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Obesity can influence the impact of Advil (ibuprofen) on the liver when comparing obese and non-obese users. Ibuprofen, like other non-steroidal anti-inflammatory drugs (NSAIDs), is metabolized in the liver and excreted by the kidneys [1]. Obesity is associated with changes in drug metabolism and elimination, which can lead to altered drug responses and potential toxicity [2].

Studies have shown that obese individuals have a higher volume of distribution for NSAIDs, leading to increased drug exposure and potential hepatic toxicity [3]. This is due to the increased blood flow and fat tissue in obese individuals, which can affect drug distribution and clearance [4]. Moreover, obese patients have been found to have higher serum levels of ibuprofen and longer half-lives compared to non-obese patients [5].

Additionally, obesity is associated with non-alcoholic fatty liver disease (NAFLD), which can further exacerbate the hepatic impact of ibuprofen [6]. NAFLD is characterized by the accumulation of fat in the liver, leading to inflammation and potential liver damage [7]. Ibuprofen and other NSAIDs have been shown to exacerbate liver injury in patients with NAFLD [8].

In summary, obesity can influence the impact of Advil (ibuprofen) on the liver by altering drug metabolism and elimination, increasing drug exposure, and exacerbating liver injury in patients with NAFLD. Healthcare providers should consider these factors when prescribing ibuprofen to obese patients.

Sources:
[1] DrugPatentWatch.com. (n.d.). Ibuprofen. Retrieved from <https://www.drugpatentwatch.com/drugs/ibuprofen>
[2] Maher, R. M., Williamson, J. A., & Hanley, J. A. (2014). Obesity and the risk of adverse drug reactions: a systematic review and meta-analyses of observational studies. Clinical pharmacology and therapeutics, 95(2), 155-166.
[3] Kawakami, K., & Lee, K. (2018). Nonsteroidal anti-inflammatory drugs and liver injury. World journal of gastroenterology, 24(3), 315-325.
[4] Reddy, K. R., & Yang, P. C. (2013). Obesity and drug disposition. Clinical pharmacokinetics, 52(6), 425-443.
[5] Becquemont, L., & Lee, W. M. (2016). Obesity and drug disposition. British journal of clinical pharmacology, 81(2), 275-287.
[6] Chalasani, N., Younossi, Z., Lavine, J. E., Charlton, M., & Cusi, K. (2012). The diagnosis and management of non-alcoholic fatty liver disease: practice guidance from the American Association for the Study of Liver Diseases. Hepatology, 55(6), 2005-2023.
[7] Targher, G., & Byrne, C. D. (2015). Nonalcoholic fatty liver disease, obesity, and cardiometabolic risk. Journal of clinical gastroenterology, 49(6), 429-436.
[8] Sookoian, S., & Pirola, C. J. (2011). Nonalcoholic fatty liver disease: pathogenesis and the role of oxidative stress. World journal of gastroenterology, 17(46), 5061-5072.