the reaction of tyrosine with peroxynitrite in paracetamol hepatotoxicity. Conclusion. Overdose of paracetamol may produce severe liver injury with hepatocellular necrosis. The most important mechanisms of cell injury are metabolic activation of paracetamol, glutathione depletion, alkylation of proteins, especially mitochondrial proteins, and formation of reactive oxygen/nitrogen species.

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Roberts, I., R. J. Flanagan, J. Strang, and L. F. Prescott. "Toxicological Studies in a Distalgesic Addict." Human Toxicology 5, no. 3 (May 1986): 207–10. http://dx.doi.org/10.1177/096032718600500310.

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1 The disposition and kinetics of paracetamol, dextropropoxyphene and their metabolites were investigated in an addict who claimed to be taking 80–100 Distalgesic tablets daily regularly. 2 Plasma concentrations of paracetamol, dextropropoxyphene and their principal metabolites were measured after an oral dose of 15 Distalgesic tablets. 3 The absorption of paracetamol and dextropropoxyphene was rapid with peak plasma concentrations at 15 and 30 min respectively. The elimination half-life for paracetamol was 2.3 h. Nordextropropoxyphene remained at steady state with very high plasma concentrations (5 mg/l). The urinary excretion of paracetamol and metabolites was not abnormal. The total recovery of paracetamol was only 31% of the dose. 4 Apart from raised plasma γ-glutamyltransferase activity there was no biochemical evidence for paracetamol-induced hepatocellular damage despite ingestion of 97.5 g of paracetamol over the 11 days of the withdrawal period.

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Bhowmik, Mithun Chandro, Mir Misbahuddin, and Habiba Akhter Bhuiyan. "Estimation of paracetamol in urine to assess the diurnal variation." Bangabandhu Sheikh Mujib Medical University Journal 11, no. 2 (May 30, 2018): 193. http://dx.doi.org/10.3329/bsmmuj.v11i2.36780.

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<p class="Abstract">The aim of the present study was to evaluate the diurnal variation of the pharmacokinetics of paracetamol by estimating the urinary free paracetamol level after single oral administration of paracetamol (500 mg) tablet to 24 healthy male volunteers (students of a Medical College). The volunteers were given paracetamol tablet at 0800, 1400 and 2000 hours in three different days (two weeks apart) and the urine samples of the volunteers were collected at just before and four hours after paracetamol administration. The samples were analyzed for free paracetamol using HPLC. The mean age was 21.1 ± 1.3 years and the body weight was 63.9 ± 10.9 kg. Three peaks were detected in the HPLC and one of them was identified for free paracetamol (RT= 4.7 min). The urine volume was nearly similar in all three times. After administration at 0800 hour, total free paracetamol excretion was significantly more than at 1400 and 2000 hours (p<0.001). The present study indicates that the dose reduction of paracetamol is required at morning than the afternoon or evening dose. </p>

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Manu, B., and S. Mahamood. "Enhanced degradation of paracetamol by UV-C supported photo-Fenton process over Fenton oxidation." Water Science and Technology 64, no. 12 (December 1, 2011): 2433–38. http://dx.doi.org/10.2166/wst.2011.804.

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For the treatment of paracetamol in water, the UV-C Fenton oxidation process and classic Fenton oxidation have been found to be the most effective. Paracetamol reduction and chemical oxygen demand (COD) removal are measured as the objective functions to be maximized. The experimental conditions of the degradation of paracetamol are optimized by the Fenton process. Influent pH 3, initial H2O2 dosage 60 mg/L, [H2O2]/[Fe2+] ratio 60 : 1 are the optimum conditions observed for 20 mg/L initial paracetamol concentration. At the optimum conditions, for 20 mg/L of initial paracetamol concentration, 82% paracetamol reduction and 68% COD removal by Fenton oxidation, and 91% paracetamol reduction and 82% COD removal by UV-C Fenton process are observed in a 120 min reaction time. By HPLC analysis, 100% removal of paracetamol is observed at the above optimum conditions for the Fenton process in 240 min and for the UV-C photo-Fenton process in 120 min. The methods are effective and they may be used in the paracetamol industry.

