Diagnostic and Interventional Imaging (2013) 94, 131—144

CONTINUING EDUCATION PROGRAM: FOCUS. . .

Lymphomas: Basic points that radiologists should

know
E. Frampas

Central Radiology and Medical Imaging Department, Hôtel-Dieu, CHU de Nantes, 1, place
Alexis-Ricordeau, 44093 Nantes cedex 1, France

KEYWORDS Abstract Lymphomas affect the lymphoid system and may be expressed in a variety of ways
Oncology; and behave in different fashions. The polymorphism of their expression, depending on the
Lymphoma; organ involved, their variable aggressiveness and their relative rarity compared with primary
Lymph nodes; or secondary diseases sometimes makes it difficult to diagnose them from imaging. Knowledge
Biopsy; of predisposing factors and radiological signs should help suggest this diagnosis and thus lead
CT scans to biopsy samples being taken to confirm it.
© 2012 Éditions françaises de radiologie. Published by Elsevier Masson SAS. All rights reserved.

Definition and nosological context of lymphomas

Lymphomatous proliferations are defined as the clonal malignant proliferation of a mature
lymphocyte from a secondary lymphoid structure, a lymph node or an extranodal struc-
ture (the spleen, structures attached to the mucosae such as Peyer’s patches). They thus
contrast with acute leukaemias or myeloproliferative syndromes arising from an immature
cell of medullary origin. They are malignant variants of lymphocytes stuck at a specific
stage in their differentiation, with their own morphological and immunophenotypic char-
acteristics. Since there are many of these stages, malignant lymphomas cover a range of
very heterogeneous conditions in terms of their forms of presentation, their development
profile and their prognosis. We shall describe a certain number of aspects of these lesions
according to the organs affected and their differential diagnoses.

E-mail address: eric.frampas@chu-nantes.fr

2211-5684/$ — see front matter © 2012 Éditions françaises de radiologie. Published by Elsevier Masson SAS. All rights reserved.
http://dx.doi.org/10.1016/j.diii.2012.11.006
132 E. Frampas

