Under a hepatic fibrosis refers to an excessive wound healing, in which intercalates amplified connective tissue in the liver. Extracellular matrix is ??produced in greater and / or poorly decomposed. Triggers are chronic lesions, especially when doing an inflammatory component plays a role. Fibrosis itself causes no symptoms but can lead to portal hypertension (scarring impairs blood flow through the liver) or cirrhosis (scarring caused a disruption of normal liver architecture and resulting in hepatic impairment) lead. Diagnosis is made by the liver biopsy. The treatment consists, if possible, to eliminate the underlying cause.
In liver fibrosis is excessive connective tissue accumulates in the liver; scarred this tissue in response to a chronic, repeated liver cell damage. In general, the fibrosis progresses, making the liver architecture and finally the function to be disturbed. Thereby regenerating hepatocytes try to replace damaged tissue and repair. If these processes are well advanced there is a cirrhosis.
Under a hepatic fibrosis refers to an excessive wound healing, in which intercalates amplified connective tissue in the liver. Extracellular matrix is ??produced in greater and / or poorly decomposed. Triggers are chronic lesions, especially when doing an inflammatory component plays a role. Fibrosis itself causes no symptoms but can lead to portal hypertension (scarring impairs blood flow through the liver) or cirrhosis (scarring caused a disruption of normal liver architecture and resulting in hepatic impairment) lead. Diagnosis is made by the liver biopsy. The treatment consists, if possible, to eliminate the underlying cause. In liver fibrosis is excessive connective tissue accumulates in the liver; scarred this tissue in response to a chronic, repeated liver cell damage. In general, the fibrosis progresses, making the liver architecture and finally the function to be disturbed. Thereby regenerating hepatocytes try to replace damaged tissue and repair. If these processes are well advanced there is a cirrhosis. Various types of chronic liver damage can cause fibrosis (see table: medical conditions and medications that can cause hepatic fibrosis). A self-limiting, acute liver injury (eg. As acute viral hepatitis A), even if it is brilliant, does not necessarily lead to changes in the architectural framework and fibrosis formation, despite the loss of hepatocytes. In the initial stages of the liver fibrosis (eg., By elimination of the virus) may regress when the cause is reversible. After months or years of chronic or recurrent injury, fibrosis becomes permanent. By a mechanical bile duct obstruction, the fibrosis developed even faster. Diseases and medications that can cause hepatic fibrosis diseases directly involving the liver autoimmune hepatitis (storage diseases and hereditary metabolic disorders Alpha-1-antitrypsin deficiency copper storage diseases (eg. B. Wilson’s disease) fructosemia galactosemia glycogen storage diseases, in particular the types III, IV, VI, IX and .. X) iron overload (hemochromatosis) lipid abnormalities (eg, Gaucher disease) Peroxisomenstörungen (eg Zellweger syndrome) tyrosinaemia Congenital hepatic fibrosis infections -. bacteria (eg, brucellosis) – Parasi Secretary (. eg echinococcosis) – viral (eg. B. Hepatitis B or C *) Non-alcoholic steatohepatitis (NASH) Primary biliary cirrhosis Primary sclerosing cholangitis diseases affecting the blood flow in the liver Budd-Chiari syndrome, heart failure, veno-occlusive disease Portal vein thrombosis drugs and chemicals alcohol * amiodarone chlorpromazine isoniazid methotrexate methyldopa oxyphenisatin tolbutamide Mechanical obstruction Scarring because of past liver surgery bile duct by gallstones * The most common causes. occasionally caused by PAs that are found in plant products such as bush teas. Pathophysiology activation of perivascular stellate cells (Ito cells that store fat) initiates fibrosis. These and neighboring cells proliferate and become contractile cells, which are called myofibroblasts. These cells produce large amounts of abnormal matrix (consisting of collagen, other glycoproteins, and glycans) and matrizellulärer proteins. Kupffer cells (macrophages), damaged hepatocytes, platelets and leukocyte aggregates produce reactive O2 species and inflammatory mediators (eg. B. platelet-dependent growth factor, transforming growth factor, connective tissue growth factor). Thus, activation of stellate cells into an altered extracellular matrix leads, both in quantity and in composition. Myofibroblasts, stimulated by endothelin-1, contribute to increased portal venous resistance in and increase the density of the abnormal matrix. By itself fibrous tissue intercalates to afferent portal veins and efferent hepatic veins, the hepatocytes are bypassed and limited in their blood supply. This fibrosis contributes both to ischemia of the liver cells (and thus to the failure of hepatocellular function) in and to the development of portal hypertension. The extent of ischemia and portal hypertension determines the liver damage. Congenital hepatic fibrosis affects z. As only the portal venous branches, while the parenchyma is spared essentially. This results in a portal Hypertens ion, wherein the hepatocellular function is not limited. Symptoms and complaints Liver fibrosis itself is asymptomatic. The symptoms can be a result of the fibrosis-causing disorder or when the fibrosis to liver cirrhosis developed to be the complications