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Department of Radiology
Seth G.S. Medical College and K.E.M. Hospital, Mumbai , India
Case of the Month
Case of the Month
Lymphoproliferative Disorder following renal transplantation
Lymphoproliferative Disorder following renal transplantation
Contributed by : Tejas Ghodasara
Contributed by : Tejas Ghodasara
Clinical Profile:
Clinical Profile:
A 20-year-old man with chronic kidney disease had had renal transplantation done in 2014. He presented with loss of weight and appetite since seven-eight months. On examination, his vitals were stable . The abdomen was soft and non-tender. The liver was mildly enlarged.
A 20-year-old man with chronic kidney disease had had renal transplantation done in 2014. He presented with loss of weight and appetite since seven-eight months. On examination, his vitals were stable . The abdomen was soft and non-tender. The liver was mildly enlarged.
Radiological Investigations:
Radiological Investigations:
Ultrasonogram of the abdomen (Fig. 1)
Ultrasonogram of the abdomen (Fig. 1)
A. The intercostal axial view of the liver shows an approximately 10x6cm sized, well-defined heterogeneously hypoechoic lesion in segments VII and VIII of the liver.
A. The intercostal axial view of the liver shows an approximately 10x6cm sized, well-defined heterogeneously hypoechoic lesion in segments VII and VIII of the liver.
B. Colour and Spectral Doppler of the same lesion shows mild internal vascularity with RI=0.60.
B. Colour and Spectral Doppler of the same lesion shows mild internal vascularity with RI=0.60.
C. Subcostal axial view of the liver shows a 5x6cm sized lesion of similar morphology in segment VI of the liver with internal vascularity.
C. Subcostal axial view of the liver shows a 5x6cm sized lesion of similar morphology in segment VI of the liver with internal vascularity.
Figure 1
A. Intercostal axial view of the liver shows an approximately 10x6cm sized, well-defined, heterogeneously, hypoechoic lesion in segment VIII of the liver.
B. Colour and Spectral Doppler of the same lesion show mild internal vascularity with RI=0.60.
C. Subcostal axial view of the liver shows a similar 5x6cm sized lesion in segment VI of the liver with internal vascularity.
Contrast-enhanced CT of the abdomen (Figs. 2,3) shows a well-defined 8.7x5.2x6cm sized hypodense lesion in segment VIII of the liver with progressive heterogeneous contrast enhancement. Another well-defined 5.2x4.2x5.3cm sized hypodense lesion in the segment VI of the liver with heterogeneous, progressive, peripheral nodular contrast enhancement. There is no enhancement in the central areas of the lesions. Both kidneys are atrophic. There is no calcification.
Contrast-enhanced CT of the abdomen (Figs. 2,3) shows a well-defined 8.7x5.2x6cm sized hypodense lesion in segment VIII of the liver with progressive heterogeneous contrast enhancement. Another well-defined 5.2x4.2x5.3cm sized hypodense lesion in the segment VI of the liver with heterogeneous, progressive, peripheral nodular contrast enhancement. There is no enhancement in the central areas of the lesions. Both kidneys are atrophic. There is no calcification.
Figure 2
Axial sections of the plain (A), arterial (B) and portovenous (C) phases of the CT abdomen show a well-defined 8.7x5.2x6cm sized hypodense lesion in segment VIII of the liver that shows progressive heterogenous contrast enhancement. There is no calcification.
Figure 3
Axial sections of the plain (A), arterial (B) and portovenous (C) phases of the CT abdomen show another well-defined 5.2x4.2x5.3cm sized hypodense lesion in segment VI of the liver that shows heterogeneous, progressive peripheral nodular contrast enhancement. The Central area of the lesion does not enhance. There is no calcification. Both the kidneys are atrophic.
