Premalignant tumours

 Premalignant tumours

Keratoacanthoma

Some argue that this rapidly growing tumour should be classed as benign, but a very few transform into a squamous cell carcinoma.

Cause

Photosensitizing chemicals such as tar and mineral oils can act as cocarcinogens with ultraviolet radiation. They may also follow therapeutic immunosuppression.

Clinical features

They occur mainly on the exposed skin of fair indi-viduals. More than two-thirds are on the face and most of the rest are on the arms. The lesion starts as a pink papule that rapidly enlarges; it may reach a diameter of 1 cm in a month or two. After 5 or 6 weeks the centre of the nodule forms either a keratinous plug or a crater (Fig. 18.23). If left, the lesion often resolves spontaneously over 6–12 months but leaves an ugly depressed scar.

Differential diagnosis

Squamous cell carcinoma is the main tumour to be distinguished from a keratoacanthoma. However, carcinomas grow more slowly and usually lack symmetry.

Histology

It is not possible to tell a keratoacanthoma from a squamous cell carcinoma histologically unless the architecture of the whole lesion can be assessed, including its base (Fig. 18.24). 

A typical lesion is symmetrical and composed of proliferating fronds of epidermis that show mitotic activity but retain a well-differentiated squamous appearance with the production of much ‘glassy’ keratin. The centre of the cup-shaped mass is filled with keratin.

Treatment

Excision or curettage and cautery are both effective. Occasionally, a further curetting may be needed but this should be performed only once; if this is still ineffective, the lesion must be excised.

Intraepidermal carcinoma (Bowen’s disease)

Usually single, these slowly expanding pink scaly plaques (Fig. 18.25) take years to reach a diameter of a few centimetres. Their border is sharply defined, with reniform projections and notches. About 3% progress into an invasive squamous cell carcinoma. 

The presence of several may be a clue to previous exposure to carcinogens (e.g. excessive sun exposure, arsenic in a tonic when young). 

Differential diagnosis

An intraepidermal carcinoma is often mistaken for psoriasis , discoid eczema, super-ficial basal cell carcinoma  or for Paget’s disease in the peri-anal region.

Treatment

These lesions are unaffected by local steroids. Small lesions may occasionally be left under observation in the frail and elderly. Cryotherapy or curettage are the treatments of choice for small lesions on a site where healing should be good (e.g. face or trunk); excision is an alternative. Photodynamic therapy  is useful for large lesions on a poor healing site (e.g. the lower legs of the elderly). Topical 5-fluorouracil or imiquimod is helpful for multiple lesions (see Guidelines in Further reading).

Actinic keratoses

These discrete rough-surfaced lesions crop up on sun-damaged skin. They are premalignant, although only a few turn into a squamous cell carcinoma.

Cause

The effects of sun exposure are cumulative. Those with fair complexions living near the equator are most at risk and invariably develop these ‘sun warts’.

A recent UK survey showed that one-third of men over 70 years had actinic keratoses. Melanin protects, and actinic keratoses are not seen in black skin. Con-versely, albinos are especially prone to develop them.

Presentation

They affect the middle-aged and elderly in temperate climates, but younger people in the tropics. The pink or grey rough scaling macules or papules seldom exceed 1 cm in diameter (Fig. 18.26). Their rough surface is sometimes better felt than seen.

Complications

Transition to a squamous cell carcinoma, although rare, should be suspected if a lesion enlarges, ulcerates or bleeds. Luckily such tumours seldom metastasize. A ‘cutaneous horn’ is a hard keratotic protrusion based on an actinic keratosis, a squamous cell papil-loma or a viral wart (Fig. 18.27).

Differential diagnosis

There is usually no difficulty in telling an actinic ker-atosis from a seborrhoeic wart, a viral wart, a keratoacanthoma, an intraepidermal carcinoma or a squamous cell carcinoma.

Investigations

A biopsy is needed if there is concern over malignant change.

Histology

Alternating zones of hyper- and parakeratosis overlie a thickened or atrophic epidermis. The normal mat-uration pattern of the epidermis may be lost and occasional pleomorphic keratinocytes may be seen. Solar elastosis is seen in the superficial dermis.

Treatment

Freezing with liquid nitrogen or carbon dioxide snow is simple and effective. Curettage is best for large lesions and cutaneous horns. Multiple lesions, including subclinical ones, can be treated with 5-fluorouracil cream (Formulary 1) after special-ist advice. The cream is applied once or twice daily until there is a marked inflammatory response in the treated area. This takes about 3 weeks and only then should the applications be stopped. Healing is rapid and most patients are very pleased with their ‘new’ smooth skin. Severe discomfort from the treatment may be alleviated by the short-term application of a local steroid. 5-Fluorouracil cream is more effective for keratoses on the face than on the arms. Altern-atively, less effective but causing less inflammation, 5-fluorouracil cream can be applied on just one or two days a week for 8 weeks. Recently, 3% sodium diclofenac made up in a hyaluronan gel has come on the market with a product licence to treat actinic keratoses but it is too early to judge its efficacy. 

Photo-dynamic therapy, using aminolaevulinic acid hydrochloride followed by blue light, is effective but requires specialist facilities. Lesions that do not respond should be regarded with suspicion, and biopsied.

Sebaceous naevi (Fig. 18.28)

A flat hairless area at birth, usually in the scalp, these naevi become yellower and more raised at puberty. Basal cell carcinomas appear on some in adult life.