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Journal articles on the topic 'Paracetamolo'

Author: Grafiati

Published: 10 March 2023

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1

Rossi, A., D. Palombo, V. Capilupi, and M. Chiapasco. "Pancreatite acuta secondaria a somministrazione di paracetamolo e codeina dopo trattamento odontoiatrico. Analisi della letteratura e caso clinico." Dental Cadmos 84, no. 5 (May 2016): 304–12. http://dx.doi.org/10.1016/s0011-8524(16)30065-4.

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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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3

Coman, Laurențiu, Horia Păunescu, Cristina Isabel Viorica Ghiță, Radu Ciprian Țincu, Sorina Vasile, Delia Cinteza, Ion Fulga, and Oana Andreia Coman. "Paracetamol-Induced Hypothermia in Rodents: A Review on Pharmacodynamics." Processes 10, no. 4 (March 31, 2022): 687. http://dx.doi.org/10.3390/pr10040687.

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Paracetamol can induce hypothermia in humans and rodents. The study’s aim is to review the mechanisms of paracetamol-induced hypothermia in rodents or the results issued from in vitro studies on the same species’ tissues (in doses that do not produce hepatic impairment) using the latest developments published in scientific journals over the last 15 years. Available human studies are also analysed. An extensive search in PubMed databases exploring the hypothermic response to paracetamol was conducted. 4669 articles about paracetamol’s effects on body temperature in mice or rats were found. After applying additional filters, 20 articles were selected for review, with 9 of them presented in tabular forms. The analysis of these articles found that the hypothermic effect of paracetamol is due to the inhibition of a cyclooxygenase-1 variant, is potentiated by endothelin receptor antagonists, and can be mediated through GABAA receptors and possibly through transient receptor potential cation channel subfamily A member 1 via N-acetyl-p-benzoquinone imine in the central nervous system. Human studies confirm the in vivo and in vitro experiments in rodents regarding the presence of a hypothermic effect after high, non-toxic doses of paracetamol. Further research is required to understand the mechanisms behind paracetamol’s hypothermic effect in humans.

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4

Begum, Shaheen, Poojitha Harisree G, and Rashida Anjum M S. "A Short Review on Biological Activities of Paracetamol Derivatives." International Journal of Pharmaceutical Sciences and Nanotechnology(IJPSN) 16, no. 1 (February 13, 2023): 6309–25. http://dx.doi.org/10.37285/ijpsn.2023.16.1.5.

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Paracetamol reduces body temperature with multiple mechanisms. Paracetamol is chemically 4-hydroxy acetanilide and has a good safety profile. Following its successful use as an over-the-counter antipyretic and analgesic medication, several attempts were made to increase the potency, mask the bitter taste, and decrease the toxicity of this drug by modifications at the phenyl ring, acetamido group, and hydroxyl group. The free hydroxyl group of paracetamols was masked to obtain prodrugs (carbonate prodrugs, ester prodrugs like alanine-prodrug, proline-prodrug, galactosylated prodrug, and mutual prodrugs with other drugs and NSAIDs). Propacetamol is a commercially available prodrug derived from paracetamol that is effective in parenteral form. Paracetamol ester prodrugs with sulfur-containing amino acids such as N-acetyl cysteine, cysteine, and methionine showed low hepatotoxicity compared to the parent drug. In addition, paracetamol derivatives including metal complexes, chalcones, Mannich bases, nucleoside analogs, hybrids with the aryl-imidazolidinyl ring, thymol, and triazole ring displayed diverse activities like antioxidant, anticancer, and antimicrobial activities.

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5

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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6

Hamed Almurisi, Samah, Khater AL-Japairai, Farhan Alshammari, Fawaz Alheibshy, Rana M. F. Sammour, and Abd Almonem Doolaanea. "Stability of Paracetamol Instant Jelly for Reconstitution: Impact of Packaging, Temperature and Humidity." Gels 8, no. 3 (February 25, 2022): 144. http://dx.doi.org/10.3390/gels8030144.

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The stability of the medicinal product is a major concern in the pharmaceutical industry and health authorities, whose goal is to guarantee that drugs are delivered to patients without loss of therapeutic properties. This study aims to evaluate the effect of environmental conditions and packaging on the stability of paracetamol instant jelly sachets based on both chemical and physical stability. The paracetamol instant jelly was packaged in plastic sachets (packaging 1) and sealed aluminium bags in screw-capped amber glass bottles (packaging 2), which were stored in real-time and accelerated stability chambers for 3 months. Samples were taken out from the chambers and were characterised for appearance, moisture content, texture, viscosity, in vitro drug release, paracetamol content, and 4-aminophenol level at different time points. The real-time storage condition at a lower temperature maintained the stability of the paracetamol instant jelly, while the accelerated condition led to a significant change in the formulation properties. In addition, the proper packaging of paracetamol instant jelly maintained the paracetamol’s stability, regardless of environmental conditions, for three months. The results show that the environmental conditions and packaging play a significant role in maintaining paracetamol instant jelly stability.

