Division of gastroenterology/hepatology, Medical College of Georgia at Augusta University Chicago, IL
Natchaya Polpichai, MD1, Emily Shu-Yen Chan, MD2, Sakditad Saowapa, MD3, Noppachai Siranart, MD4, Panisara Fangsaard, MD5 1Division of gastroenterology/hepatology, Medical College of Georgia at Augusta University, Chicago, IL; 2Weiss Memorial Hospital, Chicago, IL; 3Department of Internal Medicine, Texas Tech University Healt, Lubbock, TX; 4Brigham and Women's Hospital, Harvard Medical School, Boston, MA; 5Bassett Medical Center, Cooperstown, NY Introduction: Tigecycline (TGC) is a broad-spectrum antibiotic used for multidrug-resistant infections, including carbapenem-resistant Acinetobacter baumannii (CRAB). While gastrointestinal side effects are common, acute pancreatitis is a rare adverse reaction. We report a case of TGC-induced pancreatitis in a critically ill patient.
Case Description/
Methods: A 55-year-old female with a complex medical history—including hemorrhagic stroke with craniotomy, chronic respiratory failure requiring tracheostomy and mechanical ventilation, primary adrenal insufficiency on hydrocortisone, and multiple thromboembolic events—presented from a skilled nursing facility with fever and vomiting. Initial evaluation revealed leukocytosis (WBC 13.9 ×10⁹/L), elevated procalcitonin (0.48 ng/mL), and bilateral interstitial infiltrates on chest imaging. Blood and urine cultures were negative, but sputum culture grew CRAB.Empiric broad-spectrum antibiotics were escalated to high-dose TGC (200 mg loading dose followed by 100 mg every 12 hours) and cefiderocol. The patient subsequently developed worsening leukocytosis (WBC 45 ×10⁹/L), hypotension requiring ICU transfer, and acute kidney injury. Six days after TGC initiation, she developed nausea, vomiting, and a marked elevation in serum lipase (2132 U/L). CT imaging confirmed acute pancreatitis with diffuse peripancreatic inflammation but no necrosis or fluid collections, compared to a normal pancreas on CT abdomen eight days earlier. Alternative etiologies—including gallstones, alcohol use, hypertriglyceridemia, trauma, and other medications—were ruled out. TGC was identified as the most likely cause and was promptly discontinued. Discussion: TGC-associated pancreatitis is a rare but potentially life-threatening adverse effect. While the mechanism remains unclear, proposed theories include direct cytotoxicity and biliary excretion-related pancreatic injury. High-dose regimens may increase this risk, particularly in patients with multiple comorbidities or organ dysfunction. In this case, the temporal correlation between high-dose TGC initiation and symptom onset, the exclusion of other causes, and clinical improvement following drug discontinuation support a diagnosis of TGC-induced pancreatitis. Clinicians should remain vigilant for this adverse event, especially in critically ill patients receiving high-dose or prolonged TGC therapy. Early recognition and prompt withdrawal are essential to mitigate morbidity.
Disclosures: Natchaya Polpichai indicated no relevant financial relationships. Emily Shu-Yen Chan indicated no relevant financial relationships. Sakditad Saowapa indicated no relevant financial relationships. Noppachai Siranart indicated no relevant financial relationships. Panisara Fangsaard indicated no relevant financial relationships.
Natchaya Polpichai, MD1, Emily Shu-Yen Chan, MD2, Sakditad Saowapa, MD3, Noppachai Siranart, MD4, Panisara Fangsaard, MD5. P4417 - Navigating the Risks of Rescue Therapy: A Case of High-Dose Tigecycline (TGC)-Induced Pancreatitis, ACG 2025 Annual Scientific Meeting Abstracts. Phoenix, AZ: American College of Gastroenterology.