Acta
Neuropathologica

Acta Neuropathol (Berl) (1983) 61 : 141 - 147

9 Springer-Verlag 1983

Lymphomatoid Granulomatosis Involving the Central Nervous System:
Complication of a Renal Transplant
with Terminal Monoclonal B-Cell Proliferation
J. Michaud 1, D. Banerjee, and J. C. E. K a u f m a n n
Dept. of Pathology and Neuropathology Service, University Hospital and University of Western Ontario, London, Ontario, Canada

Summary. A 33-year-old man, an immunosuppressed
renal allograft recipient, developed fever of unknown etiology, multiple pulmonary densities, spaceoccupying lesions in the liver, confusion, disorientation, and seizures with cerebral infarcts. At autopsy,
changes classical of active l y m p h o m a t o i d granulomatosis (LYG) were found in the brain but those
studied in the lungs and liver were in the healing phase.
In addition, one cerebral focus in the right temporooccipital lobe showed a l y m p h o m a t o u s transformation.
Immunofluorescence studies done on this focus showed
monoclonal IgG-)~ cytoplasmic staining in the perivascular infiltrate. Immunoperoxidase studies confirmed the monoclonal nature of this focus but showed"
a polyclonal pattern in the other foci. This finding is
discussed along with the relationship between L Y G and
lymphoma.
Key words: L y m p h o m a t o i d granulomatosis - Central
nervous system - Immunofiuorescence - Renal
transplant - L y m p h o m a

ing a grave prognosis. The evolution and prognosis are
quite variable and unpredictable with long survival
periods or, more often, rapid deterioration and death
(Liebow et al. 1972; Katzenstein et al. 1979). "Polym o r p h o u s " l y m p h o m a or immunoblastic sarcoma are
sometimes part of the terminal picture (Liebow et al.
1972; Katzenstein et al. 1979; Cohen et al. 1979;
Bender and Jaffe 1980). No satisfactory mode of
therapy is yet available (Katzenstein et al. 1979).
We describe a case of L Y G complicating the
evolution of an immunosuppressed renal transplant
patient. The central nervous system (CNS), lungs, and
liver were involved although lesions were healing in the
latter two sites.
In addition, one cerebral focus in the right temporooccipital lobe showed l y m p h o m a t o u s transformation.
Immunofluorescence and immunoperoxidase studies
of this focus revealed the presence of a monoclonal
cytoplasmic immunoglobulin in the perivascular infiltrate. The other foci were, however, polyclonal by
immunoperoxidase studies.

Case Report
Introduction

Clinical History"

L y m p h o m a t o i d granulomatosis (LYG) described by
Liebow et al. (1972) is morphologically defined as a
necrotizing angiocentric and angiodestructive infiltrative disorder. The infiltrate is pleomorphic with
lymphocytes, plasma cells, histiocytes, and a variable
amount of atypical mononuclear cells. Lungs are
predominantly involved. Extra-pulmonary involvement is frequent and is most often clinically manifested
by cutaneous or neurologic symptoms, the latter bear-

A 33-year-old white man developed proteinuria at 15 years of age.
Chronic renal failure followed, and a diagnosis of chronic glomerulonephritis was made 10 years later. He was placed on hemodialysis.
At 30, a renal transplant had to be removed because of acute
rejection. One year prior to the final admission, bilateral nephrectomy was done and was followed by another transplant. Multiple
complications followed: cytomegalovirus pneumonia, signs of
transplant rejection, hypertension, herpetic and monilial esophagitis, right lower lobe pulmonary infiltrate secondary to papo- .
vavirus and bleeding esophageal ulcer. He had no allergies and no
history of alcohol abuse. He was a heavy smoker. The family history
was non-contributory.
His last admissionwas for fever of a few days duration, anorexia,
and abdominal discomfort of 1 month's duration. He also complained of a slight weight loss. The medications, at the time of
admission, included Prednisone 20mg daily, Inderal 160 mg b.i.d.,

1 Presentaddressandoffprintrequeststo:JeanMichaud, MD, Dept.

of Pathology, Faculty of Medicine, University of Montreal, P.O.
Box 6128, Station "A", Montreal, Que., H3C 3J7, Canada

