Islamic Fasting and Health: Difference between revisions

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{{Quote||Paracetamol-related hepatotoxicity is now the most common cause of the potentially devastating clinical syndrome of acute liver failure in many western countries. In patients who develop liver damage following moderate paracetamol overdose in the order of 5–10 g daily, recent fasting and nutritional impairment have been identified as key precipitants.
{{Quote||Paracetamol-related hepatotoxicity is now the most common cause of the potentially devastating clinical syndrome of acute liver failure in many western countries. In patients who develop liver damage following moderate paracetamol overdose in the order of 5–10 g daily, recent fasting and nutritional impairment have been identified as key precipitants.


In keeping with experience in the modest paracetamol overdose setting [6], it is likely that fasting occurring on a background of longstanding diminished caloric intake and severe malnutrition played an important role in the development of paracetamol-induced liver damage at recommended dosage of 4 g daily in this patient. Fasting and malnutrition result in reduction of hepatic levels of glutathione, required for inactivation of N-acetyl-p-benzoquinonimine, the toxic metabolite of paracetamol [6]. A 16-h period of fasting is sufficient to substantially deplete hepatic glutathione stores in mice [11]. <ref name=ParaODFast">[{{Reference archive|1http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2796.2003.01097.x/full|2=2012-10-13}} Paracetamol-induced hepatotoxicity at recommended dosage] - The Journal of Internal Medicine, Janurary 24, 2003</ref>}}
In keeping with experience in the modest paracetamol overdose setting [6], it is likely that fasting occurring on a background of longstanding diminished caloric intake and severe malnutrition played an important role in the development of paracetamol-induced liver damage at recommended dosage of 4 g daily in this patient. Fasting and malnutrition result in reduction of hepatic levels of glutathione, required for inactivation of N-acetyl-p-benzoquinonimine, the toxic metabolite of paracetamol [6]. A 16-h period of fasting is sufficient to substantially deplete hepatic glutathione stores in mice [11]. <ref name=ParaODFast">[http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2796.2003.01097.x/full Paracetamol-induced hepatotoxicity at recommended dosage] - The Journal of Internal Medicine, Janurary 24, 2003</ref>}}


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