Abstract
IntroductionBurkitt lymphoma and B cell lymphomas in childhood may arise in many atypical locations, which on rare occasions can include gastric mucosa. A case of primary gastric Burkitt lymphoma is described in a child presenting as a protein-losing enteropathy, including the direct monitoring of the disease response by sequential endoscopic biopsy and molecular analysis.Case presentationWe report a 9-year-old boy who presented with gross oedema, ascites and respiratory distress caused by a protein-losing enteropathy. Initial imaging investigations were non-diagnostic but gastroduodenal endoscopy revealed massive involvement of the gastric mucosa with a primary Burkitt lymphoma. His subsequent clinical progress and disease response were monitored directly by endoscopy and he remains in clinical remission 4 years after initial diagnosis.ConclusionsThis is the first case report of primary Burkitt lymphoma presenting as a protein-losing enteropathy. The clinical course and progress of the patient were monitored by sequential endoscopic biopsy, histology and molecular analysis by fluorescence in situ hybridisation.
Highlights
Burkitt lymphoma and B cell lymphomas in childhood may arise in many atypical locations, which on rare occasions can include gastric mucosa
A case of primary gastric Burkitt lymphoma is described in a child presenting as a protein-losing enteropathy, including the direct monitoring of the disease response by sequential endoscopic biopsy and molecular analysis
Case presentation: We report a 9-year-old boy who presented with gross oedema, ascites and respiratory distress caused by a protein-losing enteropathy
Summary
Protein-losing enteropathy (PLE) has many causes including gastrointestinal lymphoma [1,2,3], there are no reports of protein-losing enteropathy caused by a primary gastric lymphoma in childhood. Multiple raised large (2 to 3 cm in diameter) ulcerated tumours of the greater curvature of the gastric body were seen (Figure 1), and numerous smaller tumours were seen in the second and third part of the duodenum but colonoscopy was normal. Follow-up endoscopy showed complete resolution of the mucosal tumours with only residual mucosal puckering present. Abdominal CT cans were normal and, once in remission and having completed chemotherapy, the patient’s ongoing disease surveillance was by endoscopy and repeat biopsy for FISH analysis. No molecular evidence of residual disease was detected, and he remains in clinical remission with complete resolution of the protein-losing enteropathy and no treatment related sequelae 4 years from initial diagnosis
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