These are discussed earily, but are mentioned here for two reasons: first, solitary warts are some-times misdiagnosed on the face or hands of the elderly; and, secondly, a wart is one of the few tumours in humans that is, without doubt, caused by a virus. Seventy per cent of transplant patients who have been immunosuppressed for over 5 years have multiple viral warts and there is growing evidence that immunosup-pression, viral warts and ultraviolet radiation interact in this setting to cause squamous cell carcinoma.
This common tumour, arising from keratinocytes, may resemble a viral wart clinically. Sometimes an excessive hyperkeratosis produces a horn-shaped excrescence (a ‘cutaneous horn’). Excision, or curettage with cautery to the base, is the treatment of choice. The histology should be checked.
This is a common benign epidermal tumour, unrelated to sebaceous glands. The term ‘senile wart’ should be avoided as it offends many patients.
Usually unexplained but:
• multiple lesions may be inherited (autosomal dominant);
• occasionally follow an inflammatory dermatosis; or
• very rarely, the sudden eruption of hundreds of itchy lesions is associated with an internal neoplasm (Leser–Trélat sign).
Seborrhoeic keratoses usually arise after the age of 50 years, but flat inconspicuous lesions are often visible earlier. They are often multiple (Figs 18.4 and 18.5) but may be single. Lesions are most common on the face and trunk. The sexes are equally affected.
• a distinctive ‘stuck-on’ appearance;
may be flat, raised or pedunculated;
• colour varies from yellow to dark brown; and
• surface may have greasy scaling and scattered keratin plugs (‘currant bun’ appearance).
Lesions may multiply with age but remain benign.
Seborrhoeic keratoses are easily recognized. Occa-sionally they can be confused with a pigmented cel-lular naevus, a pigmented basal cell carcinoma and, most importantly, with a malignant melanoma. Some Afro-Caribbeans have many dark warty papules on their faces (dermatosis papulosa nigra; Fig. 18.6). Histologically these are like seborrhoeic warts.
Biopsy is needed only in rare dubious cases. The his-tology is diagnostic (Fig. 18.7): the lesion lies above the general level of the surrounding epidermis and consists of proliferating basal cells and horn cysts.
Seborrhoeic keratoses can safely be left alone, but ugly or easily traumatized ones can be removed with a curette under local anaesthetic (this has the advantage of providing histology), or by cryotherapy.
These common benign outgrowths of skin affect mainly the middle-aged and elderly.
This is unknown but the trait is sometimes familial. Skin tags are most common in obese women, and rarely are associated with tuberous sclerosis, acan-thosis nigricans or acromegaly, and diabetes.
Skin tags occur around the neck and within the major flexures. They look unsightly and may catch on clothing and jewellery. They are soft skin-coloured or pigmented pedunculated papules (Fig. 18.8).
The appearance is unmistakable. Tags are rarely confused with small melanocytic naevi.
Small lesions can be snipped off with fine scissors, frozen with liquid nitrogen, or destroyed with a hyfre-cator without local anaesthesia. There is no way of preventing new ones from developing.
These lesions are an example of cutaneous mosaicism and so tend to follow Blaschko’s lines (Fig. 18.9).
The term ‘naevus’ refers to a lesion, often present at birth, which has a local excess of one or more normal constituents of the skin. Melanocytic naevi (moles) are localized benign proliferations of melanocytes. Their classification (Table 18.2) is based on the site of the aggregations of naevus cells (Fig. 18.10).
The cause is unknown. A genetic factor is likely in many families, working together with excessive sun exposure during childhood.
With the exception of congenital melanocytic naevi , most appear in early childhood, often with a sharp increase in numbers during adolescence. Further crops may appear during pregnancy, oestro-gen therapy or, rarely, after cytotoxic chemotherapy and immunosuppression, but new lesions come up less often after the age of 20 years.
Melanocytic naevi in childhood are usually of the ‘junctional’ type, with proliferating melanocytes in clumps at the dermo-epidermal junction. Later, the melanocytes round off and ‘drop’ into the dermis. A ‘compound’ naevus has both dermal and junc-tional components. With maturation the junctional component disappears so that the melanocytes in an ‘intradermal’ naevus are all in the dermis (Fig. 18.10).
Congenital melanocytic naevi (Figs 18.11 and 18.12).These are present at birth or appear in the neonatal period and are seldom less than 1 cm in diame-ter. Their colour varies from brown to black or blue-black. With maturity some become protuberant and hairy, with a cerebriform surface. Such lesions can be disfiguring, e.g. a ‘bathing trunk’ naevus, and carry an increased risk of malignant transformation
Junctional melanocytic naevi (Fig. 18.13). These areroughly circular macules. Their colour ranges from mid to dark brown and may vary even within a single lesion. Most naevi of the palms, soles and genitals are of this type.
Compound melanocytic naevi (Fig. 18.14). These aredomed pigmented nodules of up to 1 cm in diameter. They may be light or dark brown but their colour is more even than that of junctional naevi. Most are smooth, but larger ones may be cerebriform, or even hyperkeratotic and papillomatous; many bear hairs.
Intradermal melanocytic naevi (Fig. 18.15). Theselook like compound naevi but are less pigmented and often skin-coloured.
Spitz naevi (juvenile melanomas; Fig. 18.16). Theseare usually found in children. They develop over a month or two as solitary pink or red nodules of up to 1 cm in diameter and are most common on the face and legs. Although benign, they are often excised because of their rapid growth.
