Description, Causes and Risk Factors:
A benign marked increase and downgrowth of epidermal cells, observed in chronic inflammatory dermatoses and over some dermal neoplasms and nevi; microscopically, it resembles well-differentiated squamous cell carcinoma.
Pseudoepitheliomatous hyperplasia is a benign condition, characterized by hyperplasia of the epidermis and adnexal epithelium, closely simulating squamous cell carcinoma. Pseudoepitheliomatous hyperplasia may be present in a number of conditions characterized by prolonged inflammation and/or chronic infection, as well as in association with many cutaneous neoplasms. Herein, we review different inflammatory, infectious, and neoplastic skin diseases, in which florid epidermal hyperplasia is a prominent histopathologic feature, and introduce a systematic approach in the interpretation of pseudoepitheliomatous hyperplasia.
Pseudoepitheliomatous hyperplasia can arise either from the epidermis or from adnexal epithelium, and is almost always associated with persistent inflammation of the subjacent dermis due to a chronic wound, ulcer, infection, malignancy, retained foreign material or an inflammatory dermatitis. It can closely mimic, abut, or degenerate into a squamous cell carcinoma. Unlike a squamous cell carcinoma, pseudoepitheliomatous hyperplasia never has atypical mitotic figures, rarely has dyskeratosis or atypical nuclei, and is never involved in vascular, lymphatic or perineural invasion. The histogenesis of pseudoepitheliomatous hyperplasia is speculated to be due to the proliferative effect of cytokines released by inflammatory or tumor cells within the subjacent dermis. The term "atypical pseudoepitheliomatous hyperplasia" is sometimes used to describe lesions similar to pseudoepitheliomatous hyperplasia, but which invade deeply into soft tissue and bone. However, atypical pseudoepitheliomatous hyperplasia lacks the cytologic atypia of a squamous cell carcinoma. There are reports of metastasis of these lesions; therefore, most consider atypical pseudoepitheliomatous hyperplasia to be a well-differentiated squamous cell carcinoma. Theories as to the histogenesis of malignant degeneration of pseudoepitheliomatous hyperplasia include that of activated keratinocytes, in which a few keratinocytes within the epidermis are intrinsically mitotically active and therefore easily proliferate when stimulated.
Six cases are described of benign thymic cysts of the anterior mediastinum showing focal pseudoepitheliomatous hyperplasia of the lining epithelium. The patients' ages ranged from 11 to 54 years; 2 cysts occurred in males and 4 in a female. Histologically, the lesions were characterized by exuberant proliferation of the cyst lining epithelium that grew as sheets and tongues of atypical squamous cells with large, hyperchromatic nuclei, prominent nucleoli, and scattered mitotic figures. The walls of the cyst adjacent to the areas of epithelial proliferation showed abundant hemorrhage, necrosis, and severe inflammatory changes. All cases were treated by local surgical excision. There was no evidence of recurrence or metastases over a follow-up period of up to 8 years (average follow-up, 4 years). It is proposed that pseudoepitheliomatous hyperplasia may develop in thymic cysts as an expression of regeneration of the lining epithelium in response to the inflammatory, hemorrhagic, and necrotizing changes which often accompany these lesions. This should not be mistaken for malignancy, and should be distinguished from the exceptional cases of true thymic neoplasms seen in association with thymic cysts.
Symptoms may include:
Slow growing flat reddish patch.
A new spot or growth that increases in size or a sore that does not heal.
A growing lump with a rough, scaly, or crusty surface.
Although this can develop on any part of the body, the most common spots are the:
Back of the hands and the arms.
Head, including the scalp, lips, ears, and mouth.
Carefully examine the lesion. Allow the appropriate time, light and perhaps magnification, to correctly identify such tumors.
Have sufficient knowledge to differentiate these from skin cancers and particularly malignant skin tumors.
Be aware of the limits of one's knowledge in this field.
Consider the amount of sun exposure the patient is generally subjected to (eg people who work mainly outside) and the site of the lesion (cancers are more likely on sun-exposed areas, such as the face).
Refer for diagnosis or biopsy lesions where there is any uncertainty of their nature.
If the diagnosis is unclear, or the lesion has an atypical appearance, dermatological referral and/or biopsy of the lesion should be considered.
Assess the history of the lesion's appearance and growth.
There is no standard or optimal treatment: inappropriate invasive modalities such as cryotherapy and CO2 laser curettage leads to an extension of the lesion area. In the three cases studied, their occurrences were associated with skin wounds: underlying tumors were excluded by histological examination. They each successively received occlusive topical steroid therapy, cryotherapy, laser curettage, and topical 5-FU. Unfortunately, these treatments were ineffective and even worsened the lesions. The patients refused surgical excision, since a large skin graft would be involved. Thus non-invasive PDT (photodynamic therapy) with its low-risk and positive cosmetic outcome was attempted. However, all the 16 lesions treated with topical PDT showed no complete response, even when given an increased photosensitizer or irradiation dose.
NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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