Case Presentation: Our patient is a 13 year old female with a 3-year history of celiac disease who presented to an outside facility with three days of fever, myalgias and RUQ pain. She had no stool changes, nausea or vomiting. Initial lab work was notable for a lipase of 1100, bilirubin of 4.9, AST of 33 and ALT of 114. An abdominal US revealed a contracted gallbladder with sludge and possible thickening. She transferred to our facility after her lipase continued to rise and fever returned. In our ED, she had a lipase of 2944, ALT of 82, AST of 33 and bilirubin of 6. Zosyn was started empirically for concern of acalculous cholecystitis. MRCP the following day demonstrated acute pancreatitis and normal biliary ducts without noted gallstones. Over the following five days her lipase and CRP improved but her total and direct bilirubin began to rise. ERCP on day 5 revealed a contracted gallbladder with sludge but no acalculous cystitis. Her pancreas, however, was found to have lobulated parenchyma which can be consistent with recurrent or chronic pancreatitis. Prior to the ERCP, her morning labs demonstrated a new increase in her ALT (130), AST (229) and Alkaline phosphatase (462) which had been normal the preceding days and signs of decreased synthetic function, with an INR of 1.4. In consultation with Rheumatolgoy and Gastroenterology, a work up was pursued for an autoimmune hepatitis but was unrevealing. Liver biopsy on hospital day 9 was consistent with drug induced hepatitis. A number of possible offending agents were discontinued, including her antibiotics. Her AST and ALT peaked at 229 and 265 respectively and bilirubin at 12.2. Given a continued rise in her transaminases and bilirubin, after stopping possible offending agents, she was started on IV methylprednisolone. Over the following 5 days she demonstrated improvement with downtrending AST, ALT, and bilirubin. Biopsy from ERCP, that resulted after discharge, revealed evidence of gluten-free diet non-compliance.
Discussion: Extraintestinal complaints have been described in patients with celiac disease thought secondary to associated inflammation or nutritional deficiencies. Patients with celiac disease may be at a two to three fold increased risk for pancreatitis and pancreatic insufficiency. Adherence to a gluten free diet helps improve pancreatic insufficiency but this does not appear to hold true with the progression to chronic pancreatitis. Our patient admitted to non-adherence to her gluten free diet later in her hospital stay. Despite a known association of Celiac disease and liver damage, given the new rise in our patient’s transaminases and bilirubin on day 7, it was important to consider an iatrogenic cause to this development. Our suspicion was confirmed when the biopsy revealed drug induced hepatitis. A number of the medications she received are known causes including piperacillin-tazobactam, ceftriaxone, ibuprofen, acetaminophen and ondansetron.
Conclusions: Our patient’s presentation demonstrates the importance of considering the extraintestinal manifestations of patients with celiac disease and risk for associated inflammatory conditions with diet non-adherence. The development of new hepatitis with cholestasis during her two week hospital course reminds us to consider iatrogenic causes of new disorders arising during hospital admission.