Anhidrosis is the inability to sweat. It can occur as a congenital (autosomal, recessive congenital insensitivity to pain with anhidrosis) or acquired disorder and in generalized or localized form. In generalized form, it is a potentially life-threatening disorder due to the associated developing body hyperthermia and heat intolerance. Local anhidrosis is usually compensated. Anhidrosis is caused by (a) peripheral eccrine sweat gland alterations [congenital (ectodermal dysplasias, incontinentia pigmenti, Bazex-Dupré-Christol syndrome, Fabry disease) or acquired (destruction from tumors, burns, radiation therapy, systemic sclerosis, morphea, Sjögren syndrome, graft-versus-host disease, acrodermatitis chronica atrophicans; obstruction from miliaria, ichthyoses, psoriasis, eczematous dermatoses, bullous diseases; chemical blockade of a selected sympathetic ganglion)] and (b) central or neuropathic diseases and/or medication that disrupt neural inputs to the gland [tumors or infarctions of the hypothalamus, pons, medulla, spinal cord; injuries or infarction; Horner syndrome; degenerative syndromes (Rosah syndrome, Shy-Drager syndrome), autoimmune autonomic neuropathy, peripheral neuropathy (diabetes, alcoholism, leprosy); drugs]. Idiopathic anhidrosis constitutes a third classification group. The term “hypohidrosis” defines a milder variant with diminished sweating.
Treatment options are limited to management, i.e., maintaining a cool environment for the patient and use of water spray bottles for cooling. For disorders due to clogged sweat glands, frequent and gentle exfoliation is useful. For disorders of cornification more aggressive exfoliation and close monitoring are required (Table 74.1). Drug-induced anhidrosis is usually reversible with discontinuation of the medication (Table 74.2). Control of peripheral neuropathy-inducing disorders may prevent worsening of anhidrosis severity.
++ Table Graphic Jump Location Table 74-1Anhidrosis Treatment ||Download (.pdf) Table 74-1 Anhidrosis Treatment
|MEDICATION NAME ||INDICATION ||MECHANISM OF ACTION ||DOSING ||ADVERSE EFFECTS ||SUGGESTED MONITORING ||LEVEL OF EVIDENCE (REFERENCE) |
|Topical Therapy |
|Tazarotenea ||Psoriasis-induced ESGOb ||Keratolytic agent ||0.05% and 0.1% cream; apply OD ||Skin irritation (>1%) ||None ||IA1 |
|Urea ||Eczema-induced ESGOb ||Keratolytic agent ||20% cream BD ||Skin irritation (<1%) ||None ||IIA2 |
|Systemic Therapy |
|Acitretin ||Ichthyosis-induced ESGOb ||Anti-inflammatory, antimicrobial ||0.25-0.5 mg kg/bw QD ||Teratogenic, skin dryness, nausea, increased lipids and liver enzymes ||CBC, CMP, serum liver enzymes and lipids, pregnancy testc ||IIA3 |
Levels of evidence are based on the Journal of the American Academy of Dermatology guidelines: level IA includes evidence from meta-analysis of randomized controlled trials; level IB includes evidence from ≥1 randomized controlled trial; level IIA includes evidence from ≥1 controlled studies without randomization; level IIB includes evidence from ≥1 other type of experimental study; level III includes evidence from nonexperimental descriptive studies, such as comparative studies, correlation studies, and case control studies; and level IV includes evidence from expert committee reports or opinions or clinical experience of respected authorities, or both.