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7

Mohamed, Ashma, Alexa Wacker, and Martin Schmidt. "Chronic Misuse of Paracetamol in OCD Without Hepatic Injury: A Case Report and Literature Review." BJPsych Open 8, S1 (June 2022): S123. http://dx.doi.org/10.1192/bjo.2022.364.

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AimsParacetamol is a commonly used antipyretic and analgesic over the counter medication. In acute or chronic overuse it is associated with dose-dependent hepatic injury. There is a narrow therapeutic margin and that consistent use of as little as 7.5 g/day may be hazardous. Unintentional overdose with paracetamol is the most common cause of acute liver failure in the United Kingdom Here we present an unusual case of a 60-year-old lady with a reported chronic history of self-medicating with an above daily recommended dose of paracetamol without evidence of hepatic injury.MethodsA 60-year-old Caucasian lady known to psychiatric services for 20 years with Recurrent Depressive disorder, Obsessive Compulsive Disorder (OCD), Dependent Personality Disorder with Borderline personality traits. She reported consuming 32 tablets of paracetamol (16gm per day) every day for the past 11 years. She experienced obsessions of fear that if she did not take a particular number of paracetamols in a day then her friends will come to harm and her anxiety was relieved by the compulsion of consuming supratherapeutic doses of paracetamol. There was no evidence of misuse of any other medications other than paracetamol. Her blood investigations revealed liver function tests within normal limits and ultrasound of the liver was unremarkable.ResultsA literature search of “paracetamol or acetaminophen” and “no liver or hepatic” and “damage or injury” found only one case report. The case reported that studies of paracetamol metabolism were performed in a 58-year-old female with rheumatoid arthritis who had consumed 15–20 g paracetamol daily for 5 years without developing liver damage and data were compared with results in seven normal volunteers. The report concluded that a combination of slow paracetamol absorption, enhanced detoxication of paracetamol (by sulphation) and reduced metabolism to potentially cytotoxic metabolites may have reduced the risk of liver damage in this patient.ConclusionIn OCD, misusing medications can be an uncommon presentation of compulsive acts to relieve anxiety. The diagnostic dilemma of factitious illness is probable, however supratherapeutic use of paracetamol without physical harm is rare but possible.

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Amirul Fauziah, Dewi rashati,. "PENGARUH VARIASI KONSENTRASI AMILUM Zea mays (L) SEBAGAI BAHAN PENGHANCUR SECARA GRANULASI BASAH TERHADAP SIFAT FISIK TABLET PARASETAMOL." JURNAL ILMIAH FARMASI AKADEMI FARMASI JEMBER 2, no. 1 (January 28, 2021): 1–6. http://dx.doi.org/10.53864/jifakfar.v2i1.15.

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This research is aims to determine the effect of variation concentration starch Zea mays (L) as disintegration agent in wet granulation to physical characteristics paracetamo. This research used eperimental method by one shot case study. Paracetamol as active ingredient, starch zea mays (L)as desintegrant agent, PVPK30 as binding agent, avicel as filler and Mg stearat as lubricants. The result of SPSS showed significant (p0,05), that means no difference in the three formulation. The first test is weight uniformity show that from column A and B qualify weight requirement range, hardness test. Showed significant (p0,05) that means nodifference in the three formulation. Friability test showed significant (p 0,05) the last is disintegration time test showed that significant (P0,05) no difference in the three formulation. The research of physic characteristic of the tablet showed that hardness test and time test not qualif. Analysis SPSS showed (p0,05) no difference in the three formulation and amilum had no effect on physical test of paracetamol tablet.Keywords: zea mays (L),paracetamol,physicial characteristic

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9

Rahimi, Omid, Nilufar Asadi Louie, Alireza Salehi, and Firouz Faed Maleki. "Hepatorenal Protective Effects of Hydroalcoholic Extract of Solidago canadensis L. against Paracetamol-Induced Toxicity in Mice." Journal of Toxicology 2022 (December 17, 2022): 1–11. http://dx.doi.org/10.1155/2022/9091605.

