Cirrhosis laboratory findings: Difference between revisions

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__NOTOC__
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{{Cirrhosis}}
{{Cirrhosis}}
{{CMG}} {{AE}} {{ADI}} {{Cherry}}


{{CMG}} ; {{AE}} {{ADI}}
==Overview==
==Overview==
A range of laboratory values may be obtained in the evaluation of [[cirrhosis]], in order to determine [[disease]] severity and [[Causality|causation]]. [[Liver function tests]], [[complete blood count]], [[basic metabolic panel]] and [[coagulation factors]] are standard in the evaluation of [[cirrhosis]]. More specific testing for markers and serum [[enzymes]] may be performed when certain [[Etiology|etiologies]] are suspected.


==Laboratory Findings==
==Laboratory Findings==
The following findings are typical in cirrhosis:
* Laboratory abnormalities may be the first indication of [[cirrhosis]].
* '''[[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
* '''[[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.
* '''[[Gamma-glutamyl transpeptidase|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.
* '''[[Globulin]]s''' - 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 [[vasopressin|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.


There is now a validated and patented combination of 6 of these markers as non-invasive biomarker 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>
* Common abnormalities include:<ref name="pmid22656328">{{cite journal |vauthors=Chalasani N, Younossi Z, Lavine JE, Diehl AM, Brunt EM, Cusi K, Charlton M, Sanyal AJ |title=The diagnosis and management of non-alcoholic fatty liver disease: practice guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology |journal=Gastroenterology |volume=142 |issue=7 |pages=1592–609 |year=2012 |pmid=22656328 |doi=10.1053/j.gastro.2012.04.001 |url=}}</ref><ref name="pmid22357834">{{cite journal |vauthors=Udell JA, Wang CS, Tinmouth J, FitzGerald JM, Ayas NT, Simel DL, Schulzer M, Mak E, Yoshida EM |title=Does this patient with liver disease have cirrhosis? |journal=JAMA |volume=307 |issue=8 |pages=832–42 |year=2012 |pmid=22357834 |doi=10.1001/jama.2012.186 |url=}}</ref><ref name="pmid27995906">{{cite journal |vauthors=Kwo PY, Cohen SM, Lim JK |title=ACG Clinical Guideline: Evaluation of Abnormal Liver Chemistries |journal=Am. J. Gastroenterol. |volume=112 |issue=1 |pages=18–35 |year=2017 |pmid=27995906 |doi=10.1038/ajg.2016.517 |url=}}</ref><ref name="pmid11853185">{{cite journal |vauthors=Cabrera-Abreu JC, Green A |title=Gamma-glutamyltransferase: value of its measurement in paediatrics |journal=Ann. Clin. Biochem. |volume=39 |issue=Pt 1 |pages=22–5 |year=2002 |pmid=11853185 |doi=10.1258/0004563021901685 |url=}}</ref><ref name="pmid2857631">{{cite journal |vauthors=Moussavian SN, Becker RC, Piepmeyer JL, Mezey E, Bozian RC |title=Serum gamma-glutamyl transpeptidase and chronic alcoholism. Influence of alcohol ingestion and liver disease |journal=Dig. Dis. Sci. |volume=30 |issue=3 |pages=211–4 |year=1985 |pmid=2857631 |doi= |url=}}</ref>
** Increased [[Bilirubin|serum bilirubin]] levels<ref name="pmid10498635">{{cite journal |vauthors=Krzeski P, Zych W, Kraszewska E, Milewski B, Butruk E, Habior A |title=Is serum bilirubin concentration the only valid prognostic marker in primary biliary cirrhosis? |journal=Hepatology |volume=30 |issue=4 |pages=865–9 |year=1999 |pmid=10498635 |doi=10.1002/hep.510300415 |url=}}</ref>
** Abnormal [[Transaminase|aminotransferase]] levels <ref name="pmid10781624">{{cite journal |vauthors=Pratt DS, Kaplan MM |title=Evaluation of abnormal liver-enzyme results in asymptomatic patients |journal=N. Engl. J. Med. |volume=342 |issue=17 |pages=1266–71 |year=2000 |pmid=10781624 |doi=10.1056/NEJM200004273421707 |url=}}</ref><ref name="pmid27995906" /><ref name="pmid20060831">{{cite journal |vauthors=Ruhl CE, Everhart JE |title=Trunk fat is associated with increased serum levels of alanine aminotransferase in the United States |journal=Gastroenterology |volume=138 |issue=4 |pages=1346–56, 1356.e1–3 |year=2010 |pmid=20060831 |pmc=2847039 |doi=10.1053/j.gastro.2009.12.053 |url=}}</ref><ref name="pmid12093239">{{cite journal |vauthors=Prati D, Taioli E, Zanella A, Della Torre E, Butelli S, Del Vecchio E, Vianello L, Zanuso F, Mozzi F, Milani S, Conte D, Colombo M, Sirchia G |title=Updated definitions of healthy ranges for serum alanine aminotransferase levels |journal=Ann. Intern. Med. |volume=137 |issue=1 |pages=1–10 |year=2002 |pmid=12093239 |doi= |url=}}</ref><ref name="pmid9581673">{{cite journal |vauthors=Piton A, Poynard T, Imbert-Bismut F, Khalil L, Delattre J, Pelissier E, Sansonetti N, Opolon P |title=Factors associated with serum alanine transaminase activity in healthy subjects: consequences for the definition of normal values, for selection of blood donors, and for patients with chronic hepatitis C. MULTIVIRC Group |journal=Hepatology |volume=27 |issue=5 |pages=1213–9 |year=1998 |pmid=9581673 |doi=10.1002/hep.510270505 |url=}}</ref><ref name="pmid12093245">{{cite journal |vauthors=Kaplan MM |title=Alanine aminotransferase levels: what's normal? |journal=Ann. Intern. Med. |volume=137 |issue=1 |pages=49–51 |year=2002 |pmid=12093245 |doi= |url=}}</ref><ref name="pmid15983331">{{cite journal |vauthors=Nannipieri M, Gonzales C, Baldi S, Posadas R, Williams K, Haffner SM, Stern MP, Ferrannini E |title=Liver enzymes, the metabolic syndrome, and incident diabetes: the Mexico City diabetes study |journal=Diabetes Care |volume=28 |issue=7 |pages=1757–62 |year=2005 |pmid=15983331 |doi= |url=}}</ref><ref name="pmid22764020">{{cite journal |vauthors=Liangpunsakul S, Chalasani N |title=What should we recommend to our patients with NAFLD regarding alcohol use? |journal=Am. J. Gastroenterol. |volume=107 |issue=7 |pages=976–8 |year=2012 |pmid=22764020 |pmc=3766378 |doi=10.1038/ajg.2012.20 |url=}}</ref><ref name="pmid520102">{{cite journal |vauthors=Cohen JA, Kaplan MM |title=The SGOT/SGPT ratio--an indicator of alcoholic liver disease |journal=Dig. Dis. Sci. |volume=24 |issue=11 |pages=835–8 |year=1979 |pmid=520102 |doi= |url=}}</ref><ref name="pmid18328931">{{cite journal |vauthors=Schuppan D, Afdhal NH |title=Liver cirrhosis |journal=Lancet |volume=371 |issue=9615 |pages=838–51 |year=2008 |pmid=18328931 |pmc=2271178 |doi=10.1016/S0140-6736(08)60383-9 |url=}}</ref><ref name="pmid19501929">{{cite journal |vauthors= |title=EASL Clinical Practice Guidelines: management of cholestatic liver diseases |journal=J. Hepatol. |volume=51 |issue=2 |pages=237–67 |year=2009 |pmid=19501929 |doi=10.1016/j.jhep.2009.04.009 |url=}}</ref>  
** Elevated [[alkaline phosphatase]] 
** Elevated [[gamma-glutamyl transpeptidase]] 
** Prolonged [[prothrombin time]]/[[Prothrombin time|INR]]
** [[Thrombocytopenia]]
** [[Hyponatremia]] 


