Gotowe bibliografie tematyczne / Toxic hepatitis

Gotowa bibliografia na temat „Toxic hepatitis”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 31 stycznia 2023

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Artykuły w czasopismach na temat "Toxic hepatitis"

Peker, Erdal, Eren Cagan i Murat Dogan. "Ceftriaxone-induced toxic hepatitis". World Journal of Gastroenterology 15, nr 21 (2009): 2669. http://dx.doi.org/10.3748/wjg.15.2669.

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Dierckx, R. I. R., i M. F. J. Vandewoude. "DONEPEZIL-RELATED TOXIC HEPATITIS". Acta Clinica Belgica 63, nr 5 (październik 2008): 339–42. http://dx.doi.org/10.1179/acb.2008.066.

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Topal, Firdevs, Ersan Özaslan, Sabiye Akbulut, Metin Küçükazman, Osman Yüksel i Emin Altiparmak. "Methylprednisolone-Induced Toxic Hepatitis". Annals of Pharmacotherapy 40, nr 10 (październik 2006): 1868–71. http://dx.doi.org/10.1345/aph.1h171.

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Baum, Susan L., i Anthony J. Suruda. "Toxic Hepatitis from Dimethylacetamide". International Journal of Occupational and Environmental Health 3, nr 1 (styczeń 1997): 1–4. http://dx.doi.org/10.1179/oeh.1997.3.1.1.

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Lança, Sara, Amanda Alves, Ana Isabel Vieira, José Barata, João de Freitas i Álvaro de Carvalho. "Chromium-induced toxic hepatitis". European Journal of Internal Medicine 13, nr 8 (grudzień 2002): 518–20. http://dx.doi.org/10.1016/s0953-6205(02)00164-4.

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Cicognani, Camilla, Mauro Malavolti, Antonio Maria Morselli-Labate, Claudia Sama i Luigi Barbara. "Flutamide-induced toxic hepatitis". Digestive Diseases and Sciences 41, nr 11 (listopad 1996): 2219–21. http://dx.doi.org/10.1007/bf02071403.

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Yang, Ha Na, Dong Joon Kim, Young Mook Kim, Byoung Ho Kim, Kyoung Min Sohn, Myung Jin Choi i Young Hee Choi. "Aloe-induced Toxic Hepatitis". Journal of Korean Medical Science 25, nr 3 (2010): 492. http://dx.doi.org/10.3346/jkms.2010.25.3.492.

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Sheikh, Israr, i Joan Culpepper-Morgan. "Sorrel Induced Toxic Hepatitis". American Journal of Gastroenterology 110 (październik 2015): S884—S885. http://dx.doi.org/10.14309/00000434-201510001-02117.

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Aydın, Mesut. "Toxic hepatitis due to heliz". Van Medical Journal 28, nr 1 (2021): 15–18. http://dx.doi.org/10.5505/vtd.2021.02328.

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Ahn, Byung-Min. "Medicinal Herbs and Toxic Hepatitis". Journal of the Korean Medical Association 48, nr 4 (2005): 318. http://dx.doi.org/10.5124/jkma.2005.48.4.318.

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Rozprawy doktorskie na temat "Toxic hepatitis"

Zhou, Ting. "Isoniazid hepatotoxicity". Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/29456.

