Steatohepatitis

from Wikipedia, the free encyclopedia
Classification according to ICD-10
K76.0 Fatty liver [fatty degeneration], not elsewhere classified
K70.1 Alcoholic hepatitis
K71 Toxic liver disease
K73 Chronic hepatitis, not elsewhere classified
K75 Other inflammatory liver diseases
K75.2 Nonspecific reactive hepatitis
ICD-10 online (WHO version 2019)

A steatohepatitis (colloquially fatty liver hepatitis ) is a disease in which inflammatory changes occur in a fatty liver (Latin steatosis hepatis). There is no infectious cause such as B. by viruses .

clinic

With a pure fatty liver there are no symptoms. With steatohepatitis , unspecific complaints occur in about half of the cases, such as tenderness with enlarged liver , loss of appetite, nausea, bloating, weight loss. In severe cases, jaundice ( jaundice ), fever and worsening of the general condition may occur.

Diagnosis

In steatohepatitis, in contrast to pure fatty liver, both the cholestasis parameters (especially gamma-GT ) and the transaminases as a sign of inflammation in the liver are increased in laboratory chemistry . Often there is also a slight increase in white blood cells ( leukocytosis ) and, under certain circumstances, a slight increase in C-reactive protein . Sonography is used in routine diagnostics for imaging diagnostics . Under certain circumstances, further examinations, such as endosonography , MRI examinations or an ERCP examination, may be necessary to complete the diagnosis and to exclude other diseases of the liver . The diagnosis is confirmed histologically by taking a biopsy as part of a liver puncture . Histologically, however, it is not possible to differentiate between alcoholic (alcohol-related) steatohepatitis (ASH) and non-alcoholic steatohepatitis (NASH).

Pathogenesis

Steatohepatitis is an inflammatory reaction due to immunological factors in pre-existing fatty liver (steatosis hepatis), which is characterized by increased fat storage in the liver cells ( hepatocytes ). Cell metabolism disorders lead to cell ballooning and cell destruction. With steatohepatitis, in addition to fatty liver, the picture of liver inflammation ( hepatitis ) occurs.

Classification

Classification according to cause

Two forms are distinguished based on the pathogenesis :

  • Alcoholic steatohepatitis (also called alcohol hepatitis or alcoholic fatty liver hepatitis, abbreviated ASH ): Excessive alcohol consumption can cause fatty liver and hepatitis.
  • Non-alcoholic steatohepatitis (or non-alcoholic fatty liver hepatitis, abbreviated NASH ): all forms of fatty liver hepatitis that are not caused by alcohol

Classification according to severity

One can distinguish two forms in relation to the severity of the disease:

  • chronic persistent hepatitis
  • the chronically active (formerly: chronically aggressive) hepatitis.

The chronic persistent hepatitis is a lighter form of steatohepatitis. In most cases it does not cause any symptoms . In some cases, however, uncharacteristic complaints such as general upper abdominal complaints, digestive disorders, pressure and / or fullness occur.

The chronically active hepatitis occurs in approx. 15–20% of all cases of fatty liver hepatitis. It is the more severe form of the disease and causes more pronounced symptoms (such as loss of appetite, nausea, weight loss, jaundice, and fever). The risk of progression into cirrhosis of the liver is significantly increased in chronic active hepatitis.

Alcoholic steatohepatitis (ASH)

root cause

Alcoholic steatohepatitis (ASH), also known as alcoholic fatty liver inflammation or alcoholic fatty liver hepatitis , occurs with regular, excessive consumption of alcohol. The delimitation results from the daily alcohol consumption. The tolerance of alcohol varies greatly from person to person and depends, among other things, on possible previous illnesses and on gender. The harmful limit is on average over 40 g of ethanol for men and over 20 g for women.

Therapy and prognosis

Alcohol abstinence also helps in the stage of acute alcohol-related steatohepatitis (ASH, alcohol hepatitis). H. the strict avoidance of any form of alcohol. As long as the liver cells have not yet been converted into scarred connective tissue, the organ can regain its functionality. While the prognosis for the chronic persistent form is quite good, for the chronically active form it appears to be dependent on the stage of the disease: With strict abstinence, on the one hand, symptoms can completely regress, on the other hand, with increasing jaundice, there is a transition to liver coma or cirrhosis possible.

Non-alcoholic steatohepatitis (NASH)

Non-alcoholic steatohepatitis (NASH) or non-alcoholic fatty liver inflammation or non-alcoholic fatty liver hepatitis is present when steatohepatitis is present, but the daily alcohol consumption is less than 40 g in men or less than 20 g in women and the liver values ​​( transaminases ) also after one three months of absolute alcohol abstinence remain elevated. NASH is much rarer than ASH, but it still occurs in around one percent of the general population. In contrast to ASH, there is no jaundice .

causes

NASH is mostly caused by metabolic disorders, but there are other, different causes.

The most common causes are:

Rarer causes are:

Occasionally, however, the cause remains unclear or several possible causes come together.

Therapy of NASH

Therapy consists of treating the underlying disease (e.g .: better control of diabetes mellitus, weight loss in the case of obesity, change of medication in case of e.g. high blood pressure or lipid metabolism disorders ). Increased physical activity and change in diet as well as a moderate weight reduction of min. 7 to 10% can cure NASH.

In some studies, pioglitazone and vitamin E led to a reduction in steatosis and inflammation, but there was no effect on fibrosis. These approaches are not recommended in the S2k guideline of the DGVS. According to the EASL guideline, pioglitazone can be considered in NASH patients with type 2 diabetes mellitus.

If liver cirrhosis has already developed, there is a possibility of therapy in liver transplantation (LTx).

Other drug approaches are being investigated in studies:

In April 2019, the US pharmaceutical company Gilead Sciences presented data from a proof-of-concept study on the fixed combination of two substances, namely the FXR agonist Cilofexor and the ACC inhibitor Firsocostat, at the international liver congress in Vienna .

See also

Web links

Individual evidence

  1. ↑ Gerd Herold: Internal Medicine 2009 . Herold-Verlag, Cologne 2009, ISBN 1-111-15195-4
  2. ↑ "www.orpha.net" , Orphanet, an EU-funded Internet database with information on rare diseases
  3. ^ Lucey et al .: Alcoholic Hepatitis. New England Journal of Medicine (2009) Volume 360 ​​(26), pp. 2758-2769
  4. ^ M. Dietel, J. Dudenhausen, N. Suttorp: Harrison's internal medicine. ABW Wissenschaftsverlagsgesellschaft, 17th edition 2008, ISBN 978-3-936072-82-2
  5. ↑ Sanyal et al .: Pioglitazone, Vitamin E, or Placebo for Nonalcoholic Steatohepatitis. In: The New Englang Journal of Medicine. May 6, 2010, accessed October 24, 2019 .
  6. ↑ Roeb et al .: S2k guideline for non-alcoholic fatty liver diseases. In: AWMF Register No. 021-025. January 2015, accessed October 24, 2019 .
  7. ↑ EASL-EASD-EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease. In: Journal of Hepatology. European Association for the Study of the Liver (EASL), European Association for the Study of Diabetes (EASD), European Association for the Study of Obesity (EASO), 2016, accessed on October 24, 2019 .
  8. ↑ Monika Rau, Andreas Geier: Non-alcoholic fatty liver disease. In: drug therapy. Baden-Württemberg Medical Association, December 2017, accessed on October 24, 2019 .
  9. ↑ Gilead Presents New Data in Nonalcoholic Steatohepatitis (NASH) at the International Liver Congress ™ 2019 , PM Gilead, April 11, 2019, accessed April 19, 2019