Abstract-
A 20-year-old man, a case of chronic kidney disease had had a renal
transplant done in 2014, and presented with loss of weight and appetite
since seven-eight months. Abdominal ultrasound showed two liver lesions
with internal vascularity. CECT abdomen showed the same liver lesions
with progressive contrast enhancement. MRI was done for further
evaluation and showed enhancing lesions in segments VI and VIII with
peripherally restricted diffusion and central necrotic component.
Ultrasound-guided biopsy was performed and histopathology showed a
high-grade Non-Hodgkin’s lymphoma.
Keywords- Post-Transplant Lymphoproliferative Disorder, PTLD,
renal transplant
Key clinical message- 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.
Case presentation :
A 20-year-old man, a case of chronic kidney disease with a renal
transplant done in 2014 presented with loss of weight and appetite since
seven-eight months. On examination, he was vitally stable and soft,
non-tender abdomen. There was mild hepatomegaly on palpation. The
patient was referred to our institution with a provisional diagnosis of
liver abscesses with unresolving symptoms on treatment with antibiotics.
On ultrasound abdomen (Figure 1), there were 10x6cm and 5x6cm sized two
heterogeneously hypoechoic lesions in segment VIII and segment VI
respectively. Both the lesions showed internal vascularity with RI=0.60.
CECT abdomen showed a well-defined 8.7x5.2x6cm (APxTRxCC) sized
hypodense lesion in segment VIII (Figure 2) of the liver with
progressive heterogenous contrast enhancement. Another well-defined
5.2x4.2x5.3cm (APxTRxCC) sized hypodense lesion in segment VI (Figure 3)
of the liver with heterogenous progressive peripheral nodular contrast
enhancement. The central part of the lesion was non-enhancing. Both
kidneys were atrophic.
MRI of the abdomen was done for further characterization of the lesion.
It showed two well-defined T2 hyperintense (Figure 4) heterogeneously
enhancing lesions. They measured
9x5.5x6cm (APxTRxCC) in segment
VIII and 4.8x5.2x5.6cm (APxTRxCC) in segment VI. There was
diffusion restriction on DWI with
a corresponding drop on ADC (Figure 5). The central necrotic component
did not show enhancement (Figure 6) or diffusion restriction. The
imaging diagnosis was made of post-transplant lymphoproliferative
disorder (PTLD).
An ultrasound-guided biopsy of the larger lesion was done.
Histopathological report showed a high-grade Non-Hodking’s Lymphoma.
Discussion :
Post-transplant lymphoproliferative disorders (PTLD) 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]. 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 [4].
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 [5].
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 [6]. Hollow viscera
involvement is similar to those of non-Hodgkin’s lymphoma, including
thickening and aneurysmal dilatation. The liver is the most frequently
involved abdominal solid organ. The most common lesions are multiple
hypodense nodules on the CT with variable peripheral enhancement. The
kidney is the most commonly involved site in renal transplant recipients
[7]. A pulmonary mass and nodules either solitary or multiple, are
the most common thoracic manifestation of PTLD. The CT and MR imaging
features of CNS PTLD closely resemble those of HIV-related lymphoma. But
hemorrhages and necrosis are more common [8].
Classic treatment is the reduction of immunosuppression particularly in
polyclonal PTLD [9]. Chemotherapy is the mainstay of treatment in
monoclonal lesions and in lesions that are unresponsive to
immunosuppression reduction.