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Eccrine and apocrine glands represent the two major types of sweat glands (see Fig. 91.1 ).
Functional from birth and activated by thermal stimuli via the hypothalamic sweat center; while their major function is thermoregulation by evaporative heat loss, they are also activated by emotional stimuli.
Innervated by sympathetic fibers that have acetylcholine as their major neurotransmitter.
Generalized distribution, with greatest concentration on the palms and soles.
The eccrine duct opens directly onto the skin surface, and the excretory product is a clear hypotonic fluid that is mostly water but also contains NaCl.
Unclear function in humans; functional development requires androgens.
More limited distribution – primarily axillae, nipples/areolae, and umbilical and anogenital regions; modified apocrine glands are found in the external auditory canals and eyelid margins.
The apocrine duct drains into the superficial portion of the hair follicle (see Fig. 91.1 ).
“Decapitation” of apocrine gland cells produces an odorless and viscous fluid; however, its degradation by flora on the skin surface can lead to an odor.
Excessive production of eccrine sweat is usually due to primary cortical (emotional) hyperhidrosis and the favored sites are the axillae or palms and soles ( Fig. 32.1 ) > the face ( Fig. 32.2 ); involvement is bilateral and symmetric ( Fig. 32.3 ).
Secondary cortical hyperhidrosis is associated with genodermatoses, including palmoplantar keratodermas and epidermolysis bullosa simplex; associated odor reflects maceration and degradation of keratin by bacteria.
Secondary hypothalamic (thermoregulatory) hyperhidrosis can be due to a number of systemic diseases, from infections to neoplasms ( Table 32.1 ).
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Secondary medullary (gustatory) hyperhidrosis can be physiologic as exemplified by the facial sweating that occurs with spicy foods, or pathologic as occurs in Frey syndrome ( Fig. 32.4 ); in the former, taste receptors send afferent impulses, whereas in the latter, disrupted nerves for sweat aberrantly connect with nerves for salivation.
Injuries or diseases affecting the spinal cord can result in segmental hyperhidrosis.
In addition to embarrassment, hyperhidrosis can lead to overhydration of the skin and a higher risk of bacterial and fungal infections.
Sweating only during waking hours points to primary cortical (emotional) hyperhidrosis; after consideration of possible underlying etiologies, topical antiperspirants containing aluminum chloride (e.g. Certain Dri®) or aluminum chloride hexahydrate (e.g. Xerac™ AC [6.25%], Drysol® [20%]) can be applied at bedtime, and if necessary, initially preceded by oral glycopyrrolate or oxybutynin. A glycopyrronium-containing cloth can also be applied daily.
Injection of botulinum toxin type A every ∼6 months is very effective for primary cortical (emotional) hyperhidrosis ( Fig. 32.5 ); tap water iontophoresis is less effective.
There are multiple etiologies of hypohidrosis and anhidrosis including the following:
A side effect of medications with anticholinergic properties (e.g. atropine, tricyclic antidepressants, glycopyrrolate)
Manifestation of inherited disorders, in particular ectodermal dysplasias (see Ch. 52 ), as well as acquired disorders such as Sjögren syndrome
Neurologic disorders, from tumors or infarcts of the hypothalamus, pons or medulla to peripheral neuropathies
Rarely, and primarily in Asians, due to acquired idiopathic generalized anhidrosis
Increased risk of developing hyperthermia.
Evaluation includes colorimetric testing (see Fig. 32.5 ) and biopsy of affected skin.
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