In 2008, more than 355,000 new cases of non-Hodgkin’s

lymphomas (NHL) were recorded worldwide, which were
responsible for 191,400 deaths [1]. Following a period of
increase until the 1990s, mainly due to NHL associated with
AIDS, the incidence in Western Europe has stabilised at
around 10.5 and 7.4/100,000 in men and women respec-
tively. NHLs are more common in developed countries. In
France, 10,800 new cases were diagnosed in 2010, NHLs
making up 3% of all cancers, and in sixth position in terms
of frequency for women and seventh for men.
The causes of the condition are still not known. Cer-
tain lymphomatogenic factors —– viral (HCV, HIV, HTLV-1,
EBV, Herpes virus) and bacterial (Helicobacter pylori) —–
have been recognised, most often restricted to certain types
of lymphoma. Other risk factors are chronic immunosup-
pression, particularly of drug origin (post-transplantation),
exposure to certain substances (dioxin, agricultural pesti-
cides) or a history of chemotherapy (alkylating agents). Figure 1. Burkitt’s lymphoma with a large tumour mass in a child.
Treatment is based on a variable combination of CT scan with injection. Diffuse infiltration of the mesentery, the
chemotherapy, radiotherapy and immunotherapy, adapted loops of the small intestine and the peritoneum, particularly in the
paracolic gutters and the lesser omentum.
to each type. In addition to classic staging of the disease,
knowledge of the various extranodal presentations is essen-
tial in order to avoid any inopportune corticosteroid therapy • through typical presentations or development profiles,
or unnecessary surgery before diagnostic confirmation. the approach to treatment following directly from them
(Table 1). It is simpler then to distinguish two groups:
◦ aggressive lymphomas (physiologically or clinically)
How are they classified?
in particular with high Ki67 proliferation marker
The diagnosis of lymphoma is based on pathological his- expression (Burkitt’s lymphoma, diffuse large B-cell
tology. Conventional examination, in the first instance, lymphoma), a large tumour mass (Fig. 1), an aggres-
distinguishes on a morphological basis between Hodgkin’s sive clinical presentation with general signs (peripheral
lymphoma (HL), characterised by the presence of Reed- T and mantle cell lymphomas), rapid development [3]
Sternberg cells (40% of lymphomas), and non-Hodgkin’s and requiring major treatment,
lymphomas (NHL) (60%), classified according to criteria ◦ indolent lymphomas of which 80% are slow growing fol-
concerning their architecture (follicular or diffuse) and licular B-cell NHLs, which may transform in 9—10 years’
morphology (small or large cells). An immunophenotypic time into high grade lymphomas (15 to 40%), where the
examination should also be used to determine the B- (85% decision concerning treatment will depend on the type
of cases) or T-cell (15%) origin, along with cytogenetic and and mass of the tumour [4];
biomolecular investigations to look for acquired character- • through being aware of the preferential frequency of
istic translocation anomalies of the different types (e.g. t the types of lymphomas depending on age, the patient’s
(14;18)(q32;q21) of follicular NHLs). According to the WHO condition or the extranodal location: Burkitt’s lym-
classification update in 2008 [2], this has resulted in 43 phoma and lymphoblastic lymphoma in children and
different conditions divided into four main groups (mature young adults, MALT lymphoma of the stomach, T-cell
B-cell, mature T-cell and NK-cell neoplasias, Hodgkin’s lym- lymphoma of the small intestine with coeliac disease,
phoma and post-transplant lymphoproliferation disorders). mantle cell lymphoma or splenic marginal zone lym-
There are several ways for the radiologist to try to learn phoma in the case of isolated splenomegaly, high grade
the broad outlines of this classification: B-cell NHL (immunoblastic, large cell, Burkitt) and

Table 1 Classification and main development profiles of non-Hodgkin’s lymphomas.

Behaviour Indolent Aggressive Highly aggressive
Type Small cell lymphoma Diffuse large B-cell NHL Burkitt
Follicular L (grade 1-2) Follicular L (grade 3) B-cell lymphoblastic L
Lymphoplasmacytic L Mantle cell lymphoma High grade B-cell L
Splenic/marginal zone lymph node L T-cell lymphoblastic L
Survival without Years Months Weeks
treatment
Curability Generally not Some Some
Treatment Delayed Yes Yes
Presentation Lymph node Medullary compression High tumour mass
Horner’s syndrome Superior vena cava obstruction
Lymphomas: Basic points that radiologists should know 133

