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Pseudolymphoma
(Cutaneous lymphoid hyperplasia)
Definition:
o Benign but persistent lymphoid proliferations in the dermis
o May be difficult to distinguish from a low-grade malignant lymphoma
o A pathological rather than a clinical appearance.
Classification ???
T-cell pseudolymphomas:
o Jessner’s lymphocytic infiltrate (a T-cell pseudolymphoma OR a
variant of cutaneous lupus erythematosus).
o Adverse drug reaction (e.g. anticonvulsants, angiotensin-converting
enzyme inhibitors, β-blockers, cytotoxics, antirheumatics, antibiotics,
antidepressants and many others).
o Persistent contact dermatitis
o Persistent nodular scabies
o Arthropod bites
B-cell pseudolymphomas:
o Lymphocytoma cutis
o Lyme disease (Borrelia burgdorferi infection)
o Tattoos (reaction to certain pigments)
o After vaccination and trauma, acupuncture
o Within scars after herpes zoster infection
Pseudo-lymphoma may rarely progress to malignant lymphoma (concept:
chronic, initially benign, reactive inflammatory conditions may very rarely
progress to frank lymphoma)
Lymphocytoma cutis
Cutaneous lymphoid hyperplasia (CLH)
Aetiopathogenesis:
Exaggerated local immunologic reaction to a stimulus (often unrecognized)
Possible triggering agents include:
o arthropod bites, metal implants, tattoos, vaccinations and medications
o infections and reactive disorders e.g. herpes simplex, post herpes
zoster infection (dermatomal) and Folliculitis (pseudolymphomatous)
Vascular disorders part 2 (Ahmad Kamel, MD) Page 29
Clinical features
o most often in adults (reported in children)
o slightly more common in women
o firm, erythematous to violaceous papules, plaques or nodules
o located on the head, neck or upper extremities
o often solitary, but may be multiple or grouped
Pathology
o The histologic features are variable and may resemble mycosis
fungoides, a B-cell lymphoma or a CD30+ anaplastic large cell
lymphoma (cause??).
o Epidermal changes:
• Epidermotropism, spongiosis, vacuolar degeneration of the basal
layer, papillary dermal edema, and red cell extravasation.
o CLH with B-cell predominance:
o superficial and deep nodular or diffuse infiltrate of lymphocytes
o admixed with histiocytes and occasional plasma cells and eosinophils.
Histopathological DD: 5 L (LE, PLE, tumid LE, L cutis, Jessner’s)
Differentiation from cutaneous lymphoma: مھم جدا
Lymphocytoma cutis Cutaneous follicle center B-
(CLH) cell lymphoma
Mixed cellular infiltrate, Predominantly lymphocytic
including eosinophils and infiltrate
plasma cells
Histopathology
Tingible-body absent
macrophages
present
T and B lymphocytes Predominance of B
lymphocytes (CD20+)
Immuno-
Mixed κ and λ expression Restricted κ or λ expression
histochemistry
(some
cases, frozen sections)
Differential diagnosis
• lymphocytic infiltrate of Jessner
• polymorphic light eruption
• LE tumidus
Vascular disorders part 2 (Ahmad Kamel, MD) Page 30
Treatment
• Cutaneous lymphoid hyperplasia is a benign, reactive condition and it
should be treated conservatively.
• Spontaneous resolution may occur without scarring.
• For persistent lesions,
o topical and/or intralesional corticosteroids
o surgical excision
o cryosurgery
o laser ablation
o radiation therapy
Jessner’s lymphocytic infiltrate ()قارن
Definition: A chronic benign T-cell lymphoproliferative disorder
Clinical features:
• More in Females
• red tumid nodules
• usually of exposed skin (usually on facial skin)
The lesions are persistent, and new lesions develop over time (may involute
spontaneously).
Histopathology:
• a lymphocytic infiltrate predominantly in the lower dermis
• concentrated tightly around blood vessels
• The epidermis and papillary dermis are relatively normal
• within the lymphocytic infiltrate there is no evidence of cellular atypia,
germinal centre or follicle formation.
• The great majority of these cells are CD4+ T cells.
Differential diagnosis: ???? DLE
• Lesions of Jessner’s lymphocytic infiltrate are smooth and non-
scarring (scaling atrophic scarring in DLE) and negative lupus band
test. However, there is a view that Jessner’s lymphocytic infiltrate is a
variant of LE.
Treatment:
o Unsatisfactory (lesions tend both to persist and to increase in numbers).
o Topical steroids, systemic steroids, PUVA, radiotherapy, dapsone,
hydroxychloroquine and gold.
Vascular disorders part 2 (Ahmad Kamel, MD) Page 31
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