Conclusion:
PTLD represents a variety of conditions with prognosis depending on the grade of lymphoid proliferation. Knowledge of the distribution and radiologic features of PTLD allows the radiologist to play a pivotal role in making an early diagnosis, in guiding biopsy, and in the surveillance of treatment response in patients with PTLD.
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]
  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]
  4. Cockfield SM. Identifying the patient at risk for post-transplant lymphoproliferative disorder. Transpl Infect Dis 2001;3:70–78.
  5. Von Schulthess GK, Steinert HC, Hany TF. Integrated PET/CT: current applications and future directions. Radiology 2006;238:405–422.
  6. Pickhardt PJ, Siegel MJ. Posttransplantation lymphoproliferative disorder of the abdomen: CT evaluation in 51 patients. Radiology 1999;213:73–78.
  7. 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.
  8. Pickhardt PJ, Wippold FJ 2nd. Neuroimaging in posttransplantation lymphoproliferative disorder. AJR Am J Roentgenol 1999;172:1117–1121
  9. Nalesnik MA. The diverse pathology of post-transplant lymphoproliferative disorders: the importance of a standardized approach. Transpl Infect Dis 2001;3:88–96
Figures :
Figure 1-Ultrasonogram of liver:
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.
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 (APxTRxCC) sized hypodense lesion in the 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 (APxTRxCC) sized hypodense lesion in the segment VI of the liver that shows heterogenous progressive peripheral nodular contrast enhancement. Central area of the lesion is non-enhancing. There is no calcification. Both the kidneys are atrophic. Figure 4: T2 weighted axial sections of the MRI abdomen show two well-defined heterogeneously hyperintense lesions in the segment VIII (A) and VI (B) of the liver. The lesion in the segment VIII measures 9x5.5x6cm (APxTRxCC) and the lesion in the segment VI measures 4.8x5.2x5.6cm (APxTRxCC). 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).