S4065 Acute Appendicitis Unmasks Incidental Cecal Adenocarcinoma in a Patient With Castleman Disease

Introduction: Castleman Disease is a complex lymphoproliferative disorder characterized by dysregulated cytokine signaling, primarily involving interleukin-6. While its link to hematologic malignancies is well-documented, associations with solid tumors are less recognized. This case illustrates the diagnostic complexity when advanced colorectal adenocarcinoma arises in the inflammatory setting of multicentric Castleman Disease, evading standard detection through both radiographic and biochemical masking. Case Description/Methods: We present the case of a 47-year-old man with multicentric Castleman Disease on siltuximab, who presented with acute non-perforated appendicitis. His medical history included well-controlled type 2 diabetes, hypertension, and dyslipidemia. A surveillance colonoscopy 4 years prior was negative for neoplasia. He underwent laparoscopic appendectomy with a prophylactic cecal wedge resection for optimal margins. Histopathology revealed a high-grade appendiceal mucinous neoplasm with dysplasia near the staple line. Four weeks later, the patient returned with abdominal pain. Imaging showed a localized abscess at the surgical site. During laparoscopic drainage, a suspicious mass was visualized, prompting conversion to open surgery. A formal ileocecectomy with anastomosis was performed. Final pathology showed stage III moderately differentiated cecal adenocarcinoma (pT4a, pN1b), with 2 of 15 lymph nodes positive. Preoperative imaging and tumor markers (CEA, CA 19-9, CA-125) remained within normal limits. Discussion: This case highlights the difficulty in distinguishing inflammation related to Castleman Disease from concurrent malignancy. The patient’s chronic inflammatory state, metabolic comorbidities, and impaired wound healing likely contributed to abscess formation, which ultimately led to the discovery of stage III cecal adenocarcinoma. The initial decision to perform a wedge resection was critical in capturing early dysplastic changes. Despite a recent negative colonoscopy, the malignancy remained undetected. Normal imaging and tumor markers further presented a misleadingly unremarkable clinical picture in this immunomodulated patient. We advocate for a lower threshold for advanced diagnostics and extended resection in Castleman patients with atypical GI symptoms. This case supports the need for disease-specific surveillance protocols using imaging, biomarker panels, and multidisciplinary oncologic care to enable early detection of solid tumors in this high-risk group.