What Is Lymphoid Hyperplasia?

Skin B-cell lymphoid hyperplasia (nodular pattern), the nodular type is usually idiopathic. Idiopathic B-cell lymphoid hyperplasia, previously known as Speigler-Fendt sarcoma.

Cutaneous B-cell lymphoid hyperplasia

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Skin B-cell lymphoid hyperplasia (nodular pattern), the nodular type is usually idiopathic. Idiopathic B-cell lymphoid hyperplasia, previously known as Speigler-Fendt sarcoma.

Chinese name

Cutaneous B-cell lymphoid hyperplasia

Foreign name

cutaneous B-cell lymphoid hyperplasia (nodular pattern

Used to be called

Speigler-Fendt sarcoma

Cause

Tattoo, Borrelia infection

Causes include tattoos, Borrelia infection,

Idiopathic and secondary localized lesions are scattered solid skin pimples or nodules, clustered or fused into plaque. It occurs mainly on the face, especially the cheeks and nose or earlobe. Second, the nodules that can invade the trunk (36%) or limbs (25%) are usually smooth. It is flesh brownish yellow, red or purple. Women are three times as likely as men, and two-thirds are under 40. Disseminated or generalized cases are rare and manifest as miliary papules. Lymphoid hyperplasia of the skin caused by Borrelia burgdorferi infections occurs infrequently at the site of a tick bite or immediately following the edge of a migratory erythema. Damage occurs up to 10 months after infection. The skin lesions were multiple nodules, with a diameter of 1 to 5 cm.

Histopathology: dense nodular infiltration is mainly located in the dermis; deep dermis and subcutaneous tissue infiltration is reduced, with head-to-foot light infiltration and a transparent zone between epidermis. Infiltration is mainly composed of mature small and large lymphocyte tissue cells, plasma cells, and eosinophils. The germinal center with clear boundaries is usually seen in the deep, with large lymphoid cells in the center, rich in cytoplasm and

According to clinical manifestations, skin lesion characteristics, and histopathological characteristics can be diagnosed. The diagnosis is confirmed by an increase in anti- Borrelia antibodies (occurring in 50% of cases) and the presence of Borrelia DNA in diseased tissues.

Most damage is asymptomatic and therefore does not require treatment. When necessary:
1. Intravenous injection of corticosteroid damage, sometimes effective. Superficial damage can also be applied topically with high-strength corticosteroids.
2. Cryotherapy, laser therapy or surgical resection.
3. Low-dose radiation therapy is very effective.
4. Interferon alpha and propaquinone treatment.
5. Disseminated damage can be treated with antimalarial drugs and PUVA. ^[1]