Ординатура / Офтальмология / Английские материалы / Clinical Medicine in Optometric Practice_Muchnick_2007

FIGURE 16-1 ■ Primary herpes simplex infection, with uniformly sized vesicles on an erythematous base.

always, topical lesions are inflammatory in nature and cause erythema, or reddening of the skin. Also common is the production of pruritus, a strong desire to scratch. Pruritus is typical of inflammatory skin conditions, such as allergic contact dermatitis.

The skin may erode, and such erosions represent a loss of epidermal tissue without loss of underlying dermis. If the dermis and epidermis both are eroded, an ulcer forms. If an underlying loss of substance

causes the intact epidermis to become depressed, this is referred to as atrophy.

Trauma and inflammation may result in scar tissue formation, a condition in which the skin is permanently changed.

Flat lesions involve the processes described in the text that follows.

Erythroderma

When the skin is reddened because of an inflammatory response, the resulting condition is referred to as erythroderma. Erythroderma is caused by a dilation of local blood vessels, thus, the area will blanch with pressure. Erythematous skin conditions are often associated with overlying erosions, pustules, and scales. The most common causes of reddened skin are cutaneous diseases, including the various types of dermatitis and psoriasis. If the reddened skin is associated with overlying plaques and located on the elbows and knees, then psoriasis should be suspected. Drug-induced erythroderma can be caused by the penicillins, sulfonamides, phenytoin, allopurinol, and captopril. An associated constellation of clinical signs including fever, chills, and lymphadenopathy is not unusual. The presence of such signs and symptoms in the context of erythroderma indicates a possible underlying systemic condition. The most common malignancy to cause erythroderma is T-cell

lymphoma. In summary, when a patient is seen with an isolated area of erythematous skin involvement, in most cases it is the result of psoriasis or dermatitis. A detailed medical history should uncover any new medications the patient ingested just before the outbreak of reddened skin. If the erythroderma occurs in conjunction with any systemic signs or symptoms, an immediate medical work-up should be done to test for an underlying systemic pathology.

This results in the white hair, gray-blue eyes, and pinkish-white skin characteristic of OCA. A defect in the P gene produces partially expressed OCA. Significant ocular findings are present in OCA patients including strabismus, amblyopia, nystagmus, and photophobia. The prototypical local hypopigmented lesion is vitiligo, which produces a patchy loss of pigmentation. In vitiligo an absolute loss of melanocytes is present within the patch.

Figurate Skin Lesions

These erythematous skin lesions form rings or arcs, are flat and nonpalpable, and are typically red, brown, or flesh-colored. A classic example is erythema migrans, the skin rash associated with Lyme disease. This annular lesion is usually larger than 10 centimeters in diameter and is usually associated with systemic manifestations of the disease including fever, headache, photophobia, and myalgias. Syphilis is another systemic disease associated with classic figurate skin lesions, which, in this case, manifest typically on the palms of the patient’s hands and soles of the patient’s feet.

Hypopigmentation

Loss of skin pigmentation can be diffuse, bodywide, or localized. Oculocutaneous albinism (OCA) is the classic example of diffuse hypopigmentation. OCA is caused by a mutation in the tyrosinase gene. In these individuals bodywide distribution of melanocytes is present with a lack of tyrosinase enzyme activity.

Hyperpigmentation

Like hypopigmentation, hyperpigmentation can be diffuse or localized. The localized forms of hyperpigmentation are caused by either a proliferation of melanocytes or an increase in pigment production. The sudden onset of multiple pigmented skin lesions may point to an underlying malignancy, usually in the gastrointestinal (GI) tract. Proliferation of melanocytes may be benign, resulting in melanocytic nevus, or malignant, resulting in melanoma. Systemic medications such as nonsteroidal antiinflammatory drugs (NSAIDs), sulfonamides, barbiturates, and antimalarials can cause localized hyperpigmentation. Hyperpigmentation may occur in Addison’s disease, hyperthyroidism, and Cushing’s disease.

Alopecia

Hair loss may be caused by an elevation in circulating androgen hormone in women and should prompt a diligent medical workup for ovarian or adrenal gland tumor. Alopecia is a frequent side effect of medications,

including vitamin A, isotretinoin, lithium, beta-blockers, amphetamines, and the blood thinners warfarin and heparin. Systemic diseases such as lupus erythematosus, thyroid disorders, sarcoidosis, HIV/AIDS, and syphilis may be an underlying cause of alopecia.

