Lymph node infarction

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Lymph node infarction

Postby patoco » Mon Aug 13, 2012 11:44 am

Lymphadenopathy and lymph node infarction as a result of gold injections

C Roberts2, P J Batstone1, J R Goodlad1

+ Author Affiliations

1Department of Pathology, Highland Acute Hospitals NHS Trust, Raigmore Hospital, Inverness, UK
2Department of Pathology, Grampian University Hospitals, Aberdeen, UK
Dr Goodlad John.Goodlad@raigmore.scot.nhs.uk.
Accepted 9 November 2000

Abstract

This report describes a case of lymphadenopathy and lymph node infarction as a consequence of intramuscular gold administered to a patient suffering from rheumatoid arthritis, to highlight this rare association. A 34 year old woman with a four year history of rheumatoid arthritis affecting multiple joints was started on intramuscular gold injections after little response to anti-inflammatory medication. After her sixth injection the patient developed enlarged neck and axillary lymph nodes. Biopsy showed subtotal infarction of a reactive node, confirmed by histochemical, immunohistochemical, and molecular techniques. The patient continued to suffer from rheumatoid arthritis with no evidence of malignant lymphoma after three years. This case provides strong evidence that lymphadenopathy with infarction is a rare complication of gold injections. In such a situation, it is particularly important to exclude a diagnosis of lymphoma, because this is the most common cause of spontaneous lymph node infarction. This can be achieved through awareness of the association, and by the use of ancillary histochemical, immunohistochemical, and molecular techniques on the biopsy material.

Although most of the side effects of gold injections are well recognised, only rarely has lymphadenopathy been described as part of an adverse reaction.1–3 Spontaneous infarction of superficial lymph nodes is also an uncommon occurrence, especially in patients who are not subsequently found to have malignant lymphoma.4, 5 Here, we describe a case of lymph node infarction presenting as lymphadenopathy during a course of intramuscular gold injections, an association described only once previously,2 to draw attention to this rare association.

Case report

The patient was a 34 year old woman with a four year history of progressive, seropositive rheumatoid arthritis affecting her hands, fingers, wrists, knees, and hips. Her past medical history included Peutz-Jeghers syndrome and an ovarian mucinous cystadenoma. Treatment of the arthritis had initially been with non-steroidal, anti-inflammatory drugs, discontinued because of gastric symptoms, and intra-articular steroid injections to the left shoulder, followed by sulfasalazine and oral prednisolone. There was little response to the latter two drugs and intramuscular gold (sodium aurothiomalate), 50 mg/week, was started. Shortly after receiving her sixth injection the patient presented with a tender enlarged lymph node measuring 2 × 2 cm in the right posterior triangle of the neck, as well as non-tender pre-auricular and left axillary lymphadenopathy. A biopsy of the enlarged neck node showed lymph node infarction. The gold injections were discontinued and the lymphadenopathy gradually resolved over the next two months. Three years later the patient was alive with no evidence of lymphadenopathy, but with persistently active rheumatoid arthritis.

Materials and methods

Tissue sections (4 μm thick) from paraffin wax embedded tissue were stained routinely with haematoxylin and eosin and immunohistochemically using a streptavidin–biotin complex immunoperoxidase technique and the following antibodies: anti-CD3 (polyclonal; Dako, Copenhagen, Denmark; diluted 1/100), anti-CD20 (monoclonal; Dako; diluted 1/400), anti-CD45 (monoclonal; Dako; diluted 1/400), and anti-CD45RO (monoclonal; Dako; diluted 1/50). Secondary antibodies and the final layer were all obtained from Dako. Antigen retrieval was performed for the detection of all antigens by pressure cooking sections in citric acid buffer.

