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POST TRANSPLANT LYMPHOPROLIFERATIVE DISORDER IN THE SMALL BOWEL WITH SPONTANEOUS PERFORATION IN A LUNG TRANSPLANT RECIPIENT
Sun Jung Oh
*, Jeong Hoon Kim
Gastroenterology, UPMC, Pittsburgh, PA
BackgroundPost-transplant lymphoproliferative disorder (PTLD) is a rare malignant condition that can arise as a complication of solid organ transplantation. Given its high density of lymphocytic cells, the gastrointestinal tract can become involved. We present an aggressive case of PTLD in a patient with lung transplant leading to spontaneous small bowel perforation and severe liver disease.
Case PresentationA 75-year-old man with a history of double lung transplantation for scleroderma-associated interstitial lung disease (10 years prior) on tacrolimus and prednisone complicated by chronic diarrhea presented with failure to thrive, worsening diarrhea and weight loss. Computed tomography (CT) abdomen/pelvis revealed an enlarged mesenteric lymph node with subsequent PET-CT with multiple mild-moderately FDG-avid mesenteric lymph nodes. EBV PCR was positive.
He underwent an EGD and colonoscopy showing penetrating ulceration and inflammation of the distal terminal ileum with patchy fibrosis and diffuse colitis. Biopsies revealed severe ileitis and active chronic colitis without clonal lesion. Four days after the colonoscopy, patient complained of sudden onset and severe abdominal pain. CT demonstrated acute small bowel perforation requiring emergent surgical resection with loop ileostomy. Several prominent lesions on the bowel along with prominent lymph nodes were biopsied, which confirmed T-cell post-transplant lymphoproliferative disorder throughout small bowel.
Following surgical intervention, the patient’s LFTs continued to uptrend precipitously. These had initially been attributed to drug-induced injury, as he had been treated with fluconazole; however, as the trend worsened, there was growing concern for infiltrative PTLD versus shock liver. CT abdomen/pelvis, right upper quadrant ultrasound, and MRCP were notable for a dysmorphic and steatotic liver, but no overt cirrhosis or biliary pathology. Hepatitis panel and AFP were negative. Autoimmune workup was positive for ANA and AMA but attributable to his underlying connective tissue disease. Finally, liver biopsy was performed and revealed extensive T-lymphocyte infiltration of sinusoid/portal areas concerning for T-cell PTLD.
Oncology was consulted and the patient was transferred to the ICU for consideration of chemotherapy, but unfortunately, given the systemic and critical illness of the patient, he elected hospice care and
Conclusions Limited literature exists on cases of enterocolitis leading to small bowel perforation and acute liver injury secondary to PTLD specifically in lung transplant patients. This case demonstrates the severity of gastrointestinal and hepatologic complications from PTLD. When the lymphoproliferative disorder presents with penetrative disease, bowel perforation must be on the differential and consideration even prior to administration of chemotherapy.
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