Nonpalpable Purpura

This condition is caused by the leaking of red blood cells into the dermis. Purpura will not blanch with pressure. Trauma and sunburn are the two most common causes of nonpalpable purpura. Systemic conditions that cause thrombocytopenia and abnormal platelet function will cause nonpalpable purpura. In addition, patients on blood thinning agents tend to develop nonpalpable purpura, even with minor trauma. Nonpalpable purpura is the cause of the classic “shiner” resulting from blunt trauma to the periorbital area. The resulting extravasation of red blood cells into the soft, thin tissue surrounding the eye produces a typical “black and blue” bruising of the skin. After immediate evaluation for orbital fracture, traumatic uveitis, hyphema, retinal detachment, and globe perforation, treatment of uncomplicated periorbital purpura involves cold compresses to reduce periorbital swelling. The patient should be advised that it can take longer than 1 month for the periorbital purpura to completely resolve.

Elevated lesions involve the processes described in the text that follows.

Urticaria

These transient lesions, more commonly known as hives, are composed of an erythematous ring surrounding a central wheal (Figure 16-3). They are in-

FIGURE 16-3 ■ Urticaria, with multiple hives of varying sizes. (From Noble J: Textbook of primary care medicine, ed 3, St Louis, 2001, Mosby.

variably pruritic and often provoke an intense desire to scratch. An outbreak of hives may be very shortlived and persist for no longer than 10 to 20 minutes. In other cases urticaria can persist for such a long time that it becomes chronic. The most common cause of hives (Box 16-2) is an allergic response. Urticaria is also often provoked by exposure to heat, cold, and sunshine. Exercise and emotional stress are also related to the production of small wheals. Systemic diseases that may underlie urticaria include hyperthyroidism, malignancy, and juvenile rheumatoid arthritis. Any outbreak of hives coincident with a fever should

prompt an immediate medical evaluation for an underlying systemic disease.

Angioedema

Subcutaneous edema typically involves the skin of the eyelids and lips. Angioedema may occur with or independent of urticaria. Angioedema presents as well demarcated, localized edema deep in the skin (Figure 16-4). Precipitating factors (Box 16-3) include inhalation of animal dander and plant pollen, and ingestion of allergenic foods and drugs. Angioedema of the upper respiratory tract may be life threatening. In angioedema the deeper layers of the skin become inflamed and inundated with lymphocytes, eosinophils, and neutrophils. The local venules dilate, causing the classic ruddy color of the skin. Treatment of angioedema is predicated on the identification and removal of the offending agent, the use of systemic antihistamines and, in severe cases, systemic glucocorticoids.

Papulonodular Lesions

These conditions involve elevated and palpable lesions that coalesce to form plaques. The diagnosis of a papulonodular lesion is made primarily on the basis of color and secondarily on location.

DERMATOLOGY 207

Skin-Colored Lesions

These lesions include inclusion cysts, lipomas, rheumatoid nodules, basal cell carcinomas, and neurofibromas.

Yellow-Colored Lesions

Typically papules or plaques, these yellow-colored lesions are often caused by systemic conditions. One of the most common of the yellow lesions is the xanthoma, which is often related to hyperlipidemia.

Purple-Colored Lesions

Kaposi’s sarcoma may be associated with cutaneous, purple-colored papules and plaques. These represent vascular tumors and their presence should prompt a diligent search for HIV infection.

Red-Colored Lesions

Insect bites often result in a reddened papule. Small, bright-red and dome-shaped papules are most often cherry hemangiomas, however, that represent benign overgrowth of capillaries. Large red plaques often form across the nose and cheeks in the classic butterfly rash associated with lupus erythematosus.

Red-Brown–Colored Lesions

Sarcoidosis can produce cutaneous lesions that are red-brown in coloration. These papules or plaques occur most commonly on the face.

FIGURE 16-4 ■ Angioedema of the eyelid.

BOX 16-3

CAUSES OF ANGIOEDEMA

Severe allergy reactions (type I): Food, drugs, stinging insect venom, pollen.

Contrast dyes and aspirin caused by direct histamine release rather than immune mechanism.

Serum sickness after exposure to the following elements:

●Heterologous serum

●Animal-derived vaccines

●Drugs (penicillin, sulfonamides, thiouracils, aminosalicylic acid, streptomycin, hydantoins, cholecystographic dyes)

Adapted from Habif TP: Clinical dermatology, ed 2, St Louis, 1990, Mosby-Year Book.