A polymerase chain reaction (PCR) for immunoglobulin heavy chain and T cell receptor γ gene rearrangements was performed on DNA extracted from 6 × 5 μm sections cut from routinely processed paraffin wax embedded tissue; the former using the primer pair FR3A and LJH (Perkin-Elmer, Warrington, UK),6 and the latter using primers Vγ11, Vγ101, Jγ12, and Jp12 (Perkin-Elmer) in two multiplex reactions.7 DNA amplification was performed in a total volume of 25 μl containing 1 μl extracted DNA, 2.5 μl buffer IV, 1.5 μl MgCl2 (25 mM), 0.75 μl dNTPs (20 mM) (all ABgene Epsom, Surrey, UK), and 1.25 μl of each primer. After five minutes denaturation at 100°C, 0.5 U enzyme (Thermoprime+; ABgene) was added. Thirty PCR cycles were then undertaken (94°C for one minute, 60°C for one minute and 30 seconds), followed by a final extension step at 72°C for five minutes. DNA from known B and T cell non-Hodgkin's lymphomas and reactive lymph nodes were used as positive and negative controls, respectively. The final products were visualised by UV transmission of ethidium bromide stained 8% polyacrylamide gels.

Pathological findings

Sections of the lymph node showed subtotal, but almost complete, infarction with only a peripheral rim of organising granulation tissue present in the region of the subcapsular sinus (fig 1), and a small focus of residual viable lymphoid tissue showing features of follicular hyperplasia. The centre of the node was filled with the ghost outlines of necrotic cells. In cortical areas, there were foci in which the nuclei of the dead cells were better preserved and appeared to be forming mantles around necrotic germinal centres, giving an impression that reactive follicles had previously been present. This interpretation was supported by a reticulin stain, which also showed preservation of the normal nodal architecture (fig 2). Immunohistochemical stains also emphasised the presence of necrotic B cell follicles surrounded by T cell areas, in keeping with normal nodal architecture. Nothing to suggest an underlying lymphoma was identified and this was borne out by PCR studies, which showed polyclonal rearrangements of immunoglobulin and T cell receptor genes.

Discussion

Spontaneous infarction of lymph nodes is rare; it has been estimated that one case of lymph node infarction will be encountered in every 13 000 routine surgical specimens.4 The most frequent association is with malignant lymphoma, accounting for approximately 40% of cases in unselected series4 and 97% of cases in specialist units.8 Even when not apparent at the time of initial presentation with an infarcted node, subsequent biopsy will reveal malignant lymphoma in a large number of patients.4, 8

In our case, lymphoma can almost certainly be ruled out as a cause of the lymph node infarction. It was not evident at the time of biopsy even when immunohistochemical and molecular studies were undertaken, both of which have been demonstrated as useful in diagnosing lymphoma in completely infarcted nodes.9, 10 Moreover, in cases where lymphoma manifests itself in a biopsy taken after one showing lymph node infarction, it invariably does so within two years.4 Our patient was alive with no evidence of lymphoma three years after initial presentation. Other potential causes of lymph node infarction include vascular thrombosis, infections, and mechanical pressure.4 There was no evidence, either clinically or in the biopsy specimen, that any of these factors were at work in the current case. All the above findings, coupled with the complete resolution of symptoms after the cessation of gold injections, argue strongly that the latter were responsible for infarction of the lymph node.

Lymph node infarction occurring during the course of gold injections has only been reported once.2 In addition, two patients have been described in whom lymphadenopathy developed as part of a reaction to gold injections.1, 3 Biopsy was only undertaken in one of these cases and this was said to show “reactive cortical hyperplasia”.3 In all these patients, including our patient, the lymphadenopathy was tender and developed in neck nodes, either in isolation or as part of a more generalised lymph node enlargement, always within a few weeks of initiating treatment. Similarly, all cases underwent complete resolution of symptoms on cessation of treatment, either spontaneously (our case, and Lowthian1 and Prichanond and Skosey3) or with concomitant steroid administration.2 In the previously described case of gold induced lymph node infarction it was postulated that a vasculitis might have been the underlying pathogenetic mechanism.2 However, there was no firm evidence of such a process in that case or in the one that we currently describe.

In summary, this case emphasises that lymphadenopathy might occur as part of a reaction to gold injections. Although lymph node enlargement commonly occurs in rheumatoid patients, the timing of its onset in the cases described and the resolution of symptoms on withdrawal of the drug mean that the relation is unlikely to be coincidental. Furthermore, gold injections appear to be a rare cause of lymph node infarction, although the mechanism leading to infarction remains to be determined.