Other laboratory studies performed in newly diagnosed [[cirrhosis]] may include:
==== Liver function tests: ====
* Serology for [[hepatitis]] viruses,
* [[Aminotransferases]]:<ref name="pmid9448172">{{cite journal |vauthors=Sheth SG, Flamm SL, Gordon FD, Chopra S |title=AST/ALT ratio predicts cirrhosis in patients with chronic hepatitis C virus infection |journal=Am. J. Gastroenterol. |volume=93 |issue=1 |pages=44–8 |year=1998 |pmid=9448172 |doi=10.1111/j.1572-0241.1998.044_c.x |url=}}</ref><ref name="pmid3135226">{{cite journal |vauthors=Williams AL, Hoofnagle JH |title=Ratio of serum aspartate to alanine aminotransferase in chronic hepatitis. Relationship to cirrhosis |journal=Gastroenterology |volume=95 |issue=3 |pages=734–9 |year=1988 |pmid=3135226 |doi= |url=}}</ref><ref name="pmid12883497">{{cite journal |vauthors=Wai CT, Greenson JK, Fontana RJ, Kalbfleisch JD, Marrero JA, Conjeevaram HS, Lok AS |title=A simple noninvasive index can predict both significant fibrosis and cirrhosis in patients with chronic hepatitis C |journal=Hepatology |volume=38 |issue=2 |pages=518–26 |year=2003 |pmid=12883497 |doi=10.1053/jhep.2003.50346 |url=}}</ref><ref name="pmid12297848">{{cite journal |vauthors=Forns X, Ampurdanès S, Llovet JM, Aponte J, Quintó L, Martínez-Bauer E, Bruguera M, Sánchez-Tapias JM, Rodés J |title=Identification of chronic hepatitis C patients without hepatic fibrosis by a simple predictive model |journal=Hepatology |volume=36 |issue=4 Pt 1 |pages=986–92 |year=2002 |pmid=12297848 |doi=10.1053/jhep.2002.36128 |url=}}</ref><ref name="pmid17567829">{{cite journal |vauthors=Vallet-Pichard A, Mallet V, Nalpas B, Verkarre V, Nalpas A, Dhalluin-Venier V, Fontaine H, Pol S |title=FIB-4: an inexpensive and accurate marker of fibrosis in HCV infection. comparison with liver biopsy and fibrotest |journal=Hepatology |volume=46 |issue=1 |pages=32–6 |year=2007 |pmid=17567829 |doi=10.1002/hep.21669 |url=}}</ref><ref name="pmid11297957">{{cite journal |vauthors=Imbert-Bismut F, Ratziu V, Pieroni L, Charlotte F, Benhamou Y, Poynard T |title=Biochemical markers of liver fibrosis in patients with hepatitis C virus infection: a prospective study |journal=Lancet |volume=357 |issue=9262 |pages=1069–75 |year=2001 |pmid=11297957 |doi=10.1016/S0140-6736(00)04258-6 |url=}}</ref><ref name="pmid15578508">{{cite journal |vauthors=Rosenberg WM, Voelker M, Thiel R, Becka M, Burt A, Schuppan D, Hubscher S, Roskams T, Pinzani M, Arthur MJ |title=Serum markers detect the presence of liver fibrosis: a cohort study |journal=Gastroenterology |volume=127 |issue=6 |pages=1704–13 |year=2004 |pmid=15578508 |doi= |url=}}</ref>
** [[Liver function tests|LFTs]] may be normal in [[cirrhosis]] patients
** [[Aspartate transaminase|Aspartate aminotransferase]] ([[Aspartate transaminase|AST]]) and [[Alanine transaminase|alanine aminotransferase]] ([[Alanine transaminase|ALT]]) are usually moderately elevated
** [[Aspartate transaminase|AST]] is more often elevated than [[Alanine transaminase|ALT]]
** '''[[Alcoholic liver disease]]''' - [[Aspartate transaminase|AST]] and [[Alanine transaminase|ALT]] are both elevated but less than 300 IU/L with a [[Aspartate transaminase|AST]]: [[Alanine transaminase|ALT]] ratio > 2.0
* [[Alkaline phosphatase]]: <ref name="pmid696683">{{cite journal |vauthors=Ellis G, Goldberg DM, Spooner RJ, Ward AM |title=Serum enzyme tests in diseases of the liver and biliary tree |journal=Am. J. Clin. Pathol. |volume=70 |issue=2 |pages=248–58 |year=1978 |pmid=696683 |doi= |url=}}</ref>
** [[Alkaline phosphatase]] is usually elevated
** Usually less than two to three times the upper limit
** High levels may be seen in patients with underlying [[Cholestasis|cholestatic]] liver disease such as:
*** [[Primary biliary cirrhosis]]
*** [[Primary sclerosing cholangitis]]
* [[Gamma-glutamyl transpeptidase]]:<ref name="pmid696683" /><ref name="pmid6104563">{{cite journal |vauthors=Goldberg DM |title=Structural, functional, and clinical aspects of gamma-glutamyltransferase |journal=CRC Crit Rev Clin Lab Sci |volume=12 |issue=1 |pages=1–58 |year=1980 |pmid=6104563 |doi= |url=}}</ref><ref name="pmid6132864">{{cite journal |vauthors=Barouki R, Chobert MN, Finidori J, Aggerbeck M, Nalpas B, Hanoune J |title=Ethanol effects in a rat hepatoma cell line: induction of gamma-glutamyltransferase |journal=Hepatology |volume=3 |issue=3 |pages=323–9 |year=1983 |pmid=6132864 |doi= |url=}}</ref>
** Non specific
** Correlates with [[Alkaline phosphatase|ALP]] levels
** Higher in [[chronic liver disease]] ([[Chronic liver disease|CLD)]] due to [[alcohol]] use:
** Mechanism of raised [[Gamma-glutamyl transpeptidase|GGT]] in [[alcoholic liver disease]]:
*** [[Alcohol]] induces [[Microsome|microsomal]] [[Gamma-glutamyl transpeptidase|GGT]] in [[liver]]
*** [[Alcohol]] causes [[Gamma-glutamyl transpeptidase|GGT]] release from [[Hepatocyte|hepatocytes]]
** [[Albumin]]:
*** [[Albumin]] levels reflect synthetic function of the [[liver]]
*** Serum [[albumin]] levels helps grade the severity of [[cirrhosis]]
*** [[Hypoalbuminemia]] is non specific for [[liver]] disease and may be seen in:
**** [[Congestive heart failure|Heart failure]]
**** [[Malnutrition]]
**** [[Protein losing enteropathy|Protein-losing enteropathy]]
**** [[Nephrotic syndrome]]
 