Pustular Dermatoses

These eruptions of pustules are most often associated with acne and are associated with the bacteria Staphylococcus aureus and the yeast Pityrosporum. The use of systemic steroids has been linked to a bodywide pustular outbreak.

Vesicular Dermatoses

Cutaneous blisters may occur in immunologically mediated skin conditions such as pemphigus vulgaris. Contact dermatitis may stimulate the formation of vesicles, and drug sensitivity may cause bullae formation characteristic of Stevens-Johnson Syndrome (SJS), or erythema multiforme major.

SELECTED FLAT SKIN LESIONS Vitiligo

This acquired and progressive cutaneous disorder is characterized by a complete absence of melanocytes within the affected area. The condition produces symmetric and extensive areas of chalky, white depigmentation, most commonly around the eyes and lips and on the distal extremities. Vitiligo is associated with

208 CLINICAL MEDICINE IN OPTOMETRIC PRACTICE

such autoimmune disorders as hypothyroidism, Graves’ disease, pernicious anemia, and Addison’s disease. Approximately one third of patients with vitiligo have thyroid gland abnormalities, and laboratory testing in these patients usually reveals antithyroidglobulin, a circulating autoantibody. The treatment of vitiligo is problematic, but patients are typically upset about their perceived cosmetic appearance. Topical glucocorticoids are useful in cases with a mild associated inflammatory condition. UV-B light treatments have met with some limited success in reducing the overall depigmented appearance of the skin. The presentation of vitiligo should prompt a diligent medical search for the associated condition of Vogt-Koyanagi- Harada syndrome (VKH). VKH encompasses the clinical signs of facial vitiligo in a patient with meningitis, granulomatous uveitis, tinnitus, and hearing loss. In VKH an underlying autoimmune disease is directed against the melanocytes of the skin and the uveal tract. The most common symptoms associated with VKH are blurred vision, ocular pain, photophobia, a stiff neck, and nausea. Clinical signs of VKH include vomiting, syncope, alopecia, and hearing loss. VKH is most common in Japan, in women, and in young adults aged 20 to 50 years. The treatment of VKH includes topical steroids and cycloplegic agents to manage the granulomatous uveitis, and cytotoxic agents such as cyclosporine for the systemic manifestations of the disorder. A retinal referral for fluorescein angiography is mandatory in VKH to monitor for retinal atrophy and choroidal involvement.

Erythema Multiforme Minor

This cutaneous condition is characterized by one or more sharply demarcated erythematous lesions in response to an ingested drug. The lesions are known as target or iris lesions. The lesions are most commonly found on the face, lips, hands, legs, or oral mucosa. An associated burning of the skin and sore throat with malaise may be present. Repeated ingestion of the drug will tend to cause repeated outbreak of the erythematous lesions in the same location. The most common drugs that elicit this reaction include NSAIDs, sulfonamides, and barbiturates. The lesions disappear with discontinuation of the inciting medication. Should a worsening of the skin condition occur on discontinuation of drug, with blistering and a systemic mucosal reaction, then Stevens-Johnson Syndrome (SJS) must be considered.

Sturge-Weber Syndrome

This congenital cutaneous condition is characterized by one or more flat, well-demarcated reddish-purple facial lesions. Known as “port-wine staining” this

skin condition results from capillary venous angiomas of the face and is usually present at or shortly after birth. The angiomas in SWS always follow the distribution of the first branch of the trigeminal nerve (V1), and may involve branches V2 and V3 as well. SWS is part of a broader group of disorders known as the phakomatoses, the typical characteristics of which include cutaneous lesions and neurologic abnormalities. In SWS, benign facial skin angiomas are present that may also be present in the choroid of the eyes and in the meninges of the brain. Complications arise caused by the presence of choroidal angiomas that result in glaucoma, and meningeal angiomas that result in childhood headaches, seizures, epilepsy, hemiparesis, developmental delay, and mental retardation. Visual fields may reveal neurologic-related hemianopsia and glaucomatoustype defects. All children seen with port-wine staining should have a complete ocular and neurologic evaluation. The eye exam should be directed at uncovering the presence of choroidal hemangiomas and related glaucoma. Treatment of the glaucoma component of SWS is best achieved with a topical prostaglandin analog, because these medications bypass the very episcleral venous system the vascular anomaly of which causes the elevated intraocular pressure. A neurologic evaluation requires neuroimaging to uncover meningeal angiomas through use of a magnetic resonance imaging (MRI) or computed tomography (CT) scan. Seizures are treated with anticonvulsant drugs such as carbamazepine, phenytoin, and topiramate. Neurosurgical intervention may be necessary in cases of unrelenting seizure activity. Pulsed-dye laser therapy is effective in the amelioration of facial port-wine staining and is often necessary to improve the patient’s self-image and confidence.

