Acquired anhidrosis and/or hypohidrosis Type CU

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Acquired anhidrosis and/or hypohidrosis Type CU

Acquired anhidrosis and/or hypohidrosis Type CU is a type of Cholinergic urticaria which refers to those who have abnormally reduced sweating.[1]

Signs and symptoms

Severe heat intolerance (e.g., nausea, dizziness, and headache), and tingling, pricking, pinchy or burning pain over the entire body on exposure to hot environments or prolonged exercise which improve after cooling the body. Occurs in the absence of any causative skin, metabolic, or neurological disorders.[2]


The wheals, hypohidrosis, and pain seems to result from the low expression levels of acetylcholinesterase (AchE) and cholinergic receptor, muscarinic 3 (CHRM3) in the eccrine gland epithelial cells.[3]

Elevated expression levels of CCL2/MCP-1, CCL5/RANTES and CCL17/TARC which result in chemoattracted CD4+ and CD8+ T cell populations to the surrounding area may be responsible for exerting a downmodulatory effect on the AchE and CHRM3 expressions.[citation needed]

Corticosteroid inhibits the expressions of CCL2/MCP-1, CCL5/RANTES and CCL17/TARC. This further support the notion that CCL2/MCP-1, CCL5/RANTES and CCL17/TARC play a crucial role.[citation needed]


Sweat is readily visualized by a topical indicator such as iodinated starch or sodium alizarin sulphonate. Both undergo a dramatic colour change when moistened by sweat. A thermoregulatory sweat test evaluates the body's response to a thermal stimulus by inducing sweating through the use of a hot box ⁄ room, thermal blanket or exercise. Failure of the topical indicator to undergo a colour change during thermoregulatory sweat testing can indicate anhidrosis and/or hypohidrosis (see Minor test).[4]

A skin biopsy may reveal cellular infiltrates in sweat glands or ducts.[citation needed]


  • First-line treatment: H1RAs are first-line therapy for patients with CholU, but many patients show only a mild to moderate response to standard H1RA doses. The addition of an H2RA was reported to be effective in patients with refractory CholU that was unresponsive to up-dosing of an H1RA. Other studies have demonstrated the efficacy of scopolamine butylbromide (an anticholinergic agent); combinations of propranolol (a b2-adrenergic blocker), antihistamines, and montelukast; and treatment and injection with botulinum toxin. [5]
  • Non-pharmacological treatment: In the absence of sweat, cold-water sprays and wet towels can be used to increase the evaporative loss of heat from the skin. Shifting to a cooler or air-conditioned environments when necessary can also reduce discomfort. In the event of severe hyperthermia (body temperature >106 °F/41 °C), drastic measures such as immersion in ice-cold water are necessary to prevent irreversible brain damage.[6]


  1. "Cholinergic Urticaria: Background, Pathophysiology, Etiology". 2021-02-12. Archived from the original on 2018-08-25. Retrieved 27 June 2021.
  2. Nakazato, Y.; Tamura, N.; Ohkuma, A.; Yoshimaru, K.; Shimazu, K. (2004). "Idiopathic pure sudomotor failure: Anhidrosis due to deficits in cholinergic transmission". Neurology. 63 (8): 1476–1480. doi:10.1212/01.wnl.0000142036.54112.57. PMID 15505168.
  3. Sawada, Y.; Nakamura, M.; Bito, T.; Sakabe, J. I.; Kabashima-Kubo, R.; Hino, R.; Kobayashi, M.; Tokura, Y. (2013). "Decreased Expression of Acetylcholine Esterase in Cholinergic Urticaria with Hypohidrosis or Anhidrosis". Journal of Investigative Dermatology. 134 (1): 276–9. doi:10.1038/jid.2013.244. PMID 23748235.
  4. Chia, K. Y.; Tey, H. L. (2012). "Approach to hypohidrosis". Journal of the European Academy of Dermatology and Venereology. 27 (7): 799–804. doi:10.1111/jdv.12014. PMID 23094789.
  5. doi=10.1007/s10286-017-0418-6
  6. Thami, G. P.; Kaur, S.; Kanwar, A. J. (2003). "Acquired idiopathic generalized anhidrosis: A rare cause of heat intolerance". Clinical and Experimental Dermatology. 28 (3): 262–264. doi:10.1046/j.1365-2230.2003.01208.x. PMID 12780708.