MRI of the abdomen (Fig. 4) shows two well-defined, T2 hyperintense, heterogeneously enhancing lesions. They measure 9x5.5x6cm in segment VIII and 4.8x5.2x5.6cm in segment VI. There is diffusion restriction on DWI with a corresponding drop on ADC. The central necrotic component does not show enhancement or diffusion restriction.
MRI of the abdomen (Fig. 4) shows two well-defined, T2 hyperintense, heterogeneously enhancing lesions. They measure 9x5.5x6cm in segment VIII and 4.8x5.2x5.6cm in segment VI. There is diffusion restriction on DWI with a corresponding drop on ADC. The central necrotic component does not show enhancement or diffusion restriction.
Figure 4
T2 weighted axial sections of the MRI show two well-defined, heterogeneously hyperintense lesions in segment VIII (A) and VI (B) of the liver. The lesion in the segment VIII measures 9x5.5x6cm and the lesion in the segment VI measures 4.8x5.2x5.6cm
Figure 5
The lesions in the segment VIII (A) and VI (B) show diffusion restriction on DWI with a corresponding drop on ADC. The central area of the lesions does not show diffusion restriction.
Figure 6
On contrast enhanced MRI of the abdomen, the lesion in segment VIII shows heterogenous enhancement (A), the lesion in segment VI shows peripheral nodular enhancement with central non-enhancing area (B).
Sagittal section of the contrast enhanced MRI abdomen (C) shows two heterogeneously enhancing lesions in the liver with a transplanted kidney in the right iliac fossa
Radiological Diagnosis:
Radiological Diagnosis:
Post transplant lymphoproliferative disorder
Post transplant lymphoproliferative disorder
Pathological diagnosis:
Pathological diagnosis:
An ultrasound-guided biopsy of the larger liver lesion was performed.
An ultrasound-guided biopsy of the larger liver lesion was performed.
Histopathological findings showed High grade non-Hodgkin's lymphoma
Histopathological findings showed High grade non-Hodgkin's lymphoma
Discussion:
Discussion:
Post-transplant lymphoproliferative disorders (PTLD) are a heterogeneous group of diseases that represent complications of transplantation that are not so common. It is an umbrella term that involves lymphoid hyperplasia to lymphoid neoplasia. It occurs in the setting of immunosuppression after transplantation. The majority of PTLDs involve B cell proliferation and related Epstein–Barr virus (EBV) infection because the EBV-infected B cells proliferate when the T cells are depleted due to therapeutic immunosuppression [1,2]. In 1968, Starzl described PTLD in renal transplant recipients [3]. Knowledge of the distribution and radiologic features of PTLD allows the radiologist to play a pivotal role in making an early diagnosis and in guiding biopsy.
Post-transplant lymphoproliferative disorders (PTLD) are a heterogeneous group of diseases that represent complications of transplantation that are not so common. It is an umbrella term that involves lymphoid hyperplasia to lymphoid neoplasia. It occurs in the setting of immunosuppression after transplantation. The majority of PTLDs involve B cell proliferation and related Epstein–Barr virus (EBV) infection because the EBV-infected B cells proliferate when the T cells are depleted due to therapeutic immunosuppression [1,2]. In 1968, Starzl described PTLD in renal transplant recipients [3]. Knowledge of the distribution and radiologic features of PTLD allows the radiologist to play a pivotal role in making an early diagnosis and in guiding biopsy.
Epidemiology and Risk factors:
Epidemiology and Risk factors:
PTLD occurs in less than 2% of the patients following transplantation. It is more common in the pediatric population with two peaks occurring at one-year post-transplant and at five years post-transplant [4]. The incidence of PTLD varies according to several factors that include the patient's age, the EBV status at the time of the transplantation, the donor source (living or non-living), the organ of transplantation, and the immunosuppressive regimen. The prevalence differs with different organ allografts, with the highest prevalence recorded in multi-visceral transplant recipients (13%–33% of cases), followed by bowel (7%–11%), heart-lung (9.4%), lung (1.8%–7.9%), heart (3.4%), liver (2.2%), and kidney (1%) recipients [5].
