Objective: The purpose of this manuscript is to identify the pathophysiology of the metabolic abnormalities observed in cirrhosis and to uncover associations, if any, to its complications, such as sarcopenia and hepatic encephalopathy (HE).Background: Liver dysfunction in cirrhosis is known to be a precipitating factor in the disruption of many physiological pathways, specifically nutrient metabolism. As a result, affected patients are highly susceptible to derangements of processes affecting multiple classes of macro-and micronutrients, including proteins, carbohydrates, electrolytes, vitamins, and minerals. These disruptions are thought to be contributory to the pathogenesis of known complications of cirrhosis.Methods: Literature research of relevant topics was conducted for the above stated objective; sources were limited to articles from peer-reviewed journals published within the last 30 years.Conclusions: This research established that there is positive correlation between nutrient derangements and the increased risk of complications of cirrhosis, which themselves carry significant morbidity and mortality risk. It also established that some nutrient and electrolyte abnormalities are independent indicators of prognosis and adverse outcomes, such as mortality. This also highlights the importance of comprehension of anomalous metabolism and its complications as it necessitates serious consideration in clinical care. In addition to medical management, cirrhotic patients also require ancillary assessment, such as comprehensive nutritional evaluation, to identify and treat reversible nutritional derangements. This consideration provides the best opportunity to achieve maximal health outcomes in the cirrhotic patient population.
Fulminant hepatic failure (FHF) carries a high mortality. We aimed to review the prognostic factors and explore the potential role of Liver Dialysis (LD).
Fifty-two patients were reviewed. The etiologies were acetaminophen toxicity (33%), viral hepatitis (18%), autoimmune (10%), idiosyncratic drug reactions (8%), others (6%) and undetermined (25%). Patients with acetaminophen had a significantly higher survival compared to the non-acetaminophen group (p=0.04). Patients with grade 3 encephalopathy had a mortality of 68%, among 5 patients with grade IV encephalopathy, 2 survived and both had had treatment with LD.
Chi-square with Fisher's exact test was used for statistical analysis.
Our study confirmed that the diagnosis of non-acetaminophen induced FHF and reduced initial serum factor V level are associated with fatal outcome. Timely OLT significantly improved the survival. The role of LD in hepatic regeneration or as a bridge to OLT needs to be further studied with prospective control trials.
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