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Paracetamol (AKA acetaminophen) is a widely used drug and is used for mild to moderate pains, such as mild osteoarthritis, toothache, headache, and pain caused by minimally invasive surgeries. Despite being a harmless drug in lower doses, acetaminophen can be toxic to the liver and kidneys if overdosed and even results in death. In this study, the therapeutic effects of Solidago canadensis L. extract (SCE) were investigated. 48 adult male Swiss albino mice (20–30 grams) were randomly divided into six groups of 8. The control group was gavaged with normal saline every 12 hours for 6 days. The second group received paracetamol at a 500 mg/kg intraperitoneally (i.p) dose on the sixth day. The third, fourth, and fifth groups were gavaged doses of 125, 250, and 500 mg/kg of SCE every 12 hours for six days, respectively, and on the sixth day, we received paracetamol at a dose of 500 mg/kg i.p. The sixth group only received SCE every 12 hours at a dose of 1000 mg/kg via gavaging for six days. On the seventh day (24 hours after paracetamol injection), blood samples were collected to measure the serum level of creatinine, uric acid, blood urea nitrogen (BUN), total protein, albumin, alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), and total and direct bilirubin, and liver and kidney tissues were also sampled for histopathological examination. It was observed that paracetamol caused a considerable increase in the ALT, AST, ALP, uric Acid, and BUN levels ( P < 0.01 ), while those in SCE-treated groups were significantly lower. In addition, various lesions in the paracetamol group were observed, while in the SCE-receiving groups, receiving prophylactic SCE inhibited the high-intense lesions such as the infiltration of inflammatory cells, hyperemia, and vacuolar degeneration, which decreased significantly in the control group in comparison with that of the paracetamol group ( P < 0.05 ). In conclusion, SCE can have substantial protective effects against paracetamol’s hepatorenal toxicity.

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10

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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11

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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Mészáros, Petra, Sára Kovács, Győző Kulcsár, Melinda Páskuj, and Attila Almási. "Investigation of Intestinal Absorption and Excretion of Paracetamol in Streptozotocin-Induced Hyperglycemia." International Journal of Molecular Sciences 23, no. 19 (October 7, 2022): 11913. http://dx.doi.org/10.3390/ijms231911913.

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The phenolic drug molecules can be metabolized, among others, by the small intestine’s enterocytes. The conjugation reactions (glucuronidation and sulfation) show great importance in these transformations, although the oxidation reactions can be significant. These processes are dependent on the substituents of the phenolic compounds or the reacting functional groups (hydroxyl or carboxyl). Pathologic conditions, e.g., permanent hyperglycemia and diabetes, can alter the activities of the conjugative and possibly the oxidative enzymes, thus forming a change in the metabolic pattern and eventually provoking oxidative stress. A rat intestinal perfusion model was used to investigate the way in which experimental hyperglycemia affects the paracetamol’s intestinal elimination and metabolism. Hyperglycemia was induced by the administration of streptozotocin. Two hundred and fifty µM paracetamol was used in the intestinal perfusion solution. For the quantitation of the paracetamol and its major metabolites in the intestinal perfusate, an isocratic high-performance liquid chromatography method with UV-Vis detection was developed. The results revealed that quantities of all of the measured metabolites (glucuronide, sulfate, cysteine, and mercapturic acid conjugates) increased as the effect of the streptozotocin-induced hyperglycemia also did. In the small intestine’s homogenate, the glutathione levels showed that there was a decrease in the hyperglycemia levels after the paracetamol administration. In contrast, the tissue levels of the cysteine were lower in the streptozotocin-induced hyperglycemia and increased after the administration of the paracetamol. The changes in the activity of the intestinal CYP 3A4, CYP 2E1, and cyclooxygenase (COX) enzymes were determined in the control and the hyperglycemic cases. Still, there was a significant observable enzyme activity elevation in the intestinal COX enzymes, but there was a decrease in the amount of activity of the intestinal CYP3A4 enzymes, and the CYP2E1 enzyme activity was practically changeless. The results on the cysteine levels in the intestinal homogenate, at least partly, can be explained by the regulation function of the cysteine during the occurrence of oxidative stress.

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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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14

&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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&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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&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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18

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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19

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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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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21

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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22

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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Sudarma, Nyoman, and I. Putu Gede Subhaktiyasa. "Analisis kadar paracetamol pada darah dan serum SIS KADAR PARACETAMOL PADA DARAH DAN SERUM." Bali Medika Jurnal 8, no. 3 (November 21, 2021): 285–93. http://dx.doi.org/10.36376/bmj.v8i3.177.