PTLD occurs in less than 2% of the patients following transplantation. It is more common in the pediatric population with two peaks occurring at one-year post-transplant and at five years post-transplant [4]. The incidence of PTLD varies according to several factors that include the patient's age, the EBV status at the time of the transplantation, the donor source (living or non-living), the organ of transplantation, and the immunosuppressive regimen. The prevalence differs with different organ allografts, with the highest prevalence recorded in multi-visceral transplant recipients (13%–33% of cases), followed by bowel (7%–11%), heart-lung (9.4%), lung (1.8%–7.9%), heart (3.4%), liver (2.2%), and kidney (1%) recipients [5].
Risk factors involve Epstein-Barr virus seronegativity at the time of transplantation, concomitant cytomegalovirus infection, allograft type, and the immunosuppressive regime (e.g.azathioprine-more common CNS involvement) [6].
Risk factors involve Epstein-Barr virus seronegativity at the time of transplantation, concomitant cytomegalovirus infection, allograft type, and the immunosuppressive regime (e.g.azathioprine-more common CNS involvement) [6].
Pathogenesis:
Pathogenesis:
The majority of PTLDs are B-lymphocyte proliferations and are related to EBV infection. In a non-immunocompromised state, EBV may precipitate infectious mononucleosis, in which massive B-lymphocyte proliferation gives rise to—and eventually subsides under the control of—an equally massive T-lymphocyte reaction. This self-limited lymphoproliferative process may be distorted in the setting of immunosuppression, in which depressed T-cell function may allow a relatively uncontrolled proliferation of EBV-infected B lymphocytes [7,8]. Although this explains EBV-associated PTLD, it does not account for a number of other features of PTLD, such as (a) occurrence in the setting of stable immunosuppression and stable past EBV infection, (b) occurrence of T-cell– or natural killer cell–derived PTLD, (c) existence of EBV-negative PTLD, (d) preferential allograft localization of PTLD, or (e) presence of donor-derived PTLD in some solid organ transplant recipients.
The majority of PTLDs are B-lymphocyte proliferations and are related to EBV infection. In a non-immunocompromised state, EBV may precipitate infectious mononucleosis, in which massive B-lymphocyte proliferation gives rise to—and eventually subsides under the control of—an equally massive T-lymphocyte reaction. This self-limited lymphoproliferative process may be distorted in the setting of immunosuppression, in which depressed T-cell function may allow a relatively uncontrolled proliferation of EBV-infected B lymphocytes [7,8]. Although this explains EBV-associated PTLD, it does not account for a number of other features of PTLD, such as (a) occurrence in the setting of stable immunosuppression and stable past EBV infection, (b) occurrence of T-cell– or natural killer cell–derived PTLD, (c) existence of EBV-negative PTLD, (d) preferential allograft localization of PTLD, or (e) presence of donor-derived PTLD in some solid organ transplant recipients.
Classification:
Classification:
The Society of Haematology and the World Health Organization recommends the current classification system, which identifies four major categories as described below.
The Society of Haematology and the World Health Organization recommends the current classification system, which identifies four major categories as described below.
Clinical features:
Clinical features:
Most patients are asymptomatic in the early stages of the disease. Clinical manifestations are nonspecific, and it is usually difficult to differentiate PTLD from infection or graft rejection. It depends on the site of the involvement. Non-specific symptoms include fever, lymphadenopathy, and weight loss [9].
Most patients are asymptomatic in the early stages of the disease. Clinical manifestations are nonspecific, and it is usually difficult to differentiate PTLD from infection or graft rejection. It depends on the site of the involvement. Non-specific symptoms include fever, lymphadenopathy, and weight loss [9].
