Aa
HIV drug Maraviroc prevents liver fibrosis
This drug is already approved for HIV & according to new research it prevents fibrosis or Hepatocellular Carcinoma.
Link : http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0053992
Link : http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0053992
... but in Mayo Clinic website .. they warn from statin side effects against liver ..
Statin side effects: Weigh the benefits and risks
Liver damage
Occasionally, statin use could cause your liver to increase its production of enzymes that help you digest food, drinks and medications. If the increase is only mild, you can continue to take the drug. Rarely, if the increase is severe, you may need to stop taking the drug. Your doctor might suggest a different statin. Certain other cholesterol-lowering drugs, such as gemfibrozil (Lopid) and niacin (Niacor, Niaspan), increase the risk of liver problems even more in people who take statins.
Although liver problems are rare, your doctor will likely order a liver enzyme test before or shortly after you begin to take a statin. You shouldn't need any additional liver enzyme tests unless you begin to have signs or symptoms of trouble with your liver. Contact your doctor immediately if you have unusual fatigue or weakness, loss of appetite, pain in your upper abdomen, dark-colored urine, or yellowing of your skin or eyes.
http://www.mayoclinic.com/health/statin-side-effects/MY00205
Statin side effects: Weigh the benefits and risks
Liver damage
Occasionally, statin use could cause your liver to increase its production of enzymes that help you digest food, drinks and medications. If the increase is only mild, you can continue to take the drug. Rarely, if the increase is severe, you may need to stop taking the drug. Your doctor might suggest a different statin. Certain other cholesterol-lowering drugs, such as gemfibrozil (Lopid) and niacin (Niacor, Niaspan), increase the risk of liver problems even more in people who take statins.
Although liver problems are rare, your doctor will likely order a liver enzyme test before or shortly after you begin to take a statin. You shouldn't need any additional liver enzyme tests unless you begin to have signs or symptoms of trouble with your liver. Contact your doctor immediately if you have unusual fatigue or weakness, loss of appetite, pain in your upper abdomen, dark-colored urine, or yellowing of your skin or eyes.
http://www.mayoclinic.com/health/statin-side-effects/MY00205
From the paper, I find this explanation about the link between fibrosis and HCC very useful:
Regardless of etiology, chronic liver disease generally involves a process of progressive destruction and regeneration of the liver parenchyma, leading to fibrosis and cirrhosis. At early stages most patients are asymptomatic and can easily go undiagnosed and untreated for decades [8]. This chronic liver injury is characterized, at the molecular level, for the rapid turnover and excessive accumulation of extracellular matrix proteins which replace the functional parenchyma by fibrotic tissue [9]. Hepatic stellate cells (HSC) are the main source of the fibrotic tissue and, upon chronic damage, they secrete numerous inflammatory mediators including chemokines CCL3, CCL4, and CCL5, among others [10], [11]. Simultaneously, HSC express several chemokine receptors such as CXCR3, CCR1, CCR3, CCR5, and CCR7 [12], [13]. Moreover, HSC express the other HIV co-receptor, CXCR4. Binding of this receptor by its endogenous ligand, CXCL12, also has pro-fibrogenic effects on HSC [14]. It seems that the paracrine and autocrine activation of these receptors promotes the fibrogenic response [15], which is characterized by increased collagen synthesis, impaired collagen degradation, and secretion of further inflammatory mediators [16]. The progressive fibrosis and persistent liver inflammation would eventually lead to HCC [17].
Regardless of etiology, chronic liver disease generally involves a process of progressive destruction and regeneration of the liver parenchyma, leading to fibrosis and cirrhosis. At early stages most patients are asymptomatic and can easily go undiagnosed and untreated for decades [8]. This chronic liver injury is characterized, at the molecular level, for the rapid turnover and excessive accumulation of extracellular matrix proteins which replace the functional parenchyma by fibrotic tissue [9]. Hepatic stellate cells (HSC) are the main source of the fibrotic tissue and, upon chronic damage, they secrete numerous inflammatory mediators including chemokines CCL3, CCL4, and CCL5, among others [10], [11]. Simultaneously, HSC express several chemokine receptors such as CXCR3, CCR1, CCR3, CCR5, and CCR7 [12], [13]. Moreover, HSC express the other HIV co-receptor, CXCR4. Binding of this receptor by its endogenous ligand, CXCL12, also has pro-fibrogenic effects on HSC [14]. It seems that the paracrine and autocrine activation of these receptors promotes the fibrogenic response [15], which is characterized by increased collagen synthesis, impaired collagen degradation, and secretion of further inflammatory mediators [16]. The progressive fibrosis and persistent liver inflammation would eventually lead to HCC [17].
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