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Surbakti, Christica Ilsana. "the PENGARUH PEMBERIAN SIMETIDIN TERHADAP PROFIL FARMAKOKINETIKA PARASETAMOL DENGAN METODE HIGH PERFORMANCE LIQUID CHROMATOGRAPHY (HPLC) TAHUN 2020." Jurnal Penelitian Farmasi & Herbal 3, no. 1 (October 31, 2020): 122–29. http://dx.doi.org/10.36656/jpfh.v3i1.362.

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Paracetamol is a safe analgesic and antipyretic drug with low side effects, effective and well tolerated. In some cases there is a drug interaction between paracetamol and other drugs. The purpose of this study is to determine the effect of cimetidine administration on paracetamol pharmacokinetic profiles. The method used in this study was an experimental method using 3 rabbits. Rabbits are divided into 3 groups. The first treatment group was given paracetamol suspension, the second treatment group was giving cimetidine 1 hour before paracetamol and the third group was giving cimetidine and paracetamol simultaneously. The dose of the drug has been adjusted to each rabbit. Measurement of plasma paracetamol drug levels was carried out using a High Performance Liquid Chromatography (HPLC) tool. The results of the study showed that the pharmacokinetic parameter values did not show any significant effect on each group. Cimetidine administration simultaneously affects paracetamol pharmacokinetic parameters but not significantly. Likewise with the administration with a time span of 1 hour, did not show any significant changes in the pharmacokinetics of paracetamol.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1204 (May 2008): 25. http://dx.doi.org/10.2165/00128415-200812040-00083.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1218 (September 2008): 25. http://dx.doi.org/10.2165/00128415-200812180-00080.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1011 (July 2004): 12. http://dx.doi.org/10.2165/00128415-200410110-00032.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1323 (October 2010): 30. http://dx.doi.org/10.2165/00128415-201013230-00102.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1283 (January 2010): 73. http://dx.doi.org/10.2165/00128415-201012830-00234.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1261 (July 2009): 23. http://dx.doi.org/10.2165/00128415-200912610-00077.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1263 (August 2009): 26. http://dx.doi.org/10.2165/00128415-200912630-00082.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1267 (August 2009): 25. http://dx.doi.org/10.2165/00128415-200912670-00075.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1279 (November 2009): 27. http://dx.doi.org/10.2165/00128415-200912790-00077.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1309 (July 2010): 33. http://dx.doi.org/10.2165/00128415-201013090-00109.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1313 (August 2010): 34. http://dx.doi.org/10.2165/00128415-201013130-00119.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 438 (February 1993): 11. http://dx.doi.org/10.2165/00128415-199304380-00044.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 455 (June 1993): 11. http://dx.doi.org/10.2165/00128415-199304550-00049.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 461 (July 1993): 10. http://dx.doi.org/10.2165/00128415-199304610-00054.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 429 (November 1992): 11. http://dx.doi.org/10.2165/00128415-199204290-00058.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 284 (January 1990): 10. http://dx.doi.org/10.2165/00128415-199002840-00048.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1088 (February 2006): 17. http://dx.doi.org/10.2165/00128415-200610880-00053.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1095 (April 2006): 22. http://dx.doi.org/10.2165/00128415-200610950-00074.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1102 (May 2006): 12. http://dx.doi.org/10.2165/00128415-200611020-00037.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1111 (July 2006): 17. http://dx.doi.org/10.2165/00128415-200611110-00055.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 778 (November 1999): 11. http://dx.doi.org/10.2165/00128415-199907780-00035.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 794 (March 2000): 9. http://dx.doi.org/10.2165/00128415-200007940-00025.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 847 (April 2001): 7–8. http://dx.doi.org/10.2165/00128415-200108470-00021.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1025 (October 2004): 12. http://dx.doi.org/10.2165/00128415-200410250-00034.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1057 (June 2005): 16. http://dx.doi.org/10.2165/00128415-200510570-00049.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1067 (September 2005): 11. http://dx.doi.org/10.2165/00128415-200510670-00026.

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