Dynamic Analysis of Histamine-Mediated Attenuation of Acetylcholine-Induced Sweating via GSK3β Activation

Matsui, Saki; Murota, Hiroyuki; Takahashi, Aya; Yang, Lingli; Lee, Jeong‐Beom; Omiya, Kouta; Ohmi, Masato; Kikuta, Junichi; Ishii, Masaru; Katayama, Ichiro

doi:10.1038/jid.2013.323

Cited by 41 publications

(48 citation statements)

References 48 publications

(48 reference statements)

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“…This effect of histamine was inhibited by a type 1-histamine receptor antagonist (5). Thus, the favourable effect of AH on the cases of patients with IPSF presented here might provide further evidence for our previous report (5). As previously mentioned, the treatment options for IPSF are limited and systemic steroid therapy has been applied to cases without spontaneous remission.…”

Section: Discussionsupporting

confidence: 82%

“…Recently, we found that the inhibitory effect of histamine on acetylcholine-induced sweating occurred via phosphorylation of glycogen synthesis kinase 3β in sweat gland acinar cells (5). This effect of histamine was inhibited by a type 1-histamine receptor antagonist (5).…”

Section: Discussionmentioning

confidence: 99%

“…Classical sedative AH that have an anticholinergic effect (6) should be avoided because this may reduce the acetylcholine-mediated sweating. In an animal study, the classical AH pyrilamine was confirmed to attenuate acetylcholine-induced sweating (5). To prove the efficacy of the more recently developed 2 nd generation AH in humans, double-blind, placebo-controlled randomised studies will be necessary in the future.…”

Section: Discussionmentioning

confidence: 99%

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Idiopathic Pure Sudomotor Failure Responding to Oral Antihistamine with Sweating Activities

Suma¹,

Murota²,

Kitaba³

et al. 2014

Acta Derm Venerol

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Idiopathic pure sudomotor failure (IPSF) is characterised by diminished sweating with sudomotor stimuli, causes hyperthermia, dry skin, and itch or tingling of the skin surface, and severely impairs patients' quality of life. The treatment options for IPSF are limited. Systemic corticosteroid has been used (1, 2), but it is not consistently effective (3). Here, we present 2 cases of patients with IPSF who responded to oral antihistamine treatment with sweating activity. CASE REPORTSCase 1. A 32-year-old male construction worker suffered from general fatigue accompanied by abnormal skin sensations, such as tingling sensation and itch after exposure to a warm environment at his work place that began in the spring. He was diagnosed with IPSF at another clinic on the basis of blood test results. Steroid pulse therapy (500 mg/day for 3 consecutive days) was given twice in one month, but did not provide a therapeutic benefit. Five months after the diagnosis of acquired idiopathic generalised anhidrosis (AIGA), the patient consulted our clinic. He had no history of cholinergic urticaria. At the first visit his body temperature was 37.0°C, and his blood levels of thyroid-stimulating hormone, free thyroxine, free triiodothyronine, immunoglobulin E, urinic acid, and HgbA1c were within normal limits. Anti-acetylcholine receptor antibody, anti-SSA antibody, and anti-SSB antibody were not detected in his serum. The result of the quantitative sudomotor axon reflex test (QSART), performed on the patient's forearm, was 0.025 mg/5 min [mean evaluation value from 26 healthy volunteers is 1.13 mg/5 min (range 0.495-4.54)], which is compatible with a diagnosis of anhidrosis. Sweat testing using minor methods (at 30ºC and 60% humidity) revealed anhidrosis on almost his entire body (Fig. 1a). Skin tissue samples were obtained from both lesional (anhidrosis) and non-lesional skin. Lymphocytic infiltration around the sweat gland and hyperkeratosis of the sweat pores were observed in both lesional and non-lesional areas (Fig. 1b, c). We assigned a diagnosis of IPSF in this case because there were no neurological signs. The first therapeutic strategy we tried, topical urea and steroid application, did not yield any improvement (Fig. S1 1 ). Next, to improve the subjective symptom of itch and tingling sensation of the skin, oral antihistamine (AH; fexofenadine) was administered at a normal dose (120 mg/day), which was gradually increased up to 3-fold the normal dose. A few days after initiation of the increased AH dose, the patient's subjective symptoms were improving (Fig. S1 1 ). We recommended the patient to engage gradually in activities that would produce sweating, such as labour or exercise, while taking AH. With this regimen, the patient can now spend his daily life without serious problems in a warm environment. By the spring and summer following his diagnosis and treatment with 240 mg/day of oral AH, his condition in the workplace was better maintained compared with his condition at the initiation of treatment. Results of QSART pe...

