Treatment for hepatitis-related cirrhosis involves medications used to treat the different types of hepatitis, such as interferon for viral hepatitis and corticosteroids for autoimmune hepatitis.Cirrhosis caused by Wilsons disease is treated by removing the copper which builds up in organs. This is carried out using chelation therapy such as penicillamine. When the cause is an iron overload, iron is removed using a chelation agent such as deferoxamine or by bloodletting.As of 2021, there are recent studies studying drugs to prevent cirrhosis caused by non-alcoholic fatty liver disease (NAFLD or NASH). A drug called semaglutide was shown to provide greater NASH resolution versus placebo. No improvement in fibrosis was observed. A combination of cilofexor/firsocostat was studied in patients with bridging fibrosis and cirrhosis. It was observed to have led to improvements in NASH activity with a potential antifibrotic effect. Lanifibranor is also shown to prevent worsening fibrosis. Preventing further liver damage
Regardless of the underlying cause of cirrhosis, consumption of alcohol and other potentially damaging substances are discouraged. There is no evidence that supports the avoidance or dose reduction of paracetamol in people with compensated cirrhosis; it is thus considered a safe analgesic for said individuals.Vaccination of susceptible patients should be considered for hepatitis A and hepatitis B. Treating the cause of cirrhosis prevents further damage; for example, giving oral antivirals such as entecavir and tenofovir where cirrhosis is due to hepatitis B prevents progression of cirrhosis.
These findings are typical in cirrhosis:

Thrombocytopenia, typically multifactorial, is due to alcoholic marrow suppression, sepsis, lack of folate, platelet sequestering in the spleen, and decreased thrombopoietin. However, this rarely results in a platelet count < 50 000/mL. Aminotransferases  AST and ALT are moderately elevated, with AST > ALT. However, normal aminotransferase levels do not preclude cirrhosis. Alkaline phosphatase – slightly elevated but less than 2–3 times the upper limit of normal. Gamma-glutamyl transferase – correlates with AP levels. Typically much higher in chronic liver disease from alcohol. Bilirubin levels are normal when compensated, but may elevate as cirrhosis progresses. Albumin  levels fall as the synthetic function of the liver declines with worsening cirrhosis since albumin is exclusively synthesized in the liver. Prothrombin time increases, since the liver synthesizes clotting factors. Globulins increase due to shunting of bacterial antigens away from the liver to lymphoid tissue. Serum sodium levels fall(hyponatremia) due to inability to excrete free water resulting from high levels of ADH and aldosterone. Leukopenia and neutropenia are due to splenomegaly with splenic margination. Coagulation defects occur, as the liver produces most of the coagulation factors, thus coagulopathy correlates with worsening liver disease. Glucagon is increased in cirrhosis. Vasoactive intestinal peptide is increased as blood is shunted into the intestinal system because of portal hypertension. Vasodilators are increased (such as nitric oxide and carbon monoxide) reducing afterload with compensatory increase in cardiac output, mixed venous oxygen saturation.