The active ingredient complex silymarin stabilizes the liver cell membrane

(shrunken liver): Progressive destruction of the liver over years, associated with nodular scarring changes and shrinkage of the liver. Liver cirrhosis is feared as the final stage of almost all liver diseases. 50% of cases are due to chronic alcohol abuse, one third to hepatitis infections and the rest to rarer causes, z. B. primary biliary cholangitis. 70% of sufferers are men, 30% women.

If the destruction cannot be stopped, the disease leads to death within months to a few years due to liver failure. For a minority of those affected, there is hope of a liver transplantation. However, in most patients – especially alcoholics – this is not possible due to their concomitant diseases.

Leading symptoms

– Fatigue, weight loss, reduced performance – Skin abnormalities such as vascular asterisks, reddened palms, lacquered tongue (ascites) – Dilated veins under the abdominal skin as a result of bypass circulation in portal hypertension – Loss of libido, breast formation in men, Irregular menstruation in women as a result of hormonal disorders – Pronounced jaundice with yellowing of conjunctiva and skin, itching all over the body – Dementia-like symptoms such as memory loss, disorientation, mood swings and inappropriate behavior as a result of brain damage.

The signs of severe liver disease such as z.B. of liver cirrhosis are: Yellow eyes, torn corners of the mouth (rhagades), scratch marks on the skin (due to itching), reddened palms (palmar erythema), growth of mammary gland tie (gynecomastia),star-shaped vascular neoplasms (spider nevi), ascites, varicose veins around the navel (caput medusae), edema in the legs, reddened and smooth tongue (varnish tongue), loss of pubic hair and shrinkage of testicles. Georg Thieme Verlag, Stuttgart

When to go to the doctor's office

In the next few days when

– Occurrence of one or more of the above symptoms

Show background information

The disease

Development of the disease and causes

Alcohol, hepatitis and some rarer pre-existing diseases lead to the death of liver cells. If the liver is permanently exposed to the harmful influences, it cannot replace the dying tie with functional liver cells, so it scars and instead forms coarse connective tie.

Hereditary metabolic diseases such as Wilson's disease and hemochromatosis are also among the pre-existing conditions that lead to liver cirrhosis. In Wilson's disease, copper metabolism is disturbed, associated with increased copper storage in the liver; in hemochromatosis, iron metabolism is disturbed, associated with increased iron deposition in the liver.

Another important cause for the development of liver cirrhosis is autoimmune liver disease, in which inflammatory processes attack the liver and bile ducts against the body's own tie. These include primary biliary cholangitis, primary sclerosing cholangitis and autoimmune hepatitis.


Once the liver tie has undergone nodular connective tie remodeling, this leads to a variety of problems:

Healthy liver cells produce many vital proteins. If liver cells are lost in favor of simple connective tie, these proteins are lacking. These include, for example, coagulation factors, i.e. proteins that are responsible for blood clotting. If too few clotting factors are produced, there is an increased tendency to bleed and thus an increased risk of hemorrhage.

The transport proteins for the blood, especially albumin, are also no longer produced in sufficient quantities. Due to this albumin deficiency in the blood, the so-called colloidosmotic prere decreases. As a result, water can no longer be held in the vessels and leaks into the surrounding tie. Depending on where it flows, edema, pleural effusion, or abdominal dropsy may result. The connective tie remodeling of the liver tie constricts. Also destroys the bile ducts located in the liver. This leads to bile flow disturbances (intrahepatic jaundice) with jaundice, itching and fat digestion disturbances.

If the blood vessels of the liver narrow as a result of the remodeling processes, the blood backs up on its way from the liver to the heart. This congestion leads to increased prere in the portal vein, the central vessel of the liver. Doctors then speak of Portal hypertension (portal hypertension). This congestion also makes itself felt in other blood vessels, e.g. B.

– in the spleen by swelling of the spleen (splenomegaly), which is associated with increased breakdown of blood cells – in the esophagus by esophageal varices, which can easily burst and lead to life-threatening bleeding – in the anus by hemorrhoids.


