Journal of Medical Cases, ISSN 1923-4155 print, 1923-4163 online, Open Access
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Case Report

Volume 16, Number 12, December 2025, pages 475-486

Cecal Involvement of Diffuse Large B-Cell Lymphoma: A Rare Extra-Nodal Presentation

Figures

↓  Figure 1. Tonsil mass biopsy histology: high-grade lymphoid neoplasm with necrosis (H&E, × 40). H&E: hematoxylin and eosin.
Figure 1.
↓  Figure 2. Tonsil mass biopsy histology. (a) CD 20 immunostain (× 40): positive in the abnormal infiltrate, confirming B-cell lineage. (b) CD3 immunostain (× 40): negative in the neoplastic B cells. Admixed CD3+ small T cells. (c) CD10 immunostain (× 40): negative in the neoplastic B cells. (d) EBER-ISH (× 40): positive in the neoplastic B cells. EBER-ISH: Epstein-Barr virus-encoded small RNA in situ hybridization.
Figure 2.
↓  Figure 3. Tonsil mass biopsy histology. (a) BCL6 immunostain (× 40): negative in the neoplastic B cells. (b) BCL2 immunostain (× 40): negative in the neoplastic B cells. (c) C-MYC immunostain (× 40): negative in the neoplastic B cells. (d) MUM1 immunostain (× 40): negative in the neoplastic B cells. (e) Ki-67 immunostain (× 40): elevated proliferative index in the large cell infiltrate. BCL2: B-cell lymphoma 2; BCL6: B-cell lymphoma 6; MUM-1: multiple myeloma oncogene 1.
Figure 3.
↓  Figure 4. Solitary 15 mm ulcer in cecum on colonoscopy. Arrows indicate the extent and dimensions of ulcer. Circle indicates distortion of ileocecal valve from the ulcer.
Figure 4.
↓  Figure 5. Cecal tumor histology. (a) H&E (× 40): cecal mucosa involved by a large atypical lymphoid infiltrate. No Hodgkin/HRS-like morphology seen. (b) H&E (× 10): cecal mucosa involved by a large atypical lymphoid infiltrate. (c) PAX5 immunostain (× 40): positive in the abnormal infiltrate, confirming B-cell lineage. (d) CD79a immunostain (× 40): positive in the abnormal infiltrate confirming B-cell lineage. H&E: hematoxylin and eosin.
Figure 5.
↓  Figure 6. Cecal tumor histology. (a) CD20 immunostain (× 40): negative in the B-cell infiltrate, consistent with anti-CD20 therapy. (b) Ki-67 immunostain (× 40): elevated proliferative index in the large cell infiltrate. (c) CD3 immunostain (× 40): negative in the neoplastic B cells. Admixed CD3+ small T cells. (d) BCL2 immunostain (× 40): positive in the neoplastic B cells. (e) C-MYC immunostain (× 20): positive (> 35%) in the neoplastic B cells. BCL2: B-cell lymphoma 2.
Figure 6.
↓  Figure 7. Cecal tumor histology. (a) BCL6 immunostain (× 40): positive in the neoplastic B cells. (b) MUM1 immunostain (× 40): positive in the neoplastic B cells. (c) EBV-LMP1 immunostain (× 40): positive in the neoplastic B cells. (d) CD10 immunostain (× 40): positive in the neoplastic B cells. BCL6: B-cell lymphoma 6; EBV-LMP1: Epstein-Barr virus latent membrane protein 1; MUM-1: multiple myeloma oncogene 1.
Figure 7.
↓  Figure 8. Infiltrative and ulcerated obstructing large cecal mass and rectal fistula. (a) Infiltrative cecal mass. (b) Partially obstructive cecal mass (arrows). (c) Ulcerated cecal mass. (d) Ulcerated fistula in rectum (arrow).
Figure 8.
↓  Figure 9. Computed tomography (CT) scan with oral and IV contrast findings. (a) Markedly distended cecum with thick-walled changes (arrows). (b) Oral contrast noted in bladder indicating a presence of a colovesical fistula (arrow). (c) Dense oral contrast material traversing colovesical fistula (arrow).
Figure 9.

Table

↓  Table 1. Timeline of Clinical Course
 
Timeline/date Clinical event/presentation Diagnostic tests and findings Treatment/intervention Outcome/notes
CT: computed tomography; DLBCL: diffuse large B-cell lymphoma; EBER-ISH: Epstein-Barr virus-encoded small RNA in situ hybridization; EBV-LMP1: Epstein-Barr virus latent membrane protein 1; FDG: F-fluorodeoxyglucose; GCB: germinal center B-cell; PET: positron emission tomography; R-CHOP: rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone; R-ICE: rituximab, ifosfamide, carboplatin, and etoposide; SUV: standardized uptake value.
Initial presentation 56-year-old male with 6-week history of sore throat, enlarging neck mass, odynophagia, dysphagia, 10-lb weight loss, night sweats CT neck: enlarged thyroid with bilateral lesions (5.5 × 4.9 cm R, 3 × 1.8 cm L), cervical lymphadenopathy, mediastinal nodes Biopsy of left tonsillar mass Histopathology: atypical lymphoid infiltrate; CD20+, high Ki-67 (80-90%), EBER-ISH positive; diagnosed aggressive DLBCL
Initial staging PET-CT whole body FDG-avid cervical nodes, hypermetabolic cecal wall thickening Bone marrow biopsy No marrow involvement
Initial treatment R-CHOP chemotherapy (six cycles over 3 months) - R-CHOP regimen -
Post-R-CHOP evaluation PET-CT Complete response in head/neck lymphadenopathy; persistent FDG uptake in cecum (SUV 23.2) Gastroenterology consult; colonoscopy 15-mm cecal ulcer biopsied; confirmed DLBCL, CD20-, PAX5+/CD79a+, Ki-67 high, EBV-LMP1+, double-expressor phenotype, GCB subtype
Disease progression and development of urologic complications Follow-up PET-CT Metabolically active diffuse cecal wall thickening; necrotic right neck lymphadenopathy; right hydroureteronephrosis; confirmation of colovesical fistula on CT Repeat colonoscopy Infiltrative, ulcerated obstructing cecal mass (14 mm); rectal fistula
Confirmed recurrent DLBCL; nephrostomy tube placement for obstructive uropathy
Salvage therapy R-ICE chemotherapy (two cycles) - Rituximab, ifosfamide, carboplatin, etoposide Did not respond; diverting loop ileostomy performed
Subsequent treatment Rituximab + polatuzumab (every 21 days) - Chemotherapy Disease continued to progress
Outcome Final - Supportive care Patient died due to lymphoma-related complications