Editing Liver function tests (section)

===Alkaline phosphatase (ALP)===
{| class="wikitable" align="right"
| Reference range
|-
| 41 to 133 IU/L<ref name="Shivaraj 2009"/>
|}
{{Main|Elevated alkaline phosphatase}}

[[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"/>