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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2014  |  Volume : 25  |  Issue : 3  |  Page : 621-624
Post-kidney transplant large bowel lymphoproliferative disorder

1 Department of Internal Medicine, Division of Nephrology, The Ohio State University Medical Center, Columbus, OH, USA
2 Department of Surgery, Division of Transplantation, The Ohio State University Medical Center, Columbus, OH, USA

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Date of Web Publication9-May-2014


Epstein-Barr virus (EBV)-associated post-transplant lymphoproliferative disorder (PTLD) is a serious complication of organ transplantation. The gastrointestinal (GI) tract is a common site involved, but non-specific signs and symptoms often delay the diagnosis. We report a case of EBV-associated GI-PTLD in a 68-year-old kidney transplant patient who received the kidney ten months earlier. He presented with chronic diarrhea and developed massive pneumo-peritoneum secondary to multiple colonic perforations.

How to cite this article:
Singh N, Samavedi S, Rajab A. Post-kidney transplant large bowel lymphoproliferative disorder. Saudi J Kidney Dis Transpl 2014;25:621-4

How to cite this URL:
Singh N, Samavedi S, Rajab A. Post-kidney transplant large bowel lymphoproliferative disorder. Saudi J Kidney Dis Transpl [serial online] 2014 [cited 2021 Oct 21];25:621-4. Available from: https://www.sjkdt.org/text.asp?2014/25/3/621/132209

   Introduction Top

Post-transplant lymphoproliferative disorder (PTLD) is a rare but potentially fatal complication of organ transplantation. The incidence of PTLD varies according to the transplanted organ, ranging from 1-3% in kidney transplants, [1],[2] to up to 20% in intestine transplants. [3] PTLD has different characteristics than lymphomas, occurring in the general population as disease is commonly extra-nodal and classical B symptoms may be absent. Majority (80-90%) of PTLDs are of B-cell origin and are associated with Epstein-Barr virus (EBV). [1] A myriad number of ways PTLDs may pose a diagnostic challenge and require a high index of suspicion and close surveillance post-transplant. In this report, we describe a case of kidney transplant recipient with gastrointestinal (GI)-PTLD who presented with chronic diarrhea and developed massive pneumoperitoneum secondary to multiple colonic perforations. Although urgent exploratory laparotomy with total colectomy was performed, the patient expired one week after the surgery.

   Case Report Top

A 68-year-old Caucasian male who received a deceased donor kidney transplant 10 months earlier presented with six-week history of intermittent diarrhea with recent worsening and weight loss. The patient had no prior history of rejection and he has had stable kidney allograft function since his transplant, with a baseline serum creatinine value of 1.5-2.0 mg/ dL. At the time transplant, he was given anti-thymocyte globulin (ATG) induction 1.5 mg/kg for five days, and subsequently was maintained on cyclosporine 100 mg BID and sirolimus 2 mg daily. On admission, he had a temperature of 99.6°F and non-tender but slightly distended abdomen. His examination further revealed a dry oral mucosa and a blood pressure of 98/46 mm Hg. Laboratory data showed: hemoglobin, 12.4 mg/dL; white cell count, 8.4 K/μL with slight leftward shift; platelets, 245 K/μL; sodium, 136 mmol/L; potassium, 4.2 mmol/L; chloride, 105 mmol/L; bicarbonate, 20 mmol/L; BUN, 54 mg/dL; and creatinine, 2.3 mg/dL. The remainder of the laboratory work-up was unremarkable. Abdominal X-ray demonstrated mild colonic distension, but no intestinal obstruction or free air [Figure 1]. Ogilvie syndrome was suspected and nasogastric suction, IV fluids and empirical antibiotics were instituted. Serum creatinine returned to the baseline value after intravenous (IV) hydration. Follow-up laboratory data showed negative blood and stool cultures and a negative Clostridium difficile toxin assay. Colonic distension persisted on serial abdominal X-rays. Colonoscopy was performed on Day 3, but no biopsy was attempted due to friable, ischemic and erythematous-looking colonic mucosa. EBV polymerase chain reaction (PCR) was reported at 38,000 copies/mL. Immunosuppresion was reduced and IV ganciclovir was added. A computed tomography scan of the abdomen and positron emission tomography scan demonstrated circumferential wall thickening of the colon and mild abdominal lymph node enlargement, raising the suspicion of large-bowel PTLD. On Day 5, the patient developed acute abdominal pain with hematochezia. A stat portable-CXR showed massive pneumoperitoneum [Figure 2]. Urgent exploratory laparotomy with total colectomy was performed due to multiple colonic perforations. The colon biopsy showed diffuse infiltration of atypical lymphoid cells of intermediate size with irregular nuclear borders [Figure 3], positive for CD20, CD30 and bcl-2 but negative for CD3, CD5, CD-10 and bcl-1 on immunohistochemical stain (not shown). In situ hybridization for Epstein-Barr virus-encoded RNA (EBER) was positive. With these data, a diagnosis of an EBV-associated B-cell PTLD, monomorphic type, was made. Post surgery, the patient was treated with anti-CD20 monoclonal antibody (rituximab), following which the serum EBV PCR decreased to 5322 copies/mL. Unfortunately, the patient died one week after the surgery due to cardiorespiratory arrest.
Figure 1: Abdominal-X ray shows mild colonic distension.

