Hepatitis C Blog

Greg Jefferys Hepatitis C blog deals with all the issues associated with hepatitis C

Is Liver Damage from Hep C Reversible

(This post is still under construction)

Hep C, Liver Damage and Liver Cirrhosis

Hepatitis C is one of the major causes of liver cirrhosis and death from liver failure. So one of the big questions that people who have had Hep C is: “Is liver damage from Hep C reversible?”

Put simply the answer is yes, liver damage from Hepatitis C can be reversed and the liver can heal from even advanced cirrhosis. The liver is very capable of regenerating from significant damage because, but various factors combined with a Hep C infection can reduce the liver’s ability to regenerate.

In this post, I will explain exactly what Hep C-induced liver cirrhosis is and give you an easy-to-understand explanation of what you can do to reverse liver damage caused by Hepatitis C once the Hep C infection is cured.

Research and Real-World Experiences on Cirrhosis Reversal

Firstly I should start out by stating that previous to the introduction of Hepatitis C treatment with DAAs the general position of the medical world was that liver cirrhosis was irreversible. Indeed many medical practitioners still believe this to be true, particularly those who did their training in the 20th century and have not kept up to date with the latest research on liver cirrhosis.


An important part of reversing liver cirrhosis is reducing or removing inflamed liver cells. The simplest way that this can be approached with known natural anti-inflammatories such as turmeric. Reducing inflammatory cells in the liver

For this, healthy hepatocytes and non-parenchymal cells change the microenvironment from a pro-inflammatory ambience (environment) to resolution, so that the presence of anti-inflammatory mediators increases. The liver macrophages become a restorative phenotype, increasing the expression of MMP and growth factors leading to hepatocyte recovery.

Macrophages, which are key cellular components of the liver, have emerged as essential players in the maintenance of hepatic homeostasis and in injury and repair processes in acute and chronic liver diseases. Upon liver injury, resident Kupffer cells (KCs) sense disturbances in homeostasis, interact with hepatic cell populations and release chemokines to recruit circulating leukocytes, including monocytes, which subsequently differentiate into monocyte-derived macrophages (MoMϕs) in the liver. Both KCs and MoMϕs contribute to both the progression and resolution of tissue inflammation and injury in various liver diseases. The diversity of hepatic macrophage subsets and their plasticity explain their different functional responses in distinct liver diseases. In this review, we highlight novel findings regarding the origins and functions of hepatic macrophages and discuss the potential of targeting macrophages as a therapeutic strategy for liver disease.


The liver is one of the only organs in the body that is able to replace damaged tissue with new cells rather than scar tissue. For example, an overdose of acetaminophen (Tylenol) can destroy half of a person’s liver cells in less than a week. Barring complications, the liver can repair itself completely and, within a month, the patient will show no signs of damage.

However, sometimes the liver gets overwhelmed and can’t repair itself completely, especially if it’s still under attack from a virus, drug, or alcohol. Scar tissue develops, which becomes difficult to reverse, and can lead to cirrhosis


Liver fibrosis

For the 52 patients with nondetectable HCV-RNA with standard methods, the biochemical tests (at a group level) indicated a statistically significant improvement (Table 2). The number of patients with fibrosis score F0–F1 increased from 19 before treatment to 41 at long-term FU. Comparisons were not possible in seven patients because of missing biopsy data at baseline (n=4) or missing TE/biopsy at FU (n=3; Table 2). Overall, the assessed fibrosis stages were significantly lower at FU (P=0.001; Fig. 2).

Greg Jefferys

Greg Jefferys

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