Efficacy and safety of anti-hepatic fibrosis drugs

Abstract

Recent progress in our understanding of the pathways linked to progression from hepatic insult to cirrhosis has led to numerous novel therapies being investigated as potential cures and inhibitors of hepatic fibrogenesis. Liver cirrhosis is the final result of prolonged fibrosis, which is an intimate balance between fibrogenesis and fibrinolysis. A number of these complex mechanisms are shared across the various etiologies of liver disease. Thankfully, investigation has yielded some promising results in regard to reversal of fibrosis, particularly the indirect benefits associated with antiviral therapy for the treatment of hepatitis B and C and the farnesoid receptor agonist for the treatment of primary biliary cholangitis and metabolic associated fatty liver disease. A majority of current clinical research is focused on targeting metabolic associated fatty liver disease and its progression to metabolic steatohepatitis and ultimately cirrhosis, with some hope of potential standardized therapeutics in the near future. With our ever-evolving understanding of the underlying pathophysiology, these therapeutics focus on either controlling the primary disease (the initial trigger of fibrogenesis), interrupting receptor ligand interactions and other intracellular communications, inhibiting fibrogenesis, or even promoting resolution of fibrosis. It is imperative to thoroughly test these potential therapies with the rigorous standards of clinical therapeutic trials in order to ensure the highest standards of patient safety. In this article we will briefly review the key pathophysiological pathways that lead to liver fibrosis and present current clinical and experimental evidence that has shown reversibility of liver fibrosis and cirrhosis, while commenting on therapeutic safety.

Exploration of nucleos(t)ide analogs cessation in chronic hepatitis B patients with hepatitis B e antigen loss

“…A considerable proportion of patients fail to achieve HBeAg seroconversion after the long-term loss of HBeAg, even if HBsAg loss occurs[ 9 , 10 ]. It remains unclear whether NAs can be discontinued in this subset of patients[ 1 - 3 , 11 , 12 ].…”

Pathophysiology and Treatment Options for Hepatic Fibrosis: Can It Be Completely Cured?

“…Advances in the understanding of the pathophysiological basis of fibrogenesis are now leading to the development of novel therapeutic approaches. Treatment options for liver fibrosis may include the use of antiviral drugs, alcohol abstinence and weight loss in case of viral hepatitis, alcoholic liver disease and obesity induced fibrosis, respectively [ 162 , 163 , 164 , 165 ]. Currently available therapies are mostly directed towards suppressing hepatic inflammation rather than reducing fibrosis.…”

Hepatoprotective Effect and Potential Mechanism of Aqueous Extract from Phyllanthus emblica on Carbon-Tetrachloride-Induced Liver Fibrosis in Rats

“…Chronic liver damage is caused by a variety of etiologies which further induce liver fibrosis, including alcohol toxicity, chemical poisons, chronic viruses, and immune damage [3]. Currently, clinical therapeutics of LF focus on either controlling the primary disease or treatment of liver fibrosis itself by routinely reducing inflammation, inhibiting oxidative stress, and promoting collagen degradation [4][5][6][7]. However, specific and high-efficiency antiliver fibrosis drugs with no obvious side effects have not yet appeared.…”