Role of imaging in diagnosis and follow-up:
Role of imaging in diagnosis and follow-up:
Since clinical features are non-specific. Imaging findings may help in identifying the lesions and guide biopsy for diagnosis. CT is the most commonly used modality because of its availability. MRI is also used depending upon the site and nature of the lesion. FDG-PET is specifically useful in the persistent lesions, and response evaluation to the therapy as it can help differentiate between residual tumor and fibrosis or necrosis [10].
Since clinical features are non-specific. Imaging findings may help in identifying the lesions and guide biopsy for diagnosis. CT is the most commonly used modality because of its availability. MRI is also used depending upon the site and nature of the lesion. FDG-PET is specifically useful in the persistent lesions, and response evaluation to the therapy as it can help differentiate between residual tumor and fibrosis or necrosis [10].
Intraabdominal involvement:
Intraabdominal involvement:
The abdominal cavity is the compartment most frequently involved by PTLD extra-nodal involvement (80% of cases) is more common than nodal involvement (20%) in intraabdominal disease [11].
The abdominal cavity is the compartment most frequently involved by PTLD extra-nodal involvement (80% of cases) is more common than nodal involvement (20%) in intraabdominal disease [11].
Gastrointestinal involvement:
Gastrointestinal involvement:
The distal small bowel is the most common site of involvement of hollow viscera, followed by the proximal large bowel, stomach, duodenum, and esophagus [11,12]. It is similar to those of non-Hodgkin’s lymphoma in immunocompetent individuals and includes wall thickening, aneurysmal dilatation, eccentric mass, and ulceration.
The distal small bowel is the most common site of involvement of hollow viscera, followed by the proximal large bowel, stomach, duodenum, and esophagus [11,12]. It is similar to those of non-Hodgkin’s lymphoma in immunocompetent individuals and includes wall thickening, aneurysmal dilatation, eccentric mass, and ulceration.
Solid organ involvement:
Solid organ involvement:
The liver is the most frequently involved abdominal solid organ. Most common lesions are multiple hypodense nodules on the CT with variable peripheral enhancement. MR imaging findings include lesions that are T1 hypointense and mildly T2 hyperintense. Sometimes ill-defined infiltrative pattern or large lesions may be seen. Overlap between the imaging features of opportunistic infections and those of PTLD at MR imaging and CT precludes confident diagnosis. Serologic markers and clinical findings may be helpful in differentiation.
The liver is the most frequently involved abdominal solid organ. Most common lesions are multiple hypodense nodules on the CT with variable peripheral enhancement. MR imaging findings include lesions that are T1 hypointense and mildly T2 hyperintense. Sometimes ill-defined infiltrative pattern or large lesions may be seen. Overlap between the imaging features of opportunistic infections and those of PTLD at MR imaging and CT precludes confident diagnosis. Serologic markers and clinical findings may be helpful in differentiation.
Splenic involvement has been reported in 10%–40% of cases, with a higher prevalence in liver transplant recipients [11,12]. The most common finding is splenomegaly, with multiple focal low-attenuation lesions (less frequent). MR imaging is useful in differentiating PTLD from opportunistic infections in the spleen. PTLD lesions are typically hypovascular and isointense on T1-weighted images and iso- to hypointense on T2-weighted images. Opportunistic lesions show T1 hypointensity and marked T2 hyperintensity relative to normal spleen parenchyma.
Splenic involvement has been reported in 10%–40% of cases, with a higher prevalence in liver transplant recipients [11,12]. The most common finding is splenomegaly, with multiple focal low-attenuation lesions (less frequent). MR imaging is useful in differentiating PTLD from opportunistic infections in the spleen. PTLD lesions are typically hypovascular and isointense on T1-weighted images and iso- to hypointense on T2-weighted images. Opportunistic lesions show T1 hypointensity and marked T2 hyperintensity relative to normal spleen parenchyma.
The kidney is the most commonly involved site in renal transplant recipients [13]. Common patterns of renal allograft involvement include heterogeneous mass or multifocal parenchymal masses. Native kidney involvement is always unilateral. Patterns of native kidney involvement include a discrete hypovascular parenchymal lesion or diffuse infiltrative disease.
