Transaminases and Liver Failure

Today’s morning report w featured a 67-year-old woman with progressive jaundice and abdominal pain on a background history of one-year of watery diarrhea.  Her only new exposure was an herbal  medication.  Her infectious, autoimmune, and imaging workup was negative.

There were lots of great learning points:

·      This patient had transaminase elevation into the thousands.  There is a relatively short differential diagnosis for this.

o   Ischemic hepatitis or “shock liver” occurs as a result of either global hypoperfusion of the liver, or arterial obstruction leading to ischemic injury.  Another vascular cause would be Budd-Chiari (hepatic vein) obstruction.

o   Viral hepatitis, typically caused by Hepatitis A or B virus (not usually hepatitis C)

o   Autoimmune hepatitis of either the type 1 or type 2 variety

o   Acute fatty liver of pregnancy typically occurs late in the pregnancy and presents with high transaminases and liver failure

o   Toxin/medication mediated – the classic here is acetaminophen toxicity, but other toxins are also possible.  Alcoholic hepatitis can also cause transaminase elevation, but generally not to the same degree (usually under 300)

o   Acute cholestatic obstruction – Although it is generally taught that this causes a cholestatic picture (elevated ALP and GGT rather than transaminases), it typically causes a very high transaminase elevation first, followed by the cholestatic picture.

·      There is a large difference between liver enzymes and liver function.  Liver enzymes are the AST, ALT, ALP and GGT that we’re all so familiar with. They are sometimes called “liver function tests” or LFTs.  More correctly, tests that examine the function of the liver are: coagulation studies, bilirubin, platelets, and clinical signs such as ascites and encephalopathy.

·      Sometimes these cases are frustratingly difficult to solve.  There are two special situations that can lead to some of these transaminase elevations:

o   Patients with HIV and HBV infection who stop their antiretrovirals (agents like tenofovir or adefovir that are active against both) can have an explosive hepatitis B reaction that can lead to progressive liver failure and death.

o   Patients with acute cholestatic obstruction which resolves can have no imaging findings on plain ultrasound.  These patients may need an MRCP to rule out a previous obstructive process.

·      The ultimate test to determine a diagnosis would be a liver biopsy.  If this patient’s transaminases had continued to rise, or she had progressive decline in liver function, then a biopsy may have been considered.

·      Pyogenic liver abscesses, especially from organisms like Echinococcus can produce symptoms including jaundice and abdominal pain.  They can rupture and produce cholestasis or even coagulation issues like Budd-Chiari syndrome.

Further Reading:

Sherman, K. E. (1991). Alanine aminotransferase in clinical practice: a review. Archives of internal medicine, 151(2), 260-265.

Khuroo, M. S., Zargar, S. A., & Mahajan, R. A. K. E. S. H. (1991). Echinococcus granulosus cysts in the liver: management with percutaneous drainage. Radiology, 180(1), 141-145.