S3536 Testosterone and Human Growth Hormone-Associated Autoimmune Pancreatitis With Persistent Biliary Stricture: A Case Report

Introduction: Autoimmune pancreatitis (AIP) is an uncommon condition of the pancreas that can closely mimic pancreatic cancer. It is histologically classified into type 1 and type 2 AIP, with type 1 being part of the IgG4-related disease spectrum. AIP can arise idiopathically or be associated with immune or environmental triggers. Herein, we present a novel case of AIP with a linkage to anabolic steroids given the proximity to case presentation. Case Description/Methods: This is the case of a 37-year-old gentleman with no significant past medical history aside from 1 year of persistent anabolic steroid usage for bodybuilding purposes presenting with painless jaundice. Laboratory demonstrated cholestatic pattern to liver injury. Imaging revealed a 4 cm mass in the head of pancreas with common bile duct (CBD) upstream dilation. Tumor markers were negative. Endoscopic retrograde cholangiopancreatography (ERCP) with CBD stenting led to improvement in the total bilirubin. Endoscopic ultrasound sampling of the pancreatic mass revealed prominent duct-centric inflammation, neutrophilic micro-abscesses, and foci of storiform fibrosis. Plasma cells were present, with up to 20-25 IgG4-positive cells per high power field (HPF), which met the diagnostic criteria for IgG-4-related disease. The overall findings were consistent with AIP, showing overlapping histologic features of both type 1 and type 2 as the IgG-4 staining pattern was somewhat equivocal. Following diagnosis, the patient underwent a 12 weeks course of oral corticosteroid with a slow taper treatment. Patient discontinued usage of the anabolic steroids. Follow up imaging revealed resolution of the pancreatic head mass and normalization of labs. Patient did require 2 subsequent ERCP with stent exchanges prior to ultimate resolution of the persistent biliary stricture after corticosteroid initiation. Discussion: AIP remains a rare pancreatic disorder, with a presentation that can closely resemble malignancy. The combination of radiologic findings, characteristic histology, and marked clinical response to corticosteroids supported the diagnosis in our patient. Prior literature related to performance enhancing substances highlight the capacity of such agents to induce pancreatic inflammation, albeit without autoimmune features. We present the first documented case of AIP potentially associated with testosterone and human growth hormone (HGH) use. Clinicians should maintain a broad differential when evaluating pancreatic masses, particularly in younger patients with atypical exposures.