Liver Shrinkage (Cirrhosis): Drug Therapy

Therapeutic target

To delay the progression (progression) of liver cirrhosis by treating the underlying disease.

Therapy recommendations

  • There is no drug therapy for cirrhosis of the liver. However, drug therapy for complications (see below) is possible to some extent:
    • Ascites (abdominal dropsy): diuretics (dehydrating drugs):for moderate ascites: potassium-sparing spironolactone (initially 100 mg/d); if the patient does not respond adequately within 2 to 3 weeks to 200 mg spironolactone, an oral loop diuretic is added. Note: In cases of marked hyponatremia (sodium deficiency;
    • Spontaneous bacterial peritonitis (SBP)/peritonitis: Antibiotic therapy (first-line norfloxacin and second-line trimethoprim-sulfamethoxazole and ciprofloxacin); Consider primary prophylaxis before liver transplantation (LTx) or in high-risk patients who have low ascites protein (< 1.5 g/dl) and another risk factor such as advanced hepatic insufficiency (Child-Pugh score > 9 with bilirubin > 3 mg/dl) or renal insufficiency (creatinine > 1.2 mg/dl, urea > 25 mg/dl, or sodium < 130 mmol/l). In case of failure of drug therapy:
      • Paracentesis (mechanical drainage of fluid)/ascites puncture or insertion of a TIPS (also TIPSS; transjugular intrahepatic portosystemic (stent) shunt).
      • During paracentesis, albumin substitution must be considered if the puncture volume is high.
    • Hepatic encephalopathy (HE) (pathological, non-inflammatory change of the brain due to severe liver dysfunction; most common complication of liver cirrhosis, with broad spectrum of neuropsychiatric disorders (impairment of: Consciousness; memory and cognition; motor ability; personality): Administration of nonabsorbable disaccharides such as lactulose (osmotically acting laxatives) or lactitol (synthetic sugar substitute); rifaximin (gut-selective antibiotic): if sole administration of a nonabsorbable disaccharide is not sufficiently effective and recurrence (recurrence of disease) has occurred without a trigger.
    • Hepatopulmonary syndrome (HPS): only therapeutic option: long-term oxygen therapy in addition to curative liver transplantation.
    • Portal hypertension (portal hypertension): vasopressin; somatostatin (derivatives); antibiosis (antibiotic therapy) should always be used in the therapy of acute variceal hemorrhage; duration of therapy 3-5 d.
    • Hepatorenal syndrome (HRS) (functional, potentially reversible renal dysfunction (severe renal dysfunction due to liver cirrhosis): vasopressin (terlipressin; alternative administration of norepinephrine under intensive care conditions)/antidiuretic hormone (ADH) and albumin; alternative: albumin + midodrine + octreotide.
  • Liver transplantation – this is indicated only when cirrhosis decompensates.
  • See also under “Further therapy”.

Further notes

  • A study demonstrates in patients with liver cirrhosis and spontaneous bacterial peritonitis/peritonitis (SBP) that non-selective ß-blockers (NSBB) lead to worsening of systemic hemodynamics (blood flow) and increase the risk of developing hepatorenal syndrome (see above) and acute renal failure. This means that transplant-free survival is reduced by.
  • In patients with liver cirrhosis and clinically significant portal hypertension/pulmonary hypertension (hepatic venous pressure gradient (HVPG) of ≥ 10 mmHg) lead non-selective beta-blockers (NSBB; here: propanolol) significantly reduced HVPG in contrast to the placebo group; furthermore, there was a significant effect on a lower rate of hepatic decompensations with development of ascites and spontaneous bacterial peritonitis (p=0.0297).
  • Patients with decompensated liver cirrhosis with additional long-term treatment with human albumin live longer than with standard treatment (follow-up of 18 months: reduction of mortality by 38%).