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Year : 2012  |  Volume : 55  |  Issue : 3  |  Page : 416-418
Gastric post transplant lymphoproliferative disorder in a cytomegalovirus positive live related renal allograft recipient: A single case study

Department of Pathology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, UP, India

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Date of Web Publication29-Sep-2012

How to cite this article:
Gupta P, Solanki A, Krishnani N. Gastric post transplant lymphoproliferative disorder in a cytomegalovirus positive live related renal allograft recipient: A single case study. Indian J Pathol Microbiol 2012;55:416-8

How to cite this URL:
Gupta P, Solanki A, Krishnani N. Gastric post transplant lymphoproliferative disorder in a cytomegalovirus positive live related renal allograft recipient: A single case study. Indian J Pathol Microbiol [serial online] 2012 [cited 2021 May 14];55:416-8. Available from: https://www.ijpmonline.org/text.asp?2012/55/3/416/101765


Majority of post transplant lymphoproliferative disorders (PTLD) are B-cell non-Hodgkin lymphoma (NHL) and occur in 1% to 20% of solid organ transplant recipients. These disorders occur in about 1% of renal transplant recipients as a consequence of chronic immunosuppression. The most common site of involvement of PTLD in a renal allograft recipient is the allograft itself followed by lymph node, liver, lung, mediastinum, intestine, central nervous system and skin. [1]

A 36 year old hypertensive male patient had undergone live related renal transplantation as a result of end stage renal disease secondary to chronic glomerulonephritis in 1999. Patient was initially on triple immunosuppression with prednisolone, cyclosporine and azathioprine and later switched to double immunosuppression with prednisolone and mycophenolate mofetil. Patient presented to gastroenterology outpatient department in October 2011 with complaints of fever and loose stool since 10 months for which he had been taking symptomatic treatment. He also complained of upper abdominal pain after meal which got relieved spontaneously after half to one hour. On examination, abdomen was soft, non tender and there was no organomegaly. No other mass was palpable. Patient underwent upper gastrointestinal endoscopy and was found to have nodular growth [Figure 1]with sloughed mucosa involving the antrum of the stomach. Endoscopic biopsy of the growth was obtained. Histopathological examination of the biopsy showed sheets of atypical lymphoid cells within the lamina propria [Figure 2]and infiltration of these cells into gastric glandular epithelium. These cells were large having anisomorphic nuclei, clumped nuclear chromatin, conspicuous nucleoli and scanty cytoplasm [Figure 3]. Mitotic activity was brisk. On immunohistochemistry tumour [Figure 4] cells were positive for leukocyte common antigen (LCA), CD20 and negative for CD3 and cytokeratin. Computed tomography (CT) of the abdomen did not show any lymphadenopathy or liver metastasis. Routine hematological examination showed hemoglobin: 9.4 gm/dl, total leukocyte count: 12,200 cells/mm 3 and differential count showed neutrophilia (neutrophils 85%, lymphocytes 14% and eosinophils 1%). Polymerase chain reaction (PCR) showed amplification of cytomegalovirus genome. Serum creatinine was 1.6 mg/dl. Following the biopsy diagnosis of diffuse large B-cell NHL of stomach patient underwent distal subtotal gastrectomy with Billroth II reconstruction and naso-jejunal intubation. Intra-operatively, growth was seen in the antrum extending into the body along the lesser curvature of stomach. Greater curvature proximal to short gastric artery appeared to be free and pancreas was not infiltrated by the growth. There was no free fluid and rest of the bowel appeared unremarkable. Transplanted kidney was visualised in the right iliac fossa.

