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Original Report |
1
Department of Radiology, University of Maryland School of Medicine, 22 S.
Green St., Baltimore, MD 21205.
4
Department of Infectious Disease, University of Maryland School of Medicine,
Baltimore, MD 21205.
5
Department of Surgery, University of Maryland School of Medicine, Baltimore,
MD 21205.
Received March 29, 1999;
accepted after revision June 4, 1999.
Address correspondence to T. Meador.
3 Present address: Danbury Radiological Associates, 24 Hospital Ave., Danbury,
CT 06810.
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CONCLUSION. The prominent image finding of PTLD in pancreas transplant recipients is diffuse allograft enlargement, an appearance that may be indistinguishable from the image findings of acute pancreatitis or transplant rejection. However, failure of response to immunosuppressive therapy, presence of intraallograft or extraallograft focal masses, or organomegaly may suggest the diagnosis of PTLD.
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CT and sonography were performed on all eight patients in our study group, and MR imaging was performed on six of the eight patients. Although the performance of the individual imaging studies varied in time from the time of histopathologic diagnosis, all patients underwent imaging by at least one technique within 2 days of their original diagnosis. The original examinations were assessed without knowledge of the specific histopathologic findings. For this study, the dictated reports were used to establish the imaging findings and the histopathologic findings were used as the standard of reference for organ involvement.
CT for all patients in the study group was performed with either conventional or helically acquired abdomen and pelvis studies with enteric contrast media administration (collimation, 7-10 mm). One patient received an IV injection of 100 ml of iohexol (Omnipaque 300; Nycomed, Princeton, NJ). In addition, thoracic CT was performed on two patients.
All patients underwent sonography using an ATL 9 or HDI 3000 scanner (Advanced Technology Laboratories; Bothell, WA), or a Sequoia scanner (Acuson; Mountain View, CA). Imaging included a combination of gray-scale, color, and power Doppler sonography. Linear and curved array transducers were used with frequencies ranging from 3 to 7 MHz. In addition, two patients underwent sonography of the right upper quadrant.
MR imaging of the pelvis was performed on six patients using a 1.5-T system (Signa; General Electric Medical Systems, Milwaukee, WI) with a phased array coil. MR imaging sequences consisted of axial conventional T1-weighted spin-echo (TR/TE, 714/20); respiratory triggered, T2-weighted fast spin-echo (4000/99) with chemical selective fat saturation; and a T1-weighted fast multiplanar spoiled gradient-recalled dynamic enhanced study (150/4.2; flip angle, 60°; 5 mm thickness without gap; field of view, 24 cm). After informed consent was obtained, 0.1 mmol/kg of gadopentetate dimeglumine (Magnevist; Berlex Laboratories, Wayne, NJ) was administered by IV injection, followed by a saline flush. For the breath-held dynamic study, an initial coronal unenhanced study was performed, followed by sequential acquisitions performed immediately after the injection and then every minute for 5 min.
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The spectrum of PTLD included polyclonal B-cell hyperplasia in six patients, polyclonal B-cell hyperplasia and B-cell lymphoma in one patient, and large cell immunoblastic lymphoma in one patient. Extraallograft disease was present in both benign and malignant grades of PTLD. All seven patients who underwent virologic studies were found to have Epstein-Barr virus antibody positive titers before transplantation.
All patients had nonspecific symptoms before diagnosis including fever, chills, malaise, nausea, and vomiting. In seven of the eight patients, mild elevation of pancreatic serum enzyme levels was noted. Explantation of the pancreas allograft was performed in seven of the eight patients after the diagnosis of PTLD was made (two patients also had explantation of the renal allograft). At follow-up (range, 3 weeks-4 years; mean, 29 months), seven patients were alive. One patient died after the explantation procedure.
Imaging Findings
Pancreas allograft disease alone.—Two of the three patients
with pancreas allograft disease alone had diffuse enlargement of the pancreas
allograft on CT, sonography, and MR imaging. The remaining patient had a focal
solid mass in the head of the pancreas transplant that was revealed on all
three imaging techniques, which was subsequently histopathologically confirmed
as PTLD (Fig. 1A,
Fig. 1B,
Fig. 1C).
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Pancreas allograft and extraallograft disease.—Three patients had allograft and extraallograft involvement (all patients had histopathology). In one patient, the liver, bone marrow, and pancreas allografts were affected. This patient had an enlarged pancreas allograft on CT, sonography, and MR imaging and mild hepatomegaly on CT. A second patient had involvement of both kidney and pancreas allografts, manifesting as an enlarged kidney and pancreas on CT. However, on sonography the pancreas and kidney allografts appeared normal except for a thick-walled renal pelvis. MR imaging was not performed. Biopsy of a palpable cervical lymph node was positive for PTLD. CT images showed many small (<1 cm in diameter) lymph nodes in the abdomen. A third patient had involvement of the pancreas and kidney allografts, as well as gallbladder involvement proven surgically. On CT images, the pancreas and kidney transplants appeared diffusely enlarged (Fig. 2A); the gallbladder had a mildly thickened wall. MR images showed enlarged kidney and pancreas allografts (Fig. 2B). Sonography showed sludge and mild gallbladder wall thickening. Although the renal transplant was enlarged on sonography, the pancreas transplant appeared normal.
