Cirrhosis laboratory findings: Difference between revisions
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* Serology for [[hepatitis]] viruses, [[autoantibody|autoantibodies]] ([[Anti-nuclear antibody|ANA]], anti-smooth muscle,[[Anti-mitochondrial antibody|anti-mitochondria]], anti-LKM) | * Serology for [[hepatitis]] viruses, [[autoantibody|autoantibodies]] ([[Anti-nuclear antibody|ANA]], anti-smooth muscle,[[Anti-mitochondrial antibody|anti-mitochondria]], anti-LKM) | ||
* [[Ferritin]] and [[transferrin saturation]] (markers of iron overload), [[copper]] and [[ceruloplasmin]] (markers of copper overload) | * [[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 | * [[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]] | * [[Cholesterol]] and [[glucose]] | ||
* [[Alpha 1-antitrypsin]] | * [[Alpha 1-antitrypsin]] | ||
Revision as of 08:50, 29 July 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 - usually slightly elevated.
- 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.
- Serum sodium - hyponatremia due to inability to excrete free water resulting from high levels of ADHand 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.
- 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
Liver biopsy
The gold standard for diagnosis of cirrhosis is a liver biopsy, through a percutaneous, transjugular, laparoscopic, or fine-needle approach. Histologically cirrhosis can be classified as micronodular, macronodular, or mixed, but this classification has been abandoned since it is nonspecific to the etiology, it may change as the disease progresses, and serological markers are much more specific. However, a biopsy is not necessary if the clinical, laboratory, and radiologic data suggests cirrhosis. Furthermore, there is a small but significant risk to liver biopsy, and cirrhosis itself predisposes for complications due to liver biopsy.[1]
- Alcoholic liver disease : Liver biopsy may show hepatocyte necrosis, Mallory bodies, neutrophilic infiltration with perivenular inflammation.
References
- ↑ Grant, A (1999). "Guidelines on the use of liver biopsy in clinical practice". Gut. 45 (Suppl 4): 1–11. PMID 10485854.
The main cause of mortality after percutaneous liver biopsy is intraperitoneal haemorrhage as shown in a retrospective Italian study of 68,000 percutaneous liver biopsies in which all six patients who died did so from intraperitoneal haemorrhage. Three of these patients had had a laparotomy, and all had either cirrhosis or malignant disease, both of which are risk factors for bleeding.
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