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Liver, Biliary Tract and Pancreatic Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
The clinical features of hepatic encephalopathy have been described above. The diagnosis is confirmed by electroencephalogram (EEG) and/or a number connection test (where the time taken to connect a series of numbered spots is measured).
Therapeutic Properties of Fermented Foods and Beverages
Published in Megh R. Goyal, Preeti Birwal, Durgesh Nandini Chauhan, Herbs, Spices, and Medicinal Plants for Human Gastrointestinal Disorders, 2023
Hepatic disease (also called hepatic encephalopathy) is a life - threatening situation of liver disease.23 The probiotic microorganisms (such as: Lb.acidophilus, Lb. plantarum, Bifidobacteria sp., Lb. casei, Lb. delbrueckii var bulgaricus, St. thermophilus and Ent. faecum) present in fermented food and milk products have the ability to disrupt the pathogenesis occurring in liver along with reducing the risk of bleeding by lowering the portal pressure due to the enzymatic action and metabolic products produced during fermentation.141, 145
Nutritional and Dietary Supplementation during Pregnancy
Published in “Bert” Bertis Britt Little, Drugs and Pregnancy, 2022
This agent is utilized as a laxative and for lowering serum ammonia in cases of hepatic encephalopathy. Although there are no human reproduction studies, this agent is not absorbed from the gastrointestinal tract for the most part, and thus is unlikely to be associated with adverse fetal effects.
Phytochemical constituents and protective efficacy of Schefflera arboricola L. leaves extract against thioacetamide-induced hepatic encephalopathy in rats
Published in Biomarkers, 2022
Ali M. El-Hagrassi, Abeer F. Osman, Mostafa E. El-Naggar, Noha A. Mowaad, Sahar Khalil, Manal A. Hamed
Hepatic encephalopathy (HE) is one of the most dangerous side effects of liver diseases. It is a neuropsychiatric syndrome that develops as a result of acute or chronic liver failure. Anxiety, shorter attention span, sleep problems, personality change, impaired consciousness levels that eventually progresses to coma may appear as a result of HE and depending on the original cause of the existing liver injury (Lopez-Franco et al. 2021). Patients with HE have an exceedingly high death rate, ranging from 50 to 90% (Allampati and Mullen 2019). The pathophysiology of HE is complicated and the variables that link hepatic and neural system damage are still unknown (Wijdicks 2016). Hyperammonemia, on the other hand, is widely accepted as the cause of HE’s clinical, pathological, and neurochemical alterations. Others have suggested that HE development is influenced by inflammation (Sun et al. 2020) and oxidative stress (Montes-Cortes et al. 2018). Therefore, finding and testing effective techniques to treat and protect against acute liver and brain injury is a challenge.
Hyperammonemia in acetaminophen toxicity
Published in Clinical Toxicology, 2022
Ryan T. Marino, Alexander M. Sidlak
Another important observation drawn from the data in this cohort is that mental status did not worsen, and encephalopathy did not develop, in patients who were not treated for hyperammonemia. The same explanation for why hyperammonemia may develop in the absence of any clinical encephalopathy may also explain the lack of benefit for conventional therapies. Lactulose, which was initiated in a majority of those patients treated, provides its benefit in hepatic encephalopathy by reducing endogenous and dietary ammonia through a cathartic and pH-altering effect in the gut lumen. Rifaximin, the second most commonly used drug in this cohort reduces urease-producing bacteria in the gut lumen and thus endogenously produced ammonia [8]. The reduction in ammonia and other poorly metabolized molecules provided by lactulose or rifaximin may not benefit patients with acetaminophen toxicity given that these therapeutic targets may not be the main cause of hyperammonemia in toxicity and hyperammonemia may not be solely responsible for the encephalopathy that develops. Acetaminophen-induced hepatotoxicity can progress to hepatic failure, which may include encephalopathy, but using ammonia as an early marker of this possibility appears to be unwise. Using an ammonia concentration alone to initiate treatment for hepatic encephalopathy that has yet to develop may lead to patient discomfort or harm rather than any benefit [11].
Endoscopic management of acute oesophageal variceal bleeding within 12 hours of admission is superior to 12–24 hours
Published in British Journal of Biomedical Science, 2021
N Mousa, A Abdel-Razik, T Sheta, A G Deiab, A Habib, M Diasty, A Eldesoky, A Taha, E Mousa, A Yassen, A Fathy, A Elgamal
Hepatic encephalopathy is a common consequence of liver cirrhosis [27]. Although there is an improvement in hepatic encephalopathy in both groups post-treatment, the results of this study showed an improvement in hepatic encephalopathy following endoscopic treatment at 12 hours post presentation versus endoscopic treatment at 12–24 hours-post presentation. These results could be explained by early cessation of bleeding and a reduction of the ammonia levels, the key factor of hepatic encephalopathy with early endoscopic treatment [28]. We speculate that early management with control of bleeding is the main source of ammonia with consequent reduction of the ammonia level that is responsible for the improvement of hepatic encephalopathy. This supports the view that early endoscopic management of acute variceal bleeding according to guidelines is an important measure to improve morbidity. Accordingly, we agree with Barkun et al. [29], who recommended early endoscopy to decrease morbidity and mortality, although some suggested that the time to endoscopy was not a significant predictor of outcome in patients with variceal bleeding [15].