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INTRODUCTION

The skin, the largest organ in the body, includes 3 primary component layers: the epidermis, which is an epithelial layer; the dermis, which provides structural support and vascular supply and contains hair follicles, sweat glands, nerves, and other structures; and the subcutis, which is composed primarily of adipose tissue. Together, these structures play many roles including interface with the external environment, temperature regulation, endocrine function, sensory input, waste excretion, and sexual function. Diseases of the skin may affect any of these functions, and it is important to consider such potential complications when planning management.

The outermost skin layer, the stratum corneum, prevents desiccation of the body in a dry atmosphere. Extensive burns, drug-induced skin necrosis (eg, toxic epidermal necrolysis), and other extensive blistering disorders represent situations in which the barrier is breached, leading to increased morbidity and mortality. In addition to providing a physical barrier to infection, the skin is an important component of the body’s immune system. Resident Langerhans cells provide immune surveillance, presenting antigens that activate lymphocytic responses.

The major endocrine function of the skin is the isomerization of provitamin D to vitamin D3, which is transported to the liver and then to the kidneys for sequential hydroxylations to form the active hormone, 1,25-dihydroxyvitamin D3. Sun exposure for the production of active vitamin D must be balanced with the risk of ultraviolet radiation–induced DNA damage. Exposure of normal keratinocytes to ultraviolet radiation causes mutations in tumor-suppressor genes, while epidermal melanin impedes transmission of ultraviolet rays. Patients with albinism who have a significant decrease in epidermal melanin have an increased risk of developing ultraviolet-induced malignancies, particularly basal cell carcinomas and squamous cell carcinomas. In patients with xeroderma pigmentosum, the repair system after ultraviolet DNA damage is defective, leading to a dramatically increased risk of cutaneous sun-induced tumors in these patients as well.

The skin’s role in thermoregulation is mediated by 2 mechanisms: evaporation of sweat secreted in response to autonomic stimuli, and shunting of blood flow to and from the skin to preserve heat or to disperse it into the environment through peripheral vasomotor control. During heat stress, the failure to sweat can lead to excessive body temperature, vasodilatation, and resultant hypovolemic shock. This may occur in genetic disorders of eccrine gland morphogenesis, such as hypohidrotic ectodermal dysplasia, or may be acquired in conditions in which eccrine ducts are destroyed or obstructed such as certain ichthyoses, atopic dermatitis associated with thick scale, and sclerotic conditions of the skin. Importantly, young infants, particularly those born prematurely, have not yet developed full capacity to sweat. In patients with cystic fibrosis, the normally hypotonic sweat becomes hypertonic, and therefore, thermal stress can induce dehydration.

The skin provides an important afferent limb to the nervous system in the interface with the external world through sensory perceptions of touch, pressure, itch, and pain. Skin, hair, and nails are highly visible ...

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