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Paracetamol merupakan golongan obat analgesik yaitu penahan rasa sakit/nyeri dengan cara kerja menghambat sintesis prostaglandin terutama di sistem saraf pusat. Paracetamol yang diberikan secara oral akan diserap cepat dan mencapai kadar serum puncak dalam waktu 30-120 menit. Tujuan penelitian ini adalah untuk mengetahui kadar paracetamol pada darah dan serum. Sampel yang digunakan adalah sampel darah dan serum dari responden yang mengkonsumsi obat paracetamol 500 mg. Sampel darah diambil 2 jam setelah mengkonsumsi obat paracetamol. Untuk mendapatkan serum, darah harus dilakukan proses sentrifugasi, dengan proses sentrifugasi zat-zat pengganggu dalam darah dapat diminimalkan. Analisis kadar paracetamol pada darah dan serum secara kualiatif dianalisis menggunakan kromatografi gas-spektrometri massa (GC-MS). Ekstraksi paracetamol pada sampel darah dan serum menggunakan metode Solid Phase Extraction (SPE). Hasil ekstraksi diderivatisasi menggunakan BSTFA yang mengandung TMCS 1% dan dianalisis menggunakan kromatografi gas-spektrometri massa (GC-MS). Analisis kuantitatif dilakukan dengan menghitung kadar paracetamol menggunakan rumus persaaman garis regresi y = 50207x + 56321.Hasil penelitian ini menunjukkan bahwa sampel darah dan serum menunjukkan positif paracetamol pada retention time 15.056 dan 15.101. Kadar paracetamol pada sampel darah yaitu 175,2 ppm dan kadar paracetamol pada sampel serum yaitu 56,7 ppm.

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KALTALIOĞLU, Kaan. "Prunus laurocerasus L. extracts prevent paracetamol-induced nephrotoxicity by regulating antioxidant status: an experimental animal model." Hittite Journal of Science and Engineering 9, no. 4 (December 31, 2022): 275–80. http://dx.doi.org/10.17350/hjse19030000280.

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Paracetamol is a popular analgesic drug and its overdose may cause toxicity in the kidney. Prunus laurocerasus L. (PL) is an important folklore medicinal plant that has antioxidant properties. This study explores effects of PL fruit water and ethanol-water extracts administrations on oxidative stress in paracetamol-induced nephrotoxicity. For this purpose, 30 rats were divided into 5 groups: control, negative control (2 g/kg paracetamol), PL fruit water extract (400 mg/kg PLW+ 2 g/kg paracetamol), PL fruit ethanol-water extract (400 mg/kg PLEW+ 2 g/kg paracetamol) and positive control (150 mg/kg NAC+ 2 g/kg paracetamol). 24 hours after the paracetamol induction, animals were sacrificed and oxidative parameters were analyzed spectrophotometrically in kidney tissue. PLW and PLEW extracts decreased MDA and NOx levels and increased SOD and CAT activities in paracetamol-induced nephrotoxicity. PL fruit extracts can restore the oxidative changes caused by paracetamol.

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Yeh, Kuan-Lin, Hung-Lin Lee, and Tu Lee. "Crystallization of Form II Paracetamol with the Assistance of Carboxylic Acids toward Batch and Continuous Processes." Pharmaceutics 14, no. 5 (May 20, 2022): 1099. http://dx.doi.org/10.3390/pharmaceutics14051099.

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Form II paracetamol has captured the interest of researchers due to its improved compressibility. However, its low stability has made it difficult to be produced on a large scale with good reproducibility. In the present study, the selective polymorphic formation of paracetamol was carried out by cooling crystallization with four types of additives: adipic acid, fumaric acid, oxalic acid, and succinic acid. It was found that: (1) the more additives that were added, the higher the probability of forming Form II paracetamol; (2) Form II paracetamol could be induced by seeding the paracetamol aqueous solution with Form II paracetamol and fumaric acid crystals, and not the other three carboxylic acids; (3) a new solution complex of paracetamol–oxalic acid, evidenced by the solubility diagram, was responsible for the selective nucleation of Form II paracetamol in the oxalic acid aqueous solution; and (4) the range of the degree of supersaturation for nucleating Form II paracetamol was extended with the assistance of oxalic acid or fumaric acid. In large-scale crystallization, Form II paracetamol was produced by the continuous crystallization of 44 mg of paracetamol/mL in 50 wt% of fumaric acid aqueous solution with a flow rate of 150 mL/min.

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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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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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Ali, Imran, Nadir Nazir, Muhammad Arshed, Ali Asgher, Arif Iftikhar, and Aqil Qayoom. "A Comparison of Mean Time to Request for First Analgesia Post-Operatively in Functional Endoscopic Sinus Surgeries (Fess) by Using Pre-Emptive Paracetamol Versus Intraoperative Paracetamol." Pakistan Journal of Medical and Health Sciences 16, no. 1 (January 30, 2022): 608–11. http://dx.doi.org/10.53350/pjmhs22161608.

