Enterogenous Endotoxemia in Chronic Hepatitis– Part 1

Enterogenous endotoxemia (EE) is a very common complication in chronic liver diseases. The incidence rate of EE in chronic hepatitis is approximately 50 to 58% with varying degress of severity. In other liver diseases such as acute hepatitis, fulminant hepatitis, and cirrhosis, the approximate ranges are 16% to 43%, 58% to 100%, and 79% to 92%, respectively. From these figures, we can see that EE is an important complication that can worsen the liver’s pathology and promote other disorders. Therefore, preventing and treating EE is an important task in the care of chronic liver diseases.

The endotoxin absorbed from the intestines passes through the barriers of the intestinal mucus membrane, Kupffer cells of the liver, serum detoxification mechanisms and finally into the systemic blood stream of the body. During active liver disease, there is often an accompanying inflammatory bowel disorders that makes the mucus membrane of intestine more penetrable. Hypertension of portal vein causes congestive intestinal disorders, in which the blood congestion, swelling, erosive lesions of mucus membrane in the intestinal wall causes the mucus membrane barrier to leak. In addition, the liver inflammation weakens the Kupffer cells' phagocytosis function, which allows the intestinal endotoxin (IE) to seep through the liver and enter the systemic circulation, bypassing the phagocytosis of Kupffer cells. Studies found that the level of IE in cirrhotic patients' liver vein was 73±110ng/L and 31± 58 ng/L in the systematic vein. The difference was statistically significant (p<0.001 and suggested that the cirrhotic liver could not clear the IE from the portal vein.

Damaged Kupffer cells can further promote liver damage. When large amounts IE enter the liver, it will directly cause liver damage when the Kupffer cells can not clear it. The IE can also trigger the release of cytokines in the damaged Kupffer cells, which will exacerbate the inflammation in the liver.  In the late stage of cirrhosis, there is portal-systemic shunt and the IE can enter the systemic circulation directly, completely bypassing the liver. This is mainly caused by the hypertension of the portal vein, which causes the lymph fluid production in the mesenterium to increase, allowing the IE to easily enter the systemic circulation via lymph circulation. Thus, EE is very common in the advanced stage of the liver disease EE.

In addition to causing direct liver damage and promoting other liver complications, EE can also obstruct bile secretion and cause bile retention. It can cause the blockage of the blood circulation in the liver vein and cause congestion in the liver. The common symptoms of EE are: fevers, failure of gastrointestinal functions, manifestations outside the liver such as kidney injuries, swelling and erosive bleeding of stomach membrane, disseminated intravenous clotting, and lung injuries. In many cases, the EE can also cause ascites and jaundice.
Treating the underlying liver disease and controlling the inflammation of the liver is the fundamental treatment for preventing and treating EE. Maintenance of regular bowel movement is also very important. To suppress the over-growth of bacteria in the intestines, Herbs such as Allicin and Coptin can be very effective. 
Detailed treatment of EE will follow in the next article.