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Intussusception Caused by Yersinia enterocolitica Enterocolitis in a Patient with Sickle Cell Anemia
Geetanjali Gupta1, Shailesh Kumar, Reecha Singh
1Department of Pathology, Mahatma Gandhi Medical College and Research Institute, Puducherry, India 607402.
Insights
Yersinia enterocolitica can cause intussusception, particularly in iron-overloaded patients. This rare case highlights the risk in children with sickle cell disease receiving blood transfusions.
Area of Science:
- Pediatric Gastroenterology
- Infectious Diseases
- Hematology
Background:
- Yersinia enterocolitica intussusception is uncommon, typically seen in iron-overloaded individuals due to the bacteria's iron utilization.
- Sickle cell disease patients often undergo transfusions, increasing iron load and potential susceptibility.
Observation:
- A 5-year-old with sickle cell disease presented with terminal ileum intussusception.
- The intussusception was caused by Yersinia enterocolitica, likely due to iron overload from monthly transfusions despite chelation therapy.
Findings:
- The patient's intussusception resulted from Yersinia enterocolitica-induced lymphoid hyperplasia and hypertrophied Peyer's patches.
- Iron serves as a critical growth factor for Yersinia enterocolitica, exacerbating infection in iron-rich environments.
Implications:
- Yersinia enterocolitica should be considered a potential pathogen in sickle cell disease patients, especially post-transfusion.
- This case underscores the importance of monitoring for Yersinia enterocolitica in immunocompromised patients with iron overload.
Abstract:
Yersinia enterocolitica intussusception is rarely encountered in patients without an underlying susceptibility and is most frequently reported in iron-overloaded patients. This is thought to be related to the unusual use of iron by this microorganism. We present a case of a 5-year old child with intussusception of the terminal ileum caused by Y. enterocolitica whose past medical history was significant for sickle cell disease. This type of presentation is extremely rare. His monthly blood transfusions may have put him at risk for Y. enterocolitica enterocolitis. The pathogenesis of this disease relates to the role of iron as an essential growth factor for Y. enterocolitica, and this patient's transfusions left him in an iron overloaded state despite treatment with Deferoxamine. Our patient's unusual presentation of intusssuception was secondary to the mass effect caused by lymphoid hyperplasia, specifically hypertrophied Peyer's patches in the ileum caused by the Y. enterocolitica infection. We believe that our case demonstrates that Y. enterocolitica should be considered a possible pathogen in patients with sickle cell disease, especially if symptoms occur shortly after blood transfusion.
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