P2596 - Spontaneous Adrenal Insufficiency in a Decompensated Cirrhotic Patient

Kazi Haque, MD¹, Andrew W. Zarker, BS¹, Jennifer Ma, MD², Stephen E. Glombicki, MD, MBA³, Jing Kees, MD⁴, Glynda Raynaldo, MD⁴, Elizabeth Lam, MD^4
1UTH Health Science Center at Houston, Houston, TX; ²McGovern Medical School at UTHealth, Houston, TX; ³University of Texas Health Science Center, Houston, TX; ⁴Baylor College of Medicine, Houston, TX

Introduction: Decompensated cirrhosis can be challenging to manage and can vary in presentation. They require close monitoring due to increased mortality risks with SBP and bleeding. Here we have a case of spontaneous adrenal insufficiency (AI) in a clinically stable cirrhotic patient.

Case Description/Methods: A 60 year-old M with hx of decompensated alcoholic cirrhosis (MELD 35) presented with encephalopathy. He was found to be hyperammonemic and septic with E. Cloacae and Klebsiella pneumonia and admitted to ICU where pressors were initiated. His home lactulose was uptitrated; he was hydrated with IV fluids and initiated on broad spectrum antibiotics which escalated to Ertapenem. After a few days, his symptoms had resolved and was transferred to the floor with the removal of pressors. He finished his antibiotics and repeat cultures were negative. He was pending discharge when he slowly became lethargic, hypotensive despite midodrine, hyponatremic to 124, and hyperkalemic to 6.1. Cultures were re-sent but were negative. Ascitic fluid via therapeutic paracentesis also ruled out SBP. He responded minimally to fluids. Endocrine was consulted and recommended hydrocortisone and fludrocortisone. His hyperkalemia, hyponatremia, blood pressures, and lethargy all resolved. ACT Stimulation test occurred days later after stopping the hydrocortisone and fludrocortisone and confirmed AI. Hydrocortisone was then restarted and the patient remained stable until discharge.

Discussion: AI presents itself with hypotension, hyperkalemia, and weakness, but usually presents with a trigger such as infection or cancer. In this patient, there were no clear triggers. Although the pathophysiology of AI in cirrhosis is unclear, there have been many proposed mechanisms that support the concept of “hepatoadrenal syndrome.” Decreased production of lipoproteins, such as HDL and apo-A1, in the setting hepatic dysfunction leads to impaired synthesis of steroidogenic acute regulatory protein (stAR), which is a key enzyme in cortisol production. Another postulated mechanism is that splanchnic vasodilation prevents adequate perfusion to the adrenal glands. Lastly, cirrhosis is a proinflammatory state that leads to the production of cytokines such as TNF-alpha and IL-6, which reduce sensitivity to cortisol in peripheral tissues and also suppresses secretion of ACTH from the anterior pituitary. Diagnosis occurs through AM cortisol testing with ACT Stimulation tests. Definitive treatment and resolution of symptoms occur through corticosteroids.


Disclosures:


Kazi Haque, MD¹, Andrew W. Zarker, BS¹, Jennifer Ma, MD², Stephen E. Glombicki, MD, MBA³, Jing Kees, MD⁴, Glynda Raynaldo, MD⁴, Elizabeth Lam, MD⁴. P2596 - Spontaneous Adrenal Insufficiency in a Decompensated Cirrhotic Patient, ACG 2023 Annual Scientific Meeting Abstracts. Vancouver, BC, Canada: American College of Gastroenterology.