of portal hypertension. These symptoms are variceal bleeding, ascites and portosystemic encephalopathy. Cirrhosis can lead to liver failure and possible, to a fatal liver failure. Diagnosis Clinical examination if necessary Blood tests and / or non-invasive imaging techniques, if necessary Liver biopsy suspected hepatic fibrosis is (chronic viral hepatitis C and hepatitis B, for example [see Table: Properties of hepatitis viruses].,) In patients with known chronic liver disease alcoholic liver disease) or abnormal liver function; In such cases, tests are performed on fibrosis and – if present – its severity (stage) is determined. The knowledge of fibrosis stage can lead to medical decisions. For example, a screening for hepatocellular carcinoma and gastroesophageal varices is indicated for confirmed cirrhosis, but generally not with mild to moderate fibrosis. Although advanced fibrosis is established in patients with hepatitis C through the liver biopsy, many clinicians push to treatment with interferons, because they assume that more effective, less toxic drugs will be available. Tests to determine the fibrosis stage are non-invasive imaging tests, blood tests, liver biopsy and newer tests assess liver stiffness. Non-invasive imaging tests are conventional ultrasound, CT and MRI and should sectional views included. These studies can give indications of cirrhosis and portal hypertension such as splenomegaly and varices. However, they are not sensitive to moderate or even advanced fibrosis when splenomegaly and varices are absent. Although fibrosis appears to be altered echogenicity on ultrasound or CT heterogeneity in the signal, these findings are non-specific and may indicate Leberparenchymfett. New technologies can increase the accuracy of ultrasound and MRI in detecting fibrosis or early cirrhosis; including ultrasound elastography, magnetic resonance elastography and “acoustic radiation force impulse imaging”. acoustic vibrations to the abdomen are given with a probe for these tests. The transmission speed of the vibration through the liver tissue is measured; this is an indication of how stiff (ie fibrotic) the liver is. Ultrasound elastography and magnetic resonance elastography win the acceptance of insurance as documentation for a fair treatment of liver fibrosis with expensive new interferon-free medicines for viral hepatitis. Liver biopsy remains the gold standard for the diagnosis and staging of liver fibrosis and for the diagnosis of the underlying liver disease that causes fibrosis. However, the liver biopsy is invasive, which with a 10-20% risk for low complications (postprocedural z. B. pain) and a 0.5-1% risk for serious complications (eg. B. serious bleeding) is connected. Also, the liver biopsy restrictions by sampling error and insufficient interobserver agreement in the interpretation of histological findings. Therefore, liver biopsy may not always be done. Blood tests include commercial tests that combine indirect markers (eg. As serum bilirubin) and direct markers of liver function. Direct markers are substances that play a role in the pathogenesis of extracellular matrix deposition, or cytokines, which induce the deposition of extracellular matrix. These tests are best used to distinguish between two levels fibrosis: No to minimal versus moderate to severe; they do not differentiate enough between moderate to severe fibrosis. Therefore, if there is suspicion of fibrosis, is an opportunity to start with one of these tests, and only to make a liver biopsy if the test result indicates moderate to severe fibrosis. Which test is performed depends on the clinical suspicion, based on clinical examination, including liver function tests. For example, non-invasive blood tests can be used to determine the indication for biopsy; in some of these cases, imaging tests are not necessary. Therapy treatment of the cause, since the fibrosis is a response to liver damage, the initial treatment should focus on the cause (removal of the cause of the liver damage). Such a treatment includes the elimination of hepatitis B virus or hepatitis C virus in chronic viral hepatitis, the absence of alcohol in alcoholic liver disease, the removal of heavy metals such as iron during hemochromatosis or copper in Wilson’s disease, as well as decompression of the bile ducts in bile duct obstruction. Such treatments can stop the progression of fibrosis and undo some fibrotic changes in some patients. Treatments that aim to regression of fibrosis, to generally toxic for long-term use (corticosteroids, penicillamine) or have no documented effect on (z. B. colchicine). Other antifibrotic therapies are currently being investigated in studies. the simultaneous application of several antifibrotic drugs is probably the most useful. Silymarin, which is present in milk thistle, is a popular alternative drug that is used to treat liver fibrosis. It seems to be sure, but it is not effective. Key points A self-limiting, acute liver injury (eg. As a result of acute viral hepatitis A), even if it is brilliant, is not prone to fibrosis formation. The most common causes of liver fibrosis are hepatitis B and C and alcohol abuse. A fibrosis causes no symptoms until progression to cirrhosis. Liver biopsy, although not perfect, the gold standard among diagnostic procedures. Non-invasive tests, including ultrasound elastography and magnetic resonance elastography, are becoming increasingly important. There is a causal treatment of fibrosis.