HIV, B-cell NHL and transplantation (Table 2) [5]. Defini- Most comparative studies are based on 18 FDG PET as the
tive typing however will still depend on histopathological reference technique. Whole body diffusion-weighted MRI
data. has produced comparable results in staging Hodgkin’s and
aggressive lymphomas, even better results for indolent lym-
phomas or in detecting visceral and bone locations [7,8].
The radiologist confronted with lymphoma Preliminary results concern small series and remain to be
validated. The place of 18 FDG PET has currently been vali-
The radiologist will be confronted with two situations. The dated for Hodgkin’s lymphomas and diffuse large B-cell NHL
first and most frequent is staging and monitoring the dis- and will be addressed in another section.
ease. CT scanning is the crucial technique for imaging, as The second situation is the discovery in imaging of tumour
it assesses the extent of the disease according to the Ann lesions where histopathological confirmation of the possible
Arbor 4-stage classification (Table 3), then allows it to be lymphomatous origin is required.
monitored according to Cheson’s 2-dimensional classic onco-
logical criteria [6]. Depending on the location, ultrasound
and MRI (central nervous system) will be indicated in addi- Forms of presentation
tion. The results of the laboratory tests, osteo-medullary
biopsy and possibly of a lumbar puncture will be added The lymph node form
to this imaging-based classification, along with the clinical
parameters for the prognostic indices for therapeutic man- The most well-known form of lymphoma is the lymph node
agement (the International Prognostic Index [IPI] score for form (Fig. 2). This is the classic form of Hodgkin’s lymphoma
aggressive NHLs, and the Follicular Lymphoma International and low grade NHLs. Any lymph node area can be affected. A
Prognostic Index [FLIPI] for indolent lymphomas). lymph node with a short axis of more than 1 cm is considered
Whole body diffusion-weighted MRI has still to find its to be pathological.
place in onco-haematology and at present is not recom- Certain complications may also reveal the disease, such
mended in current practice. The results appear promising. as superior vena cava obstruction, medullary compression or
Horner’s syndrome. These are then aggressive forms of NHL
[9].
Table 2 Contexts and particular types. The spleen, a lymphoid structure, is considered to be a
Context Frequent types lymphatic extension of the disease. It is involved in the ini-
tial stage in 30—40% of patients with Hodgkin’s disease and in
Coeliac disease and T-cell lymphoma 10—40% of those with NHL. Splenic locations mainly present
jejunal site as hypodense nodules of variable size (a few mm to several
Skin involvement Epidermotropic T-cell centimetres). A CT scan is effective for detecting splenic
lymphoma involvement, with values close to 90%, based on the detec-
Child Burkitt’s L, lymphoblastic L tion of hypodense splenic nodules or a splenic index greater
Isolated splenomegaly Mantle cell L, splenic marginal than 725 cm3 (L × W × T). When combined with 18 FDG PET,
zone L sensitivity reaches 100% with 95% specificity [10].
HIV Burkitt’s L and buccal cavity
ENT Diffuse large B-cell NHL
Post-transplantation B-cell NHL linked to EBV Presentations by organ
Gastric lesion and MALT NHL
Extranodal lymphomas, particularly in cases of NHL, can
H. pylori
involve any organ. While secondary extension from a
Auto-immune (Sjögren, MALT NHL
Hashimoto)

Table 3 Ann Arbor classification.

Stage 1 Only one supra- or subdiaphragmatic lymph
node area affected
Stage 2 Two or more lymph node areas affected on
the same side of the diaphragm
Stage 3 Lymph nodes affected on both sides of the
diaphragm
Stage 4 Visceral involvement distant from a group of
lymph nodes
Letter
A Absence of general signs (fever, nocturnal
sweating, weight loss > 10%)
B At least one general sign
E Extranodal involvement contiguous with a Figure 2. Mediastinal lymph node in stage 2 Hodgkin’s disease. CT
lymph node lesion scan with injection - coronal slice. Mediastinal and axillary lymph
node masses.
134 E. Frampas

disseminated form is the most frequent, isolated primary

lesions, although rare, are possible. The criteria for such
a primary lesion are based on the absence of distant sites
(lymph nodes outside of the adjacent drainage area, spleen,
bone marrow or any other distant lymphoid structure) and
on the absence of circulating lymphomatous cells, and thus
conflict with any possible involvement by contiguity or with
a stage IV disseminated lymphoma.
Whatever organ is concerned, these lymphoma lesions
will have a number of common imaging characteristics which
are bound to suggest this diagnosis, or challenge the more
frequent diagnoses of primary or secondary tumours, and
indicate that biopsy samples should be taken, thus avoiding
unnecessary surgery. The efficacy of radio-guided biopsy is
high at around 90% [11].

