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\begin{document}

\title{Post-Transplant Lymphoproliferative Disorder (PTLD) of the Liver
following an Allogenic Renal Transplant}



\author[1]{Sanika Patil}%
\author[2]{Padma Badhe}%
\author[3]{Tejas Ghodsara}%
\author[4]{Tejas Nikumbh}%
\affil[1]{Loyola University Health System}%
\affil[2]{Seth GS Medical College and KEM Hospital}%
\affil[3]{KEM Hospital and Seth G S Medical College}%
\affil[4]{Wright Center for Graduate Medical Education}%


\vspace{-1em}



  
  \date{May 27, 2024}


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\textbf{Title} - Post-Transplant Lymphoproliferative Disorder (PTLD) of
the Liver following an Allogeneic Renal Transplant

\textbf{Case Report}

\textbf{Authors:}

Dr. Sanika Patil

MBBS, DMRD

Research Fellow

Department of Radiology,

Loyola University, Chicago, USA

Dr. Padma V Badhe

MBBS, MD

Professor

Department of Radiology,

KEM Hospital, Mumbai, India

Dr. Tejas Ghodasara

MBBS

Radiology Resident

Department of Radiology

KEM Hospital, Mumbai, India

Dr. Tejas Nikumbh

Resident Physician,

Department of Internal Medicine,

The WrightCenter for GME,

Scranton, PA, USA

Corresponding author: drtejasnikumbh@gmail.com

\textbf{Consent statement-}

Written informed consent for publication of their clinical details
and/or clinical images was obtained from the patient.

\textbf{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.

\textbf{Keywords-} Post-Transplant Lymphoproliferative Disorder, PTLD,
renal transplant

\textbf{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.

\textbf{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.

\textbf{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.

\textbf{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.

\textbf{References} :

\begin{enumerate}
\tightlist
\item
  Nalesnik MA, Jaffe R, Starzl TE, et al.~The pathology of
  posttransplant lymphoproliferative disorders occurring in the setting
  of cyclosporine A-prednisone immunosuppression.~\emph{Am J Pathol}
  ~1988;~133:173--192.~{[}\emph{PMC free
  article}{]}~{[}\emph{PubMed}{]}~{[}\emph{Google Scholar}{]}
\item
  Nagington J, Gray J.~Cyclosporin A immunosuppression, Epstein-Barr
  antibody, and lymphoma.~\emph{Lancet} ~1980;~1:536--537.
  {[}\emph{PubMed}{]}~{[}\emph{Google Scholar}{]}
\item
  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.~\emph{Ann Surg} ~1968;~168:416--435.~{[}PMC
  free article{]}~{[}PubMed{]}~{[}Google Scholar{]}
\item
  Cockfield SM. Identifying the patient at risk for post-transplant
  lymphoproliferative disorder. Transpl Infect Dis 2001;3:70--78.
\item
  Von Schulthess GK, Steinert HC, Hany TF. Integrated PET/CT: current
  applications and future directions. Radiology 2006;238:405--422.
\item
  Pickhardt PJ, Siegel MJ. Posttransplantation lymphoproliferative
  disorder of the abdomen: CT evaluation in 51 patients. Radiology
  1999;213:73--78.
\item
  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.
\item
  Pickhardt PJ, Wippold FJ 2nd. Neuroimaging in posttransplantation
  lymphoproliferative disorder. AJR Am J Roentgenol 1999;172:1117--1121
\item
  Nalesnik MA. The diverse pathology of post-transplant
  lymphoproliferative disorders: the importance of a standardized
  approach. Transpl Infect Dis 2001;3:88--96
\end{enumerate}

\emph{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).

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