What is Nevus Spilus

Onset: They may appear at any age but usually develop before adulthood and follow a benign persistent course. Lesions can appear at birth or in early infancy as light colored café au lait macules. Pigmented macules and papules then develop over a period of months to years.
Cause: The anatomic position or time of onset is not related to sun exposure.
Origin: It has been suggested that nevus spilus is a subtype of congenital melanocytic nevus.
Size: Lesions may be very large. There is considerable variation in size, ranging from 1 to 20 cm.
Shape: Oval or irregularly shaped
Appearance: It is a common hairless, brown lesion that is dotted with darker brown-to-black spots. The brown area is usually flat, and the black dots may be slightly elevated and contain typical nevus cells.
Special features: The background hyperpigmentation histologically has the features of a lentigo or café au lait macule. The spots may be lentigines, junctional, compound, or intraepidermal nevi.
Treatment: Routine excision is not necessary. Biopsy suspicious areas. nevus spilus is flat and necessitates excision and closure if the patient desires removal.

What is Bowen's Disease

Bowen's disease, also referred to as squamous cell carcinoma in situ, appears mainly on sun-exposed sites. Lesions are found most often on the lower limbs of women and on the scalp and ears of men. Typical lesions are slightly elevated, red, scaly plaques with surface fissures and foci of pigmentation. The borders are well defined, and lesions closely resemble psoriasis, chronic eczema, superficial basal cell carcinoma, seborrheic keratosis, and malignant melanoma. The plaque grows very slowly by lateral extension and may eventually, after several months or years, invade the dermis, producing induration and ulceration. When confined to the epidermis the atypical cells, in contrast to actinic keratosis, involve epidermal appendages, particularly the hair follicle. Atypical cells are also found at the periphery of lesions in clinically uninvolved skin. Atypical cells in the epidermal lining of the hair follicle, although still confined to the epidermis, are deeper and more difficult to reach by treatment modalities such as topical 5-FU or electrosurgery, which only permit access to superficial areas.
Immunohistochemistry may sometimes be valuable in differentiating Paget's disease, superficial spreading melanoma, and Bowen's disease.
The cause of Bowen's disease is unknown, but several patients with this disease were formerly treated with arsenic. There is no evidence that Bowen's disease is a skin marker for internal malignancy.
Treatment.
Small lesions may be successfully treated with electrodesiccation and curettage, cryosurgery, or excisional surgery. Larger lesions are treated with excisional surgery or 5-FU cream applied twice a day for 4 to 8 weeks. Treatment is discontinued when erosion and superficial necrosis occur. A large area surrounding the lesion should be treated in order to destroy the clinically inapparent disease. Some authors suggest plastic occlusion to enhance penetration to the hair follicle. Acetowhitening is a useful adjunct for surgical management. Acetic acid (vinegar) applied preoperatively more clearly defines clinical margins by disclosing subclinical extension of disease. Photodynamic therapy is an effective alternative for large lesions or those in anatomically difficult areas. Photofrin (a tumor-localizing photosensitive substance) is administered intravenously and activated by light from a laser 48 hours later. Cytotoxic substances are released that destroy the malignant tumor and preserve surrounding normal tissues. The most significant side effects are moderate pain and edema. Close follow-up of patients after treatment is required because recurrences are relatively common. Recurrence is related to follicular involvement and ill-defined lateral margins. If left untreated, development of invasive carcinoma is possible but uncommon.

