3178 Augmentin-Induced Liver Injury in a Patient With Progressive Familial Intrahepatic Hepatic Cholestasis (PFIC)

Abstract

INTRODUCTION: We are reporting a case of drug induced liver injury (DILI) within 48 hours of Augmentin administration in a patient with progressive familial intrahepatic cholestasis. CASE DESCRIPTION/METHODS: 27-yo female with PMH of severe ATP8B1 protein deficiency, PFIC S/P hepatojejunostomy with external biliary diversion, not a transplant candidate due to psychosocial issues, presented with epigastric pain, vomiting and constipation. Home meds included hydroxyzine, questran and rifampin. On admission vitals were BP: 110/59, pulse: 107, temp: 98.3, O2 sat: 100% on RA. Physical exam was unremarkable except icteric sclera. Labs showed WBCs: 19.1, H&H: 14.1/41.4, PLT: 187, Total Billi: 17.9, AST/ALT/ALP of 566/398/172, normal BMP except Bicarb: 15. INR: 1.8, lipase 25, UA negative for infection. CT Abd/pelvis W/contrast did not show any acute hepatobiliary pathology, except endometrial prominence with some fluid. Rifampin was stopped, aggressive bowel regimen, IV hydration and IV antibiotics including Unasyn and doxycycline were started. Fuid from endometrial cavity was cultured. Pt's abdominal pain improved as constipation resolved. Antibiotics were switched to Augmentin for presumed endometrial infection. LFTs started rising within 48 hrs of augmentin administration. Peak LFTs were T.Billi/AST/ALT/ALP:21.5/762/528/132. Complete laboratory evaluation included negative serologies for hepatitis, A, B, C, EBV, CMV and negative assays for ANA, AMA, ASMA. Augmentin was stopped. Two weeks after discontinuation of Augmentin, patient's LFTs started to improve. DISCUSSION: DILI is a well-recognized complication of Augmentin use and multiple cases have been reported. Associated mortality can be as high as 10%, and thus prompt recognition and removal of the offending agent is of critical importance. In our patient, while systemic infection and rifampin use were other possibilities for liver injury however, worsening and improvement in LFTs correlated with Augmentin administration and discontinuation. Moreover, dose of rifampin was not changed for over a year. Several risk factors have been identified for DILI including older age, genetic determinants, preexisting liver disease and properties of certain medications. Our patient had PFIC and Augmentin use caused liver injury within 48 hrs of administration as compared to other case reports where latent period of Augmentin induced liver injury varied from days to weeks. In both DILI and PFIC, treatment options are very limited thus Augmentin should be avoided.