Complications occur when the damaged liver can no longer perform its detoxification function. syndromes such as Hepatic encephalopathy or hepatic failure coma can be explained by too much ammonia accumulating in the blood. The metabolic toxin ammonia directly impairs brain function, causing patients to exhibit various neurological and psychological abnormalities. In the beginning there is usually "only" Concentration disorders and mood swings. Due to reduced concentration and attention, people with hepatic encephalopathy also suffer from impaired responsiveness. As a result, they are more likely to commit driving errors than healthy individuals. Many traffic accidents are due to liver disease, but exact figures are not available.

In the worst case, there is a risk of impaired consciousness or even unconsciousness. Doctors refer to this as a fatal liver failure coma.

Hepatorenal syndrome. The damage associated with liver cirrhosis also results in end-stage renal failure. Signs are water retention (edema). Reduced urine output. A combined liver-. Kidney failure is usually no longer treatable.

Confirming the diagnosis

Based on the clear symptoms and the findings of the physical examination, the physician usually quickly suspects cirrhosis of the liver. Examination methods such as laboratory, ultrasound and, if necessary, laparoscopy can be used to confirm the diagnosis and assess the extent of liver damage and existing complications. Typical examinations and findings are

– Laboratory: – Ammonia elevated, due to impaired detoxification function : Anemia due to vitamin deficiency or blood loss due to coagulopathy – Blood values to search for the cause of cirrhosis: hepatitis viruses (hepatitis), autoantibodies (primary biliary cholangitis), iron (hemochromatosis), copper (Wilson's disease)

Top: Healthy liver in laparoscopy (abdominal endoscopy). The liver surface is smooth. Well perfused. Bottom: Cirrhotically altered liver in a patient with moderate cirrhosis. The nodular remodeling of the liver is easily recognizable; connective tie deposits lead to a lightening of the liver surface. Georg Thieme Verlag, Stuttgart


In addition to basic nutritional measures (compensation of vitamin or mineral deficiencies and sufficient calorie intake), the treatment of liver cirrhosis focuses on preventing further damage. These include:

– The flushing out of water in the abdominal cavity (ascites) by diuretic drugs – The sclerotherapy of varicose veins in the esophagus and stomach to prevent possible unstoppable bleeding – Strict prohibition of alcohol for the patient in order not to put more strain on the liver.

The effects of portal hypertension can also be at least reduced by treatment. One option is to place a short-circuit connection between the portal vein and the vena cava, a portosystemic shunt. Blood is diverted through it past the damaged liver, thus relieving prere. However, this procedure is associated with an increased risk of hepatic encephalopathy, because the blood is no longer sufficiently detoxified in the liver. The procedure is not without danger; the risk of death is 5-10 %, and as high as 50 % in the case of emergency surgery.

A hope for many patients is represented by the Liver transplantation dar. Unfortunately, many patients come to us due to exclusion criteria, z. B. alcohol dependence, not on the waiting lists. Even if this hurdle is cleared, waiting times are relatively long. If transplantation occurs, doctors transfer either an entire organ (cadaveric donation) or only a part of the liver (split liver transplantation, cadaveric donation and living donation possible). The 5-year survival rate is then 80%.

There is no cure or causative treatment available for hepatic encephalopathy, hepatic failure coma, and hepatorenal syndrome. In this case, doctors concentrate on ensuring circulatory function.


Prognosis depends on the extent of cirrhosis and whether complications are present. Doctors often classify liver cirrhosis into 3 classes based on 5 factors (albumin level, coagulation, bilirubin, encephalopathy and abdominal fluid; Child-Pugh score).

The 1-year survival rate is almost 100% for Child A type cirrhosis, 85% for Child B type, and 35% for Child C type. Supportive in the therapy of cirrhosis of the liver. Extracts from milk thistle are effective against other liver damages. The active ingredient complex silymarin stabilizes the liver cell membrane, stimulates the protein build-up in the liver cell and thus promotes the regeneration of the liver cells. Silymarin

Like this post? Please share to your friends:
Leave a Reply

;-) :| :x :twisted: :smile: :shock: :sad: :roll: :razz: :oops: :o :mrgreen: :lol: :idea: :grin: :evil: :cry: :cool: :arrow: :???: :?: :!: