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==Standard liver panel==
Standard liver tests for assessing liver damage include alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatases (ALPsAPs). [[Bilirubin]] may be used to estimate the excretory function of the liver and coagulation tests and albumin can be used to evaluate the metabolic activity of the liver.<ref name="Shivaraj 2009"/>
Although example reference ranges are given, these will vary depending on method of analysis used at the administering laboratory, as well as age, gender, ethnicity, and potentially unrelated health factors. Individual results should always be interpreted using the reference range provided by the laboratory that performed the test.{{citation needed|date=July 2020}}
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Measurement of total [[bilirubin]] includes both [[Unconjugated bilirubin|unconjugated]] (indirect) and conjugated (direct) bilirubin. Unconjugated bilirubin is a breakdown product of [[heme]] (a part of [[hemoglobin]] in red blood cells). The liver is responsible for clearing the blood of unconjugated bilirubin, by 'conjugating' it (modified to make it water-soluble) through an enzyme named [[UDP-glucuronyl-transferase]]. When the total bilirubin level exceeds 17 μmol/L, it indicates liver disease. When total bilirubin levels exceed 40 μmol/L, bilirubin deposition at the sclera, skin, and mucous membranes will give these areas a yellow colour, thus it is called [[jaundice]].<ref name="Shivaraj 2009">{{cite journal|display-authors=3|last1=Shivaraj|first1=Gowda|last2=Prakash|first2=B Desai|last3=Vinayak|first3=V Hull|last4=Avinash|first4=AK Math|last5=Sonal N|first5=Venekar|last6=Shruthi S|first6=Kulkarni|title=A review on laboratory liver function tests|journal=The Pan African Medical Journal|date=22 November 2009|volume=3|issue=17|pages=17|pmid=21532726|pmc=2984286}}</ref>
The increase in predominantly unconjugated bilirubin is due to overproduction, reduced hepatic uptake of the unconjugated bilirubin and reduced conjugation of bilirubin. Overproduction can be due to the reabsorption of a [[haematoma]] and ineffective [[erythropoiesis]] leading to increased red blood cell destruction. [[Gilbert's syndrome]] and [[Crigler–Najjar syndrome]] have defects in the [[UDP-glucuronyl-transferase]] enzyme, affecting bilirubin conjugation.<ref name="Shivaraj 2009"/>
In [[acute appendicitis]], total bilirubin can rise from 20.52 μmol/L to 143 μmol/L. In pregnant women, the total bilirubin level is low in all three trimesters.<ref name="Shivaraj 2009"/>
The measurement of bilirubin levels in the newborns is done through the use of bilimeter or transcutanoeus bilirubinometer instead of performing LFTs. When the total serum bilirubin increases over 95th percentile for age during the first week of life for high risk babies, it is known as [[hyperbilirubinemia]] of the newborn ([[neonatal jaundice]]) and requires [[light therapy]] to reduce the amount of bilirubin in the blood. Pathological jaundice in newborns should be suspected when the serum bilirubin level rises by more than 5 mg/dL per day, serum bilirubin more than the physiological range, clinical jaundice more than 2 weeks, and conjugated bilirubin (dark urine staining clothes). [[Hemolytic disease of the newborn|Haemolytic jaundice]] is the commonest cause of pathological jaundice. Those babies with Rh hemolytic disease, [[ABO incompatibility]] with the mother, [[Glucose-6-phosphate dehydrogenase]] (G-6-PD) deficiency and minor blood group incompatibility are at increased risk of getting haemolytic jaundice.<ref>{{cite journal|last1=Sana|first1=Ullah|last2=Khaista|first2=Rahman|last3=Mehdi|first3=Hedayati|title=Hyperbilirubinemia in Neonates: Types, Causes, Clinical Examinations, Preventive Measures and Treatments: A Narrative Review Article|journal=Iranian Journal of Public Health|date=May 2016|volume=45|issue=5|pages=558–568|pmid=27398328|pmc=4935699}}</ref>
===Alanine transaminase (ALT)===
| 7-56 IU/L<ref name="Shivaraj 2009"/>
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Apart from being found in high concentrations in the liver, ALT is found in the [[kidneys]], heart, and muscles. It catalyses the [[transamination]] reaction, and only exists in a cytoplasmic form. Any kind of liver injury can cause a rise in ALT. A rise of up to 300 IU/L is not specific to the liver, but can be due to the damage of other organs such as the kidneys or muscles. When ALT rises to more than 500 IU/L, causes are usually from the liver. It can be due to hepatitis, ischemic liver injury, and toxins that causes liver damage. The ALT levels in [[hepatitis C]] rises more than in hepatitis A and B. Persistent ALT elevation more than 6 months is known as [[chronic hepatitis]]. [[Alcoholic liver disease]], [[non-alcoholic fatty liver disease]] (NAFLD), fat accumulation in liver during childhood obesity, [[steatohepatitis]] (inflammation of fatty liver disease) are associated with a rise in ALT. Rise in ALT is also associated with reduced insulin response, reduced glucose tolerance, and increased free [[fatty acid]]s and [[triglyceride]]s. Bright liver syndrome (bright liver on ultrasound suggestive of fatty liver) with raised ALT is suggestive of [[metabolic syndrome]].<ref name="Shivaraj 2009"/>