The kidney is the most commonly involved site in renal transplant recipients [13]. Common patterns of renal allograft involvement include heterogeneous mass or multifocal parenchymal masses. Native kidney involvement is always unilateral. Patterns of native kidney involvement include a discrete hypovascular parenchymal lesion or diffuse infiltrative disease.
Adrenal gland involvement findings include diffuse infiltration with enlargement and a homogeneous low-attenuation mass.
Adrenal gland involvement findings include diffuse infiltration with enlargement and a homogeneous low-attenuation mass.
Pancreatic involvement is rare and only reported in the pancreatic allograft. Imaging features are non-specific including diffuse enlargement that is indistinguishable from acute graft rejection or pancreatitis.
Pancreatic involvement is rare and only reported in the pancreatic allograft. Imaging features are non-specific including diffuse enlargement that is indistinguishable from acute graft rejection or pancreatitis.
Nodal involvement:
Nodal involvement:
There is non-specific nodal enlargement, similar to other lymphomas most commonly affecting the mediastinum or retroperitoneum [14].
There is non-specific nodal enlargement, similar to other lymphomas most commonly affecting the mediastinum or retroperitoneum [14].
CNS involvement:
CNS involvement:
The CT and MR imaging features closely resemble those of HIV-related lymphoma. But hemorrhages and necrosis are more common [15]. Most cases manifest as a solitary mass that typically affects the periventricular region. On NCCT, the lesion is hyperdense secondary to hypercellularity or hemorrhage. The lesion is typically hypo- to isointense on T1-weighted MR images. On T2-weighted images, the lesion appears hypointense due to hypercellularity. It shows peripheral enhancement.
The CT and MR imaging features closely resemble those of HIV-related lymphoma. But hemorrhages and necrosis are more common [15]. Most cases manifest as a solitary mass that typically affects the periventricular region. On NCCT, the lesion is hyperdense secondary to hypercellularity or hemorrhage. The lesion is typically hypo- to isointense on T1-weighted MR images. On T2-weighted images, the lesion appears hypointense due to hypercellularity. It shows peripheral enhancement.
Thoracic involvement:
Thoracic involvement:
A pulmonary mass and nodules either solitary or multiple, are the most common thoracic manifestation of PTLD. Other findings include nodal enlargement, airspace consolidation, and less commonly pleural/pericardial effusions. Many of the thoracic manifestations are nonspecific for PTLD and can also be seen with transplantation-related complications, particularly infection. FDG-PET can increase specificity. A biopsy is still necessary for confirmation [16].
A pulmonary mass and nodules either solitary or multiple, are the most common thoracic manifestation of PTLD. Other findings include nodal enlargement, airspace consolidation, and less commonly pleural/pericardial effusions. Many of the thoracic manifestations are nonspecific for PTLD and can also be seen with transplantation-related complications, particularly infection. FDG-PET can increase specificity. A biopsy is still necessary for confirmation [16].
Treatment and prognosis:
Treatment and prognosis:
The treatment is variable and depends on the site, nature of the involvement, and histological type. Classic treatment is the reduction of immunosuppression particularly in polyclonal PTLD [17]. Chemotherapy is the mainstay of treatment in monoclonal lesions and in lesions that are unresponsive to immunosuppression reduction. The common regimen is cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP). Other options include rituximab and anti B-cell receptor antibodies. Surgical resection of the localized disease may be considered.
The treatment is variable and depends on the site, nature of the involvement, and histological type. Classic treatment is the reduction of immunosuppression particularly in polyclonal PTLD [17]. Chemotherapy is the mainstay of treatment in monoclonal lesions and in lesions that are unresponsive to immunosuppression reduction. The common regimen is cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP). Other options include rituximab and anti B-cell receptor antibodies. Surgical resection of the localized disease may be considered.
