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Contents

   



(Top)
 


1 Lymph node anatomy  





2 Cutaneous hyperplasia  





3 Follicular hyperplasia  





4 Paracortical hyperplasia  





5 Sinus hyperplasia  





6 Complications  





7 See also  





8 References  














Lymphoid hyperplasia







 

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From Wikipedia, the free encyclopedia
 


Lymphoid hyperplasia is the rapid proliferation of normal lymphocytic cells that resemble lymph tissue which may occur with bacterial or viral infections.[1] The growth is termed hyperplasia which may result in enlargement of various tissue including an organ, or cause a cutaneous lesion.[2]

Lymph node anatomy

[edit]

Alymph node is small, capsulated lymphoid organ that is present along the lymphatic system. It is composed of cortex and medulla. The cortex is also divided into outer cortex and inner cortex (also known as the paracortex). The outer cortex is composed of follicles of B cells so that it is called the B-cell zone. Similarly, the inner cortex has T cells and is called the T-cell zone.[citation needed]

Cutaneous hyperplasia

[edit]

Cutaneous lymphoid lesions may be observed in follicular, granulomatous or lymphoreticular pathologic patterns. Cutaneous lymphoid hyperplasia is generally not malignant, but in rare cases an association has been observed.[2]

Follicular hyperplasia

[edit]

Follicular hyperplasia is a stimulation of the B cell compartment. It is caused by an abnormal proliferation of secondary follicles and occurs principally in the cortex without broaching the lymph node capsule. The follicles are cytologically polymorphous, are often polarized, and vary in size and shape.[3] Follicular hyperplasia must be distinguished from follicular lymphoma (bcl-2 protein is expressed in neoplastic follicles, but not reactive follicles).[citation needed]

Paracortical hyperplasia

[edit]

Paracortical hyperplasia is the preferential stimulation of the T cell compartment. It is caused by an abnormal expansion of the interfollicular zones but is confined within the lymph node capsule. The population of the compartment is cytologically polymorphous. Paracortical hyperplasia may be accompanied by vascular proliferation. Must be distinguished from monomorphous T cell lymphoma.[citation needed]

Sinus hyperplasia

[edit]

Sinus hyperplasia is the preferential stimulation of the histiocytic (tissues macrophage) compartment. Histological features include distention or engorgement of both subcapsular and intraparenchymal sinuses by benign histiocytes which may be hemophagocytic. Sinus hyperplasia may be associated with non-hematolymphoid malignancy. Other features include presence of white spaces and lymphocytes (large cells) within sinuses.[citation needed]

Complications

[edit]

It is one common source of appendicitis, as it may cause an obstruction of the appendiceal lumen, resulting in the subsequent filling of the appendix with mucus, causing it to distend and internal pressure to increase. Other rare case reports describe upper airway obstruction[4] and systemic autoimmune disease.[5]

See also

[edit]

References

[edit]
  1. ^ "Lymphoid hyperplasia". MedlinePlus Medical Encyclopedia.
  • ^ a b Caro WA, Helwig HB (September 1969). "Cutaneous lymphoid hyperplasia". Cancer. 24 (3): 487–502. doi:10.1002/1097-0142(196909)24:3<487::aid-cncr2820240310>3.0.co;2-7. PMID 5343388.
  • ^ Torigian DA, Levine MS, Gill NS, Rubesin SE, Fogt F, Schultz CF, Furth EE, Laufer I (July 2001). "Lymphoid hyperplasia of the stomach: radiographic findings in five adult patients". AJR. American Journal of Roentgenology. 177 (1): 71–5. doi:10.2214/ajr.177.1.1770071. PMID 11418401.
  • ^ Sands NB, Tewfik M (2011). "Benign lymphoid hyperplasia of the tongue base causing upper airway obstruction". Case Reports in Otolaryngology. 2011: 625185. doi:10.1155/2011/625185. PMC 3420505. PMID 22937372.
  • ^ Onoda N, Ohsawa M, Kawajiri H, Noda S, Kashiwagi S, Takashima T, Hirakawa K (July 2014). "Reactive lymphoid hyperplasia of the thyroid followed by systemic autoimmune diseases: a case report". Journal of Medical Case Reports. 8 (1): 247. doi:10.1186/1752-1947-8-247. PMC 4096417. PMID 25005726.

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