In pregnancy, ALT levels would rise during the second trimester. In one of the studies, measured ALT levels in pregnancy-related conditions such as [[hyperemesis gravidarum]] was 103.5 IU/L, [[pre-eclampsia]] was 115, [[HELLP syndrome]] was 149. ALT levels would reduce by greater than 50% in three days after child delivery. Another study also shows that [[caffeine]] consumption can reduce the risk of ALT elevation in those who consume alcohol, overweight people, impaired glucose metabolism, and viral hepatitis.<ref name="Shivaraj 2009"/>
[[Alkaline phosphatase]] (ALP) is an enzyme in the cells lining the [[biliary tract|biliary ducts]] of the liver. It can also be found on the mucosal epithelium of the small intestine, [[proximal convoluted tubule]] of the kidneys, bone, liver, and placenta. It plays an important role in lipid transposition in small intestines and calcification of bones. 50% of all the serum ALP activities in blood are contributed by bone. Acute viral hepatitis usually has normal or increased ALP. For example, hepatitis A has increased ALP due to [[cholestasis]] (impaired bile formation or bile flow obstruction) and would have the feature of prolonged itching. Other causes include: infiltrative liver diseases, granulomatous liver disease, abscess, [[amyloidosis]] of the liver and [[peripheral arterial disease]]. Mild elevation of ALP can be seen in liver cirrhosis, hepatitis, and [[congestive cardiac failure]]. Transient [[hyperphosphataemia]] is a benign condition in [[infant]]s, and can reach normal level in 4 months. In contrast, low levels of ALP is found in [[hypothyroidism]], [[pernicious anemia]], [[zinc deficiency]], and [[hypophosphatasia]].<ref name="Shivaraj 2009"/>
ALP activity is significantly increased in the third trimester of [[pregnancy]].<ref name="Gronowski2004" /> This is due to increased synthesis from the [[placenta]] as well as increased synthesis in the [[liver]] induced by large amounts of [[estrogens]].<ref name="Gronowski2004" /><ref name="McCombBowersPosen1979">{{cite book | title = Alkaline Phosphatase | last1 = McComb | first1 = Robert B. | last2 = Bowers | first2 = George N. | last3 = Posen | first3 = Solomon | chapter = Clinical Utilization of Alkaline Phosphatase Measurements | date = 1979 | pages = 525–786 | publisher = Springer US | doi = 10.1007/978-1-4613-2970-1_9 | isbn = 978-1-4613-2972-5 | url = }}</ref><ref name="pmid14236214">{{cite journal | vauthors = Mueller MN, Kappas A | title = Estrogen pharmacology. I. The influence of estradiol and estriol on hepatic disposal of sulfobromophthalein (BSP) in man | journal = J Clin Invest | volume = 43 | issue = 10| pages = 1905–14 | date = October 1964 | pmid = 14236214 | pmc = 289635 | doi = 10.1172/JCI105064 | url = }}</ref> Levels in the third trimester can be as much as 2-fold greater than in non-pregnant women.<ref name="Gronowski2004">{{cite book | title = Handbook of Clinical Laboratory Testing During Pregnancy | last1 = Gronowski | first1 = Ann M. | chapter = Human Pregnancy | date = 2004 | pages = 1–13 | publisher = Humana Press | doi = 10.1007/978-1-59259-787-1_1 | isbn = 978-1-4684-9862-2 | url = }}</ref> As a result, ALP is not a reliable marker of hepatic function in pregnant women.<ref name="Gronowski2004" /> In contrast to ALP, levels of ALT, AST, GGT, and [[lactate dehydrogenase]] are only slightly changed or largely unchanged during pregnancy.<ref name="Gronowski2004" /> [[Bilirubin]] levels are significantly decreased in pregnancy.<ref name="Gronowski2004" />
In pregnancy conditions such as hyperemesis gravdirum, ALP levels can reach 215 IU/L, meanwhile, in [[pre-eclampsia]], ALP can reach 14 IU/L, and in HELLP syndrome ALP levels can reach 15 IU/L.<ref name="Shivaraj 2009"/>
===Gamma-glutamyltransferase (GGT)===
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{{Main|Alpha-fetoprotein}}
[[Alpha-fetoprotein]] (AFP) is significantly expressed in foetal liver. However, the mechanism that led to the suppression of AFP synthesis in adults is not fully known. Exposure of the liver to cancer-causing agents and arrest of liver maturation in childhood can lead to the rise in AFP. AFP can reach until 400–500 μg/L in [[hepatocellular carcinoma]]. AFP concentration of more than 400 μg/L is associated with greater tumour size, involvement of both lobes of liver, portal vein invasion and a lower median survival rate.<ref name="Shivaraj 2009"/>
===Coagulation test===
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