SUN-524 - Unraveling the Masquerade: When LADA Mimics Neuroendocrine Tumors, Chron'S, and Malabsorptive Syndromes

Introduction:
Latent autoimmune diabetes in adults (LADA) is an underrecognized autoimmune β-cell disorder that may mimic type 2 diabetes or present atypically with gastrointestinal, dermatologic, and systemic inflammatory features. This case uniquely demonstrates transient octreotide responsiveness and systemic inflammation in LADA, mimicking inflammatory bowel disease, celiac disease, and neuroendocrine tumors, resulting in extensive evaluation and diagnostic delay.

Case Presentation:
A 38-year-old Caucasian man, recently relocated from Florida to Georgia, presented with four months of non-bloody diarrhea (4–5 episodes/day), 60-lb unintentional weight loss, chronic intermittent pruritic rash, poor appetite, and persistent depression. He had a history of hyperglycemia (A1c >15) without a formal diabetes diagnosis and experienced seven emergency department visits and hospitalizations for similar complaints. Laboratory evaluation revealed elevated CRP (48 mg/dL) and ESR (103 mm/hr) with normal fecal calprotectin. CT enterography showed mild small bowel thickening and gastric distension. Colonoscopy revealed mild terminal ileitis. Pancreatic elastase was low (47 mcg/g), consistent with mild exocrine insufficiency. Celiac disease was excluded by negative serologies and normal intestinal histopathology.
Given chronic diarrhea, weight loss, and systemic symptoms, neuroendocrine tumors including VIPoma, glucagonoma, and carcinoid syndrome were strongly considered. An empiric trial of octreotide led to transient improvement in stool frequency and glycemic excursions, further reinforcing suspicion for a neuroendocrine process. However, biochemical evaluation, including VIP, glucagon, serotonin, 5-HIAA, and chromogranin A, was normal. HIV and thyroid testing were unremarkable, and no unifying diagnosis emerged.
Persistent severe hyperglycemia (up to 600 mg/dL) prompted further evaluation. C-peptide was markedly low (0.37 ng/mL; normal 0.8–3.85), and GAD-65 antibodies were elevated (33 IU/mL; normal < 5), confirming LADA. The patient was initiated on basal–bolus insulin therapy and continuous glucose monitoring. Short courses of steroids and mesalamine provided modest symptom relief but were limited by glycemic instability. Depression was managed with sertraline, and the patient remains under close outpatient follow-up.

Discussion:
Accounting for 5–10% of adult-onset diabetes, LADA should be considered in adults with brittle hyperglycemia, systemic inflammation, and atypical presentations. Early screening with GAD antibodies and C-peptide is crucial for timely diagnosis and appropriate management.This case highlights the need for heightened clinical suspicion for autoimmune diabetes in adults with multisystem involvement, as delayed recognition may lead to unnecessary testing, inappropriate therapies, and prolonged morbidity.

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