* [[Bilirubin]]:
** [[Bilirubin]] levels may be normal or raised
* [[Prothrombin time]]: <ref name="pmid25009372">{{cite journal |vauthors=Chrostek L, Panasiuk A |title=Liver fibrosis markers in alcoholic liver disease |journal=World J. Gastroenterol. |volume=20 |issue=25 |pages=8018–23 |year=2014 |pmid=25009372 |pmc=4081671 |doi=10.3748/wjg.v20.i25.8018 |url=}}</ref>
** [[Prothrombin time]] reflects the degree of [[Liver|hepatic]] synthetic function.
** Worsening [[coagulopathy]] correlates with the severity of [[Liver|hepatic]] dysfunction.
* Metabolic panel:
** [[Hyponatremia]]<ref name="pmid2217672">{{cite journal |vauthors=Papadakis MA, Fraser CL, Arieff AI |title=Hyponatraemia in patients with cirrhosis |journal=Q. J. Med. |volume=76 |issue=279 |pages=675–88 |year=1990 |pmid=2217672 |doi= |url=}}</ref>
*** common in patients with [[cirrhosis]] and [[ascites]] and is related to an inability to excrete free water.
*** Reflects poor prognosis
*** Due to [[Antidiuretic hormone|ADH]] elevation
** Progressive rise in serum [[creatinine]]: may be indicative of [[hepatorenal syndrome]]
'''Hematologic abnormalities:'''  <ref name="pmid19281860">{{cite journal |vauthors=Qamar AA, Grace ND, Groszmann RJ, Garcia-Tsao G, Bosch J, Burroughs AK, Ripoll C, Maurer R, Planas R, Escorsell A, Garcia-Pagan JC, Patch D, Matloff DS, Makuch R, Rendon G |title=Incidence, prevalence, and clinical significance of abnormal hematologic indices in compensated cirrhosis |journal=Clin. Gastroenterol. Hepatol. |volume=7 |issue=6 |pages=689–95 |year=2009 |pmid=19281860 |pmc=4545534 |doi=10.1016/j.cgh.2009.02.021 |url=}}</ref>
* [[Thrombocytopenia]]: most common hematologic abnormality in [[cirrhosis]]
** Rarely results in a [[Platelet|platelet count]] < 50,000/mL 
** Mechanism of [[thrombocytopenia]]:
*** caused by [[portal hypertension]] with congestive [[splenomegaly]]: sequesters circulating [[Platelet|platelets]] 
*** decreased [[thrombopoietin]] levels
 