Acknowledgments
The authors would like to thank Dr C Yiu, Hurley Clinic, London for providing follow up clinical information on this patient.

http://jcp.bmj.com/content/54/7/562.full

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Lymph node infarction. An immunohistochemical study of 11 cases.

Strauchen JA, Miller LK.
Source
Department of Pathology, Mount Sinai School of Medicine, New York, NY 10029, USA. james.strauchen@msnyuhealth.org

Abstract

CONTEXT:
The etiology of lymph node infarction may be difficult or impossible to determine by histologic examination. Lymph node infarction is followed by malignant lymphoma in some but not all patients. The role of immunohistochemistry in the evaluation of lymph node infarction is not well defined. Although it is widely believed that necrotic tissue is not suitable for immunohistochemical study, this view may be inaccurate.

OBJECTIVE:
To determine whether lymphoid antigens are preserved in infarcted lymph nodes and to determine the utility of immunohistochemical staining in the evaluation of lymph node infarction.

DESIGN:
Retrospective immunohistochemical study of infarcted lymph nodes using archival formalin-fixed, paraffin-embedded tissue.

SETTING:
Academic medical center.

PATIENTS:
Eleven adult patients with lymph node infarction retrieved from pathology files.

MAIN OUTCOMES MEASURES:
Results of immunohistochemistry, diagnosis of lymphoma.

RESULTS:
Preservation of lymphoid antigens was observed in 4 of 6 cases of lymph node infarction associated with malignant lymphoma, including 3 of 5 cases of diffuse large B-cell lymphoma and 1 case of peripheral T-cell lymphoma. Nonspecific staining was not encountered. In 1 case, in which an infarcted lymph node showed a benign pattern of lymphoid antigen expression, lymphoma has not developed after 5 years.

CONCLUSION:
Lymphoid antigens are frequently preserved in cases of lymph node infarction, and immunohistochemical study of infarcted lymph nodes may provide clinically useful information.

http://www.ncbi.nlm.nih.gov/pubmed/12521368

Main Article

Lymph node infarction refers to a syndrome of spontaneous coagulative necrosis of lymph nodes that is frequently associated with concurrent or subsequent malignant lymphoma.1–5 Lymph node infarction may also follow fine-needle aspiration biopsy. The incidence of malignant lymphoma in patients with lymph node infarction varies from as high as 89% to as low as 32% in published series.1,2 Some cases of lymph node infarction may occur due to vascular compromise or other undetermined causes in the absence of malignant lymphoma.2

The diagnosis of malignant lymphoma in extensively necrotic lymph nodes may be difficult or impossible on morphologic grounds alone. There is little published data on the role of immunohistochemistry in the evaluation of lymph node infarction. Although it is widely believed that necrotic tissue is unsuitable for immunophenotypic studies because of loss of antigenicity and nonspecific staining,6 this view has been challenged.7–9 Preservation of antigens in some cases of lymph node infarction associated with malignant lymphoma of B- or T-cell type7,8 and with metastatic carcinoma or melanoma9 has been reported. In these cases, however, lymphoma was diagnosed concurrently with lymph node infarction, and cases of lymph node infarction of benign or undetermined etiology were not studied.

To further define the role of immunohistochemistry in the evaluation of infarcted lymph nodes, we studied 11 cases of lymph node infarction of varied etiology using a panel of monoclonal antibodies to lymphoid and epithelial antigens detectable in routinely processed, formalin-fixed, paraffin-embedded tissue.

METHODS AND MATERIALS

Lymph Nodes

Lymph nodes with a diagnosis of lymph node infarction or lymph node necrosis, with or without concurrent lymphoma, were retrieved from the files of the Mount Sinai Hospital from 1994 to 2002. No cases were excluded. Cases studied dated from 1995 to 2002. Sections for immunohistochemistry were prepared from routinely processed, formalin-fixed, paraffin-embedded tissue.

Antibodies
Antibodies used were anticytokeratins CAM5.2 (Becton Dickinson, Mountain View, Calif) and AE1/AE3 (Signet Laboratories Inc, Dedham, Mass), epithelial membrane antigen, leukocyte common antigen (anti-CD45RB), L26 (anti-CD20), UCHL-1 (anti-CD45RO), Ber-H2 (anti-CD30), anti-CD3(P), anti-CD43, and anti-CD79a (Dako Corporation, Carpinteria, Calif).