The digestive tract Figure 3. Gastric MALT lymphoma. CT scan with injection. Cir-
cumferential hypodense antral thickening with no luminal stenosis.
Digestive involvement occurs in 10—30% of NHL patients, in
Associated intra-abdominal effusion.
decreasing order affecting the stomach, the small intestine,
the pharynx, the colon and the oesophagus [12]. Iden-
tified risk factors include infection by H. pylori, coeliac
disease, chronic inflammatory diseases and post-transplant
immunosuppression. The prevalence of the various types of
lymphoma varies depending on the site. B-cell and MALT
NHLs are the most common. Irrespective of the site, cer-
tain common characteristics can be seen: hypovascularity
of the lesions (masses, infiltration), the classic absence of
occlusive repercussions despite the large size of the lesions
due to the absence of an associated desmoplastic reaction,
preservation of the fat planes, multifocal lesions, associated
lymph node masses [13].
The stomach is the most frequent site of extranodal lym-
phomas. In this location, they are mainly MALT lymphomas
associated with chronic infection by H. pylori with a low
to high grade sequence, followed by diffuse large B-cell
NHL. While there is normally no lymphoid structure in the
stomach, chronic H. pylori infection is associated with the
development of lymphoid structures in the lamina propria
Figure 4. Gastric linitis. Injected CT scan. Parietal thickening
which are the origin of the lymphomatous process. Diagno- with moderate, fibrous homogeneous enhancement accompanied
sis is essentially by endoscopy. Radiology techniques may by parietal retraction and a reduction in gastric volume.
show gastric involvement as ulcers (50% of cases), masses
(36%) or mucous nodules with central ulceration [14]. The
lymphomas make up 0.4% of tumours. The majority are
main differential diagnosis is gastric adenocarcinoma. In the
B-cell NHLs. Possible lesions described include polypoid
case of parietal infiltration with thickening of the folds,
masses, circumferential infiltrations, cavitary masses, thick-
retained gastric distensibility is an argument against gastric
ening of the haustra and mucous nodules [16] (Figs. 7 and 8).
linitis (Figs. 3 and 4). Preservation of perilesional fat planes,
Complications may be invagination when the caecum is
particularly where there is a large mass, and the pres-
involved, ulcerations and fistulae. Rectal or appendicular
ence of voluminous lymphadenopathies beyond the adjacent
lesions have also been described.
drainage area (under the renal hilum) point to a lymphoma.
In the small intestine, B-cell NHLs predominate in the
ileum, T-cell NHLs being more frequently found in the The liver
jejunum associated with coeliac disease [15]. Different Unlike the visceral hepatic extension of stage IV lymphomas,
basic forms are possible: single or multiple mucous nod- present in 15% of cases, primary lymphomas of the liver are
ules, diffuse or focal parietal infiltration and thickening. The rare (< 1% of extranodal lymphomas) [17]. They are mainly
most suggestive is aneurysmal parietal thickening (Fig. 5). large B-cell NHLs. The other types described (immunoblas-
The differential diagnoses are mainly adenocarcinoma and tic, lymphoblastic, Burkitt’s, MALT lymphomas) represent
stromal tumours (Fig. 6). A widespread or multifocal appear- less than 5% of cases. Aetiological factors reported include
ance, the absence of occlusive repercussions despite a HCV (21% of cases in France), EBV and HIV infection, as well
large tumour volume, and the absence of hypervasculari- as auto-immune diseases for MALT lymphomas [18,19]. They
sation are signs pointing towards a lymphoma. In the large are typically discovered at a mean of 55 years (5—87 years),
intestine, predominantly in the caecal and rectal regions, with a male/female ratio of 2.3/1, in a context of
Lymphomas: Basic points that radiologists should know 135

Figure 5. Forms of B-cell non-Hodgkin’s lymphomas found in the small intestine. CT scan with injection. a: infiltration of the final loop
and contact mesenteric extension. Absence of occlusion despite the size of the tumour; b: circumferential involvement of the final loop.
The ileal lumen is preserved; c: aneurysmal form. Slightly enhanced circumferential thickening contrasting with the luminal distension at
this point.