* [[Anemia]]
** Mechanism of [[anemia]]:
** Acute and chronic gastrointestinal [[blood]] loss 
** [[Folic Acid|Folate]] deficiency
** [[Hemolysis]]
** [[Anemia of chronic disease]] 
** Direct toxicity due to [[alcohol]] 
** [[Splenomegaly|Hypersplenism]] 
** [[Bone marrow]] suppression ( [[hepatitis]]-associated [[aplastic anemia]]) 
* [[Leukopenia]]/[[neutropenia]]: due to [[Splenomegaly|hypersplenism]] with [[Spleen|splenic]] margination
* '''[[Coagulation defects]]''' - the [[liver]] produces most of the [[Coagulation|coagulation factors]] and [[coagulopathy]] correlates with worsening [[liver]] disease
 
* '''Other abnormalities''' :
** [[Globulin|Globulins]]: increase due to shunting of bacterial antigens away from the [[liver]] to [[Lymphatic system|lymphoid tissue]] which induces [[immunoglobulin]] production.<ref name="pmid4123153">{{cite journal |vauthors=Triger DR, Wright R |title=Hyperglobulinaemia in liver disease |journal=Lancet |volume=1 |issue=7818 |pages=1494–6 |year=1973 |pmid=4123153 |doi= |url=}}</ref> 
** [[Disseminated intravascular coagulation]] 
** [[Vitamin K]] deficiency
** [[Diabetes]]: seen in patients with [[hemochromatosis]] <ref name="pmid8020880">{{cite journal |vauthors=Bianchi G, Marchesini G, Zoli M, Bugianesi E, Fabbri A, Pisi E |title=Prognostic significance of diabetes in patients with cirrhosis |journal=Hepatology |volume=20 |issue=1 Pt 1 |pages=119–25 |year=1994 |pmid=8020880 |doi= |url=}}</ref><ref name="pmid8119686">{{cite journal |vauthors=Petrides AS, Vogt C, Schulze-Berge D, Matthews D, Strohmeyer G |title=Pathogenesis of glucose intolerance and diabetes mellitus in cirrhosis |journal=Hepatology |volume=19 |issue=3 |pages=616–27 |year=1994 |pmid=8119686 |doi= |url=}}</ref>
** [[Insulin resistance]]: seen in [[Non-alcoholic fatty liver disease|nonalcoholic fatty liver disease]]
** [[Familial dysfibrinogenemia|Dysfibrinogenemia]]
** [[Fibrinolysis]] 
 
* '''[[Ascitic fluid analysis]]:'''
** A diagnostic [[paracentesis]] may be performed if the [[ascites]] is new or if the [[patient]] with ascites is being admitted to the hospital.
** The [[fluid]] is analysed for the following:
*** Gross appearance
*** [[Protein]] level
*** [[serum albumin|Albumin]]
*** [[White blood cells|WBC]], [[Red blood cell|RBC]] counts
*** [[Gram stain]]
*** [[cytology]]<ref name="OTM">Warrell DA, Cox TN, Firth JD, Benz ED. ''Oxford textbook of medicine''. Oxford: Oxford University Press, 2003. ISBN 0-19-262922-0.</ref>
** '''[[Serum-ascites albumin gradient]]''' ([[Serum-ascites albumin gradient|SAAG]]) is probably a better discriminant than older measures ([[transudate]] versus [[exudate]]) for the causes of [[ascites]].<ref>Runyon BA, Montano AA, Akriviadis EA, Antillon MR, Irving MA, McHutchison JG. The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites. ''Ann Intern Med'' 1992;117:215-20. PMID 1616215.</ref>
** A high gradient (> 1.1 g/dL) indicates the [[ascites]] is due to [[portal hypertension]]
** A low gradient (< 1.1 g/dL) indicates [[ascites]] of non-portal hypertensive etiology
** [[Ascites]] is broadly classified as two types based on the [[Serum-ascites albumin gradient]] (SAAG):
*** [[Transudate]] - [[Serum-ascites albumin gradient|SAAG]] > 1.1 g/dL (indicates the [[ascites]] is due to [[portal hypertension]])
*** [[Exudate]] - [[Serum-ascites albumin gradient|SAAG]] < 1.1 g/dL (indicates the [[ascites]] is due to non-portal hypertension etiology)
 
