Why is alp elevated in cholestasis

Decreases in both ALP and magnesium observed in the postcardiac surgery patients appeared to be a consequence of cardiopulmonary bypass and not hemodilution alone. Magnesium is a cofactor for ALP activity, but the addition of magnesium to serum samples from postoperative cardiac surgery patients did not restore ALP activity, suggesting that something other than magnesium was affected by cardiopulmonary bypass.

Low plasma ALP level returns to normal after thyroid replacement therapy. Pernicious anemia is associated with cobalamin deficiency. Cobalamin deficiency is associated with lower ALP concentrations because osteoblast activity is dependent on cobalamin.

Low ALP activity during estrogen replacement therapy for postmenopausal women with osteoporosis is attributed to inhibition of bone resorption by estrogen. Specimen requirement is one SST tube of blood. If blood is collected in a citrate or EDTA tube, ALP activity will be almost totally inhibited due to the chelation of zinc and magnesium, which are necessary enzyme cofactors.

Lum G. Significance of low serum alkaline phosphatase activity in a predominantly adult male population. Clin Chem.

Liver Enzymes: No trivial elevations, even if asymptomatic. The results of the study are presented as fold elevations above the designated ULN. For the purpose of this study, patients with two or more hepatocellular or cholestatic liver diseases were excluded unless otherwise indicated. Also, to eliminate the effects of liver disease treatments on serum liver enzyme levels, only laboratory results from the untreated patient's initial visit to the clinic were analyzed.

The diagnostic criteria for each disorder were as follows: NAFLD, histology or radiologic imaging in keeping with fatty infiltration of the liver and no history of excess alcohol intake, use of medications associated with fatty infiltration of the liver and negative testing for hepatitis C virus HCV.

In the majority of NAFLD cases where autoantibodies were present, a biopsy was obtained to rule out concurrent immune-mediated liver disease. Liver enzyme values were available from a total of diagnosed patients, with hepatocellular and with cholestatic liver disorders. Overall, the mean age of study subjects was Causes of liver disease and demographic features of the study population.

With the exception of AIH patients where ALP levels were consistently higher than predicted values for other causes of liver disease p 0. Liver enzyme abnormalities in patients with varying degrees of hepatocellular liver disease. Liver enzyme abnormalities in patients with varying degrees of cholestatic liver disease. To determine whether predicted ranges of ALP in hepatocellular disease patients and ALT in cholestatic patients aid in identifying patients with both types of disorders, the results of liver enzyme testing in 56 patients with concurrent hepatocellular and cholestatic diseases were analyzed.

The gender distribution and mean age in these patients are shown in Table 4. Demographic features, underlying liver disease and beyond predicted liver enzyme levels in those with both hepatocellular and cholestatic liver disorders. The results of this study provide clinicians with predicted ranges for cholestatic liver enzymes in patients with common causes of hepatocellular disease and aminotransferase levels for patients with common causes of cholestasis.

The results reveal that serum ALP levels are increased in proportion to the severity of hepatocellular liver injury and aminotransferases to the severity of cholestasis. In addition, the findings suggest the profile of elevated liver enzymes can help determine which patients have concurrent hepatocellular and cholestatic forms of liver disease. The mechanism s whereby hepatocellular liver injury results in increased serum ALP levels remains to be determined.

However, certain conditions such as ischaemic hepatitis can be associated with marked elevations in serum aminotransferases yet normal or near normal ALP levels [6,7].

Thus, the explanation for why serum ALP levels are increased in some but not all patients with hepatocellular injury is unclear. Also remaining to be determined is why serum aminotransferases are elevated in patients with common cholestatic liver diseases. That ALT and AST values increased in proportion to the severity of the underlying cholestatic liver disease are in keeping with both explanations. The explanation for this relates to the nonspecificity of AST and GGT values and with the exception of ALD, the limited sensitivity of AST in documenting the extent of hepatocellular liver injury in common causes of hepatitis [1].

In terms of assisting diagnostic accuracy, it is important to note that aside from higher serum ALP levels being documented in AIH patients, the predicted changes in ALP levels were consistent amongst the various common causes of hepatocellular disease. Translating these findings into clinical practice one could advise that in the majority of patients with common causes of hepatocellular disease, concurrent cholestatic liver disease should be considered if the serum ALP level exceeds 1.

Clearly, prospective studies are required to support these general guidelines. Likely contributing to this finding was the probability the second co-existing disorder was in its early stages when patients first presented to the clinic and liver enzyme abnormalities were not yet fully manifest. None-the-less, either disproportionate increases in serum ALP and ALT levels were present in the majority of patients with concurrent hepatocellular and cholestatic liver diseases and therefore, could serve to alert physicians to the possibility that a second disorder existed in these patients.

There are a number of limitations to this study that warrant emphasis. First, this was a retrospective analysis and larger, prospective studies are required to confirm the findings.

Second, not all causes of hepatocellular disease and cholestasis were analyzed. Fourth, in order to eliminate the impact of disease treatment, only one set of liver enzymes values was utilized the patients initial laboratory findings and therefore, transient elevations due to sample collection, storage or circadian rhythm could not be excluded [10].

Fifth, it could not be reliably ascertained whether patients were fasting when tested. This may be particularly relevant to Lewis-positive secretors of blood types B or O in that serum ALP levels can increase in these patients following meals [11,12]. Finally, liver histology was not available to support the use of serum enzyme levels as reflecting the severity or stage of liver disease.

However, the intent of the study was to determine what the predicted serum levels of liver enzymes would be in patients with various types of liver disease and not necessarily the histologic severity or stage of disease.

In conclusion, the results of this study provide clinicians with predicted ranges of liver enzymes in patients with hepatocellular or cholestatic liver disease.

In doing so, they may enhance a clinician's ability to identify patients with both forms of liver disease. Abbreviations ALT alanine aminotransferase. The authors have no conflicts of interest to declare. The authors wish to thank Ms R. Vizniak for her prompt and accurate typing of the manuscript.. This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors..

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The relative expression of hepatocellular and cholestatic liver enzymes in adult patients with liver disease. Download PDF. Corresponding author. This item has received. It is a very sensitive test of hepatobiliary disease both hepatocellular and cholestatic injuries. However, its specificity is poor as GGT elevation can be seen in a wide range of non-hepatic diseases, including alcoholism, pancreatic disease, chronic obstructive pulmonary disease and renal failure.

Because GGT is not elevated in bone disease, it is mainly used to confirm the liver as the source of increased alkaline phosphatase. Although 5'N has a wide body distribution, its elevation is generally associated with hepatobiliary pathology. Like GGT, 5'N is not elevated in bone disease and it is therefore useful in confirming hepatic origin of alkaline phosphatase.