Nevus

This cutaneous disorder is produced by a proliferation of melanocytes, whereas the common “freckle,” or “ephelis,” is caused by an enlargement of the melanocytes. The nevus has a definite relationship to sun exposure, particularly in the adult. Melanocytic nevi can be grouped into three general categories: (1) the dysplastic nevus, or atypical mole; (2) the congenital melanocytic nevus, that ranges in size from small to medium to giant (greater than 20 cm in diameter); and

(3) the acquired nevus (Table 16-1).

Benign acquired nevi are typically a uniform brown or tan, and have a round shape with sharp, well-delineated borders. Acquired nevi are usually flat, but some noticeable elevation is possible. These benign skin lesions are usually less than 6 mm in

diameter and number from 10 to 40 in the typical adult. Acquired nevi may be present anywhere on the skin and are found most often on sun-exposed areas of the body. The least involved areas are the scalp, breasts, and buttocks. Benign nevi are present in 85% of the world’s population.

Dysplastic nevi are atypical moles that are precursors for melanoma (Box 16-4). Dysplastic nevi are transmitted through family members by an autosomal dominant trait involving chromosome 9p16. From one to hundreds of dysplastic nevi may be present on a single individual. Atypical moles have hazy and indistinct borders, and the border pigment may fade off into the surrounding skin. Dysplastic nevi possess variable pigmentation within the lesion, and colors may range from tan, brown, and black to red and pink, all within a single nevus (Figure 16-5). Atypical moles are usually larger than 6 mm in size, and can even reach diameters of 10 mm or more. When dysplastic nevi are present, often more than a hundred are present on a single individual. They are most commonly located on sun-exposed areas of the body, but unlike benign acquired nevi, dysplastic nevi may be present on the scalp, breasts, and buttocks.

Congenital melanocytic nevi are differentiated on the basis of size. The giant congenital melanocytic nevus and small congenital melanocytic nevus are less frequent precursors of melanoma than the dysplastic nevus. Congenital melanocytic nevi are present at birth or shortly after delivery. The giant form can cover half the body, and characteristically have sharp borders and associated hair. The small and medium congenital melanocytic nevi can be slightly raised, are dark brown in color, and have a smooth surface.

TABLE 16-1 CLINICAL CHARACTERISTICS OF NEVI

DERMATOLOGY 209

BOX 16-4

CLINICAL CHARACTERISTICS

OF DYSPLASTIC NEVI

Simultaneously flat and elevated Pebbled or “fried egg” surface Haphazard colors

Regular or irregular borders Symmetric or asymmetric shape “Macular tan shoulder”

No hypertrichosis

FIGURE 16-5 ■ Dysplastic nevi. (From Goldman L, Ausiello D: Cecil textbook of medicine, ed 22, Philadelphia, 2004, W.B. Saunders.)

Biopsy of a nevus is necessary in all cases in which detectable growth or changes in shape of the lesion have occurred.

Several other benign nevi can masquerade as melanoma, and both appearance and biopsy are necessary for differentiation. These nevi have been well described by Finberg. Color is a major discriminating characteristic and serves to classify the pigmented lesions that must be distinguished from cutaneous melanoma into two varieties: blue and brown.

210 CLINICAL MEDICINE IN OPTOMETRIC PRACTICE

The blue nevus is seen as a cerulean blue or gunmetal color. This bluish gray lesion, which does not grow over time and ranges in size from 3 mm to 1 cm, typically occurs on the hands and feet. A domeshaped, reddish-purple, or blue nodule that blanches from pressure is a hemangioma. The hemangioma is easily confused with a nodular melanoma.

