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
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
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.