This article provides background information on chronic liver disease and states that it can be caused by many things, including alcohol abuse, chronic viral hepatitis, and metabolic factors. Over time, fibrotic tissue develops and without treatment, causes chronic injury and becomes fibrotic. Fibrosis then impairs the normal oxygenation and vasculature to the liver tissue. The author states that according to a large study, cirrhosis is the fourth leading cause of death due to non-communicable diseases worldwide. The total number of deaths due to cirrhosis has increased by 50 million over the past two decades. This is accredited to late diagnosis and the fact that compensated state of cirrhosis can remain asymptomatic for a long period of time.
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Ironically, the addition of portal hypertension plays a significant role in the transformation of compensated cirrhosis to the decompensated stage. The author suggests that early diagnosis of the compensated phase and an accurate risk stratification are the key to moving toward personalized medicine. The author states that this can be done not by the current standard method of diagnosis, which includes liver biopsy, hepatic venous pressure gradient measurement and endoscopy, but rather, reconsider the non-invasive ultrasound elastography that may enhance the detection of early diagnosis. Perhaps this will be key to identifying compensated cirrhosis before it becomes decompensated and causes increased risk of complications. The author suggests that simple, diagnostic methods, such as the ultrasound and elastography, are easy ways to provide bedside screening and first risk stratification. She admits; however, that in patients with compensated cirrhosis and potential hepatocellular carcinoma, the hepatic venous pressure gradient is the best method to stage the portal hypertension. When addressing advancements in therapy, it is concluded that pharmacological and non-pharmalogical therapies markedly reduce further decompression. In compensated cirrhosis, the goal of treatment should be to decrease the intra-hepatic resistance. Treatment should be focused on the vasculature and sinusoidal endothelial
Ironically, the addition of portal hypertension plays a significant role in the transformation of compensated cirrhosis to the decompensated stage. The author suggests that early diagnosis of the compensated phase and an accurate risk stratification are the key to moving toward personalized medicine. The author states that this can be done not by the current standard method of diagnosis, which includes liver biopsy, hepatic venous pressure gradient measurement and endoscopy, but rather, reconsider the non-invasive ultrasound elastography that may enhance the detection of early diagnosis. Perhaps this will be key to identifying compensated cirrhosis before it becomes decompensated and causes increased risk of complications. The author suggests that simple, diagnostic methods, such as the ultrasound and elastography, are easy ways to provide bedside screening and first risk stratification. She admits; however, that in patients with compensated cirrhosis and potential hepatocellular carcinoma, the hepatic venous pressure gradient is the best method to stage the portal hypertension. When addressing advancements in therapy, it is concluded that pharmacological and non-pharmalogical therapies markedly reduce further decompression. In compensated cirrhosis, the goal of treatment should be to decrease the intra-hepatic resistance. Treatment should be focused on the vasculature and sinusoidal endothelial