Figure 6. Differential diagnoses of lymphomas of the small intestine. CT scan with injection. a: aneurysmal shaped stromal tumour. Unlike
in lymphomas, the tumoral wall has a vascularised appearance with an increase in the calibre of the vessels supplying it; b: adenocarcinoma
of the small intestine. Stenosing jejunal thickening associated with infiltration of the mesentery at this point.
136
Figure 7. Colic forms of lymphoma. Coronal CT scans with injection. a: endoluminal mass in the right colon (Burkitt’s lymphoma). Multiple
adenomegalies of the axis of the right colon; b and c: multiple parietal nodules extending over the whole of the colon (B-cell NHL) and into
the rectum.
abdominal pain or discomfort [20]. Jaundice is uncommon
(10—20% of cases). The often large, solitary nodular form,
which can measure more than 10 cm, is the most com-
mon (50—60% of cases), followed by the multinodular form
in 40% of cases, the diffuse infiltrating form being excep-
tional [21,22]. With ultrasound, the nodules are usually
hypoechoic, sometimes anechoic. In a CT scan, these spon-
taneously hypodense lesions exhibit variable behaviour after
injection (absence of enhancement in half of the cases,
in patches for one third, possibly with a necrotic centre,
ring enhancement in 16—29% of cases, with a trend towards
isodensity in the late stage) (Fig. 9). After chemotherapy,
calcification is possible. In MRI, there is spontaneous T1
hypointensity, often marked T2 hyperintensity, as with dif-
fusion weighting, enhancement being again variable. Forms
of diffuse infiltration are possible [21]. Given its rarity,
the most frequent diagnoses suggested are hepatocellu-
lar carcinoma, particularly when there is hepatitis C, and
hepatic metastases. Median survival time in the literature is
E. Frampas
15.3 months [20,23]. After liver transplantation, two forms
are described: a rapidly progressing precocious form, mainly
involving the pedicular region and which may locally invade
the liver in connection with EBV and respond favourably to a
reduction in or discontinuation of immunosuppressants, and
a later, EBV negative form with a poorer prognosis.
The pancreas
While peripancreatic and pancreatic extensions of a
retroperitoneal or mesenteric lymphomatous lymph node
infiltration do not in general pose a problem, isolated
involvement of the pancreas can still be a diagnostic trap
(Fig. 10). Analysis of the literature shows that the diagnosis
was made from biopsies in 28% of cases and by laparotomy
in 65% of cases. Ablation surgery was performed in 21% of
cases [24].
Pancreatic lymphomas are rare, representing less than
1% of NHL. They make up only 1.3 to 1.5% of malignant
Lymphomas: Basic points that radiologists should know 137

Figure 8. Differential diagnosis of colic forms. a: undifferentiated carcinoma of the right colon with a pseudoaneurysmal form. The colloid
forms of colic adenocarcinomas may appear hypodense similarly to lymphomatous infiltrations; b and c: rectal linitis. In the CT scan, the
hypodense parietal infiltration is stenosing. In the MRI, there is marked contrast uptake pointing towards a carcinomatous infiltration.

