Lymph nodes & spleen, nonlymphoma
Lymph node-nonspecific findings
Reactive lymphadenopathy
Author: Jayalakshmi Balakrishna, M.D.
Last author update: 1 December 2016
Last staff update: 5 November 2024 (update in progress)
Copyright: 2003-2024, PathologyOutlines.com, Inc.
PubMed search: Hyperplasia[TI] lymph nodes[TI]
Table of Contents
Definition / general | Essential features | Terminology | ICD coding | Epidemiology | Sites | Pathophysiology | Etiology | Clinical features | Diagnosis | Laboratory | Radiology description | Prognostic factors | Treatment | Gross description | Microscopic (histologic) description | Microscopic (histologic) images | Cytology description | Positive stains | Negative stains | Flow cytometry description | Molecular / cytogenetics description | Differential diagnosis | Additional referencesCite this page: Balakrishna J. Reactive lymphadenopathy. PathologyOutlines.com website. https://www.pathologyoutlines.com/topic/lymphnodesreactivegeneral.html. Accessed November 27th, 2024.
Definition / general
- Lymph node enlargement due to hyperplasia of cellular components reflecting antigenic stimulation
- Benign and reversible process.
Essential features
- Clinically manifests as lymph node enlargement
- No clonal process
- No cytologic or architectural atypia
Terminology
- Reactive lymphoid hyperplasia
- Reactive follicular hyperplasia
- Diffuse paracortical hyperplasia
- Sinus histiocytosis
ICD coding
Epidemiology
- Represents the reaction of lymphoid tissue to intrinsic or environmental antigens
- Most lymph node enlargements are reactive
- In children, most lymphadenopathies are benign; in adults, chance of malignancy increases with age
Sites
- Any lymph node group can be affected depending on the stimulation
Pathophysiology
- Lymph nodes filter lymph drained from tributary regions
- Substances carried by lymph reach the nodes; these may be antigenic and cause an immune reaction
- Bacteria and fungi cause predominantly inflammatory reactions; viruses and drugs cause predominantly immune reactions
- 4 patterns of reactive hyperplasia have been described, depending on the etiology: follicular, paracortical / diffuse, sinus and mixed
Etiology
- Multiple etiologic factors, including:
- Bacteria
- Fungi
- Viruses
- Chemicals
- Environmental pollutants
- Drugs: phenytoin, allopurinol, atenolol, gold, penicillin, quinidine
- Altered tissue components
- Other antigens or allergens
- Definitive identification of etiologic agent is possible only in a small subset of cases
Clinical features
- Clinical syndrome usually reflects the underlying disorder
- Generally, of short duration but may be prolonged
- Enlargement of lymph node(s) may be painful or tender
- Associated symptoms include fever, weight loss, malaise, loss of appetite
- Nodes are soft or fluctuant in inflammation and suppuration
Diagnosis
- Histopathology
- Exclude specific causes by clinical, laboratory and imaging studies
Laboratory
- Depends on the etiologic agent
Radiology description
- Enlarged lymph node(s)
Prognostic factors
- Benign, self limiting process
- Prognosis depends on the etiology
Treatment
- Treatment of the underlying disorder
Gross description
- Enlarged, soft, lymph node with tan homogenous cut surfaces
Microscopic (histologic) description
- Reactive follicular hyperplasia
- B cell response pattern
- Enlarged follicles, varying in size and shape, may coalesce and display different configurations
- Prominent germinal center and mantle zone
- Germinal centers show mixed small and large lymphocytes - centrocytes and centroblasts
- Centroblasts polarize to the medial pole forming the darker zone and centrocytes accumulate at the peripheral pole forming the lighter zone
- Centroblasts are 3 - 4 times larger than the inactivated lymphocytes and show narrow rim of basophilic cytoplasm and large, round to oval vesicular nuclei with 1 - 3 prominent peripheral nucleoli
- Mitotic figures are frequent
- Centrocytes are smaller lymphocytes with scant cytoplasm, cleaved nuclei, clumped chromatin and small or absent nucleoli
- Numerous tingible body macrophages are a characteristic feature of follicular hyperplasia
- Diffuse paracortical hyperplasia
- T cell response pattern
- T cell zones, paracortical or interfollicular are expanded with a heterogeneous population of cells, including numerous small lymphocytes and admixed immunoblasts resulting in a starry sky or moth eaten appearance
- Immunoblasts in some cases may resemble Reed-Sternberg cells
- Proliferation of high endothelial venules is another characteristic finding
- Sinus histiocytosis
- Sinuses are prominent and are lined by hyperplastic sinus histiocytes
- Mixed
- Follicular, diffuse and sinus patterns coexist in one lymph node
Microscopic (histologic) images
Images hosted on other servers:
Reactive lymphoid hyperplasia
Cytology description
- Cellular smears with mixed small and large lymphocytes and numerous tingible body macrophages
- No cytologic atypia
Positive stains
Negative stains
- BCL2 is negative in reactive follicular centers (in contrast to follicular lymphoma, in which neoplastic follicles are BCL2+)
Flow cytometry description
- No aberrant immunophenotype
Molecular / cytogenetics description
- Gene rearrangement - polyclonal pattern
Differential diagnosis
- Atypical lymphoid hyperplasia: cellular atypia
- Follicular lymphoma: effaced architecture, back to back nodules which invade surrounding tissues and capsule; no tingible body macrophages, no mantle zones; germinal center is BCL2+; follicular cells are monoclonal, t(14;18) present
- Hodgkin lymphoma: Reed-Sternberg cells and variants are present
- Other non-Hodgkin lymphomas: monotonous population of atypical lymphoid cells, invasion of capsule and surrounding tissues, monoclonal nature and specific surface markers
