Cirrhosis laboratory findings: Difference between revisions
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==Laboratory Findings== | ==Laboratory Findings== | ||
The following findings are typical in cirrhosis: | The following findings are typical in cirrhosis: | ||
* '''[[Transaminase|Aminotransferase]]s''' - AST and ALT are moderately elevated, with AST > ALT | * '''[[Transaminase|Aminotransferase]]s''' - 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 | ** '''[[Alcoholic liver disease]]''' - AST and ALT are both elevated but less than 300 IU/L with a AST:ALT ratio > 2.0 | ||
* '''[[Alkaline phosphatase]]''' - | * '''[[Alkaline phosphatase]]''' - It is 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. | ||
* '''[[Gamma-glutamyl transpeptidase|GGT]]''' -- correlates with AP levels. | * '''[[Gamma-glutamyl transpeptidase|GGT]]''' -- correlates with AP levels. It is typically much higher in chronic liver disease from alcohol. | ||
* '''[[Bilirubin]]''' - may elevate as cirrhosis progresses. | * '''[[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 | * '''[[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. | * '''[[Prothrombin time]]''' - increases since the liver synthesizes clotting factors. | ||
* '''[[Globulin]]s''' - | * '''[[Globulin]]s''' - increase 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 [[vasopressin|ADH]] and [[aldosterone]]. | * '''Serum [[sodium]]'''- [[hyponatremia]] due to inability to excrete free water resulting from high levels of [[vasopressin|ADH]] and [[aldosterone]]. | ||
* '''[[Thrombocytopenia]]''' - due to both congestive [[splenomegaly]] as well as decreased [[thrombopoietin]] from the [[liver]] | * '''[[Thrombocytopenia]]''' - due to both congestive [[splenomegaly]] as well as decreased [[thrombopoietin]] from the [[liver]], however this rarely results in a platelet count < 50,000/mL. | ||
* '''[[Leukopenia]]''' and '''[[neutropenia]]''' - due to [[splenomegaly]] with splenic margination. | * '''[[Leukopenia]]''' and '''[[neutropenia]]''' - due to [[splenomegaly]] with splenic margination. | ||
* '''[[Anemia]]''' - multifactorial in origin. | * '''[[Anemia]]''' - multifactorial in origin. | ||
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* '''[[Coagulation defects]]''' - the [[liver]] produces most of the coagulation factors and thus coagulopathy correlates with worsening liver disease. | * '''[[Coagulation defects]]''' - the [[liver]] produces most of the coagulation factors and thus coagulopathy correlates with worsening liver disease. | ||
There is now a validated and patented combination of 6 of these markers as non-invasive | There is now a validated and patented combination of 6 of these markers as non-invasive biomarkers of fibrosis (and so of cirrhosis) : [[FibroTest]].<ref name="pmid18973844">{{cite journal |author= Halfon P, Munteanu M, Poynard T|title= FibroTest-ActiTest as a non-invasive marker of liver fibrosis |journal= Gastroenterol Clin Biol |volume=32|issue=6 |pages=22–39 |year=2008 |pmid= 18973844 |doi=10.1016/S0399-8320(08)73991-5}}</ref> | ||
Other laboratory studies performed in newly diagnosed [[cirrhosis]] may include: | Other laboratory studies performed in newly diagnosed [[cirrhosis]] may include: | ||
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**'''[[Anti-mitochondrial antibody]]''' - present in primary biliary cirrhosis | **'''[[Anti-mitochondrial antibody]]''' - present in primary biliary cirrhosis | ||
** '''[[Anti-LKM]]''' | ** '''[[Anti-LKM]]''' | ||
* '''[[Total iron]], [[TIBC]], [[transferrin saturation]]''', and '''[[ferritin]]''' - elevated [[totat iron]], reduced [[TIBC]], elevated [[transferrin saturation]], and elevated [[ferritin]] in | * '''[[Total iron]], [[TIBC]], [[transferrin saturation]]''', and '''[[ferritin]]''' - elevated [[totat iron]], reduced [[TIBC]], elevated [[transferrin saturation]], and elevated [[ferritin]] in [[hemochromatosis]]. | ||
*'''Serum [[ceruloplasmin]]'''- low in Wilson's disease | *'''Serum [[ceruloplasmin]]'''- low in Wilson's disease | ||
* '''[[Immunoglobulin]]''' levels (IgG, IgM, IgA) - these are non-specific but may assist in distinguishing various causes. | * '''[[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 | ** '''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 or not patients will need antiviral therapy. | ||
*'''Serum [[protein electrophoresis]]''' - alpha-1 band absent in alpha-1 antitrypsin deficiency | *'''Serum [[protein electrophoresis]]''' - alpha-1 band absent in alpha-1 antitrypsin deficiency. | ||
* '''[[Cholesterol]]''' and '''[[glucose]]''' | * '''[[Cholesterol]]''' and '''[[glucose]]''' | ||
* '''[[Alpha 1-antitrypsin]]''' - reduced in alpha-1 antitrypsin deficiency. | * '''[[Alpha 1-antitrypsin]]''' - reduced in alpha-1 antitrypsin deficiency. | ||
Revision as of 14:06, 7 September 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [2]
Overview
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 - It is 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. It is 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 - increase 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 a 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.
There is now a validated and patented combination of 6 of these markers as non-invasive biomarkers of fibrosis (and so of cirrhosis) : FibroTest.[1]
Other laboratory studies performed in newly diagnosed cirrhosis may include:
- Serology for hepatitis viruses.
- Autoantibodies
- ANA - present in autoimmune hepatitis
- Anti-smooth muscle antibody - present in autoimmune hepatitis
- Anti-mitochondrial antibody - present in primary biliary cirrhosis
- Anti-LKM
- Total iron, TIBC, transferrin saturation, and ferritin - elevated totat iron, reduced TIBC, elevated transferrin saturation, and elevated ferritin in hemochromatosis.
- Serum ceruloplasmin- low in Wilson's disease
- 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 or not patients will need antiviral therapy.
- Serum protein electrophoresis - alpha-1 band absent in alpha-1 antitrypsin deficiency.
- Cholesterol and glucose
- Alpha 1-antitrypsin - reduced in alpha-1 antitrypsin deficiency.
References
- ↑ Halfon P, Munteanu M, Poynard T (2008). "FibroTest-ActiTest as a non-invasive marker of liver fibrosis". Gastroenterol Clin Biol. 32 (6): 22–39. doi:10.1016/S0399-8320(08)73991-5. PMID 18973844.