Gross examination of the resected specimen showed a proliferative growth measuring 12×9 cm involving the antrum and body of the stomach [Figure 1]. On cut surface growth appeared greyish white and was seen infiltrating beyond muscularis propria. Tumour was however away from both the proximal and distal resection margin of partial gastrectomy specimen. Histopathological examination was concordant with the biopsy findings. The mucosa was ulcerated and tumour cells were seen to infiltrate transmurally up to serosal fat. Heliobacter pylori was also evident within the gastric glands. All the seven perigastric lymphnodes retrieved from adjacent fat were free of tumour. Immunohistochemistry showed tumour cells to be immune-reactive for LCA and CD20 and negative for CD3.
Figure 1: Gross photograph showing partial gastrectomy specimen with nodular growth present in the antropyloric region and body of stomach

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Figure 2: Photomicrograph showing atypical lymphoid cells infi ltrating the lamina propria along with lymphoepithelial lesion (haematoxylin and eosin, × 100)

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Figure 3: Photomicrograph showing sheets of atypical lymphoid cells with dispersed nuclear chromatin, conspicuous nucleoli at places, brisk mitosis (haematoxylin and eosin, × 200)

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Figure 4: Photomicrograph showing tumour cells to be positive for CD20 (IHC, × 200)

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Immunosuppression results in almost 100 fold increase in the risk of malignancy following solid organ transplantation. Non Hodgkin lymphoma is the second most common malignancy in this group of patients and comprises about 20% of all malignancies. [1] It has been observed that gastric PTLD is more common in renal allograft recipients compared to other solid organ transplantation but the exact cause of this difference is not well understood. [2] Gastrointestinal PTLD usually involve the small and large intestine and most common presentation is fever, abdominal pain or perforation. [3] The exact incidence of gastric PTLD in renal allograft recipients is not well known and only few cases are reported in world literature. [4],[5]

Clinical presentation in PTLD can be of two different types; an infectious mononucleosis like illness in young patients presenting with fever, pharyngitis and lymphadenopathy early in the post transplant period and the second is in the form of extra nodal mass in older individuals usually more than six months after transplantation with more aggressive clinical course. In this group of patients with delayed presentation, the pathogenesis of PTLD may be related to complex interplay of various factors including chronic antigenic stimulation induced by the graft, accompanying immunosuppression and Ebstein Bar virus (EBV) infection. Apart from surgical measures, treatment of post-transplant lymphoproliferative disorders may include reduction or withdrawal of immunosuppression in low-risk patients. [1],[4] In addition, rituximab, a monoclonal antibody directed against CD20 antigen of B cells, can obtain response in two-third of PTLD. In the present case, the patient was surgically treated by distal subtotal gastrectomy with optimisation of immunosuppression, however didn't receive rituximab.

Present case highlights that gastric post transplant lymphoproliferative disorders although rare should be considered as an important differential diagnosis in renal allograft recipients who present with abdominal symptoms and gastric mass lesion.

   References Top

1.Schooler VC, Ragland B, Lazenby A, Eloubeidi MA. Post-transplantation lymphoproliferative disorder. Gastrointest Endosc 2004; 60:989-90.  Back to cited text no. 1
2.Ponticelli C, Passerini P. Gastrointestinal complications in renal transplant recipients. Transpl Int 2005;18:643-50.  Back to cited text no. 2
3.Caillard S, Dharnidharka V, Agodoa L, Bohen E, Abbott K. Posttransplant lymphoproliferative disorders after renal transplantation in the United States in era of modern immunosuppression. Transplantation 2005;80:1233-43.  Back to cited text no. 3
4.Hsi ED, Singleton TP, Swinnen L, Dunphy CH, Alkan S. Mucosal associated lymphoid tissue-type lymphomas occurring in post transplantation patients. Am J Surg Pathol 2000;24:100-6.  Back to cited text no. 4
5.Lasmar EP, Coelho LG, Lasmar MF, Lasmar LF, Lima PV, Nogueira AF. Mucosa-associated lymphoid tissue gastric lymphoma regression in a renal transplant patient after conversion of the immunosuppression to sirolimus: A case report. Transplant Proc 2009;3:959-61.  Back to cited text no. 5

Correspondence Address:
Narendra Krishnani
Pathology Department, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow - 226014
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0377-4929.101765

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

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