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Extraallograft involvement only.—Two patients had extraallograft disease only (lymph nodes, n = 1; liver, n = 1). The first patient's CT images showed many mildly enlarged (1-2 cm in diameter) lymph nodes located in the abdomen and pelvis, particularly in the paraaortic and subdiaphragmatic regions; chest evaluation revealed no lymph node enlargement. The kidney and pancreas allografts appeared normal. Sonographic images showed a slightly enlarged pancreas allograft with heterogeneous texture. The second patient had liver involvement identified through a biopsy performed during surgery for allograft explantation. CT images showed no liver abnormality.
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Patients with PTLD usually have Epstein-Barr virus (as seen in all seven of our patients for whom virologic data was available), Epstein-Barr virus has been strongly implicated as the cause of PTLD [2, 4, 6]. However, a direct causal link between the Epstein-Barr virus and PTLD has not been proven. The development of PTLD is also thought to be related to the use of certain immunosuppressive agents, including cyclosporine A (Sandiummune IV; Sandoz Canada, Quebec City, Quebec, Canada), Muromonab-CD3 (Orthoclone OKT3; Ortho Pharmaceuticals, Raritan, NJ), and tacrolimus (FK506; Fujisawa USA, Deerfield, IL) [1, 9, 10]. In our study, six patients received cyclosporine A, six received OKT3, and six received tacrolimus. Of the four patients who received all three medications, three developed polymorphic B-cell hyperplasia and the fourth developed malignant lymphoma.
In our study, 2.4% of all pancreas transplant recipients developed PTLD. The incidence of PTLD was much more common in pancreas-alone allografts (3.8%) as compared with pancreas after kidney (0.9%) or simultaneously placed pancreas and kidney (2.8%) transplants. To the best of our knowledge, no study has analyzed the frequency of PTLD in relation to the type of pancreas allograft transplantation. Although the sample size is small, our data suggest that patients with a pancreas transplant alone are at greater risk of developing PTLD. This trend could possibly be attributed to the fact that pancreas transplantation is associated with a high incidence of allograft rejection and steroid-resistant rejection, conditions that require large doses of immunosuppressive agents [1].
In examining the rate of occurrence of PTLD in the allograft after various solid organ transplantations, Hanto et al. [6] found the allograft was the site of PTLD in 37% of renal transplant recipients. Nalesnik et al. [4] reported allograft involvement in 17% of renal transplants and in 8.6% of liver transplants, and no occurrence of PTLD in heart transplants. In our study, six (66%) of the eight patients had involvement of the pancreas allograft.
The lack of specific radiologic findings contributes to the diagnostic difficulty in examining allograft recipients for PTLD. In prior series of solid organ transplants, PTLD has shown a variable imaging appearance: focal mass or masses, diffuse tissue involvement, wall thickening of the gastrointestinal tract, organomegaly, or lymphadenopathy [3, 11]. Of the eight patients in our study, five showed a diffusely enlarged allograft, a finding that may be radiographically indistinguishable from acute rejection or pancreatitis [12]. In addition, seven of the eight patients in our series developed an elevated level of serum amylase, a nonspecific finding that adds to the diagnostic difficulty. Only one patient had a focal mass involving the head of the pancreas allograft.
Our study showed that PTLD typically involved the pancreas allograft, whereas extraallograft involvement was less prominent. Of our patients with liver involvement, one presented with mild hepatomegaly and the other showed no abnormalities on CT images. Two patients had biopsy-proven lymph node involvement. One patient had palpable cervical lymphadenopathy but did not have significant abdominal or pelvic lymphadenopathy. The other patient had paraaortic and subdiaphragmatic lymph nodes that were slightly enlarged, with an average size of 1.5 to 2 cm (maximum diameter). Interestingly, no confluent nodal masses were seen, as would be expected with lymphoma involving the abdomen and pelvis. Pickhardt and Siegel [11] described abdominal manifestations of PTLD in which lymph node involvement was more commonly retroperitoneal than intraperitoneal. In their study, retroperitoneal lymph node involvement appeared as a discrete mass or as an infiltrative lesion with areas of central low attenuation consistent with necrosis.
When we compared the three imaging techniques used to assess PTLD in this study, CT of the abdomen and pelvis revealed virtually all histologically identified abnormalities. The exception was that liver and bone marrow involvement was not seen on CT images for two patients. Six of our eight patients underwent MR imaging to evaluate the allografts. The multiplanar capacity of MR imaging improved the visualization of abnormalities in some cases, but no additional findings were seen on MR imaging that were not seen with CT. In two of our eight patients, sonography failed to detect allograft involvement by PTLD.
Because of the rarity of PTLD in allograft recipients, our study is limited by a small patient population. In addition, because the study was performed at a single institution and immunosuppressive regimens may differ, institutional variation may occur. However, in our study, PTLD in pancreas allografts most commonly appeared as diffuse allograft enlargement. This appearance may be indistinguishable from the typical imaging findings of acute pancreatitis or allograft rejection. A mass lesion involving the pancreas allograft was seen in only one patient. The diagnosis of PTLD should be considered in pancreas transplant recipients who have allograft enlargement that does not respond to antiinflammatory or antirejection therapy or in whom extraallograft masses or organomegaly are present.
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