Four brown cutaneous lesions appear similar to cutaneous melanoma: the compound and junctional nevi, and the juvenile and solar lentigines. The round or oval-shaped compound nevus has well-demarcated borders. This dome-shaped lesion ranges in color from flesh-colored to dark brown, and within a single lesion the colors do not tend to vary (Figure 16-6). Another brown lesion is the junctional nevus, which is flat or barely elevated and has sharp borders (Figure 16-7). The junctional nevus differs from the compound nevus in its stippled pigmentary appearance. The dermal nevus is the most elevated of all nevi, and is attached to the underlying dermis by a stalk (Figure 16-8). These nevi often have associated hair and a lobulated appearance. Juvenile and solar lentigines are freckles acquired after birth or from sun exposure. These brown lesions also have sharp borders and measure from 2 mm to larger than 1 cm. The solar lentigo occurs most often on sun exposed areas of the skin. The freckle results from

FIGURE 16-6 ■ Compound nevus, with elevated contour, slightly lobulated surface, and regular borders. (From Bolognia JL, Jorizzo JL, Rapini RP: Dermatology, St Louis, 2003, Mosby.)

FIGURE 16-7 ■ Junction nevus, with smooth surface, regular borders, and little elevation. (From Bolognia JL, Jorizzo JL, Rapini RP: Dermatology, St Louis, 2003, Mosby.)

an enlargement of the melanocytes within the basal layer and it has no malignant potential.

Melanoma

This cutaneous malignancy results from a proliferation of melanocytes. Cutaneous melanomas may be deadly, and must be distinguished from the benign skin lesions listed above. There are several factors that raise the suspicion of malignancy (Box 16-5). More than 45,000 new cases of skin melanoma are diagnosed each year in the United States. Every year more than 7000 people in the United States die of skin melanoma. The tumor occurs at any age and is most common in fairskinned, blond-haired, blue-eyed individuals with freckles. Melanoma is increasing in prevalence, most likely because of increased sun exposure and a weakening ozone layer in the atmosphere. At present rates, by the year 2010, the lifetime risk of melanoma is expected to be greater than 1% (Table 16-2). According to Finberg, four types of skin melanoma exist, and three of these spread radially first, before becoming deeply invasive. Lentigo maligna melanoma, a brown or tan lesion, occurs most frequently on the sun-exposed surfaces of the cheek and temple in patients who are 70 years or older (Box 16-6). This lesion has a good prognosis and patients are expected to survive 5 to

FIGURE 16-8 ■ Dermal nevus, with marked elevation, lobulated surface, and broad attachment (From Goldman L, Ausiello D: Cecil textbook of medicine, ed 22, Philadelphia, 2004, W.B. Saunders.)

20 years or longer (Figure 16-9). Superficial spreading melanoma, a brown or bluish-red lesion, may have a part that is elevated and occurs at any site in patients typically ages 40 to 50 years (Box 16-7). This lesion has a poorer prognosis, with expected survival of 1 to 7 years (Figure 16-10). Nodular melanoma is a reddishblue mixed with brown lesion occurring at any site in patients aged 40 to 50 years (Box 16-8). These patients have a poor prognosis, with expected survivorship from months to less than 5 years (Figure 16-11). The

TABLE 16-2 RELATIVE RISKS OF MALIGNANT MELANOMA

Adapted from Rhodes AR, et al: Risk factors for cutaneous melanoma: a practical method of recognizing predisposed individuals, JAMA 258:3146, 1987.

BOX 16-6

CHARACTERISTICS OF LENTIGO MALIGNA MELANOMA

Color

●Usually variants of tan or brown

●White, gray-white (regression)

●Reticulated or flecked brown or black

●Variegation of colors

Borders

●Irregular everywhere on lesion

●Extremely convoluted

●Surface characteristics

●Perfectly flat when lentigo maligna

●Largest surface area of melanomas

Signs of invasion

●Irregular surface

●Elevation

●Nodule (brown, black, blue-black)

FIGURE 16-9 ■ Lentigo maligna melanoma, with irregular, flat areas of lentigo maligna (Hutchinson’s freckle) and nodule with friable surface. (From Yanoff M: Ophthalmology, ed 2, St Louis, 2004, Mosby.)

fourth type of melanoma is acral-lentiginous melanoma, which typically occurs on the palms or soles of the feet in patients aged 60 years or older. This melanoma is seen as a flat, dark-brown lesion, but may occur as raised plaques that appear bluish-black. These patients have an expected survival of 1 to 10 years. Patients who observe suspicious moles will note an increase in size or a change in color before the melanoma is ultimately diagnosed. Many cutaneous lesions can be confused for malignant melanoma (Box 16-9). The likelihood of metastases is correlated to thickness of the tumor, with a low-risk tumor having a thickness less than a millimeter. Of patients with melanomas greater than 4 mm in thickness, half of these individuals will develop metastases and die. Tumor satellites