Immunohistochemistry
Immunohistochemistry was performed on deparaffinized sections by standard avidin-biotin-complex (ABC) immunoperoxidase technique with diaminobenzidine (DAB) chromogen, following antigen retrieval by microwaving in 10 mmol/L citric acid at pH 6.0 for 15 minutes. Sections were counterstained with hematoxylin.

RESULTS
Six cases of lymph node infarction were associated with the development of malignant lymphoma, either concurrently (cases 2, 5, and 6) or following a brief interval (cases 1, 3, and 4) (Table 1). Diagnosis of concurrent lymphoma was based on examination of another viable lymph node for which a biopsy had been procured at the same time. Five cases were diagnosed as diffuse large B-cell lymphoma, and 1 case was diagnosed as peripheral T-cell lymphoma. Lymphoma developed at the same site as the lymph node infarction in all cases. Lymphoid antigens were preserved in the infarcted lymph nodes in 4 of 6 cases (Table 2). Lymphoid antigens were preserved in 3 of 5 cases of lymph node infarction associated with diffuse large B-cell lymphoma (Figures 1 and 2) and in 1 case associated with peripheral T-cell lymphoma (Figures 3 and 4). Lymphoid antigen expression in infarcted tissue accurately predicted lymphoma immunophenotype. CD79a was more consistently preserved in infarcted tissue than CD20. CD3(P), CD45RO, and CD43 were equally well preserved (Table 2).

Three cases of lymph node infarction were of undetermined etiology. Lymphoid antigens were preserved in each case. In 2 cases, “ghosts” of lymphoid follicles were apparent (Figures 5 and 6). Follow-up was benign at 5 years in 1 case (case 7), and subsequent lymph node biopsy showed only reactive follicular hyperplasia in another case (case 9). In the third case (case 8), sheets of cells staining for B-cell antigens were apparent; in this case, follow-up is too short to exclude malignant lymphoma.

Two cases of lymph node infarction were associated with metastatic carcinoma, an axillary lymph node with metastatic carcinoma of the breast (case 10) and a mediastinal lymph node with metastatic small cell carcinoma (case 11). Epithelial antigens (cytokeratins CAM5.2 and AE1/AE3, and epithelial membrane antigen) were not preserved in these cases. Nonspecific staining for lymphoid antigens was not encountered.

COMMENT
Lymph node infarction, a syndrome of spontaneous coagulative necrosis of lymph nodes, may be the presenting manifestation of malignant lymphoma.1–5 The reported incidence of malignant lymphoma following lymph node infarction has ranged from nearly 90% to less than one third in published series.1,2 Cleary et al1 reported the occurrence of malignant lymphoma in 16 (89%) of 18 patients with lymph node infarction, occurring either concurrently or within 2 to 6 months. Maurer et al2 reported the occurrence of malignant lymphoma in 20 (39%) of 51 cases of lymph node infarction from their own multicenter series; these cases occurred either concurrently (14 cases) or developed within 2 years (6 cases). These authors also reported the occurrence of malignant lymphoma in 26 (32%) of 81 cases of lymph node infarction gathered from other pathologists and the literature. The variation in the reported incidence of malignant lymphoma associated with lymph node infarction may be due to inconsistency in the inclusion of cases of concurrent malignant lymphoma and lymph node infarction. Lymph node infarction may also occur due to vascular compromise or other undetermined causes.2