==== FibroTest ====
* A validated and patented combination of six [[serum]] markers as non-invasive biomarkers of [[fibrosis]] are included in the [[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>
* The [[FibroTest|FibroTest score]] is correlated with the degree of [[liver]] damage in people with a variety of [[liver]] diseases
* [[FibroTest|FibroTest score]] is calculated combining the following six [[serum]] markers with the age and gender of the [[patient]]:
** Alpha-2-[[macroglobulin]]
**  [[Haptoglobin]]
**  [[Apolipoprotein A1]]
**  [[Gamma-glutamyl transpeptidase]] (GGT)
** Total [[bilirubin]]
** [[Alanine transaminase]] ([[Alanine transaminase|ALT]])
 
==== Other laboratory studies performed in newly diagnosed [[cirrhosis]] may include: ====
* '''[[Serology]] for [[hepatitis]] viruses'''.
*'''[[autoantibody|Autoantibodies]]'''
*'''[[autoantibody|Autoantibodies]]'''
**'''[[Anti-nuclear antibody|ANA]]'''-present in autoimmune hepatitis
**'''[[Anti-nuclear antibody|ANA]]''' - present in [[autoimmune hepatitis]]
**'''[[Anti-smooth muscle antibody]]'''-present in autoimmune hepatitis
**'''[[Anti-smooth muscle antibody]]''' - present in [[autoimmune hepatitis]]
**'''[[Anti-mitochondrial antibody]]'''-present in primary biliary cirrhosis
**'''[[Anti-mitochondrial antibody]]''' - present in [[primary biliary cirrhosis]]
** '''[[Anti-LKM]]'''
** '''[[Anti-LKM]]'''
* [[Ferritin]] and [[transferrin saturation]] (markers of iron overload),
* '''[[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 patient will need antiviral therapy.
** '''Chronic [[hepatitis B]]''' - [[Hepatitis B|Chronic hepatitis B]] can be diagnosed with detection of [[Hepatitis B surface antigen|HBsAg]] > 6 months after initial [[infection]].
*'''Serum [[protein electrophoresis]]'''-alpha-1 band absent in alpha-1 antitrypsin deficiency
** HBeAg and HBV DNA are determined to assess whether or not patients will need [[Antiviral|antiviral therapy]].
* [[Cholesterol]] and [[glucose]]
*'''Serum [[protein electrophoresis]]''' - alpha-1 band absent in [[Alpha 1-antitrypsin deficiency|alpha-1 antitrypsin deficiency]].
* '''[[Alpha 1-antitrypsin]]'''-reduced in alpha-1 antitrypsin deficiency.
* '''[[Cholesterol]]''' and '''[[glucose]]'''
* '''[[Alpha 1-antitrypsin]]''' - reduced in [[Alpha 1-antitrypsin deficiency|alpha-1 antitrypsin deficiency]].
 
===Combinations of tests===
* [[Clinical prediction rule]]s exist to help diagnosis cirrhosis according to a [[systematic review]] by the [[Rational Clinical Examination]] project.<ref name="pmid22357834">{{cite journal| author=Udell JA, Wang CS, Tinmouth J, FitzGerald JM, Ayas NT, Simel DL et al.| title=Does this patient with liver disease have cirrhosis? | journal=JAMA | year= 2012 | volume= 307 | issue= 8 | pages= 832-42 | pmid=22357834 | doi=10.1001/jama.2012.186 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22357834  }} </ref>
* Pohl's Index:
** [[Cirrhosis]] is very likely when [[Aspartate transaminase|AST]]/[[Alanine transaminase|ALT]] ratio ≥1 and [[Platelet|platelet count]] ≤ 150,000/mm<sup>3</sup> <ref name="pmid16918883">{{cite journal| author=Borroni G, Ceriani R, Cazzaniga M, Tommasini M, Roncalli M, Maltempo C et al.| title=Comparison of simple tests for the non-invasive diagnosis of clinically silent cirrhosis in chronic hepatitis C. | journal=Aliment Pharmacol Ther | year= 2006 | volume= 24 | issue= 5 | pages= 797-804 | pmid=16918883
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=16918883 | doi=10.1111/j.1365-2036.2006.03034.x }}</ref>
 
* The [http://jama.ama-assn.org/content/307/8/832/F3.expansion.html Bonacini score] is based on the [[Alanine transaminase|ALT]]/[[Aspartate transaminase|AST]] ratio, [[Platelet|platelet count]], and [[Prothrombin time|INR]].<ref name="pmid16437635">{{cite journal| author=Colli A, Colucci A, Paggi S, Fraquelli M, Massironi S, Andreoletti M et al.| title=Accuracy of a predictive model for severe hepatic fibrosis or cirrhosis in chronic hepatitis C. | journal=World J Gastroenterol | year= 2005 | volume= 11 | issue= 46 | pages= 7318-22 | pmid=16437635 | doi= | pmc= | url= }} </ref>
** A score of > 7 or 8 makes [[cirrhosis]] more likely.<ref name="RCE">[http://jama.ama-assn.org/content/307/8/832.full Does this patient have cirrhosis?] JAMA 2012</ref>
** A score of < 3 makes [[cirrhosis]] less likely.<ref name="RCE">[http://jama.ama-assn.org/content/307/8/832.full Does this patient have cirrhosis?] JAMA 2012</ref>
 