142
Aldomet 250 mg q.i.d., Imuran 75 mg daily, and Lasix 40 mg daily.
Physical examination revealed a patient in no acute distress. The
blood pressure was 120/90mm Hg, temperature was 38.9~ The
head, neck, chest, and cardiovascular system were unremarkable.
Abdominal palpation revealed a non-tender kidney in the right lower
quadrant. The neurologic examination was totally unremarkable.
Laboratory investigation revealed a normochromic normocytic
anemia with hemoglobin (Hb) of 8.9 rag/100 ml. The white cell count
(WBC) was 3,800cells/mm 3 with a normal differential count.
Rehydration corrected slightly elevated creatinine and BUN levels.
Electrolytes, bilirubin, serum calcium, iron, vitamin B12, and serum
and red cell (RBC) folate were normal. The blood coagulation studies
were also normal. A renal scan and an i.v. pyelogram were
unremark able.
The evolution was mostly characterized by a fever varying
between 38.1~ and 39.2~ All blood, throat urine, and fecal
cultures remained negative for bacteria and fungi. Sputum was
repeatedly negative for acid-fast bacilli. Numerous studies were done
to rule out the following : adenovirus, herpes simplex, varicella-zoster,
cytomegalovirus, influenza A/B, papopavirus, mycoplasma, toxoplasmosis, blastomyeosis, coccidioidomycosis, cryptococcosis, histoplasmosis, psittacosis, rickettsia, and Q fever. All tests were
negative. WBC remained between 2,200 and 3,800 cells/ram3 with a
normal differential count.
The admission chest X-ray revealed a density in the right upper
lobe, approximately 2 cm in diameter. Repeated chest X-rays were
suggestive of a tuberculous process. Although repeated sputum
examinations were negative for acid-fast bacilli, a trial of Isoniazid
and Rifampin was begun in addition to the initial medication. Fever
persisted and the trial was discontinued. A percutaneous needle
biopsy of the right lung was not contributory. Subsequently, he
developed a right lower lobe consolidation and several nodules in the
left lower lobe. A bronchoscopy showed inflamed right middle and
lower lobe bronchial mucosa. Cultures from washing and brushing
specimens remained negative. An open lung biopsy showed focal
necrotizing pneumonitis. Tissue cultures were negative. Tests for
Legionnaire's disease were also negative.
Hepatomegaly and a slight elevation of the hepatic enzymes were
also noted. A computerized axial tomography (CAT) body scan
showed space-occupying lesions in the liver. A biopsy revealed only
hemosiderosis and tissue cultures remained negative.
Three weeks prior to his death, he developed disorientation and
confusion with a suggestion of hallucinations. Five days later, a grand
real seizure occurred with head and eyes deviated to the right but
without other signs of localization. A CAT scan was negative.
A lumbar puncture showed 82RBC, 4WBC, a glucose level of
80mg/100ml, and a protein level of 72mg/100ml. Cultures were
negative. Six days later, another seizure occurred. The CAT scan
showed a possible infarct in the right parieto-occipital region. He
improved temporarily. Five days prior to his death, however, neck
stiffness and disorientation occurred with a rapid deterioration. A
lumbar puncture showed 5 RBC, 59WBC (all mononuclears), a
glucose level of 32 rag/100 ml, and a protein level of 103 rag/100 ml.
Cultures remained negative. A brain needle biopsy was done in the
right temporal lobe. The tissue was very scanty and smears only were
done at the time. No organisms were found but a few atypical cells
suggested the possibility of a neoplasm. Permanent sections revealed
areas of necrosis, a few atypical cells, and two small vessels with a
definite fibrinoid necrosis. A vasculitis was suggested without further
characterization due to the small amount of tissue available. Tissue
cultures were also negative. Profound coma preceded his death and a
complete autopsy was performed.

Methods
Representative paraffin sections were studied with one or more of the
following stains: hematoxylin-eosin (HE), Gordon and Sweet,

J. Michaud et al. : Lymphomatoid Granulomatosis Involving the CNS

Fig. 1. Coronal section, left temporal lobe. Softening and petechiae
involving the left hippocampus

Martius scarlet blue, methyl green-pyronin, luxol fast blue, Gram,
periodic acid-Schiff (PAS), methenamine silver, Dieterle (for
Legionnaire's disease), Ziehl-Nielson, and Warthin-Starry (for
spirochetes).
For immunofluorescence, fresh tissue from the right temporal
lobe was snap-frozen in a liquid nitrogen-isopentane slurl~j and
stored at - 80~ until processed. Frozen sections were cut, picked up
on gelatinized slides, dried at 4~ overnight, and stained for
immunoglobulins and C3 using a direct immunofluorescence
method. Fluorescence was visualized with a Leitz Orthoplan fluorescent microscope with an HBO 100W high pressure mercury light
source, using transmitted illumination, hnmunoperoxidase studies
were performed using the peroxidase-anti-peroxidase (PAP) method
on formaldehyde-fixed paraffin-embedded cerebral tissue. This technique as well as its various control methods has been described before
in detail by Taylor (1978a).