The prognosis depends on the grade of the lymphoma, and cell type: the low-grade lymphoid proliferation of polyclonal B-cell origin has a better prognosis than other cell types of a higher grade.
The prognosis depends on the grade of the lymphoma, and cell type: the low-grade lymphoid proliferation of polyclonal B-cell origin has a better prognosis than other cell types of a higher grade.
References :
References :
1. Nalesnik MA, Jaffe R, Starzl TE, et al. The pathology of posttransplant lymphoproliferative disorders occurring in the setting of cyclosporine A-prednisone immunosuppression. Am J Pathol 1988; 133:173–192. [PMC free article] [PubMed] [Google Scholar]
1. Nalesnik MA, Jaffe R, Starzl TE, et al. The pathology of posttransplant lymphoproliferative disorders occurring in the setting of cyclosporine A-prednisone immunosuppression. Am J Pathol 1988; 133:173–192. [PMC free article] [PubMed] [Google Scholar]
2. Nagington J, Gray J. Cyclosporin A immunosuppression, Epstein-Barr antibody, and lymphoma. Lancet 1980; 1:536–537. [PubMed] [Google Scholar]
2. Nagington J, Gray J. Cyclosporin A immunosuppression, Epstein-Barr antibody, and lymphoma. Lancet 1980; 1:536–537. [PubMed] [Google Scholar]
3. Murray JE, Wilson RE, Tilney NL, et al. Five years’ experience in renal transplantation with immunosuppressive drugs: survival, function, complications, and the role of lymphocyte depletion by thoracic duct fistula. Ann Surg 1968; 168:416–435. [PMC free article] [PubMed] [Google Scholar]
3. Murray JE, Wilson RE, Tilney NL, et al. Five years’ experience in renal transplantation with immunosuppressive drugs: survival, function, complications, and the role of lymphocyte depletion by thoracic duct fistula. Ann Surg 1968; 168:416–435. [PMC free article] [PubMed] [Google Scholar]
4. Castellano-Sanchez AA, Li S, Qian J et-al. Primary central nervous system posttransplant lymphoproliferative disorders. Am. J. Clin. Pathol. 2004;121 (2): 246-53. doi:10.1309/N82C-TQ1J-0XEV-EFQB - Pubmed citation
4. Castellano-Sanchez AA, Li S, Qian J et-al. Primary central nervous system posttransplant lymphoproliferative disorders. Am. J. Clin. Pathol. 2004;121 (2): 246-53. doi:10.1309/N82C-TQ1J-0XEV-EFQB - Pubmed citation
5. Cockfield SM. Identifying the patient at risk for post-transplant lymphoproliferative disorder. Transpl Infect Dis 2001;3:70–78.
5. Cockfield SM. Identifying the patient at risk for post-transplant lymphoproliferative disorder. Transpl Infect Dis 2001;3:70–78.
6. Brennan KC, Lowe LH, Yeaney GA. Pediatric central nervous system posttransplant lymphoproliferative disorder. AJNR Am J Neuroradiol. 2005;26 (7): 1695-7. Pubmed citation
6. Brennan KC, Lowe LH, Yeaney GA. Pediatric central nervous system posttransplant lymphoproliferative disorder. AJNR Am J Neuroradiol. 2005;26 (7): 1695-7. Pubmed citation
7. Hislop AD, Taylor GS, Sauce D, Rickinson AB. Cellular responses to viral infection in humans: lessons from Epstein-Barr virus. Annu Rev Immunol 2007; 25:587–617.
7. Hislop AD, Taylor GS, Sauce D, Rickinson AB. Cellular responses to viral infection in humans: lessons from Epstein-Barr virus. Annu Rev Immunol 2007; 25:587–617.
