A 54-year-old woman presents with severe abdominal pain lasting 3 hours. The pain came on suddenly and was 10/10 in severity. It was in her right upper quadrant radiating to her back. She has had a 50-pound weight loss in the past year. Her medications include sertraline, phentermine-topiramate, and simvastatin.

She is evaluated in the emergency department, and labs show the following: aspartate aminotransferase, 450; alanine aminotransferase, 500; alkaline phosphatase, 100; bilirubin, 1.2. She receives morphine for her pain with minimal relief. An ultrasound shows no gallstones and no dilated common bile duct (CBD).

Her pain resolves 3 hours after arriving in the ED. Repeat labs 15 minutes after pain resolution show the following: AST, 900; ALT, 1,000; alk phos, 130; bili, 1.2.

What is the most likely diagnosis?

A. Acetaminophen toxicity.

B. Hepatitis A.

C. Ischemic hepatitis.

D. Simvastatin.

E. Passage of gallstone.

The correct answer in this case is passage of a gallstone.

The patient has had weight loss, which increases the risk of gallstone formation, and the pain pattern is consistent with passage of a gallstone through the common bile duct.

I have seen a number of cases where the diagnosis was missed when the lab pattern is similar to the labs in this case. The high transaminases and the absence of significant alkaline phosphatase elevation can be confusing. We are taught in our medical training that alkaline phosphatase is a lab value that goes up with obstruction, and that transaminases are liver injury labs. What are the data on liver labs in the setting of acute obstruction as seen with the passage of a gallstone?

Frederick Kiechle, MD, and colleagues reported that alkaline phosphatase levels, either alone or in conjunction with bilirubin levels, were not useful in determining the presence of common bile duct stones.1 Ming-Hsun Yang et al. found that normal gamma-glutamyl transferase results had the highest negative predictive value for the presence of a common bile duct stone (97%).2 The sensitivity for ultrasound detection of CBD stone in this study was only 35%.

Keun Soo Ahn and colleagues found that, in patients with symptomatic CBD stones, the average AST was 275, and the average ALT was 317 – about six to seven times the upper limit of normal for these lab tests.3 In the same study, the average alkaline phosphatase was 213, which is about twice the upper limit of normal.

Sometimes, extremely high transaminase elevations can occur with choledocholithiasis. Saroja Bangaru et al. reported on a case series of patients who all had transaminase values greater than 1,000 with symptomatic choledocholithiasis.4 All of the patients had normal or just mildly elevated alkaline phosphatase levels.

Rahul Nathwani, MD, and colleagues also reported on a series of 16 patients with choledocholithiasis and transaminase levels greater than 1,000.5 All patients were symptomatic, and the average alkaline phosphatase levels were 2.5 times the upper limit of normal.

Ala Sharara, MD, et al. looked at 40 patients in a retrospective study of patients found to have choledocholithiasis who presented within 12 hours of pain onset.6 Levels of AST and ALT both significantly correlated with duration of pain (P less than .001), whereas there was no significant correlation with alkaline phosphatase and bilirubin levels.

Pearl: AST and ALT elevations in patients with acute abdominal pain could be due to choledocholithiasis, even if there are minimal or no abnormalities in alkaline phosphatase. Marked elevations (greater than 1,000) can occur.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu .

References

1. Am J Emerg Med. 1985 Nov;3(6):556-60 .

2. Surg Endosc. 2008 Jul;22(7):1620-4 .

3. World J Surg. 2016 Aug;40(8):1925-31 .

4. J Clin Gastroenterol. 2017 Sep;51(8):728-33 .

5. Am J Gastroenterol. 2005 Feb;100(2):295-8 .

6. Clin Gastroenterol Hepatol. 2010 Dec;8(12):1077-82 .

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