Cirrhosis laboratory findings

Cirrhosis Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Cirrhosis from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Study of Choice
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
Chest X Ray
CT
MRI
Echocardiography or Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Tertiary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case studies
Case #1
Cirrhosis laboratory findings On the Web
Most recent articles
cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Cirrhosis laboratory findings All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Cirrhosis laboratory findings
CDC on Cirrhosis laboratory findings
Cirrhosis laboratory findings in the news
Blogs on Cirrhosis laboratory findings
Directions to Hospitals Treating Cirrhosis
Risk calculators and risk factors for Cirrhosis laboratory findings

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [2]

Laboratory Findings

The following findings are typical in cirrhosis:

• Aminotransferases - AST and ALT are moderately elevated, with AST > ALT. However, normal aminotransferases do not preclude cirrhosis.
  • Alcoholic liver disease - AST and ALT are both elevated but less than 300 IU/L with a AST:ALT ratio > 2.0
• Alkaline phosphatase - Elevated but usually less than two to three times the upper limit. Patients with Primary biliary cirrhosis and Primary sclerosing cholangitis may have higher levels.
• GGT -- correlates with AP levels. Typically much higher in chronic liver disease from alcohol.
• Bilirubin - 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 - increased due to shunting of bacterial antigens away from the liver to lymphoid tissue which induces immunoglobulin production.
• Serum sodium- hyponatremia due to inability to excrete free water resulting from high levels of ADH and aldosterone.
• Thrombocytopenia - due to both congestive splenomegaly as well as decreased thrombopoietin from the liver. However this rarely results in platelet count < 50,000/mL.
• Leukopenia and neutropenia - due to splenomegaly with splenic margination.
• Anemia - multifactorial in origin.
  • Acute and chronic GI bleeding
  • Folate deficiency
  • Direct toxicity of alcohol
  • Hypersplenism
  • Bone marrow suppression
  • Anemia of chronic disease
  • Hemolysis
• Coagulation defects - the liver produces most of the coagulation factors and thus coagulopathy correlates with worsening liver disease.

Other laboratory studies performed in newly diagnosed cirrhosis may include:

• Serology for hepatitis viruses, autoantibodies (ANA, anti-smooth muscle,anti-mitochondria, anti-LKM)
• Ferritin and transferrin saturation (markers of iron overload), copper and ceruloplasmin (markers of copper overload)
• Immunoglobulin levels (IgG, IgM, IgA) - these are non-specific but may assist in distinguishing various causes.
  • Chronic hepatitis B. Chronic hepatitis B can be diagnosed with detection of HBsAG > 6 months after initial infection. HBeAG and HBV DNA are determined to assess whether patient will need antiviral therapy.
• Cholesterol and glucose
• Alpha 1-antitrypsin
• Prothrombin time, albumin
• Platelets
• Lytes/Creatinine (Cr)- hyponatremia suggests severe disease