BOX 16-7

CHARACTERISTICS OF SUPERFICIAL SPREADING MELANOMA

Color variegation

●Tan, brown, dark brown

●Pink, rose, red (inflammation)

●Blue, blue-gray, purple

●White (regression)

●Haphazard arrangement of colors

●Disorganized combinations of brown

Borders

●Circular outline

●Usually irregular

●Increasing irregularity with enlargement

●Margins often elevated, palpable

Surface

●Irregularly elevated, palpable

●Possible nodules (pink-gray, dark gray)

●Possible yellow-brown, warty surface

FIGURE 16-10 ■ Superficial spreading malignant melanoma, with regression and nodule development. (From Townsend C, et al: Sabiston textbook of surgery, ed 17, Philadelphia, 2004, W.B. Saunders.)

typically occur in the dermis or subcutaneous fat near the melanoma. The presence of these satellites tends to indicate spread to the regional lymph nodes. From here the melanomas spread by the lymphatic channels or into the bloodstream. Target organs for spread of melanoma include the liver, bone, lungs, brain, and anterior chamber of the eye. Metastasis of the melanoma has a low cure rate. Prevention of melanoma involves the use of sun block on all individuals in all stages of life. In addition, patients should be educated on the evaluation of atypical moles, and the characteristics that raise suspicion of melanoma. A wide surgi-

BOX 16-8

CHARACTERISTICS OF NODULAR MELANOMA

Color Blue-gray Purple-blue

“Thundercloud gray” Blue-black Reddish-blue Rose-gray

Black

Pale gray-blue (amelanotic) Contour

Spherical

Polypoid

Nodule (elevated)

No flat component to the nodule Often symmetrical shape

Elevated, irregular, blue-black plaque (rare) Surface

Smooth Ulcerated

Hyperkeratotic (uncommon) Irregular (uncommon)

DERMATOLOGY 213

BOX 16-9

DIFFERENTIAL DIAGNOSIS OF MALIGNANT MELANOMA

Acquired nevi

Junction nevus

Compound nevus

Dermal nevus

Blue nevus

Halo nevus

Spitz nevus (benign juvenile melanoma)

Dysplastic nevus

Lentigo

Lentigo simplex

Solar lentigo

Dermatofibroma

Pigmented seborrheic keratosis

Pigmented actinic keratosis

Pigmented basal cell carcinoma

Merkel cell carcinoma

Hemangioma

Hemorrhage into cyst, nevus, or nailbed

Kaposi’s sarcoma

Ulcerated pyogenic granuloma

curable, with survival limited to less than a year. Metastases to the brain are treated with radiation and glucocorticoids for reduction of symptomology.

FIGURE 16-11 ■ Nodular melanoma, with surrounding flat component. (From Townsend C, et al: Sabiston textbook of surgery, ed 17, Philadelphia, 2004, W.B. Saunders.)

cal excision is necessary to remove all elements of the cutaneous melanoma. Regional node dissection can confirm spread to the lymphatic system, and surgical excision of the nodal micrometastases may reduce the risk of spread and improve survival. In patients with nodal spread of their melanoma, high-dose interferon has been shown to be effective in some cases after surgical excision. Metastatic melanoma is considered in-

SELECTED ELEVATED SKIN LESIONS Benign Cutaneous Lesions

Atopic Dermatitis

This cutaneous response is an expression of hypersensitivity without known physical contact with an environmental allergen. Atopy is a cutaneous form of allergic response to exogenous substances in genetically susceptible individuals. If both parents have atopic dermatitis (AD), then more than 80% of their children will develop the condition. AD is very common, occurring in 2% of the human population. AD occurs most often in childhood and in patients with a family history of asthma, hay fever, or dermatitis. Of children with AD, 80% ultimately develop asthma or allergic rhinitis later in life. In fact, nearly one fourth of all Norwegian school children have atopic dermatitis. The disease is immunologically characterized by a decrease in T-lymphocyte cellular immunity and an abnormal and elevated immunoglobulin E (IgE) antibody response. The lesions appear anywhere on the skin as patchy scales. In the acute phase crusts, erythema, and fine scaling of the skin with indistinct borders is present. In the chronic stage lichenification, or thickening, of the skin caused by rubbing or scratching is present. The most common complaint among patients with AD is itching. The most common sites of