pancreatic tumours [25,26]. They are more common in men
(male/female ratio 13/3). Clinical signs are not very spe-
cific, being mainly weight loss and abdominal pain. An
epigastric mass was however observed in more than half of
the cases and measured more than 6 cm in 70% of patients
[27]. Imaging characteristics are those common to lym-
phoma lesions: hypoechoic masses that are hypointense with
poor enhancement, often well delimited, and usually homo-
geneous. Certain diffuse infiltrating forms (12% of cases)
may look like acute pancreatitis, with enlargement of the
gland, peripancreatic infiltration and elevation of blood
amylase, but without the clinical symptoms of pancreatitis.
Enlargement of the gland can sometimes lead one astray
towards a diagnosis of auto-immune pancreatitis. In MRI,
the homogeneous nature, more marked hyperintensity with
T2-weighting, the absence of late enhancement and of a
capsule point towards a lymphoma [28]. No case of calci-
fication has been described in the absence of treatment.
Laboratory results are not very specific, with CA19-9 levels
being normal or slightly raised. However, when faced with
a pancreatic mass, various signs should attract attention,
including a discordant large mass with no jaundice despite
a predominantly cephalic location, moderate dilatation of
the pancreatic duct, few vascular repercussions, a raised
serum LDH concentration, or lymphadenopathies present
below the level of the renal veins, and suggest the possibility
of a lymphoma rather than an adenocarcinoma [29,30].
Urogenital involvement
In cases of known lymphoma, while renal involvement is
frequent, being present in nearly a third of cases, and reach-
ing 30 to 60% on autopsy [31], it is rarely symptomatic
(pain in the side, haematuria, nocturnal sweating, fever).
It usually occurs during extension of diffuse NHL (interme-
diate to high grade B-cell NHL, Burkitt’s lymphoma). Diffuse
infiltration can also be the cause of renal impairment by
compressing the tubules. Despite this high frequency, less
than 8% of patients have lesions detected by CT scans. Most
renal involvement results from haematogenous dissemina-
tion or extension from the neighbouring retroperitoneum,
and isolated primary lesions are rare (< 1% of extranodal lym-
phomas) [32]. The most common forms are intermediate or
high grade B-cell or Burkitt’s lymphomas. Various forms are
described in imaging: intraparenchymal hypoechoic multiple
nodules or solitary masses, only slightly enhanced follow-
ing administration of contrast agent, perirenal infiltration,
infiltrative nephromegaly. In a CT scan, acquisition in the
138 E. Frampas

Figure 9. Classic forms of lymphoma in the liver. Injected CT scans. a: multiple hypodense nodules of a stage 4 large B-cell NHL; b: large
hypodense mass with no distal biliary repercussions, no capsular retraction nor vascular invasion; c: perihilar hypodense infiltration with
no vascular repercussions on the portal structures; d: hypodense nodules in a patient with a kidney transplant for polycystosis. The main
nodule of the right lobe of the liver has a rosette-like appearance.

nephrographic (venous) phase is essential for detection of

these hypovascular or poorly enhanced lesions, particularly
those in the medullary portion of the kidneys (Fig. 11). The
secretory phase is necessary when there is sinus infiltra-
tion [33]. In MRI, lymphomatous lesions appear hypointense
with T1-weighting and hyperintense with T2-weighting and
appear poorly vascularised [34]. The differential diagnoses
to consider in the case of isolated lesions are pyelonephritic
foci, usually hyperdense in the delayed phase, renal emboli
and infarction, and renal metastases (breast, stomach,
melanoma). Where there is a solitary tumour, the hypo-
vascular character and the absence of venous invasion can
suggest a lymphoma and indicate that the tumour should
be biopsied. Isolated perirenal lesions in the form of tissue
sheathing and/or compressing the kidney are rare. Diffuse
infiltration of the kidneys is still a form which is difficult
to diagnose. Combined with nephromegaly, a loss of corti-
comedullary differentiation, infiltration of the sinus fat, or
sheathing of the cavities may be seen.
Figure 10. Peripancreatic lymphomatous infiltration by a follicu-
Primary testicular lesions occur between 60—70 years of
lar lymphoma.
age as gradual painless hypertrophy. It is the commonest
aetiology for testicular masses after the age of 60 [35].
With ultrasound the lesion appears as infiltration or a
Lymphomas: Basic points that radiologists should know
Figure 11. Classic forms of renal lymphomatous involvement. a: hypodense renal nodule corresponding to a follicular NHL; b: renal lesion
of the inferior pole invading the perirenal fat and responsible for dilatation of the superjacent renal pelvis (large B-cell NHL); c: pedicle
infiltration in a stage 4 HL; d: retroperitoneal infiltration invading the paravertebral gutter and the left kidney (diffuse large B-cell NHL).
hypoechoic mass. Ovarian lesions are B-cell NHLs, and are
found particularly in the context of Burkitt’s lymphoma [36].
The thorax
Thoracic lymphomas are the main expression of mediastinal
lymph node involvement which is present in 80% of HLs [37].
Pulmonary involvement is only found in 5% of NHL patients.
Primary thoracic extranodal lesions are mainly MALT NHLs.
This type is typically found in the stomach, the small intes-
tine, the eye and salivary glands and is associated with
auto-immune diseases (Hashimoto’s thyroiditis). While ade-
nomegalies are frequent in the initial stage if there are
pulmonary lesions of HL, an isolated pulmonary lesion is pos-
sible in NHL [38]. The main pulmonary forms mimic many
tumoral or inflammatory conditions and include nodules and
masses with or without cavitation, condensations, ground
glass opacities, endobronchial masses and reticular inter-
stitial syndrome (Fig. 12) [39]. In the particular context
of immunosuppression, the most frequently encountered
lesions are multiple nodules. Pleural involvement in the form
139
of thickening, isolated or multiple nodules occurs in 16% of
NHLs, essentially as disseminated or recurring forms [40].
Effusions are more common, either through direct lesions or
by lymphatic obstruction originating from lymph nodes.
Cardiac involvement is rare, whether by direct exten-
sion (corresponding to Ann Arbor stage E) or haematogenous
or lymphatic diffusion (Fig. 13). Right atrial cavity lesions
are the most frequent, often associated with extension
involving more than one cavity and the pericardium. In
MRI these masses appear isointense with T1-weighting,
heterogeneously hyperintense with T2-weighting and are
heterogeneously enhanced after gadolinium injection [41].
The prognosis for these forms is poor.
The central nervous system
The CNS is involved in 10—15% of systemic lymphomas,
mainly in the form of a leptomeningeal lesion in large B-
cell NHLs. Primary lesions represent less than 1% of cases of
NHL. The most common locations for the single or multiple
masses are the deep grey matter, the corpus callosum, the
140 E. Frampas