8. Snow AL, Martinez OM. Epstein-Barr virus: evasive maneuvers in the development of PTLD. Am J Transplant 2007;7:271–27
8. Snow AL, Martinez OM. Epstein-Barr virus: evasive maneuvers in the development of PTLD. Am J Transplant 2007;7:271–27
9. Bakker NA, van Imhoff GW, Verschuuren EA, van Son WJ. Presentation and early detection of posttransplant lymphoproliferative disorder after solid organ transplantation. Transpl Int 2007;20:207–218.
9. Bakker NA, van Imhoff GW, Verschuuren EA, van Son WJ. Presentation and early detection of posttransplant lymphoproliferative disorder after solid organ transplantation. Transpl Int 2007;20:207–218.
10. Von Schulthess GK, Steinert HC, Hany TF. Integrated PET/CT: current applications and future directions. Radiology 2006;238:405–422.
10. Von Schulthess GK, Steinert HC, Hany TF. Integrated PET/CT: current applications and future directions. Radiology 2006;238:405–422.
11. Pickhardt PJ, Siegel MJ. Posttransplantation lymphoproliferative disorder of the abdomen: CT evaluation in 51 patients. Radiology 1999;213:73–78.
11. Pickhardt PJ, Siegel MJ. Posttransplantation lymphoproliferative disorder of the abdomen: CT evaluation in 51 patients. Radiology 1999;213:73–78.
12. Harris KM, Schwartz ML, Slasky BS, Nalesnik M, Makowka L. Post transplantation cyclosporineinduced lymphoproliferative disorders: clinical and radiologic manifestations. Radiology 1987;162: 697–700.
12. Harris KM, Schwartz ML, Slasky BS, Nalesnik M, Makowka L. Post transplantation cyclosporineinduced lymphoproliferative disorders: clinical and radiologic manifestations. Radiology 1987;162: 697–700.
13. Caillard S, Lelong C, Pessione F, Moulin B. Posttransplant lymphoproliferative disorders occurring after renal transplantation in adults: report of 230 cases from the French Registry. Am J Transplant 2006;6:2735–2742.
13. Caillard S, Lelong C, Pessione F, Moulin B. Posttransplant lymphoproliferative disorders occurring after renal transplantation in adults: report of 230 cases from the French Registry. Am J Transplant 2006;6:2735–2742.
14. Camacho JC, Moreno CC, Harri PA et-al. Posttransplantation lymphoproliferative disease: proposed imaging classification. Radiographics. 2014;34 (7): 2025-38. doi:10.1148/rg.347130130 - Pubmed citation
14. Camacho JC, Moreno CC, Harri PA et-al. Posttransplantation lymphoproliferative disease: proposed imaging classification. Radiographics. 2014;34 (7): 2025-38. doi:10.1148/rg.347130130 - Pubmed citation
15. Pickhardt PJ, Wippold FJ 2nd. Neuroimaging in posttransplantation lymphoproliferative disorder. AJR Am J Roentgenol 1999;172:1117–1121
15. Pickhardt PJ, Wippold FJ 2nd. Neuroimaging in posttransplantation lymphoproliferative disorder. AJR Am J Roentgenol 1999;172:1117–1121
16. Reams BD, McAdams HP, Howell DN, Steele MP, Davis RD, Palmer SM. Posttransplant lymphoproliferative disorder: incidence, presentation, and response to treatment in lung transplant recipients. Chest 2003;124:1242–1249
16. Reams BD, McAdams HP, Howell DN, Steele MP, Davis RD, Palmer SM. Posttransplant lymphoproliferative disorder: incidence, presentation, and response to treatment in lung transplant recipients. Chest 2003;124:1242–1249
17. Nalesnik MA. The diverse pathology of post-transplant lymphoproliferative disorders: the importance of a standardized approach. Transpl Infect Dis 2001;3:88–96
17. Nalesnik MA. The diverse pathology of post-transplant lymphoproliferative disorders: the importance of a standardized approach. Transpl Infect Dis 2001;3:88–96
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