There is little published data on the immunohistochemistry of lymph node infarction. It is generally believed that necrotic tissue should be avoided for immunohistochemistry because of loss of antigenicity and nonspecific staining 6; however, this view has been challenged.7–9 Norton et al7 studied 11 cases of lymph node infarction occurring concurrently with malignant lymphoma. Using a panel of monoclonal antibodies to antigens detectable in routinely processed formalin-fixed, paraffin-embedded tissue, they found preservation of lymphoid antigens in 8 cases of lymph node infarction concurrent with non-Hodgkin lymphoma, including 6 of 7 cases of B-cell lymphoma and 2 of 3 cases of T-cell lymphoma; 1 case of Hodgkin disease showed preservation of lymphoid antigens on background T lymphocytes but not on Reed-Sternberg cells. These authors concluded that immunostaining of infarcted lymphoid tissue provided valuable information that was not available from conventional light microscopy. Vega et al8 reported preservation of lymphoid antigens in a single case of lymph node infarction associated with B-cell lymphoma. In these studies, however, cases of lymph node infarction occurring prior to the diagnosis of malignant lymphoma, cases of lymph node infarction of undetermined etiology, and cases of lymph node infarction due to other causes (eg, metastatic carcinoma) were not studied. Nasuti et al9 reported preservation of antigens in 2 cases of metastatic squamous carcinoma and 1 case of metastatic melanoma associated with lymph node infarction following fine-needle aspiration.

In the present study, we describe 11 cases of lymph node infarction of varied etiology studied by immunohistochemistry with a panel of monoclonal antibodies to lymphoid and epithelial antigens detectable in routinely processed, formalin-fixed, paraffin-embedded tissue. Lymphoid antigens were preserved in 4 of 6 cases of lymph node infarction associated with malignant lymphoma, including 2 of 3 concurrent cases and 2 of 3 cases preceding malignant lymphoma. Lymphoid antigens were preserved in 3 of 5 cases associated with diffuse large B-cell lymphoma and in 1 case associated with peripheral T-cell lymphoma. The detection of lymphoid antigens in infarcted lymph nodes accurately predicted the lymphoma phenotype (B cell in 3 cases, T cell in 1), and nonspecific staining was not encountered. CD79a was more consistently preserved than CD20. Poor preservation of CD20 in necrotic tissue was also noted by Norton et al.7 The T-cell antigens CD3(P), CD45RO, and CD43 were equally preserved.

Lymphoid antigens were also preserved in 3 cases of lymph node infarction of undetermined etiology. In 2 cases (cases 7 and 9), immunohistochemical staining demonstrated ghosts of B-cell follicles, suggesting an intact lymph node architecture. In 1 of these cases, follow-up after 5 years was benign (case 7), and in the other case, biopsy of another lymph node showed only reactive follicular hyperplasia (case 9). In the third case (case 8), a pattern of staining similar to that observed in cases of lymph node infarction associated with B-cell lymphoma was observed. This patient had an enlarged retroperitoneal lymph node discovered at time of surgery for an abdominal aortic aneurysm, suggesting a possible vascular etiology; however, follow-up in this case is too short to exclude the development of lymphoma.

In 2 cases of lymph node infarction associated with metastatic carcinoma (cases 10 and 11), epithelial antigens (cytokeratins CAM5.2 and AE1/AE3, and epithelial membrane antigen) were not preserved. This observation is in contrast to a previous study, in which preservation of antigens in metastatic squamous cell carcinoma (2 cases) and malignant melanoma (1 case) was reported in cases of lymph node infarction following fine-needle aspiration.9 The difference may relate to the brief interval between infarction and biopsy in the latter cases.

In summary, lymphoid antigens are frequently preserved in cases of lymph node infarction. Immunohistochemical staining of infarcted tissue cannot be used to establish a definitive diagnosis of malignant lymphoma, but may be useful in directing further clinical evaluation. Immunohistochemical staining of infarcted lymph nodes may give clinically useful information when conventional histology is inconclusive.

http://www.archivesofpathology.org/doi/ ... -9985(2003)127%3C60:LN%3E2.0.CO;2

===================

Lymph Node Infarction Simulating Acute Appendicitis

ABSTRACT
A number of diseases can present as acute right iliac region pain. Lymph node infarction, located adjacent to the cecum,
mimicking acute appendicitis in a 13-year-old boy is presented here.

[i]Key words:[/i] Lymph node infarction, Acute appendicitis, Pain right iliac region

INTRODUCTION
A number of diseases have been reported to present with
acute pain in right iliac region, simulating acute
appendicitis [1]. Infarction of lymph nodes has been
reported with many neoplastic and non-neoplastic
conditions. In patients with malignant lymphoma,
infarction of the lymph nodes has been reported quite
frequently [2,3]. Lymph node infarction located adjacent
to the cecum is a condition reported hitherto, the purpose
of which is to add another cause of pain abdomen
simulating acute appendicitis.

