Reactive T-cell Hyperplasia

Transcription

2/15/2013
Welcome to Mayo Medical Laboratories Hot Topics. These presentations provide
short discussion of current topics and may be helpful to you in your practice.
Our speaker for this program is Dr. Dragan Jevremovic, Co-Director of the Cell Kinetics
Laboratory in the Division of Hematopathology. Dr. Jevremovic presents a case in
which the patient was diagnosed with reactive T-cell hyperplasia in the lymph node
using multiple techniques.
Thank you for the introduction.
©2013 Mayo Foundation for Medical
Education and Research. All rights
reserved.
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I have nothing to disclaim regarding this case.
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This is a case of a 47-year-old male that presented acutely with a shortness of breath.
The patient had a long-standing history of asthma and allergies, and imaging revealed
mediastinal, periaortic, and inguinal lymphadenopathy. The clinicians went ahead and
biopsied inguinal lymph node.
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This is a low-power picture of a H&E stain of the lymph node, which shows a
disorganized architecture bordering on effacement. There is also prominent vascular
proliferation.
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: Intermediate power shows marked vascular proliferation and paracortical
hyperplasia of predominantly small cells.
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On an even higher magnification, there is a mixture of small, intermediate, and large
lymphocytes, as well as mixed in plasma cells and eosinophils.
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High magnification shows that there are some large atypical cells with prominent
nucleoli, which can raise possibility that these are Reed-Sternberg cells. This could
also be activated immunoblasts. Neutrophil margination is seen in the vessels.
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A panel of immunohistochemical stains was performed. CD3 stain showed that the
majority of paracortical cells are small CD3 positive T cells.
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CD20 stain highlights B-cells organizing follicles supporting the notion that the
architecture is not effaced. In addition, there are scattered CD20-positive larger cells
in the paracortex and these represent immunoblasts.
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We already saw that the majority of cells in the paracortex were CD3-positive T cells.
CD4 stain shows that the majority of these T cells are CD4 cells.
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There’s also a relatively small CD8-positive component of the T cells.
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The T cells showed normal expression of pan T-cell markers, which are CD2,
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CD5,
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and CD7.
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CD30 stain highlighted only scattered immunoblasts, which showed only weak
staining with CD30 antigen.
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CD21 stain showed preserved follicular dendritic cell architecture without expansion.
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CD279 or PD1 is a follicular T-cell marker and is strongly positive in follicular T-helper
cells, which are shown in the upper part of the slide. The paracortical T cells showed
only a partial weak staining for CD279, which is nonspecific.
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Epstein-Barr virus staining was negative by in situ hybridization, and so was staining
for CD10 in the T cells. CD10 can be seen positive in marginalized neutrophils within
the vessels. The vast majority of the T cells expressed alpha-beta T-cell receptor and
were negative for gamma-delta T-cell receptor.
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T-cell receptor gene rearrangements for both beta and gamma regions showed
polyclonal T cells.
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The diagnosis was made of paracortical hyperplasia of reactive T cells
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Paracortical hyperplasia is a T-cell response to infection, usually viral, and can also be
seen in hypersensitivity reaction. It is characterized by heterogeneous cell population
that includes small lymphocytes, immunoblasts, monocytoid B-cells, as well as
eosinophil, plasma cells, and neutrophils. On low power, paracortical hyperplasia has
a “moth-eaten” appearance with vascular proliferation and sometimes sinus
histiocytosis.
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Differential diagnosis is the most important in the cases of reactive T-cell hyperplasia.
In this case, the most difficult differential diagnosis was differentiating this
hyperplasia from T-cell lymphoma, in particular, angioimmunoblastic T-cell lymphoma
and peripheral T-cell lymphoma. What makes this case a reactive lymphoid
hyperplasia is that:
• The atypical cells were only scattered
• The immunohistochemistry showed still-preserved architecture
• That CD279 or PD1 stain was very weak outside the follicles
• There was no expansion of follicular dendritic cells meshworks and
• The T-cell receptor gene rearrangements were negative.
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This is for contrast a case of angioimmunoblastic T-cell lymphoma, which shows
effaced architecture by perforation of intermediate-sized cells with slight atypia and
abundant clear cytoplasm. The background is polymorphic, and there is a prominent
vascular proliferation similar to our case. However, the atypical cells would be
strongly positive for CD279, and measure a loss of 1 or more pan T-cell antigens.
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This is CD21 stain in cases of angioimmunoblastic T-cell lymphoma and shows marked
expansion of follicular dendritic cell meshworks.
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Another potential differential diagnostic entity is classical Hodgkin lymphoma. Our
case did not raise strong suspicion for classical Hodgkin lymphoma because there was
preserved architecture on immunohistochemical stains. Cells in our case showed a
spectrum in cell size, and when there’s a spectrum the cells are much more likely to
be immunoblasts than Reed-Steinberg cells. Our case had the very weak and variable
expression of CD30 in these immunoblasts, and these cells were also CD45 positive.
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This is for example and for contrast, a case of classical Hodgkin lymphoma, which
shows that there are large atypical cells, surrounded by small cells; therefore, there is
clear dichotomy in cell size and morphology, unlike seen in reactive proliferation
which shows spectrum in size and morphology. There is also background mixed
inflammation and fibrosis. The atypical cells express CD30 and PAX5, often express
CD15, and they are negative of CD45.
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The other potential differential diagnostic entities that could be confused with
paracortical T-cell hyperplasia include reactive lymphoid hyperplasias with a specific
etiology, often include Epstein-Barr virus, cytomegalovirus, or toxoplasma. EpsteinBarr virus infections often go with follicular hyperplasia, in addition to paracortical
hyperplasia, but in situ hybridization or immunostains would be necessary for making
this diagnosis.
Cytomegalovirus lymphadenitis is characterized by nuclear acidophilic inclusions and
presence of monocytoid B-cells. Toxoplasma lymphadenitis comes with triad of
follicular hyperplasia, hyperplasia monocytoid B-cells, and presence of epithelioid
histiocytes, which often infiltrate germinal centers.
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The patient that was presented in this case was followed-up 3 months postbiopsy.
Radiologic studies showed significant decrease in lymphadenopathy to less than half
of original size without any treatment. The patient is being followed.
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In summary, reactive and atypical lymphoid hyperplasia can mimic many neoplastic
entities. The clue to diagnosis is preserved architecture, even if it can be shown only
on immunostains, and spectrum in cell size, which favor reactive over lymphoma.
Immunohistochemistry is necessary to exclude Hodgkin lymphoma and T-cell
lymphoma. Sometimes molecular studies are necessary to make sure that the
proliferation is reactive and not neoplastic. Advice is to always look at clinical history;
in this case, long-standing presence of autoimmune disorders was helpful in making
diagnosis of reactive proliferation. And, if in doubt, its always better to call
proliferation atypical and wait, then to overcall a lymphoma.
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Reactive T-cell Hyperplasia

Transcription

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