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Objective: To compare mean time required to request for first analgesia post-operatively in functional endoscopic sinus surgeries (FESS) by using pre-emptive paracetamol versus intra-operative paracetamol. Study Design: Comparative Observational Study. Sampling Technique: Non probable, consecutive sampling Place & Duartion: This Study was conducted in the Department of Anesthesiology, Sindh employee’s social security hospital landhi Karachi, From June, 2018 to January, 2019. Materials and Methods: In this study 64 patients of both genders included. 36 patients were male and 28 were females. They were aged between 18 and 70 years. This study was conducted from June, 2018 to January, 2019. Patients were distributed into two different groups, Group-1 (pre-emptive paracetamol) and Group-2 (intra-operative paracetamol). 32 patients were included in each group. In Group-1 (pre-emptive paracetamol), patients received 1 Gm. I/V paracetamol, 15 minutes prior to induction of general anesthesia and in Group-2 (intra-operative paracetamol), patients received 1gm. I/V paracetamol just before removal of endotracheal tube. Post-operatively patients were observed in Post-Anesthesia Care Unit (PACU) with standard monitoring. Time for first request for analgesia in minutes was noted. Result: SPSS 16 version used for statistical analysis. Chi squire test applied. Mean age of in pre-emptive paracetamol group (group-1) was 51.53 + 18.90 years and mean age of patients in intra-operative paracetamol group, was 50.43 + 19.10 years (p-value 0.819). Mean weight of patients in pre-emptive paracetamol was 66.65 + 10.74 kg and mean weight of the patients in intra-operative paracetamol was 67.71 + 10.78 kg. (P-value was 0.694). ASA status 1 was found in 36 (56.30%) patients and ASA status II was found in 28 (43.80%) patients. Mean time required for first analgesia in pre-emptive paracetamol group was 192.90 + 8.70 minutes and mean time required for first analgesia in intra-operative paracetamol group was 163.93 + 13.57 minutes and p-value found < 0.001 (significant). Conclusion: Significant variance was observed in the mean time required to request for first analgesia post-operatively in functional endoscopic sinus surgeries (FESS) by using pre-emptive paracetamol versus intra-operative paracetamol. Keywords: pre-emptive versus intraoperative paracetamol, functional endoscopic sinus surgeries, time required to request for first analgesia post-operatively.

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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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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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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1377 (November 2011): 29–30. http://dx.doi.org/10.2165/00128415-201113770-00098.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 700 (May 1998): 10. http://dx.doi.org/10.2165/00128415-199807000-00033.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 738 (February 1999): 10. http://dx.doi.org/10.2165/00128415-199907380-00028.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 741 (March 1999): 12. http://dx.doi.org/10.2165/00128415-199907410-00044.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1174 (October 2007): 22–23. http://dx.doi.org/10.2165/00128415-200711740-00065.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1184 (January 2008): 29. http://dx.doi.org/10.2165/00128415-200811840-00089.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1187 (February 2008): 22–23. http://dx.doi.org/10.2165/00128415-200811870-00072.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1194-1195 (March 2008): 29. http://dx.doi.org/10.2165/00128415-200811940-00106.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1133 (January 2007): 20–21. http://dx.doi.org/10.2165/00128415-200711330-00072.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1134 (January 2007): 21. http://dx.doi.org/10.2165/00128415-200711340-00071.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1139 (February 2007): 18. http://dx.doi.org/10.2165/00128415-200711390-00056.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1143 (March 2007): 20. http://dx.doi.org/10.2165/00128415-200711430-00067.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1148 (April 2007): 27. http://dx.doi.org/10.2165/00128415-200711480-00086.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1149 (April 2007): 20. http://dx.doi.org/10.2165/00128415-200711490-00063.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1149 (April 2007): 21. http://dx.doi.org/10.2165/00128415-200711490-00064.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1155 (June 2007): 14–15. http://dx.doi.org/10.2165/00128415-200711550-00041.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1156 (June 2007): 20–21. http://dx.doi.org/10.2165/00128415-200711560-00063.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1357 (June 2011): 27. http://dx.doi.org/10.2165/00128415-201113570-00088.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1359 (July 2011): 30. http://dx.doi.org/10.2165/00128415-201113590-00118.

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&NA;. "Paracetamol." Reactions Weekly &NA;, no. 1361 (July 2011): 32. http://dx.doi.org/10.2165/00128415-201113610-00117.

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