CASE REPORT
A 13-year-old boy presented with acute pain in right iliac
region for a day. The pain initially felt in the periumbilical
region. There was no associated fever, anorexia, nausea
or vomiting. On palpation of the abdomen, there was
muscle guarding, localized abdominal tenderness in the
right iliac fossa with rebound tenderness. Laboratory tests
showed hemoglobin 11gm/dl and WBC count 13700/cmm
with predominant polymorphonuclear cells. Ultrasound of
abdomen was reported as normal. The score on Alvarado
scale was 7, indicating probable appendicitis.

At operation, normal looking appendix was observed.
Appendectomy was done. The Meckel’s diverticulum was
not present. Further exploration revealed an enlarged
lymph node adjacent to the cecal wall. The connective
tissue over the lymph node was incised that revealed a
necrosed lymph node (Fig. 1). Specimens of the
appendix and lymph node were sent for histopathology.
The histopathology report showed an appendix
measuring 6x0.5cm with lymphoid hyperplasia but no
signs of acute inflammation. The lymph node biopsy
revealed hemorrhagic necrosis of its parenchyma. The
few preserved areas of lymph node were free of any
malignant cells (Fig. 2,3). The patient had an uneventful
recovery. He is counseled for diligent follow-up with
repeated ultrasound abdomen. He is doing well at 6
months follow-up.

DISCUSSION
Pain in RIF has many differential diagnoses [1]. The
Alvarado score in our case was 7 which had a high
probability of acute appendicitis, however, a distinct
infarcted lymph node lying adjacent to the cecal wall was
the only pathology observed in presence of histologically
normal appendix. On the other hand, the histopathology
of the infarcted lymph node showed extensive
hemorrhagic necrosis.

There are multiple causes of lymph node infarction and
can be categorized as iatrogenic, non-neoplastic and
neoplastic. Lymphoma is a frequently reported neoplastic
cause of lymph node infarction with an incidence of 32-
89%.The lymphoma may be synchronously present or
develop after months to years of initial event. Therefore a
long term follow up is advised in such cases [2,3].
To the best of our knowledge, such a presentation of
infarcted lymph node is not reported before. In addition
infarction of lymph node must be kept in differential
diagnosis of acute right iliac region pain.

http://www.apspjcaserep.com/documents/2 ... 1-2-18.pdf

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Lymph Node Infarction Associated with Infectious Mononucleosis

August 2011

Report of a Case Resembling Lymph Node Infarction Associated with Malignant Lymphoma
Masaru Kojima, MD
Department of Pathology and Clinical Laboratories, Gunma Cancer Center Hospital, 617-1, Takabayashinishi-cho Ohta, 373-8550, Japan; Department of Pathology, Dokkyo University School of Medicine, Mibu, Japan
Shigeo Nakamura, MD
Department of Pathology and Genetics, Aichi Cancer Center Hospital, Nagoya, Japan
Shiro Sugihara, MD
Department of Pathology and Clinical Laboratories, Gunma Cancer Center Hospital, Ohta, Japan
Noriyuki Sakata, MD
Second Department of Pathology, Fukuoka University School of Medicine, Fukuoka, Japan
Nobuhide Masawa, MD
Department of Pathology, Dokkyo University School of Medicine, Mibu, Japan

Abstract

A completely infarcted lymph node should alert the pathologist to the high possibility of malignant lymphoma. The lymph node lesion of infectious mononucleosis (IM) shows marked histologic diversity and occasionally may be confused with malignant lymphoma. We report a rare case of IM showing extensive lymph node infarction whose lymph node lesion was similar to lymph node infarction associated with maligant lymphoma. This case describes a 32-year-old Japanese man who had signs and symptoms consistent with IM, which he was later proven serologically to have, but whose cervical lymph node showed extensive lymph node infarction with a thin area of granulation tissue beneath the capsule. The infarcted tissue contained numerous eosinophilic ghosts of large lymphoid cells. The thin granulation tissue was composed of numerous small lymphocytes, plasma cells, and histiocytes, in addition to large lymhoid cells including immunoblasts and granulocytes. CD20, CD3, and CD45RO imunostains revealed the mixed Bnd T-cell nature of the ghosts of large lymphoid cells in the infarcted tissue as well as viable large cells in the granulation tissue. The patient was free from disease after 50 months' follow-up.