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Isoniazid (INH), one of the most effective agents in the treatment and prophylaxis of tuberculosis associated with a mild increase in liver transaminases in up to 20% of treated patients and severe hepatotoxicity in up to 2% of treated patients. Since the 1970's, a number of studies have been reported on the mechanism of INH-induced hepatotoxicity. The original studies in rats suggested that the hepatotoxic effect of INH was due to the microsomal metabolism of acetylhydrazine (AcHz, a metabolite of INH) to a reactive intermediate. More recently other workers have been unable to reproduce the original results in the rat, or other mechanistic models have been proposed. Therefore, it is necessary to establish a reproducible animal model which resembles INH hepatotoxicity in the human being. In these experiments,, male New Zealand white rabbits were used, and divided into 12 treatment groups of 6-8 rabbits each. Serum argininosuccinate lyase (ASAL) levels and histological changes in liver slides were chosen as indices of hepatotoxicity. After the determination of acetylator phenotype for each rabbit, INH and its metabolites, acetylisoniazid (AcINH), hydrazine (Hz) and AcHz were administered in a two-day regimen orally or subcutaneously. The results showed that the serum ASAL level in rabbits is a sensitive and specific enzyme marker which parallels the incidence of hepatic necrosis seen on histology. The serum ASAL control values 4.3±2.6 (SD) Takahara units were maintained until about 24 hrs after the first challenge of INH in the two-day regimen (0.36+3x0.26 mmol/kg/dx2d, s.c.); peak values of up to 2674 Takahara units occurred at about 72 hrs. No significant difference between the toxicity of INH given orally and subcutaneously was detected. Phenobarbital (PB) (0.1 mg/kgx3d, i.p.) pretreatment increased the elevation of serum ASAL level caused by INH (0.36+3x0.26 mmol/kg/dx2d, p.o.) significantly (p<0.05, F test) compared with the group without PB pretreatment. The 65 experimental rabbits were classified into populations of acetylator phenotype by measuring their acetylation rate of sulfamethazine (SMZ): fast acetylators with a SMZ t[formula omitted] of 12.8±4.4 (SD) (n=54) and slow acetylators with a SMZ t[formula omitted] of 50.3±10.4 (SD) (n=ll). Among the rabbits challenged with INH (0.36+3x0.26 mmol/kg/dx2d, p.o. or s.c.) with or without PB pretreatment, no correlation was found between the peak serum ASAL values and acetylation rate represented by SMZ t[formula omitted (r=0.05, n=18). This lack of this correlation was also present in rabbits challenged with AcINH and Hz. Among INH and its metabolites, AcINH, Hz and AcHz, Hz is the most potent hepatotoxin. Its effect is dose-dependent over the dose range (0.10+3x0.07, 0.14+3x0.10 and 0.19+3x0.14 mmol/kg/dx2d, p.o.). AcHz (0.36+3x0.26 mmol/kg/dx2d, s.c.), produced no significant hepatotoxic effect, which is contradictory to the results reported by other authors. AcINH (0.28+3x0.20 mmol/kg/dx2d, s.c, 0.42+3x0.30 mmol/kg/dx2d, s.c. or p.o.) had a intermediate hepatotoxic effect which is similar to that of INH. The results showed that (1) the rabbit is a reproducible animal model for studying INH hepatotoxicity; (2) the release of ASAL to serum and pathological changes resemble that seen in human beings; (3) the hepatotoxicity of INH is potentiated by PB pretreatment which is in accordance with the evidence in human beings of an increased risk in the presence of microsomal enzyme inducers; (4) the acetylation rate does not affect the hepatotoxicity of INH; (5) among the metabolites tested, Hz was most potent. These data indicate that the hypothesis that INH hepatotoxicity is due to microsomal metabolism of AcHz is probably incorrect. We think that it is more likely that Hz is responsible. Further studies are required to elucidate the exact mechanism in the rabbit model.
Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate

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Митус, Н. В., i К. І. Чепілко. "Токсичні гепатити в практиці інфекціоніста". Thesis, Видавництво СумДУ, 2011. http://essuir.sumdu.edu.ua/handle/123456789/15035.

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Захворювання печінки переважають сьогодні над усіма захворюваннями органів травлення. Вони реєструються у третьої частини людей, вдвічі частіше у жінок. Враховуючи роль печінки в метаболізмі хімічних речовин, можна апріорі стверджувати, що не існує ксенобіотиків, котрі при певних умовах не викликали б її ураження. Багаточисельні відомості про можливу гепатотоксичну дію різних етіологічних чинників дозволяють зробити висновок, що токсичне ураження печінки – одна з важливих проблем гепатології. При цитуванні документа, використовуйте посилання http://essuir.sumdu.edu.ua/handle/123456789/15035

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Медвідь, І. І., i Л. С. Фіра. "Досліджування впливу густого екстракту з листя шовковиці (Morus alba, Morus nigra) на метаболічні порушення у тварин з токсичним гепатитом". Thesis, Видавництво СумДУ, 2011. http://essuir.sumdu.edu.ua/handle/123456789/14470.

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Lenga, E. L. "Effects of melatonin on the content of reduced glutation in the blood under toxic hepatitis". Thesis, БДМУ, 2020. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18371.

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Wright, Paul F. A. "Systemic oxidant stress and its effects on hepatotoxicity /". Title page, contents and abstract only, 1988. http://web4.library.adelaide.edu.au/theses/09PH/09phw952.pdf.

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Alfaifi, Mohammed. "Cell therapy for acute liver injury : in vivo efficacy of mesenchymal stromal cells in toxic and immune-mediated murine hepatitis". Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8330/.