* Another method is the Lok index<ref name="pmid15986415">{{cite journal| author=Lok AS, Ghany MG, Goodman ZD, Wright EC, Everson GT, Sterling RK et al.| title=Predicting cirrhosis in patients with hepatitis C based on standard laboratory tests: results of the HALT-C cohort. | journal=Hepatology | year= 2005 | volume= 42 | issue= 2 | pages= 282-92 | pmid=15986415 | doi=10.1002/hep.20772 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15986415  }} </ref>
 
* Online calculators are available ([http://static.inpractice.com/medcalc/LokIndex.htm link 1] and [http://ebmcalc.com/LokIndex.htm link 2]).
 
* In diagnosis of [[cirrhosis]] (Ishak scores, 5-6) in patients with [[hepatitis C]], the [[Aspartate transaminase|aspartate aminotransferase]] to [[platelet]] ratio index (APRI) ratio > 1 suggests [[cirrhosis]] with an accuracy of:<ref name="pmid23142332">{{cite journal| author=Gara N, Zhao X, Kleiner DE, Liang TJ, Hoofnagle JH, Ghany MG| title=Discordance among transient elastography, aspartate aminotransferase to platelet ratio index, and histologic assessments of liver fibrosis in patients with chronic hepatitis C. | journal=Clin Gastroenterol Hepatol | year= 2013 | volume= 11 | issue= 3 | pages= 303-308.e1 | pmid=23142332 | doi=10.1016/j.cgh.2012.10.044 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23142332  }} </ref>
** Sensitivity = 79%
** Specificity = 78%
 
* A more recent meta-analysis has focused on the diagnosis of [[cirrhosis]] among patients with [[hepatitis C]]<ref name="pmid23732714">{{cite journal| author=Chou R, Wasson N| title=Blood tests to diagnose fibrosis or cirrhosis in patients with chronic hepatitis C virus infection: a systematic review. | journal=Ann Intern Med | year= 2013 | volume= 158 | issue= 11 | pages= 807-20 | pmid=23732714 | doi=10.7326/0003-4819-158-11-201306040-00005 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23732714  }} </ref> using the Lok index:
** < 0.2 has negative likelihood ratio of 0.21
** > 0.6 has positive likelihood ratio of 4.4


==References==
==References==
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{{reflist|2}}
[[Category:Gastroenterology]]
[[Category:Hepatology]]
[[Category:Disease]]


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Latest revision as of 10:35, 13 December 2017

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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] Sudarshana Datta, MD [3]

Overview

A range of laboratory values may be obtained in the evaluation of cirrhosis, in order to determine disease severity and causation. Liver function tests, complete blood count, basic metabolic panel and coagulation factors are standard in the evaluation of cirrhosis. More specific testing for markers and serum enzymes may be performed when certain etiologies are suspected.

Laboratory Findings

  • Laboratory abnormalities may be the first indication of cirrhosis.

Liver function tests:

Hematologic abnormalities:  [29]

FibroTest

Other laboratory studies performed in newly diagnosed cirrhosis may include:

Combinations of tests

  • Another method is the Lok index[39]
  • A more recent meta-analysis has focused on the diagnosis of cirrhosis among patients with hepatitis C[41] using the Lok index:
    • < 0.2 has negative likelihood ratio of 0.21
    • > 0.6 has positive likelihood ratio of 4.4

