“…Thirdly, paracetamol and cannabinoids have several intense interactions with difficult-to-judge clinical importance. Finally, there are suggestions of cannabinoids contributing to nonalcoholic liver disease, fibrosis, and inflammation, but the data are conflicting and inconclusive [298,299].…”
Section: Liver Effects In the Context Of Cannabinoid Usementioning
Increased usage of recreational and medically indicated cannabinoid compounds has been an undeniable reality for anesthesiologists in recent years. These compounds’ complicated pharmacology, composition, and biological effects result in challenging issues for anesthesiologists during different phases of perioperative care. Here, we review the existing formulation of cannabinoids and their biological activity to put them into the context of the anesthesia plan execution. Perioperative considerations should include a way to gauge the patient’s intake of cannabinoids, the ability to gain consent properly, and vigilance to the increased risk of pulmonary and airway problems. Intraoperative management in individuals with cannabinoid use is complicated by the effects cannabinoids have on general anesthetics and depth of anesthesia monitoring while simultaneously increasing the potential occurrence of intraoperative hemodynamic instability. Postoperative planning should involve higher vigilance to the risk of postoperative strokes and acute coronary syndromes. However, most of the data are not up to date, rending definite conclusions on the importance of perioperative cannabinoid intake on anesthesia management difficult.
“…Thirdly, paracetamol and cannabinoids have several intense interactions with difficult-to-judge clinical importance. Finally, there are suggestions of cannabinoids contributing to nonalcoholic liver disease, fibrosis, and inflammation, but the data are conflicting and inconclusive [298,299].…”
Section: Liver Effects In the Context Of Cannabinoid Usementioning
Increased usage of recreational and medically indicated cannabinoid compounds has been an undeniable reality for anesthesiologists in recent years. These compounds’ complicated pharmacology, composition, and biological effects result in challenging issues for anesthesiologists during different phases of perioperative care. Here, we review the existing formulation of cannabinoids and their biological activity to put them into the context of the anesthesia plan execution. Perioperative considerations should include a way to gauge the patient’s intake of cannabinoids, the ability to gain consent properly, and vigilance to the increased risk of pulmonary and airway problems. Intraoperative management in individuals with cannabinoid use is complicated by the effects cannabinoids have on general anesthetics and depth of anesthesia monitoring while simultaneously increasing the potential occurrence of intraoperative hemodynamic instability. Postoperative planning should involve higher vigilance to the risk of postoperative strokes and acute coronary syndromes. However, most of the data are not up to date, rending definite conclusions on the importance of perioperative cannabinoid intake on anesthesia management difficult.
“…Similar to NAFLD, ALD also comprises symptoms including liver injury accompanied by simple steatosis or steatohepatitis, which can progress to liver cirrhosis and HCC [ 24 ]. Indeed, as for HFD, excessive and chronic alcohol consumption causes hepatic immune disturbances, and the excessive activation of inflammatory caspases in proinflammatory Kupffer cells, resulting in pyroptosis with the secretion of inflammatory cytokines, and oxidative stress with the production of ROS, and it is accompanied by the metabolic dysfunction of hepatocytes and abnormal lipogenesis, which leads to hepatic steatosis [ 4 , 24 ]. Given the underlying similarities in ALD and NAFLD/NASH pathogenesis, it is not surprising that alcohol intake can also induce changes in the eCBS [ 71 ].…”
Section: The Endocannabinoid System In Chronic Liver Diseasesmentioning
confidence: 99%
“…Treating alcohol-fed mice with CBD inhibited the activation of NLRP3 inflammasome, reduced the pyroptosis and liver inflammation, and protected the mice livers against steatohepatitis [ 34 ]. Accordingly, these findings suggest that, by activating hepatic CB1R, chronic alcohol intake stimulates the secretion of 2-AG by activated HSCs, which, in turn, promotes hepatic lipogenesis, on the one hand, and, on the other hand, inhibits fatty acid oxidation, thereby creating a disbalance between lipogenesis and lipid oxidation and resulting in chronic fat accumulation in the liver and steatosis [ 4 , 71 , 72 , 73 ]. Moreover, the activation of the hepatic CB1R by excessive alcohol intake also drives the activation of the key processing pathways involved in the setting of alcohol-induced steatohepatitis and liver inflammation [ 34 ].…”
Section: The Endocannabinoid System In Chronic Liver Diseasesmentioning
confidence: 99%
“…Meanwhile, prolonged alcohol abuse causes the development of ALD through complex signaling pathways by perturbating the immune response at the hepatic site with an aberrant activation of Kupffer cells, which secrete high amounts of proinflammatory cytokines, such as tumor necrosis factor alpha (TNF-α), and the recruitment of other innate immune cells at the hepatic site [ 4 ]. Alcoholic liver intoxication is also accompanied by mitochondrial dysfunctions and an increase in oxidative stress with the production of reactive oxygen species (ROS), which all lead to the establishment of a deleterious inflammatory microenvironment in the liver and the apoptosis of hepatocytes [ 4 ]. This liver inflammation is also accompanied by the progressive dysfunction of liver metabolism with an increase in abnormal lipogenesis, which promotes steatosis and acute hepatitis cirrhosis [ 2 ].…”
Nonalcoholic fatty liver disease (NAFLD), alcohol-induced liver disease (ALD), and viral hepatitis are the main causes of morbidity and mortality related to chronic liver diseases (CLDs) worldwide. New therapeutic approaches to prevent or reverse these liver disorders are thus emerging. Although their etiologies differ, these CLDs all have in common a significant dysregulation of liver metabolism that is closely linked to the perturbation of the hepatic endocannabinoid system (eCBS) and inflammatory pathways. Therefore, targeting the hepatic eCBS might have promising therapeutic potential to overcome CLDs. Experimental models of CLDs and observational studies in humans suggest that cannabis and its derivatives may exert hepatoprotective effects against CLDs through diverse pathways. However, these promising therapeutic benefits are not yet fully validated, as the few completed clinical trials on phytocannabinoids, which are thought to hold the most promising therapeutic potential (cannabidiol or tetrahydrocannabivarin), remained inconclusive. Therefore, expanding research on less studied phytocannabinoids and their derivatives, with a focus on their mode of action on liver metabolism, might provide promising advances in the development of new and original therapeutics for the management of CLDs, such as NAFLD, ALD, or even hepatitis C-induced liver disorders.
“… 29 In their review of the mechanisms of cannabinoid receptor signaling in hepatic pathogenesis, Yang, Choi, and Jeong summarize evidence in support of cannabinoid-based treatments for alcohol-associated liver disease. 30 Lees, Debenham, and Squeglia present a comprehensive overview of longitudinal neuropsychological and neuroimaging studies on the independent and combined effects of cannabis and alcohol use on the developing human brain. 31 Several articles review findings on the impact of cannabis use on alcohol consumption and consequences, and how this association may differ by cannabis formulation or by user characteristics, 32 with a specific focus on simultaneous alcohol and cannabis use, and contextual characteristics of co-use in young adults.…”
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