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The ability of umbilical cord-derived mesenchymal stromal cells (UC-MSCs) to immunomodulate offers therapeutic potential in liver injury but the inherent heterogeneity of unsorted MSC populations may explain varied/reduced function as well as posing regulatory challenges. Thus, we aimed to evaluate the therapeutic potential of purified CD362+ MSC infusion in murine models of acute liver injury. UC-MSCs were injected intravenously into mice injured by single dose of Carbon tetrachloride (CCl4) & OVA-BIL mice. MSC used were either unsorted or sorted CD362+. The extent of liver damage was determined by liver histology, serum analysis, gene expression and FACS analysis 3 or 5 days after cell infusion. Homing and bio-distribution of stem cells was determined by whole mouse cryo-imaging of Q-dot labelled MSC following infusion of UC-MSC into injured mice. CD362+ MSC were as effective as unsorted MSC in ameliorating liver injury, with reductions in serum ALT seen in both models. In contrast heat-inactivated MSC had no effect on liver injury. MSC also led to a reduction in CD45+staining on liver sections in both models of liver injury corroborated by an accompanying reduction in hepatic CD45+ cells in (FACS analysis of liver digest). In addition, there was a significant reduction in hepatic CD19+ B cells in digested liver in CCl4 injury. CD362+ MSCs were found to have the ability to reduce the level of adhesion molecules (ICAM and VCAM) in Ova-Bil mice. Cryo-imaging of time-course in both animal models indicated that MSC had migrated to the lung within 1 hour and were then cleared rapidly, although there was a liverspecific increase in MSC 2-3 day in Ova-Bil mice. CD362+ human MSC exert potent anti-inflammatory activity in toxic and immune-mediated murine liver injury with demonstrable reductions in infiltrating inflammatory leucocytes and B cells.

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Пришляк, А. М., С. І. Яворська, Т. К. Головата i Б. Я. Ремінецький. "Стан вільнорадикальних процесів організму щурів та морфологічні зміни в товстій кишці при змодельованому токсичному гепатиті". Thesis, Сумський державний університет, 2017. http://essuir.sumdu.edu.ua/handle/123456789/65580.

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Вступ. Підвищене поступлення галенових сполук до організму людини та тварини може спровокувати розвиток функціональних порушень та патологічних змін органів травної системи і товстої кишки зокрема. Матеріали та методи дослідження. Метою дослідження було встановити стан вільнорадикальних процесів організму та морфологічні зміни у товстій кишці при змодельованому токсичному гепатиті.

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He, Wencan. "Etude du rôle de la Cytolethal Distending Toxin dans la carcinogenèse digestive et la survie cellulaire". Thesis, Bordeaux, 2020. http://www.theses.fr/2020BORD0087.

