Antihistamine

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The chemical structure of histamine

Antihistamines are a class of substances that inhibit the action of histamine. Antihistamines are commonly used to relieve allergies and to promote sleep.^[1] Recreationally, very high doses of most first-generation antihistamines can be used to induce delirium and achieve a hallucinogenic effect in which the user sees and hears fully-formed, extremely convincing hallucinations. However, this experience is typically considered highly unpleasant by most users.

H1 antihistamines are classified as first- and second-generation compounds. First-generation compounds cross the blood–brain barrier (BBB) causing sedation and they commonly cause antimuscarinic anticholinergic effects such as delirium, dry mouth and dysfunctional urine voiding. Second-generation compounds cross the BBB to a minimal degree and are less sedating and do not cause delirium.^[2]

The toxicity of recreational antihistamine use is poorly understood, although there is some evidence that abuse may cause cognitive deficits and other health issues.^[3]

Pharmacology

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Most antihistamines act as inverse agonists on histamine receptors, meaning they inhibit the action of histamine by preventing it from binding to them. They may also inhibit the enzymatic activity of histidine decarboxylase which catalyzes the transformation of histidine into histamine.^{[citation needed]}

First-generation antihistamines readily cross the blood–brain barrier (BBB) and occupy H1-receptors located on postsynaptic membranes of histaminergic neurons throughout the central nervous system (CNS). Most of these drugs have antimuscarinic anticholinergic effects, some have alpha-adrenergic blocking effects, and others can inhibit both histamine and 5-HT activity. Second-generation H1-antihistamineshave significantly less affinity for muscarinic cholinergic and alpha-adrenergic receptors and cross the BBB to a minimal degree, penetrate poorly into the CNS, and typically occupy fewer than 20% of CNS H1-receptors.^{[citation needed]}

The promotion of sleep by antihistamines with sedative properties may partially be due to the antagonism of histamine receptors in the ventrolateral preoptic area (VLPO) located in the hypothalamus. When the VLPO is stimulated, it increases the frequency of GABAergic activity within other wake-promoting sites of the brain as an inhibitory process to wakefulness. In contrast, the VLPO is inhibited by histaminergic activity, primarily from the tuberomammillary nucleus (TMN); deactivating the VLPO in order to promote wakefulness (primarily in the transition from sleep to wake).^[4]

Examples

Antihistamines are found throughout organic chemistry and include psychoactive and anti-allergenic compounds.

First-generation antihistamines

Second-generation antihistamines

Cetirizine
Loratadine
Desloratadine
Fexofenadine

Other

Toxicity and harm potential

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First-generation H1-antihistamines potentially cause adverse effects in multiple body systems. CNS adverse effects of antihistamines are due to inverse agonism at CNS H1-receptors, inhibition of neurotransmission in histaminergic neurons, and impairment of alertness, cognition, learning, and memory that is not necessarily associated with sedation, fatigue, or somnolence. After an overdose, some first-generation H1-antihistamines potentially lead to sinus tachycardia, prolongation of the QT interval, ventricular arrhythmias, and torsade de pointes.^[2]

In contrast to first-generation H1-antihistamines, second-generation H1-antihistamines are relatively free from antihistaminic adverse CNS effects and from antimuscarinic, antiserotonin, and anti–α-adrenergic effects. Massive overdoses of second-generation H1-antihistamines, such as cetirizine, fexofenadine, and loratadine, have not been causally linked with seizures, coma, respiratory depression, or fatality.^[2]

External links

Antihistamine (Wikipedia)

Literature

Emanuel, M. B. (1999). Histamine and the antiallergic antihistamines: a history of their discoveries. Clinical & Experimental Allergy, 29(S3), 1-11. https://doi.org/10.1046/j.1365-2222.1999.00004.x-i1

References

↑ Sicherer, S. H. (2006). Understanding and managing your child’s food allergies. A Johns Hopkins Press health book. Johns Hopkins University Press. ISBN 9780801884917.
↑ ^2.0 ^2.1 ^2.2 Simons, F. E. R., Simons, K. J. (1 December 2011). "Histamine and H1-antihistamines: Celebrating a century of progress". Journal of Allergy and Clinical Immunology. 128 (6): 1139–1150.e4. doi:10.1016/j.jaci.2011.09.005. ISSN 0091-6749.
↑ Gray, S. L., Anderson, M. L., Dublin, S., Hanlon, J. T., Hubbard, R., Walker, R., Yu, O., Crane, P. K., Larson, E. B. (1 March 2015). "Cumulative Use of Strong Anticholinergics and Incident Dementia: A Prospective Cohort Study". JAMA Internal Medicine. 175 (3): 401. doi:10.1001/jamainternmed.2014.7663. ISSN 2168-6106.
↑ Yu Wei, Liu; Jing, Li; Jiang-Hong, Ye (2010). "Histamine regulates activities of neurons in the ventrolateral preoptic nucleus". The Journal of Physiology. 588 (21): 4103–4116. doi:10.1113/jphysiol.2010.193904. ISSN 0022-3751.

[1] Sicherer, S. H. (2006). Understanding and managing your child’s food allergies. A Johns Hopkins Press health book. Johns Hopkins University Press. ISBN 9780801884917.

[H1-antihistamines-2] 2.0 ^2.1 ^2.2 Simons, F. E. R., Simons, K. J. (1 December 2011). "Histamine and H1-antihistamines: Celebrating a century of progress". Journal of Allergy and Clinical Immunology. 128 (6): 1139–1150.e4. doi:10.1016/j.jaci.2011.09.005. ISSN 0091-6749.

[3] Gray, S. L., Anderson, M. L., Dublin, S., Hanlon, J. T., Hubbard, R., Walker, R., Yu, O., Crane, P. K., Larson, E. B. (1 March 2015). "Cumulative Use of Strong Anticholinergics and Incident Dementia: A Prospective Cohort Study". JAMA Internal Medicine. 175 (3): 401. doi:10.1001/jamainternmed.2014.7663. ISSN 2168-6106.

[4] Yu Wei, Liu; Jing, Li; Jiang-Hong, Ye (2010). "Histamine regulates activities of neurons in the ventrolateral preoptic nucleus". The Journal of Physiology. 588 (21): 4103–4116. doi:10.1113/jphysiol.2010.193904. ISSN 0022-3751.

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