Radiation effects of Sun exposure

The sun emits electromagnetic rays comprising a continuous spectrum of short to long waves. Only a narrow range of wavelengths between 400 nm and 770 nm react with photocells in the retina and observed as the various colors of the rainbow. Beyond red (770 nm) is infrared. Heat is due to infrared radiation, which can be felt. Below violet (400 nm) are the ultraviolet (200–400 nm) and X-rays. Most short wavelengths, that can neither be seen nor felt, are filtered out by the Earth's thick atmosphere which includes ozone and water vapour. Therefore, as there is less atmosphere above mountain tops, the danger of radiation exposure is greater. The content of water vapor in the atmosphere varies, which accounts for protection from sunburn in winter, cloudy days, the early morning, or late evening sun. Glass filters out wavelengths below 320 nm, so that the closed windows of a car will protect even in a tropical desert unless one is sensitive to the longer wavelengths of ultraviolet radiation. Porphyria is, for example, a disease triggered by UVA radiation and is thus difficult to protect against by shade, cloud, or glass.
Ultraviolet radiation (UVR) is arbitrarily divided into UVC (200–280 nm), UVB (280–320), and UVA (320–400 nm). The principal effects of ultraviolet light on the skin are elastic fibre damage and cutaneous ageing, apoptosis, immunosuppression, suntan, sunburn, and carcinogenesis. While each subclass of UVR can produce all of these effects, UVC is relatively more likely to cause cancer, UVB relatively more likely to produce burning, and UVA relatively more likely to produce ageing. UVA is estimated to be 10 times less effective than UVB at producing a suntan and 100 times less effective than UVB at producing non-melanoma skin cancer. This is the basis of so-called ‘safe tanning’ using UVA light in solariums. However, high-dose UVA does cause non-melanoma skin cancer. In addition, the spectrum responsible for producing melanoma has not been established and may include UVA. UVR immunosuppression may suppress tumour surveillance and thereby enhance carcinogenesis.
The diagnosis of UVR damage is determined by recognizing the distribution of the rash as being typical of exposure. Thus the head, nose, and cheeks are principally affected, but there is often sparing below the eyebrows, under a forelock, beneath and behind the ears, and below the chin. The sides and back of the neck are picked out, but there is a sharp border to the sun damage where the collar shields the skin from sunlight. Much, of course, depends on the style of clothing as well as on the direction of irradiation. The backs of the hands and dorsum of the feet are often caught by the sun; however, there may be some tolerance of such skin previously exposed and tanned so that skin not so tolerant is clearly more prone to burning. Mediation of sunburn erythema is partly due to the generation of prostaglandins.

What are Dermal Nevi

Onset: mainly after adolescence
Site: generally appear on the face
Origin: Nests and cords of nevus cells are found within the dermis; they may extend into the subcutaneous fat
Size: vary in size from a few millimeters to a centimeter
Shape: Dome-shaped lesions are the most common, The variety of shapes reflects the evolutionary process in which moles extend downward with age and nevus cells degenerate or become replaced by fat and fibrous tissue
Appearance: elevated, fleshy, and slightly or moderately pigmented papules, may appear as a soft, flabby, wrinkled sack
Surface: smooth, may be white or translucent, with telangiectatic vessels
Color: brown or black, but may become lighter or flesh-colored with time
Border: symmetric, white borders may appear, creating a halo nevus
Special features: Pigmentation may be arranged in flecks. Coarse, dark, terminal hairs may grow from the nevus. may be warty or polypoid. Pedunculated lesions with a narrow stalk are located on the trunk, neck, axilla, and groin
Complications: prone to trauma from clothing and other stimuli, often causing them to bleed
Progress: Degeneration into melanoma is rare
Differential Diagnosis: 1- dermal nevi may resemble nodular melanoma, 2- trauma causing them to bleed and inflame, influencing some patients to suspect malignancy. 3- telangiectatic vessels on the surface mimicking basal cell carcinoma.


Histologically Dermal Nevi are composed of nests and cords of nevus cells are found within the dermis; they may extend into the subcutaneous fat. Melanocytic cells are pale, uniform in size and are found in cords or clusters surrounded by collagen bundles in the dermis.

What are Compound Nevi

Origin: both at the dermoepidermal junction and within the dermis
Appearance: slightly or markedly raised pigmented papules
Surface: smooth or slightly papillomatous
Border: have an irregular border but are symmetric
Special features: Hair may be present, the center tends to be more heavily pigmented than the periphery, If a white halo appears at the periphery of the lesion, it is referred to as a halo nevus
Progress: tend to increase in thickness and pigmentation in late childhood and adolescence.