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L’homme est fréquemment exposé à des génotoxines bactériennes impliquées dans les cancers digestifs, comme la colibactine et la toxine CDT (Cytolethal Distending Toxin). Ces toxines endommagent l'ADN des cellules hôtes et constituent un facteur prédisposant au développement de cancers. Les Helicobacter entérohépatiques, tels que Helicobacter hepaticus et Helicobacter pullorum, sont associés à plusieurs maladies intestinales et hépatiques. Leur principal facteur de virulence est la toxine CDT. Nous avons étudié les mécanismes d'action de la génotoxine CDT dans l'activation des processus procancéreux et la survie cellulaire, en utilisant l'infection à Helicobacter hepaticus comme modèle. Nous avons démontré que le remodelage nucléaire induit par la sous-unité active CdtB de la CDT de Helicobacter implique la surexpression de l'oncoprotéine MAFB qui est ensuite associée à une forte localisation nucléaire et périnucléaire dans les noyaux distendus en réponse à la CDT/CdtB, ainsi qu’à la formation de gros lamellipodes, des extensions cellulaires connues pour être impliquées dans la migration cellulaire et la production de métastases. Nous avons également montré que le remodelage nucléaire induit par CDT/CdtB peut être associé à la formation de réticulum nucléoplasmique (NR) enrichi en particules ribonucléoprotéiques. Ces structures dynamiques et transitoires induites par la génotoxine pourraient correspondre à une passerelle privilégiée pour la synthèse d'ARNm sélectionnés, qui seraient préférentiellement transportés du noyau à travers les pores nucléaires et traduits à l'intérieur du NR. Le NR induit par la CDT (et aussi par la colibactine) pourrait permettre à la cellule de s'arrêter et de réparer les dommages à l'ADN causés par les génotoxines bactériennes afin de maintenir la survie cellulaire. L'identiﬁcation à base de MicroArrays des gènes régulés par la CdtB a aussi montré une régulation de l'autophagie par cette toxine. Nous avons montré que la CdtB stimulait le flux autophagique et induisait une autophagie de survie suite aux dommages à l'ADN induits par la CDT/CdtB. Nous avons montré que la CDT/CdtB favorise la formation d'agrégats cytoplasmiques SQSTM1/P62 parfois profondément invaginés dans les noyaux distendus ainsi que des vésicules extra-cellulaires SQSTM1/P62-positives. La formation de NR suite aux dommages à l'ADN induits par la CDT est associée à l'induction de l'autophagie, qui joue un rôle de survie dans ce contexte. Les particules SQSTM1/P62 ont un rôle clé dans ces effets. Ces résultats offrent de nouvelles perspectives dans le contexte de la formation du NR et de la survie cellulaire en réponse aux dommages à l'ADN, une caractéristique commune à de nombreux cancers, qui apparaissent non seulement en réponse aux dommages à l'ADN induits par les thérapies mais aussi plus tôt en réponse aux bactéries génotoxiques. De nouvelles études sont nécessaires pour identifier les structures cytosoliques entourées et englouties par P62/SQSTM1 ainsi que pour déchiffrer le rôle de cette protéine cargo dans la survie des cellules dont l'ADN est endommagé et, plus particulièrement, son rôle dans la formation de NR à la lumière de sa fonction de protéine de liaison à l’ARN récemment démontrée. Les résultats issus de cette thèse confortent l’idée que les génotoxines bactériennes pourraient être à l’origine de cancers
Humans are frequently exposed to bacterial genotoxins, colibactin and Cytolethal Distending Toxin (CDT), involved in digestive cancers. These toxins damage the DNA of host cells and constitute a predisposing factor for the development of cancer. Enterohepatic Helicobacters, such as Helicobacter hepaticus and Helicobacter pullorum, are associated with several intestinal and hepatic diseases. Their main virulence factor is CDT.We studied the mechanisms of action of CDT genotoxin in the activation of pro-cancerous processes and cell survival, using Helicobacter hepaticus infection, as a model. We demonstrated that the nuclear remodeling induced by Helicobacter CdtB active subunit of CDT involves MAFB oncoprotein overexpression which is subsequently associated with a strong nuclear and perinuclear localization of MAFB protein in CDT/CdtB-distended nuclei, and with the formation of large lamellipodia, corresponding to cellular extensions known to be involved in cell migration and arousal of metastases. We also showed that the nuclear remodeling induced by CDT/CdtB could be associated to the formation of transient rich-messenger ribonucleoprotein nucleoplasmic reticulum (NR). These genotoxin-induced dynamic structures may correspond to a privileged gateway for the synthesis of selected mRNA, preferentially transported from the nucleus, through pores and translated therein. CDT-induced NR may allow the cell to pause and repair DNA damage caused by bacterial genotoxins in order to maintain cell survival. Microarray-based identiﬁcation of diﬀerentially-expressed genes pointed a CdtB regulation of autophagy. We showed that CdtB stimulated autophagic flux and enhanced pro-survival autophagy following CDT-induced DNA damage. CDT promoted the formation of cytoplasmic SQSTM1/P62 aggregates, sometimes deeply invaginated in distended nuclei, as well as SQSTM1/P62-positive extra-cellular like vesicles. NR formation following DNA damage induced by CDT is associated with the induction of autophagy, which plays a survival role in this context. SQSTM1/P62 have a key role in these effects.These findings offer new insights into the context of NR formation and cell survival in response to DNA damage, a common feature of many cancers, which not only appears in response to therapies-induced DNA damage, but also earlier in response to genotoxic bacteria.Further studies are required identify the cytosolic structures surrounded and engulfed by P62/SQSTM1 and to decipher the role of this cargo protein in the prosurvival of cells whose DNA is damaged, and more particularly its role in NR formation in light with its recently demonstrated RNA-binding protein function.The results of this thesis support the idea that bacterial genotoxins could cause cancer

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Wright, Paul F. A. (Paul Frank Albert). "Systemic oxidant stress and its effects on hepatotoxicity". 1988. http://web4.library.adelaide.edu.au/theses/09PH/09phw952.pdf.

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Wright, Paul F. A. (Paul Frank Albert). "Systemic oxidant stress and its effects on hepatotoxicity / by Paul F.A. Wright". Thesis, 1988. http://hdl.handle.net/2440/18808.