Figure 12. CT scans of pulmonary lymphoma lesions. a: irregular MALT lymphoma nodule; b: diffuse B-cell NHL nodule; c: atelectatic
condensation of a MALT lymphoma; d: right lower lobe excavated opacity and posterior segmental condensation of the right middle lobe in
Hodgkin’s disease.

periventricular and subependymal zones, and the cerebral

Figure 13. Pericardial and pleural extension in an aggressive lym-
phoblastic NHL.
hemispheres. MRI is the preferred technique for explor-
ing and staging central nervous system lymphomas. In MRI,
these lesions appear iso-or hypointense with T1 weighting,
enhancing after injection (Fig. 14) [42]. The principal differ-
ential diagnoses are secondary lesions and abscesses where
there are multifocal lesions, and glioblastomas in perical-
losal sites.
Spinal forms include epidural extensions from a peri-
spinal or spinal column lesion and focal or disseminated
extra and intramedullary intradural lesions. The main dif-
ferential diagnoses are metastases of intra or extranervous
origin and granulomatoses (neurosarcoidosis).
ENT involvement concerns Waldeyer’s ring structures (the
tongue, palate and tonsils), the sinus cavities and the orbit.
The absence of lymph node necrosis and contact bone
erosion points to a lymphomatous disease rather than a squa-
mous cell carcinoma. When the salivary glands or thyroid
are affected, there is frequently an associated auto-immune
condition (Sjögren, Hashimoto).
Lymphomas: Basic points that radiologists should know 141

Figure 14. Cerebral lymphoma. T2-weighted SE sequence (a) and T1-weighted axial slice with injection of gadolinium (b). Lesion showing
hyperintensity with T2-weighting, infiltrating the splenium of the corpus callosum, enhancing heterogeneously after gadolinium injection.

