Tests of Hepatic Function

The true LFTs reflect the synthetic capacity of the liver. Although conjugation and excretion of bilirubin is one such test, there are other variables that affect bilirubin levels, including the rate of production outside of the liver. Bile acids measured in the serum can be a useful tool to measure hepatic function. Because the pool of bile acids is much greater than bilirubin and enterohepatic cycling occurs, any change in the serum values will reflect even small changes in hepatic function. The main difficulty in establishing clinical utility for serum bile acids has been the lack of a true advantage in diagnostic capabilities over standard liver tests. The use of postprandial serum bile acid measurements is cumbersome requiring multiple blood draws, and is affected by changes in portal venous blood flow in the setting of portal hypertension. Hence, although the sensitivities of serum bile acids are high in detecting liver disease, there is no real advantage to routine clinical use.

PT is a very useful marker of hepatic function, and in acute liver failure it can impart prognostic information. Coagulation factors made in the liver include I, II, V, VII, IX, and X. Notably, factor VIII is not made in the liver and can be used to distinguish disseminated intravascular coagulation from liver related abnormalities in bleeding parameters, though this is rarely a clinical dilemma. More importantly, since factor V production is not dependent on vitamin K presence, measurement can be used to distinguish vitamin K deficiency as a cause of prolonged PT from liver disease-related causes. Vitamin K dependent factors are II, VII, IX, and X. Although prolonged PT is not specific for liver diseases, the other causes of prolonged PT, such as consumptive coagulapathy, vitamin K deficiency states, or medication-related causes, are generally simple to rule out. Hence, PT becomes a critical test for liver synthetic function. In fact, the international normalization ratio (INR) is now one of three tests used in the current liver cadaveric organ allocation scheme which uses a logarithmic calculation (model for end-stage liver disease) to categorize patients into 1 of 34 levels of illness and prioritizes their medical need for a transplant. The other two values used in the assessment are total bilirubin and creatinine.

Albumin is synthesized in the liver at a rate of 10 to 15 g daily with a pool of roughly 500 g. Although not useful as a marker of acute liver disease, it is very useful as an indicator of chronic liver disease, and is used in the Child-Turcotte-Pugh scoring systems. Because levels of albumin are depressed in malnourished states, nephrotic syndromes, and protein losing enteropathies, its clinical utility should be assessed in the setting of other tests of synthetic liver function.

Lipid and lipoprotein synthesis occurs in the liver, and levels of various lipid molecules change with both acute and chronic liver disease. For example, in cholestatic forms of liver disease, cholesterol levels rise, whereas in acute liver injury, plasma triglycerides are often elevated. In advanced liver disease, cholesterol levels are frequently low. Unfortunately, because of individual differences in these lipid values, as well as their dependence on nutritional status, there is no reliable way to use them to assess hepatic function.

Finally, several quantitative hepatic function assessments have been developed and remain experimental for the most part. These include the indocyanine green clearance test, aminopyrine breath test, antipyrine clearance, and caffeine clearance among others. None of these have any proven utility over standard tests in clinical practice, and they are difficult to perform compared to serum blood tests.

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