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Książki na temat "Toxic hepatitis"

J, Manning Frederick, i Swartz Morton N, red. Review of the Fialuridine (FIAU) clinical trials. Washington, DC: National Academy Press, 1995.

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1957-, Emanuel Ezekiel J., red. Exploitation and developing countries: The ethics of clinical research. Princeton, N.J: Princeton University Press, 2008.

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Jean-Paul, Fillastre, Institut national de la santé et de la recherche médicale (France) i Université de Rouen. Centre du médicament, red. Hépatoxicité médicamenteuse. [Paris]: Editions INSERM, 1986.

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Leung, Doris G. Neuropathies Associated with Infection or Toxic Exposure. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0113.

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Among the many causes of peripheral neuropathy are those mediated by environmental exposure to infectious and toxic agents. The most common neuropathy associated with HIV is HIV-associated distal sensory polyneuropathy (HIV-DSP). The clinical presentation of HIV-DSP is one of a distal, symmetric, often painful, small-fiber sensory axonal polyneuropathy. Other infectious causes of neuropathy include hepatitis C, leprosy, Lyme disease, rabies, and diphtheria, and antibiotic drugs such as isoniazid can also cause neuropathy. Heavy metals and a variety of other toxins including chemotherapeutic agents such as platinum, vincristine, and thalidomide disrupt peripheral nerve function. High doses of pyridoxine can cause damage to the dorsal root ganglia and foodbourne toxins such as saxitoxins found in shellfish.

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C, Sahu Saura, red. Hepatotoxicity: From genomics to in vitro and in vivo models. Chichester, England: John Wiley & Sons, 2007.

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Levy, Barry S. Liver Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190662677.003.0030.

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This chapter describes occupational and environmental liver disorders. It describes the types of liver function and types of liver damage, and how these functions and this damage can be assessed. Workers in healthcare and solid waste management are at increased risk hepatitis B virus and hepatitis C virus infections. Occupational exposure to swine is associated with hepatitis E virus infection. More than 100 industrial chemicals can be acutely hepatotoxic in experimental animals or humans. Metabolic reactions may affect the hepatotoxicity of chemicals. Occupational exposure to organic solvents can cause toxic hepatitis. Occupational exposure to vinyl chloride monomer has been causally associated with toxicant-associated fatty liver disease as well as a form of non-cirrhotic portal hypertension. Several agents can cause cancer of the liver or bile ducts. Vinyl chloride monomer is causally associated with angiosacoma of the liver. Arsenic causes liver cancer. Dietary exposure to aflatoxins can cause hepatoceulluar carcinoma.

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C, Sahu Saura, red. Hepatotoxicity: From genomics to in vitro and in vivo models. Chichester, England: John Wiley & Sons, 2007.

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Hepatotoxicity: From Genomics to In Vitro and In Vivo Models. Wiley, 2008.

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Sahu, Saura. Hepatotoxicity. Wiley & Sons, Incorporated, John, 2010.

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Brennfleck, Shannon Joyce, red. Liver disorders sourcebook: Basic consumer health information about the liver and how it works; liver diseases, including cancer, cirrhosis, hepatitis, and toxic and drug related diseases; tips for maintaining a healthy liver; laboratory tests, radiology tests, and facts about liver transplantation; along with a section on support groups, a glossary, and resources listings. Detroit, Mich: Omnigraphics, 2000.

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Części książek na temat "Toxic hepatitis"

Raj, Satish R., S. R. Wayne Chen, Robert S. Sheldon, Arti N. Shah, Bharat K. Kantharia, Ulrich Salzer, Bodo Grimbacher i in. "Toxic Hepatitis, Acute". W Encyclopedia of Molecular Mechanisms of Disease, 2095. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_45.

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Scharnagl, Hubert, Winfried März, Markus Böhm, Thomas A. Luger, Federico Fracassi, Alessia Diana, Thomas Frieling i in. "Acute Toxic Hepatitis". W Encyclopedia of Molecular Mechanisms of Disease, 31. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_9020.

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Stolz, Andrew. "Toxic and Drug-Induced Hepatitis". W Modern Concepts of Acute and Chronic Hepatitis, 201–15. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4615-9519-9_14.

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Cioffi, William G., Michael D. Connolly, Charles A. Adams, Mechem C. Crawford, Aaron Richman, William H. Shoff, Catherine T. Shoff i in. "Toxin Induced Hepatitis". W Encyclopedia of Intensive Care Medicine, 2244. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_2309.