Autopsy Findings
Central Nervous System. The brain weighed 1,410 g. ExtemaI examination revealed a mild flattening of gyri without significant uncal or
cerebellar tonsil herniation. Several loci of softening with petechiae
were seen over the lateral and inferior temporal and occipital lobes.
One, at the tip of the left temporal lobe, was covered by a yellow green
meningeal exudate.
Coronal sections of the brain showed multiple loci of petechiae
with or without associated softening. They involved both hemispheres, all cerebral artery territories, and the cortex and white
matter. The most prominent foci were located in the left occipital lobe
and in the inferior portion of the fight temporo-occipital lobe where
the softening was significantly more extensive. The genu of the corpus
eallosum was involved on the right side and the hippocampus on the
left (Fig. 1). The deep gray matter was spared. A small hematoma
filled the biopsy site in the right temporal lobe.
External examination of the cerebellum, brainstem, and spinal
cord was unremarkable. However, sagittal and parasagittal sections
of the cerebellum revealed two large foci of hemorrhagic softening,
one in the central vermis and the other in the left posterior
hemisphere. Transverse sections of the brainstem and spinal cord
were grossly normal.
Microscopic examination showed a patchy but rather dense
infiltrate in the meninges and cerebral parenchyma giving a picture of
meningo-encephalitis (Fig. 2). The infiltrate had a predominantly
perivascular distribution. Several vessels showed complete fibrinoid
necrosis of the wall with narrowing or occlusion of the lumen by

J. Michaud et al. : Lymphomatoid Granulomatosis Involving the CNS

143

Fig. 3. Photomicrograph of a cortical vessel, left frontal lobe, showing
fibrinoid necrosis and perivascular pleomorphic infiltrate and necrosis. HE, x 120

Fig. 2. Meninges and cortex, right occipital lobe, with meningeal,
perivascular and parenchymal infiltrate. One cortical vessel shows
fibrinoid necrosis (arrow). HE, x 65

fibrin. Small and medium-sized vessels were involved (Fig. 3).
Surrounding necrosis of the cerebral parenchyma was seen more
often in sections taken from the temporal and occipital lobes and the
cerebellum.
The infiltrate was pleomorphic with small lymphocytes, plasma
cells, histiocytes, and atypical mononuclear cells (Fig. 3). The latter
varied in number from one field to another. In the right temporooccipital lobe, however, the atypical mononuclear cells were the
majority (Fig. 4). Mitoses were seen along with bi- or trinucleated
cells. No Reed-Sternberg cells were found. Pyroninophilia was seen in
plasma cells and in some atypical mononuclear cells. Russell bodies
were occasionally seen in plasma cells. Reticulin deposition was
increased around vessels with a thick perivascular infiltrate, in the
right temporo-occipital lobe (Fig. 4, insert).
Microscopically, the most severely involved structures were the
meninges of the cerebral hemispheres and midbrain, and the cortex
and subcortical white matter of the cerebellum and cerebrum.
However, similar changes were seen focally in the left mammillary
body, the substantia nigra, the left basis pontis, the pontine tegmentum and medulla dorsal to the pyramids, the fourth cranial nerve, and
one cranial nerve at the medullary level. No organisms or viral
inclusions were found.
The spinal cord, pituitary gland, eyes, common peroneal nerve,
and gastrocnemius muscle were not involved. Finally, a mild anoxic
encephalopathy was seen in both hippocampi and in the left frontal
lobe.

Fig.4. Photomicrograph of a cortical vessel, right temporal lobe,
showing numerous atypical mononuclear cells. HE, • 190. Insert.
Increased reticulin deposition, around vessel with thick perivascular
infiltrate. Reticulin, x 50

Other Systems. The fight and left lungs weighed 950 and 970 g,
respectively. All lobes were distended and firm. On cut sections, a few
yellow-whitenodules, measuring between 1,0 and 3.5 cm, were seen in
both upper and lower lobes, bilaterally. Microscopically, they
consisted of necrotic tissue surrounded by granulation tissue with
occasional multinucleate giant cells. Some totally necrotic vessels
surrounded by nuclear debris were observed. One vessel was also
surrounded by degenerated and ghost-like irregular mononuclear
cells. The liver was markedly enlarged and weighed 2,800 g. On cut
sections, several yellow-white irregularly circumscribed lesions varying from 1.0 to 2.0cm were present. Microscopically, they were
similar to the pulmonary lesions. Increased fibrosis was present in the
surrounding periportal regions. No viral inclusions and no organisms
were found in both liver and lung sections.
The lymph nodes showed a non-specific mild reactive hyperplasia. The spleen showed congestion, and the bone marrow was
normal. The skin was normal. The other significant changes found at
autopsy were: moderate chronic rejection of kidney transplant with
arteriolonephrosclerosisand a few infarcts, thrombotic non-bacterial
endocarditis of the mitral valve and acute bronchopneumonia.