References

  1. ↑ Chalasani N, Younossi Z, Lavine JE, Diehl AM, Brunt EM, Cusi K, Charlton M, Sanyal AJ (2012). "The diagnosis and management of non-alcoholic fatty liver disease: practice guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology". Gastroenterology. 142 (7): 1592–609. doi:10.1053/j.gastro.2012.04.001. PMID 22656328.
  2. ↑ 2.0 2.1 Udell JA, Wang CS, Tinmouth J, FitzGerald JM, Ayas NT, Simel DL, Schulzer M, Mak E, Yoshida EM (2012). "Does this patient with liver disease have cirrhosis?". JAMA. 307 (8): 832–42. doi:10.1001/jama.2012.186. PMID 22357834.
  3. ↑ 3.0 3.1 Kwo PY, Cohen SM, Lim JK (2017). "ACG Clinical Guideline: Evaluation of Abnormal Liver Chemistries". Am. J. Gastroenterol. 112 (1): 18–35. doi:10.1038/ajg.2016.517. PMID 27995906.
  4. ↑ Cabrera-Abreu JC, Green A (2002). "Gamma-glutamyltransferase: value of its measurement in paediatrics". Ann. Clin. Biochem. 39 (Pt 1): 22–5. doi:10.1258/0004563021901685. PMID 11853185.
  5. ↑ Moussavian SN, Becker RC, Piepmeyer JL, Mezey E, Bozian RC (1985). "Serum gamma-glutamyl transpeptidase and chronic alcoholism. Influence of alcohol ingestion and liver disease". Dig. Dis. Sci. 30 (3): 211–4. PMID 2857631.
  6. ↑ Krzeski P, Zych W, Kraszewska E, Milewski B, Butruk E, Habior A (1999). "Is serum bilirubin concentration the only valid prognostic marker in primary biliary cirrhosis?". Hepatology. 30 (4): 865–9. doi:10.1002/hep.510300415. PMID 10498635.
  7. ↑ Pratt DS, Kaplan MM (2000). "Evaluation of abnormal liver-enzyme results in asymptomatic patients". N. Engl. J. Med. 342 (17): 1266–71. doi:10.1056/NEJM200004273421707. PMID 10781624.
  8. ↑ Ruhl CE, Everhart JE (2010). "Trunk fat is associated with increased serum levels of alanine aminotransferase in the United States". Gastroenterology. 138 (4): 1346–56, 1356.e1–3. doi:10.1053/j.gastro.2009.12.053. PMC 2847039. PMID 20060831.
  9. ↑ Prati D, Taioli E, Zanella A, Della Torre E, Butelli S, Del Vecchio E, Vianello L, Zanuso F, Mozzi F, Milani S, Conte D, Colombo M, Sirchia G (2002). "Updated definitions of healthy ranges for serum alanine aminotransferase levels". Ann. Intern. Med. 137 (1): 1–10. PMID 12093239.
  10. ↑ Piton A, Poynard T, Imbert-Bismut F, Khalil L, Delattre J, Pelissier E, Sansonetti N, Opolon P (1998). "Factors associated with serum alanine transaminase activity in healthy subjects: consequences for the definition of normal values, for selection of blood donors, and for patients with chronic hepatitis C. MULTIVIRC Group". Hepatology. 27 (5): 1213–9. doi:10.1002/hep.510270505. PMID 9581673.
  11. ↑ Kaplan MM (2002). "Alanine aminotransferase levels: what's normal?". Ann. Intern. Med. 137 (1): 49–51. PMID 12093245.
  12. ↑ Nannipieri M, Gonzales C, Baldi S, Posadas R, Williams K, Haffner SM, Stern MP, Ferrannini E (2005). "Liver enzymes, the metabolic syndrome, and incident diabetes: the Mexico City diabetes study". Diabetes Care. 28 (7): 1757–62. PMID 15983331.
  13. ↑ Liangpunsakul S, Chalasani N (2012). "What should we recommend to our patients with NAFLD regarding alcohol use?". Am. J. Gastroenterol. 107 (7): 976–8. doi:10.1038/ajg.2012.20. PMC 3766378. PMID 22764020.
  14. ↑ Cohen JA, Kaplan MM (1979). "The SGOT/SGPT ratio--an indicator of alcoholic liver disease". Dig. Dis. Sci. 24 (11): 835–8. PMID 520102.
  15. ↑ Schuppan D, Afdhal NH (2008). "Liver cirrhosis". Lancet. 371 (9615): 838–51. doi:10.1016/S0140-6736(08)60383-9. PMC 2271178. PMID 18328931.
  16. ↑ "EASL Clinical Practice Guidelines: management of cholestatic liver diseases". J. Hepatol. 51 (2): 237–67. 2009. doi:10.1016/j.jhep.2009.04.009. PMID 19501929.
  17. ↑ Sheth SG, Flamm SL, Gordon FD, Chopra S (1998). "AST/ALT ratio predicts cirrhosis in patients with chronic hepatitis C virus infection". Am. J. Gastroenterol. 93 (1): 44–8. doi:10.1111/j.1572-0241.1998.044_c.x. PMID 9448172.
  18. ↑ Williams AL, Hoofnagle JH (1988). "Ratio of serum aspartate to alanine aminotransferase in chronic hepatitis. Relationship to cirrhosis". Gastroenterology. 95 (3): 734–9. PMID 3135226.
  19. ↑ Wai CT, Greenson JK, Fontana RJ, Kalbfleisch JD, Marrero JA, Conjeevaram HS, Lok AS (2003). "A simple noninvasive index can predict both significant fibrosis and cirrhosis in patients with chronic hepatitis C". Hepatology. 38 (2): 518–26. doi:10.1053/jhep.2003.50346. PMID 12883497.
  20. ↑ Forns X, Ampurdanès S, Llovet JM, Aponte J, Quintó L, Martínez-Bauer E, Bruguera M, Sánchez-Tapias JM, Rodés J (2002). "Identification of chronic hepatitis C patients without hepatic fibrosis by a simple predictive model". Hepatology. 36 (4 Pt 1): 986–92. doi:10.1053/jhep.2002.36128. PMID 12297848.