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Krichbaum, Michelle, i Maura Miller. "Pain Management in Liver Disease". W Pain, 345–52. Oxford University Press, 2022. http://dx.doi.org/10.1093/med/9780197542873.003.0041.

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Chronic liver disease accounts for approximately 1 million deaths annually, with an additional 1 million deaths from liver cancer and acute hepatitis. Accurate estimates of mortality are important in determining timing of care interventions, including pain control. End-stage liver disease can be a challenge to manage because pain and symptoms are often multifactorial, including abdominal distention, muscle cramps, dyspnea from excess fluid, altered mentation, and nociceptive, neuropathic, and visceral pain. Considerations for analgesia should account for the protein binding of medications, active or toxic metabolites, and renal adjustments if the patient progresses to hepatorenal syndrome. Interventional pain and symptom management incorporates the use of paracentesis and transjugular intrahepatic portosystemic shunts (TIPS) for the relief of suffering.

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M., Halima, Ihsana Banu Ishthiaq, Sneha Unnikrishnan i Karthikeyan Ramalingam. "Nanoemulsion-Based Antiviral Drug Therapy". W Handbook of Research on Nanoemulsion Applications in Agriculture, Food, Health, and Biomedical Sciences, 194–212. IGI Global, 2022. http://dx.doi.org/10.4018/978-1-7998-8378-4.ch009.

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Nanoemulsions are an attractive approach for the delivery of antiviral drugs in the treatment of various viral infections. Nanoemulsions are easy to plan and develop, and their components exhibit high variability. Nanoemulsion system and its components have certain biophysical properties which could increase the efficacy of drug therapy. Pulmonary surfactant (PS)-assisted antiviral drug delivery by nanoemulsion system could be another effective approach for the treatment of COVID-19. Antiviral drug delivery of nebulization using an animation system could increase the efficacy of antiviral drug against COVID-19. Ginkgo biloba polyprenol nanoemulsion was also found to be stable, non-toxic, and had strong antiviral activity against influenza A H3N2 and hepatitis B virus in vitro. Nanoemulsion systems possess certain properties that make their system suitable for drug delivery by mobilization and hence would be promising systems for therapeutics in the future.

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Okwudiri Ihegboro, Godwin, i Chimaobi James Ononamadu. "Drug-Induced Hepatotoxicity". W Hepatotoxicity [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.103766.

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This chapter aims at discussing the consequential effects of drug-induced hepatotoxicity on man. The liver carries out drug detoxification among other roles, but sometimes, drug toxicity can occur caused by either medication overdose or imbalance drug metabolic reactions (Phase 1 & 2), resulting in the formation of reactive (toxic) metabolites (electrophilic compounds or free radicals) that binds covalently to hepatocytes, leading to liver injury/diseases like acute and chronic hepatitis, cholestasis, steatosis among others. Mitochondrial dysfunction, oxidative stress and lipid peroxidation are some of the mechanisms of liver injury. Furthermore, drug hepatotoxicity results in hepatocellular, gastroenterological, cholestatic as well as immunological disorders. The clinical manifestations of drug toxicity arise from the abnormalities observed in liver’s biochemical and molecular indicators. Our findings, revealed that in the event of liver injury, liver function indices like aspartate and alanine aminotransferases, ALP (alkaline phosphatase) and gamma glutamyl transferase (GGT) activities, intracellular calcium (Ca2+) and lipid peroxidation increases whereas indices of oxidative stress such as glutathione and its allies, catalase and superoxide dismutase activity deplete. At molecular level, the gene expression levels of Bcl-2 mRNA and microRNA genes (miR-122, 192 and 194) reduces while mitochondrial genes (MMP-2 and MMP-9) overexpresses. Since drug abuse is deleterious to human health, therefore, adherence to doctors’ prescription guidelines should be followed.

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Kayyal, Mohamad K. "Estimation of Amounts of Waste Generated from Healthcare Facilities". W Environmental Information Systems in Industry and Public Administration, 215–26. IGI Global, 2001. http://dx.doi.org/10.4018/978-1-930708-02-0.ch014.