144

J. Michaud et al. : LymphomatoidGranulomatosis Involvingthe CNS

Fig. 5 A, B. Immunoperoxidasestudy of monoclonalfocus. A Lambda staining is present in several cells (arrowheads) : B no reaction is present
with Kappa fight chain. Immunoperoxidase:A x 630, B x 400

Gram-negative rods wereseen in the fociof acute bronchopneumonia
and cultures grew Escherichia coli.
Immunohistochemical Studies. The mononuclear infiltrate showed

cytoplasmicstaining for IgG-2only,by immunofluorescence,and for
light chain only by immnnoperoxidase (Fig. 5). However, in the
polyclonal foci, cytoplasmic staining was detected with both immunoglobulin light and heavy chains (Fig.6). By immunofluorescence, deposits of IgG and C3 were found in affected vessels.
Electron Microscopy. The fibrinoid necrosisof blood vesselwalls and
the pleomorphic infiltrate were confirmed. No viral structures or
other organisms were found. However, these studies did not contribute further to the evaluation of the morphologicalchanges and did
not provide new data.

Discussion
The present case demonstrated clinically a n d morphologically several features of lymphomatoid granulomatosis (LYG): fever of unknown origin; multiple
organ involvement: lungs, liver, and brain (including
cranial nerves); striking vasculitis with parenchymal
necrosis and pleomorphic perivascular infiltrate includ-

ing atypical mononuclear cells. These features were first
described by Liebow et al. (1972). Clinical manifestations of LYG, prognostic factors, and results of
various therapeutic regimens in 152 patients were further documented by Katzenstein et al. (1979). In about
one of six of these patients, associated diseases were
present before or during the development of LYG. The
nature of these illnesses was quite variable. However,
most of them either required the use of immunosuppressive drugs or were commonly associated with
immunologic disturbances (Katzenstein et al. 1979).
Immunosuppressed renal transplant recipients
would therefore fall in a group susceptible to develop
LYG. However, only three previous reports of such a
combination have been made (Hammar and
Mennemeyer 1976; Gardiner 1979; Walter et al. 1979).
If one excludes the problems of rejection, renal
transplantation is more often complicated by infections
or by secondary malignancies.
Malignancies complicating renal transplantation
are rising in frequency. After cancers of the skin and
lips, lymphomas are the most frequent. The majority

J. Michaudet al. : LymphomatoidGranulomatosisInvolvingthe CNS

| 45

Fig.6A, B. Immunoperoxidasestudyof one polyclonalarea. Lambda(A) and Kappa (B) stainingis seen in occasionalcells (arrow heads).
Immunoperoxidase, x 400

are large-cell lymphomas (Penn 1977). Contrary to the
lymphomas diagnosed in the general population, the
renal transplant lymphomas have a high predilection
for the CNS: 43 of 103 in Penn's series. Furthermore,
this system is frequently the only one involved by the
process (Penn 1977).
Lymphomatoid granulomatosis has also a predilection for the CNS (Liebow et al. 1972; Katzenstein
et al. 1979; Pena 1977; Verity and Wolfson 1976;
Simon et al. 1981). Sometimes, neurologic symptoms
are its only manifestation (Kokman et al. 1977). More
often, the CNS involvement arrives when the disease is
well established in the other systems or while it is being
treated. Bone et al. (1978) emphasized that point in
reviewing 13 cases published in the literature, including
their own. They also noted that in six of them,
pulmonary lesions were clearing after the development
of the CNS lesions. This feature was present in our case.
Both pulmonary and hepatic lesions were healing at the
time of autopsy and were therefore not diagnostic. The
fact that CNS lesions develop so frequently during
treatment indicates resistance to treatment at least in

that system. It also emphasizes the bad prognosis of
CNS involvement, as already indicated by Katzenstein
et al. (1979).
The present case stresses the close relationship
between LYG and lymphomas because one focus in the
right temporo-occipital lobe was morphologically a
lymphoma. This area, studied by immunofluorescence,
showed monoclonal IgG-2 cytoplasmic staining. The
PAP method confirmed this finding while showing the
polyclonal nature of the other loci. Deposition of
reticulin in the perivascular lymphomatous cuffing is
also a classical feature of intracerebral lymphomas
(reticulin cell sarcoma-microglioma). In a large series of
LYG, 12 % of patients developed malignant lymphoma
(Katzenstein et al. 1979). Focal lymphomatous transformation in LYG has rarely been studied immunohistochemically.
Reddick et al. (1978) studied a case of systemic
LYG with immunoblastic sarcoma in the brain. The
cerebral lesion showed only a few cells staining with
IgG or IgM and both k and 2 chains. The lymph nodes
showed a polyclonal pattern, but the typical LYG