  21. ↑ Vallet-Pichard A, Mallet V, Nalpas B, Verkarre V, Nalpas A, Dhalluin-Venier V, Fontaine H, Pol S (2007). "FIB-4: an inexpensive and accurate marker of fibrosis in HCV infection. comparison with liver biopsy and fibrotest". Hepatology. 46 (1): 32–6. doi:10.1002/hep.21669. PMID 17567829.
  22. ↑ Imbert-Bismut F, Ratziu V, Pieroni L, Charlotte F, Benhamou Y, Poynard T (2001). "Biochemical markers of liver fibrosis in patients with hepatitis C virus infection: a prospective study". Lancet. 357 (9262): 1069–75. doi:10.1016/S0140-6736(00)04258-6. PMID 11297957.
  23. ↑ Rosenberg WM, Voelker M, Thiel R, Becka M, Burt A, Schuppan D, Hubscher S, Roskams T, Pinzani M, Arthur MJ (2004). "Serum markers detect the presence of liver fibrosis: a cohort study". Gastroenterology. 127 (6): 1704–13. PMID 15578508.
  24. ↑ 24.0 24.1 Ellis G, Goldberg DM, Spooner RJ, Ward AM (1978). "Serum enzyme tests in diseases of the liver and biliary tree". Am. J. Clin. Pathol. 70 (2): 248–58. PMID 696683.
  25. ↑ Goldberg DM (1980). "Structural, functional, and clinical aspects of gamma-glutamyltransferase". CRC Crit Rev Clin Lab Sci. 12 (1): 1–58. PMID 6104563.
  26. ↑ Barouki R, Chobert MN, Finidori J, Aggerbeck M, Nalpas B, Hanoune J (1983). "Ethanol effects in a rat hepatoma cell line: induction of gamma-glutamyltransferase". Hepatology. 3 (3): 323–9. PMID 6132864.
  27. ↑ Chrostek L, Panasiuk A (2014). "Liver fibrosis markers in alcoholic liver disease". World J. Gastroenterol. 20 (25): 8018–23. doi:10.3748/wjg.v20.i25.8018. PMC 4081671. PMID 25009372.
  28. ↑ Papadakis MA, Fraser CL, Arieff AI (1990). "Hyponatraemia in patients with cirrhosis". Q. J. Med. 76 (279): 675–88. PMID 2217672.
  29. ↑ Qamar AA, Grace ND, Groszmann RJ, Garcia-Tsao G, Bosch J, Burroughs AK, Ripoll C, Maurer R, Planas R, Escorsell A, Garcia-Pagan JC, Patch D, Matloff DS, Makuch R, Rendon G (2009). "Incidence, prevalence, and clinical significance of abnormal hematologic indices in compensated cirrhosis". Clin. Gastroenterol. Hepatol. 7 (6): 689–95. doi:10.1016/j.cgh.2009.02.021. PMC 4545534. PMID 19281860.
  30. ↑ Triger DR, Wright R (1973). "Hyperglobulinaemia in liver disease". Lancet. 1 (7818): 1494–6. PMID 4123153.
  31. ↑ Bianchi G, Marchesini G, Zoli M, Bugianesi E, Fabbri A, Pisi E (1994). "Prognostic significance of diabetes in patients with cirrhosis". Hepatology. 20 (1 Pt 1): 119–25. PMID 8020880.
  32. ↑ Petrides AS, Vogt C, Schulze-Berge D, Matthews D, Strohmeyer G (1994). "Pathogenesis of glucose intolerance and diabetes mellitus in cirrhosis". Hepatology. 19 (3): 616–27. PMID 8119686.
  33. ↑ Warrell DA, Cox TN, Firth JD, Benz ED. Oxford textbook of medicine. Oxford: Oxford University Press, 2003. ISBN 0-19-262922-0.
  34. ↑ Runyon BA, Montano AA, Akriviadis EA, Antillon MR, Irving MA, McHutchison JG. The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites. Ann Intern Med 1992;117:215-20. PMID 1616215.
  35. ↑ 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.
  36. ↑ Borroni G, Ceriani R, Cazzaniga M, Tommasini M, Roncalli M, Maltempo C; et al. (2006). "Comparison of simple tests for the non-invasive diagnosis of clinically silent cirrhosis in chronic hepatitis C." Aliment Pharmacol Ther. 24 (5): 797–804. doi:10.1111/j.1365-2036.2006.03034.x. PMID 16918883.
  37. ↑ Colli A, Colucci A, Paggi S, Fraquelli M, Massironi S, Andreoletti M; et al. (2005). "Accuracy of a predictive model for severe hepatic fibrosis or cirrhosis in chronic hepatitis C.". World J Gastroenterol. 11 (46): 7318–22. PMID 16437635.
  38. ↑ 38.0 38.1 Does this patient have cirrhosis? JAMA 2012
  39. ↑ Lok AS, Ghany MG, Goodman ZD, Wright EC, Everson GT, Sterling RK; et al. (2005). "Predicting cirrhosis in patients with hepatitis C based on standard laboratory tests: results of the HALT-C cohort". Hepatology. 42 (2): 282–92. doi:10.1002/hep.20772. PMID 15986415.
  40. ↑ Gara N, Zhao X, Kleiner DE, Liang TJ, Hoofnagle JH, Ghany MG (2013). "Discordance among transient elastography, aspartate aminotransferase to platelet ratio index, and histologic assessments of liver fibrosis in patients with chronic hepatitis C." Clin Gastroenterol Hepatol. 11 (3): 303–308.e1. doi:10.1016/j.cgh.2012.10.044. PMID 23142332.
  41. ↑ Chou R, Wasson N (2013). "Blood tests to diagnose fibrosis or cirrhosis in patients with chronic hepatitis C virus infection: a systematic review". Ann Intern Med. 158 (11): 807–20. doi:10.7326/0003-4819-158-11-201306040-00005. PMID 23732714.

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