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Figure 2: Chest-X ray with massive pneumoperitoneum.

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Figure 3: Colon biopsy shows diffuse infiltration of atypical lymphoid cells suggestive of posttransplant lymphoproliferative disorder.

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The patient had received an EBV-positive donor kidney, although he himself was EBV-seropositive as well. Post transplant, his risk of developing EBV viremia was considered low. Consequently, he did not receive prophylactic antiviral therapy and no routine monitoring for EBV was performed post transplant.

   Discussion Top

The GI tract has been reported to be one of the most common sites of PTLD among kidney transplant recipients. [4] Manifestations are often non-specific, and include GI bleeding, diarrhea, weight loss, malabsorption [5],[6] and chronic intestinal pseudo-obstruction, which mimics small bowel occlusion in the absence of demonstrable mechanical obstruction. [7] Involvement of the entire thickness of the intestinal wall may lead to perforation of the bowel wall with pneumoperitoneum, [8] which was seen in our patient as well. A high index of clinical suspicion for PTLD in transplant patients presenting with GI symptoms, and a careful interpretation of subtle early radiological findings like colonic distension or mild ileus, may help in making an early diagnosis and possibly preventing the high morbidity and mortality associated with this serious complication of organ transplantation.

The risk of PTLD increases with age, level and duration of immunosuppression, antilymphocyte therapy, EBV-seronegative recipient with EBV-seropositive donor, cytomegalovirus disease, HLA mismatch and Caucasian race. Although the staging of PTLD has not been formally defined, the World Health Organization (WHO)classification [9] is commonly used and divides PTLD into four major categories: Early lesions, polymorphic PTLD, monomorphic PTLD and classical Hodgkin Lymphoma (CHL)-type PTLD. The British Committee for Standard in Haematology and the British Transplantation Society have reviewed the available literature and made recommendations for the diagnosis and management of PTLD in adult recipients of solid organ transplants. [10],[11]

In conclusion, GI involvement is common in PTLD with often non-specific symptoms and signs. Our patient presented with subtle and non-specific symptoms, and, in spite of medical and surgical interventions, did not survive. An accurate diagnosis of PTLD should be made early, and this requires a high index of suspicion and awareness of clinical features to avoid fatal complications.

   References Top

1.Taylor AL, Marcus R, Bradley JA. Post-transplant lymphoproliferative disorders (PTLD) after solid organ transplantation. Crit Rev Oncol Hematol 2005;56:155-67.  Back to cited text no. 1
2.Opelz G, Henderson R. Incidence of non-Hodgkin lymphoma in kidney and heart transplant recipients. Lancet 1993;342:1514-6.  Back to cited text no. 2
3.Cockfield SM. Identifying the patient at risk for post-transplant lymphoproliferative disorder. Transpl Infect Dis 2001;3:70-8.  Back to cited text no. 3
4.Opelz G, Dohler B. Lymphomas after solid organ transplantation: A collaborative transplant study report. Am J Transplant 2004;4: 222-30.  Back to cited text no. 4
5.Younes BS, Ament ME, McDiarmid SV, Martin MG, Vargas JH. The involvement of the gastrointestinal tract in posttransplant lymphoproliferative disease in pediatric liver transplantation. J Pediatr Gastroenterol Nutr 1999;28:380-5.  Back to cited text no. 5
6.Cao S, Cox K, Esquivel CO, et al. Posttransplant lymphoproliferative disorders and gastrointestinal manifestations of Epstein-Barr virus infection in children following liver transplantation. Transplantation 1998;66:851-6.  Back to cited text no. 6
7.De Giorgio R, Ricciardiello L, Naponelli V, et al. Chronic intestinal pseudo-obstruction related to viral infections. Transplant Proc 2010; 42:9-14.  Back to cited text no. 7
8.Hsu YC, Liao WC, Wang HP, Yao M, Lin JT. Catastrophic gastrointestinal manifestations of post-transplant lymphoproliferative disorder. Dig Liver Dis 2009;41:238-41.  Back to cited text no. 8
9.Swerdlow SH, Webber SA, Chadburn A, Ferry JA. Post-transplant lymphoproliferative disorders (PTLD). In: Swerdlow SH, Campo E, Harris NL, et al., eds. WHO Classification of Tumours of Haematopoietic and Lymphoid Tissue,. 343-50. IARC, Lyon.  Back to cited text no. 9
10.Parker A, Bowles K, Bradley JA, et al. Diagnosis of post-transplant lymphoproliferative disorder in solid organ transplant recipients - BCSH and BTS Guidelines. Br J Haematol 2010;149:675-92.  Back to cited text no. 10
11.Parker A, Bowles K, Bradley JA, et al. Management of post-transplant lymphoproliferative disorder in adult solid organ transplant recipients - BCSH and BTS Guidelines. Br J Haematol 2010;149:693-705.  Back to cited text no. 11

Correspondence Address:
Dr. Neeraj Singh
Department of Internal Medicine, Division of Nephrology, The Ohio State University Medical Center, Columbus, OH
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DOI: 10.4103/1319-2442.132209

PMID: 24821162

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  [Figure 1], [Figure 2], [Figure 3]


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