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In response to government and public pressures, the healthcare industry has in the past few years directed a significant effort toward the proper and safe management of its medical waste streams. Medical waste is classified as a biohazardous waste, which according to a study published by the United States Agency for Toxic Substances and Disease Registry (1990), may result in human infection and transfer of disease. This includes injury and infection with the Hepatitis B Virus (HVB) and the Human Immunodeficiency Virus (HIV), by janitorial and laundry workers, nurses, emergency medical personnel, and refuse workers who may come into contact with medical waste. In a recent survey conducted in the United States and Japan, and reported by the World Heath Organization (WHO) (1994), it was found that injuries by sharps constitute about 1% to 2% per annum for nurses and maintenance workers and 18% per annum for outside waste management workers. In Japan, the survey indicated that injuries by sharps constitute about 67% for in-hospital waste handlers and 44% for outside waste management workers. In order to reduce the risks associated with medical waste, proper management mechanisms should be adopted by healthcare facilities to protect the health of the staff within the medical facility, waste collectors/workers, and the public once the waste has left the facility for final disposal. These mechanisms include waste identification, segregation, storage, and treatment. However, and as a first step in the implementation of a waste management system, the management of a medical facility should conduct an audit of the generated waste streams.

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Marjot, Thomas. "Liver disorders". W Best of Five MCQS for the European Specialty Examination in Gastroenterology and Hepatology, 208–58. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780198834373.003.0008.

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This chapter covers core curriculum topics relating to liver disorders including the anatomy, physiology, and biochemistry of the liver as it relates to disease processes. There is a focus on the investigation and management of acute hepatitis including viral, drug- and toxin-induced, and the risk stratification of patients with acute liver failure. All major chronic liver diseases are discussed including non-alcoholic fatty liver disease, autoimmune liver disease, alcohol related liver disease and chronic viral hepatitis. There is also education on managing the complications of cirrhosis including renal dysfunction, hepatic encephalopathy, variceal haemorrhage, and spontaneous bacterial peritonitis. Additional important topics covered include nutrition in liver disease, hepatocellular carcinoma, liver transplantation indications and assessment, and complications following liver transplantation. Additional curriculum material regarding liver disorders will also be covered in the mock examination chapter.

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Li, Jie Jack. "Sofosbuvir (Sovaldi)". W Top Drugs. Oxford University Press, 2015. http://dx.doi.org/10.1093/oso/9780199362585.003.0017.

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Viruses are humanity’s invisible enemy. They wreak daily havoc by causing the flu, measles, rabies, hepatitis, smallpox, polio, and even human immunodeficiency virus (HIV). Although viruses have existed on the earth much longer than humans, it was not until in 1892 when the concept of virus took root when Chamberland experimented with viruses using the Pasteur–Chamberland filter. Solid evidence emerged when tobacco mosaic virus (TMV) crystal was isolated in 1935. However, human ingenuity afforded successful measures to combat viruses long before 1892. For instance, Jenner successfully pioneered a vaccination for preventing smallpox in 1796, nearly one hundred years before Chamberland’s exploits and before Pasteur developed the first vaccination for rabies in 1885. The scourge of polio has been nearly wiped out thanks to Salk’s inactivated polio vaccine (IPV) available since 1954 and Sabin’s oral poliovirus vaccine (OPV) popularized in 1960. The 1951 the Nobel Prize in Physiology or Medicine was awarded to Theiler for his contributions to yellow fever vaccines. In terms of small molecule antiviral drugs, the nucleoside iododeoxyuridine (IDU, 2), a simple analog of thymidine (3), was first synthesized and used as an antiviral drug in 1959 by Prusoff. Unfortunately, due to its systemic cardiotoxicities, IDU is now only used topically to treat herpes simplex keratitis. A similar antiviral nucleoside, trifluorothymidine (TFT, Viroptic, 4), is less toxic than 2, and is also primarily used topically in eyes to kill the herpes simplex virus (HSV). Under the leadership of future Nobel laureate Elion, Burroughs Wellcome introduced the nucleoside analog acyclovir (Zovirax, 5) in 1978 for the treatment of HSV infection.3 While not the first antiviral agent on the market, Zovirax (5) was the first small molecule drug to be widely used to control a viral infection. Introduction of valacyclovir (Valtrex, 6), a prodrug of Zovirax (5) with higher oral bioavailability, afforded the patient a more convenient regimen because it does not have to be taken as frequently as the parent drug Zovirax (5).

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Streszczenia konferencji na temat "Toxic hepatitis"

Kudryavtsev, Vladimir, Anatoly Shatrov i Alexey Vishnyakov. "Mathematical modeling of toxic hepatitis in male Wistar rats". W 2022 IEEE International Multi-Conference on Engineering, Computer and Information Sciences (SIBIRCON). IEEE, 2022. http://dx.doi.org/10.1109/sibircon56155.2022.10016912.