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Idiopathic Pure Sudomotor Failure Responding to Oral Antihistamine with Sweating Activities

Suma¹,

Murota²,

Kitaba³

et al. 2014

Acta Derm Venerol

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“…Histamine is a factor common to both pathological conditions. It plays a major role in the pathogenesis of urticaria and also inhibits acetylcholine‐induced sweating . Through histamine H1 receptors, histamine inhibits secretion of sweat from secretory cells of sweat glands to suppress sudomotor activity .…”

Section: Treatment and Clinical Questionsmentioning

confidence: 99%

Revised guideline for the diagnosis and treatment of acquired idiopathic generalized anhidrosis in Japan

Munetsugu

Fujimoto

Oshima

et al. 2016

The Journal of Dermatology

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131

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Acquired idiopathic generalized anhidrosis (AIGA) is characterized by an acquired impairment in total body sweating despite exposure to heat or exercise. Severe cases may result in heatstroke. Most cases of AIGA have been reported in Asia, especially in Japan. However, there is limited information on the epidemiology of this condition, and no diagnostic criteria or appropriate treatment options have been established. This guideline was developed to fill this gap. It contains information on the etiology, diagnosis, evaluation of disease severity and evidencebased recommendations for the treatment of AIGA. Appropriate treatment according to disease severity may relieve the clinical manifestations and emotional distress experienced by patients with AIGA.

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“…Beyond unambiguously showing aggravation of histamine-induced neurogenic flare starting at 2 min post-histamine pricks and lasting throughout the assessment period, this study also showed a significantly increased sudomotor activity on the fingertips during the conditioning pain stimulation indicative of increased sympathetic efferent fiber activity. The decrease in skin conductance within the prick area suggests a local histamine-induced desiccation of the skin immediately around the prick site (which was offset by a slight increase evoked by pressure conditioning stimulation), in line with the known hypohydrotic effect of histamine (Matsui et al 2014a(Matsui et al , 2014bMurota et al 2015).…”

Section: The Neurogenic Inflammatory Response Is Increased By Heterotmentioning

confidence: 58%

Conditioning pain stimulation does not affect itch induced by intra-epidermal histamine pricks but aggravates neurogenic inflammation in healthy volunteers

Andersen

Imai

Petersen

et al. 2016

Somatosensory & Motor Research

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This study investigated whether itch induced by intra-epidermal histamine is subjected to modulation by a standardized conditioned pain modulation (CPM) paradigm in 24 healthy volunteers. CPM was induced by computer-controlled cuff pressure algometry and histamine was introduced to the volar forearm by skin prick test punctures. Moreover, neurogenic inflammation and wheal reactions induced by histamine and autonomic nervous system responses (heart rate variability and skin conductance) were monitored. CPM did not modulate the intensity of histamine-induced itch suggesting that pruriceptive signaling is not inhibited by pain-recruited endogenous modulation, however, CPM was found to aggravate histamine-induced neurogenic inflammation, likely facilitated by efferent sympathetic fibers.

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Dynamic Analysis of Histamine-Mediated Attenuation of Acetylcholine-Induced Sweating via GSK3β Activation

Cited by 41 publications

References 48 publications

Idiopathic Pure Sudomotor Failure Responding to Oral Antihistamine with Sweating Activities

Idiopathic Pure Sudomotor Failure Responding to Oral Antihistamine with Sweating Activities

Revised guideline for the diagnosis and treatment of acquired idiopathic generalized anhidrosis in Japan

Conditioning pain stimulation does not affect itch induced by intra-epidermal histamine pricks but aggravates neurogenic inflammation in healthy volunteers

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