Disorders of the Sweat Glands

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Chapter 653 Disorders of the Sweat Glands

Joseph G. Morelli

Eccrine glands are found over nearly the entire skin surface and provide the primary means, through evaporation of the water in sweat, of cooling the body. These glands have no anatomic relationship to hair follicles and secrete a relatively large amount of odorless aqueous sweat. In contrast, apocrine sweat glands are limited in distribution to the axillae, anogenital skin, mammary glands, ceruminous glands of the ear, Moll glands in the eyelid, and selected areas of the face and scalp. Each apocrine gland duct enters the pilosebaceous follicle at the level of the infundibulum and secretes a small amount of a complex, viscous fluid that, on alteration by microorganisms, produces a distinctive body odor. Some disorders of these two types of sweat glands are similar pathogenetically, whereas others are unique to a given gland.

Anhidrosis

Neuropathic anhidrosis results from a disturbance in the neural pathway from the control center in the brain to the peripheral efferent nerve fibers that activate sweating. Disorders in this category, which are characterized by generalized anhidrosis, include tumors of the hypothalamus and damage to the floor of the 3rd ventricle. Pontine or medullary lesions may produce anhidrosis of the ipsilateral face or neck and ipsilateral or contralateral anhidrosis of the rest of the body. Peripheral or segmental neuropathies, caused by leprosy, amyloidosis, diabetes mellitus, alcoholic neuritis, or syringomyelia, may be associated with anhidrosis of the innervated skin. Various autonomic disorders are also associated with altered eccrine sweat gland function.

At the level of the sweat gland, anticholinergics (drugs such as atropine and scopolamine) may paralyze the sweat glands. Acute intoxication with barbiturates or diazepam has produced necrosis of sweat glands, resulting in anhidrosis with or without erythema and bullae. Eccrine glands are largely absent throughout the skin or are present in a localized area among patients with anhidrotic ectodermal dysplasia or localized congenital absence of sweat glands, respectively. Infiltrative or destructive disorders that may produce atrophy of sweat glands by pressure or scarring include scleroderma, acrodermatitis chronica atrophicans, radiodermatitis, burns, Sjögren syndrome, multiple myeloma, and lymphoma. Obstruction of sweat glands may occur in miliaria and in a number of inflammatory and hyperkeratotic disorders, such as the ichthyoses, psoriasis, lichen planus, pemphigus, porokeratosis, atopic dermatitis, and seborrheic dermatitis. Occlusion of the sweat pore may also occur with the topical agents aluminum and zirconium salts, formaldehyde, or glutaraldehyde.

Diverse disorders that are associated with anhidrosis by unknown mechanisms include dehydration; toxic overdose with lead, arsenic, thallium, fluorine, or morphine; uremia; cirrhosis; endocrine disorders such as Addison disease, diabetes mellitus, diabetes insipidus, and hyperthyroidism; and inherited conditions such as Fabry disease, Franceschetti-Jadassohn syndrome, which combines features of incontinentia pigmenti and anhidrotic ectodermal dysplasia, and familial anhidrosis with neurolabyrinthitis.

Anhidrosis may be complete, but in many cases, what appears clinically to be anhidrosis is actually hypohidrosis caused by anhidrosis of many but not all eccrine glands. Compensatory, localized hyperhidrosis of the remaining functional sweat glands may occur, particularly in diabetes mellitus and miliaria. The primary complication of anhidrosis is hyperthermia, seen primarily in anhidrotic ectodermal dysplasia or in otherwise normal preterm or full-term neonates who have immature eccrine glands.

Hyperhidrosis

Etiology/Pathogenesis

Hyperhidrosis is excessive sweating beyond what is physiologically necessary for temperature control and occurs in 3% of the population with about half having axillary hyperhidrosis. The numerous disorders that may be associated with increased production of eccrine sweat may also be classified into those with neural mechanisms involving an abnormality in the pathway from the neural regulatory centers to the sweat gland and those that are non-neurally mediated and occur by direct effects on the sweat glands (Table 653-1).

Table 653-1 CAUSES OF HYPERHIDROSIS

CORTICAL

Familial dysautonomia

Congenital ichthyosiform erythroderma

Epidermolysis bullosa

Nail-patella syndrome

Jadassohn-Lewandowsky syndrome

Pachyonychia congenita

Palmoplantar keratoderma

HYPOTHALAMIC

Chronic illness

Diabetes mellitus

Hyperpituitarism

Hyperthyroidism

Infantile scurvy

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