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Dzhioev, I. G., F. E. Batagova, O. V. Remizov, E. A. Gutsaeva i I. I. Akhmadov. "The Effect of the Course Intake of Hilak Mineral Water on Liver Function in Experimental Toxic Hepatitis and Intrahepatic Cholestasis". W Proceedings of the International Conference on Health and Well-Being in Modern Society (ICHW 2019). Paris, France: Atlantis Press, 2019. http://dx.doi.org/10.2991/ichw-19.2019.21.

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Kondufor, O. V., i YA A. Sockaya. "Dynamics of the isoenzyme spectrum of lactate dehydrogenase in patients with chronic toxic hepatitis ethanol etiology in combination with cerebrovascular pathology". W SCIENCE OF RUSSIA: TARGETS AND GOALS. "Science of Russia", 2019. http://dx.doi.org/10.18411/sr-10-10-2019-14.

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Raporty organizacyjne na temat "Toxic hepatitis"

Gidengil, Courtney, Matthew Bidwell Goetz, Margaret Maglione, Sydne J. Newberry, Peggy Chen, Kelsey O’Hollaren, Nabeel Qureshi i in. Safety of Vaccines Used for Routine Immunization in the United States: An Update. Agency for Healthcare Research and Quality (AHRQ), maj 2021. http://dx.doi.org/10.23970/ahrqepccer244.

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Objective. To conduct a systematic review of the literature on the safety of vaccines recommended for routine immunization in the United States, updating the 2014 Agency for Healthcare Research and Quality (AHRQ) report on the topic. Data sources. We searched MEDLINE®, Embase®, CINAHL®, Cochrane CENTRAL, Web of Science, and Scopus through November 9, 2020, building on the prior 2014 report; reviewed existing reviews, trial registries, and supplemental material submitted to AHRQ; and consulted with experts. Review methods. This report addressed three Key Questions (KQs) on the safety of vaccines currently in use in the United States and included in the Centers for Disease Control and Prevention’s (CDC) recommended immunization schedules for adults (KQ1), children and adolescents (KQ2), and pregnant women (KQ3). The systematic review was supported by a Technical Expert Panel that identified key adverse events of particular concern. Two reviewers independently screened publications; data were extracted by an experienced subject matter expert. Studies of vaccines that used a comparator and reported the presence or absence of adverse events were eligible. We documented observed rates and assessed the relative risks for key adverse events. We assessed the strength of evidence (SoE) across the existing findings from the prior 2014 report and the new evidence from this update. The systematic review is registered in PROSPERO (CRD42020180089). Results. A large body of evidence is available to evaluate adverse events following vaccination. Of 56,608 reviewed citations, 189 studies met inclusion criteria for this update, adding to data in the prior 2014 report, for a total of 338 included studies reported in 518 publications. Regarding vaccines recommended for adults (KQ1), we found either no new evidence of increased risk for key adverse events with varied SoE or insufficient evidence in this update, including for newer vaccines such as recombinant influenza vaccine, adjuvanted inactivated influenza vaccine, and recombinant adjuvanted zoster vaccine. The prior 2014 report noted a signal for anaphylaxis for hepatitis B vaccines in adults with yeast allergy and for tetanus, diphtheria, and acellular pertussis vaccines. Regarding vaccines recommended for children and adolescents (KQ2), we found either no new evidence of increased risk for key adverse events with varied SoE or insufficient evidence, including for newer vaccines such as 9-valent human papillomavirus vaccine and meningococcal B vaccine. The prior 2014 report noted signals for rare adverse events—such as anaphylaxis, idiopathic thrombocytopenic purpura, and febrile seizures—with some childhood vaccines. Regarding vaccines recommended for pregnant women (KQ3), we found no evidence of increased risk for key adverse events with varied SoE among either pregnant women or their infants following administration of tetanus, diphtheria, and acellular pertussis vaccines during pregnancy. Conclusion. Across this large body of research, we found no new evidence of increased risk since the prior 2014 report for key adverse events following administration of vaccines that are routinely recommended. Signals from the prior report remain unchanged for rare adverse events, which include anaphylaxis in adults and children, and febrile seizures and idiopathic thrombocytopenic purpura in children. There is no evidence of increased risk of adverse events for vaccines currently recommended in pregnant women. There remains insufficient evidence to draw conclusions about some rare potential adverse events.

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