146
lesions in the lungs were not studied. Bender and Jaffe
(1980), using an indirect immunoperoxidase method,
demonstrated a predominantly mixed pattern of all
immunoglobulins in two typical cases of pulmonary
LYG. One of these had one focus consistent with
immunoblastic sarcoma and this one showed only
IgG/k. Two atypical cases were also studied, one
showing a mixed pattern and the other no staining at
all. They noticed that these results were similar to other
benign lymphoproliferative disorders with malignant
potentials, e.g., angioimmunoblastic lymphadenopathy, with an original polyclonal pattern sometimes
evolving in a monoclonal proliferation. These few
studies do not permit, however, definite conclusions.
Interestingly, primary intracranial lymphomas,
without organ transplantation or immunosuppressive
therapy, seem to be more consistently monoclonal
( H o u t h o f f et al. 1978; Taylor et al. 1978 b; Hassoun et
al. 1981 ; Jardon-Jeghers and Reznik 1982). Even if a
certain number of cases show results difficult to
interpret or no staining at all, these results are in
accordance with those of a large series of extra-cranial
B-cell lymphomas (Taylor 1979).
Distinction between L Y G and lymphomas has been
already commented upon several times (Liebow et al.
1972; Bone et al. 1978; Katzenstein et al. 1979;
Pasquier et al. 1980; Bender and Jaffe 1980; Colby and
Carrington 1982). Most authors agree so far that there
are significant differences and that both entities should
be kept separate until new information is obtained on
the etiology and pathogenesis of these diseases. The
striking vasculitis and the tendency for L Y G to spare
lymph nodes, spleen, and bone m a r r o w are important
differentiating features. It is possible, however, that
some cases of L Y G could be lymphomas from the
beginning. De Remee et al. (1978) and Stamemkovic et
al. (1981) who compared L Y G with polymorphic
reticulosis and more recently Colby and Carrington
(1982) who studied 20primary lung lymphomas
simulating L Y G suggested that the latter is probably a
l y m p h o m a defying recognition by the usual criteria.
The polymorphic infiltrates and the polyclonal pattern
by immunofluorescence in some reported cases could
then be explained by the presence of a secondary
inflammatory response to the tumor. Even the vasculitis could be the result of local antigen-antibody (AgAc) complexes in the presence of complement (C1).
Deposits of I g G and C a were found in the vessel walls in
our case and these are consistent with an Ag-Ac-C x
reaction.
Whether L Y G is a lymphoproliferative disorder
resulting from a chronic antigenic stimulation with
l y m p h o m a as a possible outcome or a l y m p h o m a from
the beginning remains to be settled. It stresses a need for
not only more immunohistochemical studies of large

J. Michand et al. : Lymphomatoid Granulomatosis Involving the CNS
series of L Y G but also for prospective in vivo immunologic evaluation. The role of Epstein-Barr virus (EBV)
as a possible etiologic factor should also be evaluated as
a case of L Y G was recently linked with this virus. Veltri
et al. (1982) reported a patient with L Y G presenting
initially as a reactivated EBV infection.
EBV is an ubiquitous B-cell-tropic virus which has
been linked with a variety of lymphoproliferative
conditions including those arising in renal transplant
recipients (RTR). Approximately 80 ~ of R T R secrete
EBV in saliva compared to 1 5 - 2 0 ~ in the general
population. A large collaborative studies recently
demonstrated EBV genome in tissues of all R T R tested
(Purtilo 1981). Furthermore, H a n t o et al. (1981)
showed evidence that EBV was the probable cause of
the lymphoproliferative disorders found in six RTR.
Although not demonstrated, this is a very likely
possibility in our case.

Acknowledgements. Dr. P. Keown expressed his encouragement by
facilitating our accessto the clinicaldata. Mrs. C. Bernierand Mr. W.
Scarrow provided secretarial and technical assistance.

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Received December 21, 1982/Accepted May 2, 1983