In hepatic fibrosis, excessive connective tissue builds up in the liver; this tissue represents scarring in response to repetitive chronic liver cell injury. Fibrosis often progresses and compromises the structure and eventually function of the liver as regenerating hepatocytes attempt to replace and repair damaged tissue. When this alteration is disseminated, cirrhosis is confirmed.
Several types of chronic liver injury can cause fibrosis. Self-limited acute liver injury (eg, acute viral hepatitis A), even if fulminant, does not necessarily distort the basic structure of the liver and thus does not promote the development of fibrosis despite loss of hepatocytes. In its early stages, liver fibrosis may regress if the cause is reversible (eg, after viral clearance). If the patient is exposed to several months or years of chronic or repetitive injury, the fibrosis becomes permanent. Fibrosis develops at an even faster rate in the presence of mechanical obstruction of the bile ducts.
Activation of perivascular stellate cells of the liver (Ito cells, which store lipids) promotes the development of fibrosis. These and adjacent cells proliferate and become contractile cells called myofibroblasts. These cells produce excessive amounts of abnormal matrix (made up of collagen, other glycoproteins, and glycans) and cell matrix proteins. Kupffer cells (resident macrophages), injured hepatocytes, platelets, and leukocytes aggregate. As a consequence, reactive oxygen species and inflammatory mediators (eg, platelet-derived growth factor, transforming growth factors, connective tissue growth factor) are released. Consequently, the activation of stellate cells promotes the development of an abnormal extracellular matrix, both in quantity and composition.
Endothelin-1-stimulated myofibroblasts contribute to increased resistance in the portal vein and increase the density of the abnormal matrix. The fibrous tracts join with branches of the afferent portal veins and efferent hepatic veins, allowing them to bypass hepatocytes and limiting their blood supply. Thus, fibrosis contributes to both hepatocyte ischemia (with subsequent hepatocellular dysfunction) and portal hypertension. The magnitude of ischemia and portal hypertension determine liver involvement. For example, congenital hepatic fibrosis involves the branches of the portal vein and spares little parenchyma. As a result, portal hypertension develops, but with normal hepatocellular function.
- Clinical evaluation
- Sometimes blood tests and/or noninvasive imaging tests
- Sometimes liver biopsy
Liver fibrosis is suspected if patients have known chronic liver disease (eg, chronic viral hepatitis C or chronic hepatitis B, alcoholic liver disease) if liver test results are abnormal; in such cases, tests are done to check for fibrosis and, if fibrosis is present, to determine its severity (stage). Knowledge of the stage of fibrosis can guide medical decisions. For example, screening for hepatocellular carcinoma and gastroesophageal varices is indicated if cirrhosis is confirmed, but is generally not indicated for mild or moderate fibrosis. Evaluation of the degree of liver fibrosis helps to assess the prognosis of patients with chronic viral hepatitis. However, due to the widespread availability of direct-acting antiviral drugs, knowing the degree of fibrosis has become much less important in deciding when to start antiviral therapy.
Tests used to stage fibrosis include noninvasive imaging tests, blood tests, liver biopsy, and newer tests that assess liver stiffness.
Non-invasive imaging tests include conventional ultrasound, CT, and MRI. These tests can detect evidence of cirrhosis and portal hypertension, such as liver surface nodularity, splenomegaly, and varices. However, they are not sensitive for moderate or even advanced fibrosis and may fail to detect some cases of cirrhosis in the absence of splenomegaly and varices. Although fibrosis may present as altered echogenicity on ultrasound or signal heterogeneity on CT, these findings are nonspecific and may indicate only fatty tissue in the liver parenchyma.
CBD oil for Hepatic Fibrosis
If we look at a hepatic liver, we can see how the condition appears when hepatic stellate cells are activated, which multiply excessively and produce collagen in excessive amounts, which is what leads to hepatic fibrosis. CBD has been shown to cause the death of these activated hepatic stellate cells, making CBD an effective treatment for liver fibrosis.
In a study with mice suffering from hepatic encephalopathy, the use of CBD shows that a better treatment can be developed. Hepatic encephalopathy occurs when acute or chronic liver failure occurs, leading to this neuropsychiatric disorder.
Mice treated with CBD for this particular disease showed an improvement in their liver functions, as cannabidiol restored plasma levels of ammonia, liver enzymes and bilirubin. At the same time, CBD administration helped normalize brain function in the same mice, which is considered possible due to the dual action of CBD on both the brain and liver at the same time. This indicates that the use of CBD products may help in the treatment of this disease in humans.
What is the posology of CBD for Hepatic Fibrosis?
It always depends of many factors, like the CBD composition, the CBD concentration, the weight, etc..
Our suggestion with our CBD oil at 20% is start with 3 drops in the morning, another 2-3 at lunch time and a little higher in the evening just 4-5 for a rest sleep.
We always say that is necessary to talk with your doctor about the CBD and a control of the dosage. Too much CBD will not be absorbed by the body and as it comes in it will go out. Not for taking a lot of CBD means that will help you faster. Remember that this is natural and the effects on the body are not the same as a chemical pill. CBD will never leave you a residue or will give you a side effect.
I leave you the direct link if you would like to try one of our CBD oils. This one is a 20% CBD concentration with less than 0.1´8% of THC for a fast result. Let us a comment at the bottom and a suggestion if you like. Catch you on the next post!