http://ijs.sagepub.com/content/10/3/223.abstract

===================

Lymph node infarction: Role of underlying malignancy, tumor proliferation fraction and vascular compromise- A study of 35 cases and comprehensive review of the literature.
2012

Keywords:
Lymph nodes;infarction;lymphoma;proliferation fraction;ischemia;recanalized thrombi

Abstract

Aim:  To determine the role of presence of malignancy, tumor proliferation fraction, vascular compromise and therapeutic and diagnostic manipulations in lymph node infarction (LNI).

Methods and Results: Thirty-five cases of LNI were identified from the pathology records over a 20-year period. 31/35 (89%) of these patients had underlying malignancy: 27/31 (87%) were hematologic malignancies, the rest being metastatic carcinoma (2), melanoma, and seminoma. Of the four patients without evidence of malignancy, two were diagnosed with viral infection, one had LNI adjacent to a thrombosed pancreas graft, and one patient was lost to follow-up. Ki-67 immunostaining in viable tumor demonstrated a range (5% to 60%) of proliferation fractions. A history of fine needle aspiration alone was present in 7/35 (20%), that of chemotherapy alone in 11/35 (31%), and of both in 2/35 (5.7%) patients. Factor-VIII immunostaining highlighted thrombosed and recanalized vessels next to the infarction.

Conclusions:  Infarction of lymph nodes is associated with previous, concurrent, or subsequent diagnosis of malignancy in the vast majority of cases. Chemotherapy or previous fine needle aspiration can precipitate infarction in some cases, but infarction may occur without such intervention possibly due to an underlying subacute or chronic vascular compromise produced by vascular thrombosis.

http://onlinelibrary.wiley.com/doi/10.1 ... x/abstract

===================

Lymph Node Infarction in Classical Hodgkin’s Lymphoma

May 2012

Eiichiro Mori, 1,2,5) Yasunori Enomoto, 1) Hirokazu Nakamine, 3) Takahiko Kasai, 1) Maiko Takeda, 1) Masato Takano, 1)
Kouhei Morita, 1) Toshizo Koizumi, 4) and Akitaka Nonomura 1)

Among lymphoproliferative disorders, lymph node infarction appears to be most frequently seen in diffuse large B-cell
lymphoma, followed by follicular lymphoma, with other types beingrare. We experienced one such case, classical Hodgkin’s
lymphoma (cHL) associated with lymph node infarction, in which Reed-Sternberg(RS) cells were positive for CD15, CD30,
fascin, PAX-5, p53, latent membrane protein-1 (LMP-1), Bcl-2, and EBV-encoded small non-polyadenylated RNAs.

Furthermore, RS cells in the infarcted area were still positive for CD30, fascin, p53, and Bcl-2. For definitive diagnosis of nodal lymphomas including Hodgkin’s lymphoma, identification of the effacement of normal nodal architecture is essential.

Although this could not be evaluated in our case because of predominant reactive follicular hyperplasia with interfollicular distribution of RS cells, the presence of large cells with RS cell-related molecules together with the distorted distribution of cCD3-positive cells and CD20-positive cells led us to make a definitive diagnosis of cHL. It is, therefore, considered that immunohistochemical evaluation of the infarcted lymph node is, at least on some occasions, still informative for more accurate diagnosis of lymphoid neoplasia. Hodgkin’s lymphoma should also be considered when one encounters lymph node infarction. 〔J Clin Exp Hematopathol 52(1) : 35-39, 2012〕

Keywords: lymph node infarction, malignant lymphoma, Hodgkin’s lymphoma, immunohistochemistry

FULL TEXT ARTICLE MAY BE FOUND: http://www.jsltr.org/journal/52-1/5201_05.pdf

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