Blue naevi (Fig. 18.17). So-called because of theirstriking slate grey-blue colour, blue naevi usually
appear in childhood and adolescence, on the limbs, buttocks and lower back. They are usually solitary.
Mongolian spots. Pigment in dermal melanocytes isresponsible for these bruise-like greyish areas seen on the lumbosacral area of most Down’s syndrome and many Asian and black babies. They usually fade during childhood.
Atypical mole syndrome (dysplastic naevus syndrome;Fig. 18.18).
Clinically atypical melanocytic naevi can occur sporadically or run in families as an autosomal dominant trait, with incomplete penetrance, affecting several generations. Some families with atypical naevi are melanoma-prone. Genes for susceptibility to melanoma have been mapped to chromosomes 1p36 and 9p13 in a few of these families. The many large irregularly pigmented naevi are most obvious on the trunk but some may be present on the scalp. Their edges are irregular and they vary greatly in sizeamany being over 1 cm in diameter. Some are pinkish and an inflamed halo may surround them. Some have a mamillated surface. Patients with multiple atypical melanocytic or dysplastic naevi with a positive family history of malignant melanoma should be followed up 6-monthly for life.
• Malignant melanomas. This is the most importantpart of the differential diagnosis. Melanomas are very rare before puberty, single and more variably pigmented and irregularly shaped (other features are listed below under Complications).
• Seborrhoeic keratoses. These can cause confusionin adults but have a stuck-on appearance and are warty. Tell-tale keratin plugs and horny cysts may be seen with the help of a lens.
• Lentigines. These may be found on any part of theskin and mucous membranes. More profuse than junctional naevi, they are usually grey-brown rather than black, and develop more often after adolescence.
• Ephelides (freckles). These are tan macules less than
5 mm in diameter. They are confined to sun-exposed areas, being most common in blond or red-haired people.
• Haemangiomas. Benign proliferations of bloodvessels, including haemangiomas and pyogenic gran-ulomas, may be confused with a vascular Spitz naevus or an amelanotic melanoma.
Most acquired lesions fit into the scheme given in Fig. 18.10: orderly nests of benign naevus cells are seen in the junctional region, in the dermis, or in both. However, some types of melanocytic naevi have their own distinguishing features. In congenital naevi the naevus cells may extend to the subcutaneous fat, and hyperplasia of other skin components (e.g. hair follicles) may be seen.
A Spitz naevus has a histology worry-ingly similar to that of a melanoma. It shows dermal oedema and dilatated capillaries, and is composed of large epithelioid and spindle-shaped naevus cells, some of which may be in mitosis.
In a blue naevus, naevus cells are seen in the mid and deep dermis.
The main features of clinically atypical (‘dysplastic’) naevi are lengthening and bridging of rete ridges, and the presence of junctional nests showing melanocytic dysplasia (nuclear pleomorphism and hyperchroma-tism). Fibrosis of the papillary dermis and a lympho-cytic inflammatory response are also seen.
• Inflammation. Pain and swelling are common butare not features of malignant transformation. They are caused by trauma, bacterial folliculitis or a foreign body reaction to hair after shaving or plucking.
• Depigmented halo (Fig. 18.19). So-called ‘halo naevi’are uncommon but benign. There may be vitiligo elsewhere. The naevus in the centre often involutes spontaneously before the halo repigments.
Malignant change. This is extremely rare exceptin congenital melanocytic naevi, where the risk has been estimated at between 3 and 6% depending on their size (Fig. 18.20), and in the atypical naevi of melanoma-prone families. It should be considered if the following changes occur in a melanocytic naevus
• increased or decreased pigmentation;
• altered shape;
• altered contour;
• ulceration; or
If changing lesions are examined carefully, remember-ing the ‘ABCDE’ features of malignant melanoma (Table 18.3), few malignant melanomas should be missed.
Excision is needed when:
1 a naevus is unsightly;
2 malignancy is suspected or is a known risk, e.g. in a large congenital melanocytic naevus; or
3 a naevus is repeatedly inflamed or traumatized.
Often incorrectly called ‘sebaceous cysts’, these are common and can occur on the scalp, face, behind the ears and on the trunk. They often have a central punctum; when they rupture, or are squeezed, foul-smelling cheesy material comes out. Histologically, the lining of a cyst resembles normal epidermis (an epidermoid cyst) or the outer root sheath of the hair follicle (a pilar cyst). Occasionally an adjacent foreign body reaction is noted. Treatment is by excision, or by incision followed by expression of the contents and removal of the cyst wall.
Milia are small subepidermal keratin cysts (Fig. 18.21). They are common on the face in all age groups and appear as tiny white millet seed-like papules of from 0.5 to 2 mm in diameter. They are occasionally seen at the site of a previous subepidermal blister (e.g. in epidermolysis bullosa and porphyria cutanea tarda). The contents of milia can be picked out with a sterile needle without local anaesthesia.
This terminological mouthful is, strictly, not a neo-plasm, but a chronic inflammation. A painful nodule develops on the helix or antehelix of the ear, most often in men. It looks like a small corn, is tender and prevents sleep if that side of the head touches the pillow. Histologically, a thickened epidermis overlies inflamed cartilage. Wedge resection under local anaesthetic is effective if cryotherapy or intralesional triamcinolone injection fails.
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