Abstract
Ischaemic Hepatitis (IH) or Hypoxic Hepatitis (HH) also known as centrilobular liver cell necrosis is an acute liver injury characterized by a rapid increase in serum aminotransferase. The liver injury typically results from different underlying medical conditions such as cardiac failure, respiratory failure and septic shock in which the liver becomes damaged due to deprivation of either blood or oxygen. IH is a potentially lethal condition that is often preventable if diagnosed timely. The role of mechanisms that cause IH is often not well understood, making it difficult to diagnose or accurately quantify the patterns of related biomarkers. In most patients, currently, the only way to determine a case of IH is to rule out all other possible conditions for liver injuries. A better understanding of the liver's response to IH is necessary to aid in its diagnosis, measurement, and improve outcomes. The goal of this study is to identify mechanisms that can alter associated biomarkers for reducing the density of damaged hepatocytes, and thus reduce the chances of IH. We develop a mathematical model capturing dynamics of hepatocytes in the liver through the rise and fall of associated liver enzymes aspartate transaminase (AST), alanine transaminase (ALT) and lactate dehydrogenase (LDH) related to the condition of IH. The model analysis provides a novel approach to predict the level of biomarkers given variations in the systemic oxygen in the body. Using IH patient data in the US, novel model parameters are described and then estimated for the first time to capture real-time dynamics of hepatocytes in the presence and absence of IH condition. The results may allow physicians to estimate the extent of liver damage in an IH patient based on their enzyme levels and receive faster treatment on a real-time basis.
Highlights
Ischaemic Hepatitis (IH) is a critical liver injury due to centrilobular liver cell necrosis with a massive increase in serum aminotransferase [1, 2]
The goals of this study are to: (i) provide a framework of relevant biomarkers and hepatocytes in order to study patterns of IH condition, (ii) estimate average decay and growth parameters related to concentration of biomarkers during IH, (iii) predict real time peak levels of different biomarkers, namely aspartate transaminase (AST), alanine transaminase (ALT), and lactate dehydrogenase (LDH), due to liver injury caused by IH at varied oxygen levels in the body as well as varied treatment frequency, and (iv) identify threshold conditions for time to reach the critical concentration level of hepatocytes for irreversible damage for varied initial oxygen level in the body
We model the production of aspartate aminotransferase-AST (S), alanine aminotransferase-ALT (L) and lactate dehydrogenase-LDH (D) which are all important bio-markers and byproducts of liver damage
Summary
Ischaemic Hepatitis (IH) is a critical liver injury due to centrilobular liver cell necrosis with a massive increase in serum aminotransferase [1, 2]. Over a long period of time, this increased blood flow to the hepatic vein causes congestion of the vein, eventually building to a point of failure resulting in IH [7,8,9]. For this reason, there are no chronic cases of IH, just chronic conditions that can cause it. A few such conditions are kidney disease, heart disease, and liver disease [6, 10, 11]
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