Bone and soft tissue involvement

There is bone involvement in 5% of diffuse lymphomas.
the moderate repercussions on the actual organ
These cases only represent less than 5% of primary bone
(digestive tube, liver, kidneys).
tumours and are essentially NHLs [43,44]. The lesions are • A biopsy, usually guided by imaging, will confirm the
typically lytic (70%) but mixed forms have been reported.
diagnosis and type the lymphoma.
A solitary metaphyseal/diaphyseal lesion with a periosteal • Certain situations (post-transplantation,
reaction (60% of cases) associated with a soft tissue mass
immunosuppression, coeliac disease, Helicobacter
is suspect. In MRI, definite hyperintensity in T2-weighted
pylori infection) are conducive to the development
and STIR sequences and T1-weighted hypointensity suggests
of lymphomatous conditions and should evoke the
these lesions [45].
diagnosis.
• Staging using imaging is based on a thoracic-
abdominal-pelvic CT scan.
Conclusion • Extension of the disease is assessed using the Ann
Primary forms of lymphoma can be diagnostic traps Arbor classification.
• Therapeutic management is based on typing, staging
because of their polymorphism and rarity. Lymph node
forms occur most frequently. CT scans are the crucial and the clinical-laboratory scores.
radiological exploration technique for staging and monitor-
ing.

TAKE-HOME MESSAGES
• The lymph node form of lymphomas is the most
frequent.
• Primary extranodal lymphomas are rare and pose
problems of differential diagnosis with primary or
secondary lesions. Certain common signs will suggest
this condition: a frequent hypovascular appearance,
discordance between the volume of the tumour and
Clinical case
You are confronted with four hypodense hepatic lesions in
the portal phase found in a CT scan (Figs. 15—18).
Questions
1. What is your analysis of the images?
2. What are your hypotheses?
3. What are the signs for or against a lymphomatous origin?
142
Figure 15. CT scan with injection - axial slice. Hypodense tumoral
lesion of hepatic segment VIII in a 70-year-old woman.
Figure 16. CT scan with injection - axial slice. Voluminous lesion
occupying the entire right lobe of the liver, heterogeneously hypo-
dense, with central calcification.
Answers
These four lesions appear hypodense in the portal phase.
Certain criteria will act as pointers.
E. Frampas
Figure 17. CT scan with injection - axial slice. Nodule of 3 cm
diameter in segment II, hypodense in the portal phase.
Patient 1 (Fig. 15) has a large lesion with discretely lob-
ulated contours. No vascular structure is visible within it.
The liver does not appear to be dysmorphic. The absence
of contrast uptake by fibrous stroma does not point towards
an intrahepatic cholangiocarcinoma. In the first instance, a
secondary hepatic lesion is suggested.
Patient 2 (Fig. 16) has a large lesion in the right lobe
of the liver. There is central calcification and clumps of
peripheral enhancement can be seen. Calcifications within
lymphomatous lesions are rare and found following treat-
ment. An angioma is strongly suspected here. Additional MRI
will provide the diagnostic confirmation.
Patient 3 (Fig. 17) has signs of chronic liver disease with
dysmorphia and portal hypertension. In the first instance
therefore, this suggests a primary hepatocellular carcinoma
with washout in the portal phase. To comply with the
non-invasive diagnostic criteria of HCC with cirrhosis, arte-
rialisation is necessary prior to washout to confirm the latter
(CT scan or MRI).
Patient 4 (Fig. 18) has a discretely hypodense homoge-
neous lesion. No capsular or biliary repercussions are visible.
Above all, there are no distortions within it in size or direc-
tion of the vascular structures of the portal and hepatic
veins. This is highly suggestive of an infiltrating lymphoma.
MRI may show hyperintensity in a T2-weighted sequence and
diffusion of the lesion. A biopsy will provide the diagnosis
(here a lymphoplasmacytic lymphoma).
Lymphomas: Basic points that radiologists should know
Figure 18. Man of 60 years of age. CT scan with injection - axial slice: MPR (a) and MIP (b). Hypodense nodule in the right lobe of the
liver discovered by chance.
Disclosure of interest
The author declares that he has no conflicts of interest con-
cerning this article.
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