Analysis of coagulation factor VIII in liver failure syndromes

Kumar, Sandeep; Nair, Sukesh C.; Zachariah, Uday; Geevar, Tulasi; Eapen, C.E.; Goel, Ashish

doi:10.1016/j.jceh.2021.10.126

Cited by 1 publication

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“…Although the exact root cause of the increase in FVIII levels in liver diseases is not known, there are several hypotheses regarding why FVIII levels changed [ 175 , 176 , 177 ]. The release of cytokine from necrotic cirrhotic liver tissue might result in elevated FVIII synthesis [ 178 ].…”

Section: Possible Interaction Mechanisms Among Coagulation Dyshomeost...mentioning

confidence: 99%

Coagulation Dysfunctions in Non-Alcoholic Fatty Liver Disease—Oxidative Stress and Inflammation Relevance

Robea,

Balmus,

Girleanu

et al. 2023

Medicina

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Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases. Its incidence is progressively rising and it is possibly becoming a worldwide epidemic. NAFLD encompasses a spectrum of diseases accounting for the chronic accumulation of fat within the hepatocytes due to various causes, excluding excessive alcohol consumption. In this study, we aimed to focus on finding evidence regarding the implications of oxidative stress and inflammatory processes that form the multifaceted pathophysiological tableau in relation to thrombotic events that co-occur in NAFLD and associated chronic liver diseases. Recent evidence on the pathophysiology of NAFLD suggests that a complex pattern of multidirectional components, such as prooxidative, proinflammatory, and prothrombotic components, better explains the multiple factors that promote the mechanisms underlying the fatty acid excess and subsequent processes. As there is extensive evidence on the multi-component nature of NAFLD pathophysiology, further studies could address the complex interactions that underlie the development and progression of the disease. Therefore, this study aimed to describe possible pathophysiological mechanisms connecting the molecular impairments with the various clinical manifestations, focusing especially on the interactions among oxidative stress, inflammation, and coagulation dysfunctions. Thus, we described the possible bidirectional modulation among coagulation homeostasis, oxidative stress, and inflammation that occurs in the various stages of NAFLD.

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