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Although pruritus is the critical symptom of atopic dermatitis that profoundly affect the patients' quality of life, controlling and management of prurirtus still remains as unmet needs mainly due to the distinctive multifactorial pathogenesis of pruritus in atopic dermatitis. Based on the distinct feature of atopic dermatitis that psychological state of patients substantially influence on the intensity of pruritus, various psychotropic drugs have been used in clinic to relieve pruritus of atopic dermatitis patients. Only several psychotropic drugs were reported to show real antipruritic effects in atopic dermatitis patients including naltrexone, doxepin, trimipramine, bupropion, tandospirone, paroxetine and fluvoxamine. However, the precise mechanisms of antipruritic effect of these psychotropic drugs are still unclear. In human skin, serotonin receptors and serotonin transporter protein are expressed on skin cells such as keratinocytes, melanocytes, dermal fibroblasts, mast cells, T cells, natural killer cells, langerhans cells, and sensory nerve endings. It is noteworthy that serotonergic drugs, as well as serotonin itself, showed immune-modulating effect. Fenfluramine, fluoxetine and 2, 5-dimethoxy-4-iodoamphetamine significantly decreased lymphocyte proliferation. It is still questionable whether these serotonergic drugs exert the immunosuppressive effects via serotonin receptor or serotonin transporter. All these clinical and experimental reports suggest the possibility that antipruritic effects of selective serotonin reuptake inhibitors in atopic dermatitis patients might be at least partly due to their suppressive effect on T cells. Further studies should be conducted to elucidate the precise mechanism of neuroimmunological interaction in pruritus of atopic dermatitis.
Pubmed ID: 24009842
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THIS RESOURCE IS NO LONGER IN SERVICE. Documented on January 5, 2023. Database of information on the abilities of drugs to interact with an expanding number of molecular targets. It serves as a data warehouse for published and internally-derived Ki, or affinity, values for a large number of drugs and drug candidates at an expanding number of G-protein coupled receptors, ion channels, transporters and enzymes. The query interface is designed to let you search by any field, or combination of them to refine your search criteria. The flexible user interface also provides for customized data mining. The database is regularly updated. If you know of Ki data you would like to add, you can select Direct Ki Entry at the grey panel. If you would like, however, your own data (published or not) added, Send them a Reference at the grey panel, or send an email to Dr. Bryan Roth or Estela Lopez. Most common targets: 5-HT2A, DOPAMINE D1, DOPAMINE D2, 5-HT2C, 5-HT1A, Cholinergic, muscarinic M1, 5-HT Transporter, HISTAMINE H1, 5-HT2B, OPIOID Mu, 5-HT6, adrenergic Beta2, 5-HT7, OPIATE Delta, adrenergic Alpha1A, OPIOID Kappa, 5-HT3, m-AChR, adrenergic Beta1, adrenergic Alpha2A, 5-HT1, Acetylcholinesterase, AChE, Thromboxane A2, n-AChR, Opiate non-selective, CANNABINOID CB1, HERG, Dopamine, cocaine site, adrenergic Alpha2C, M3, Norepinephrine Uptake, Monoamine Oxidase A, Monoamine Oxidase B, 5-HT4, adrenergic Alpha1, 5-HT1E, B1 BRADYKININ, 5-HT2, 5-HT2C-INI, DOPAMINE D4, ANGIOTENSIN AT1, Neurokinin NK1, HISTAMINE H3, Sigma-1, VIP, Dopamine2-like, metabotropic glutamate 5, 5-HT2c VGI, Carbonic Anhydrase Isozymes, CA I, DOPAMINE D2 Long, adrenergic Alpha2, adrenergic Alpha2B, adrenergic Alpha2D, GABA A alpha1, CANNABINOID CB2, adrenergic Alpha1B, 5-HT5a, Melatonin, HISTAMINE H4, NMDA, 5-HT4a, Glucocorticoid, Interleukin 1-beta, Sodium Channel, Benzodiazepine central, Cholinergic, muscarinic M5, Neuropeptide Y1, GABA A alpha5, Galanin R2, Neurokinin NK3, 5-HT1B, M2, DOPAMINE D3, Angiotensin, Dopamine1-like, Neurokinin NK2, adrenergic Beta, Dopamine D1 high, Dopamine D1A, MAP kinase, ADENOSINE A2a, 5-HT7b, Nitrogen oxide synthase - neuronal, Sigma-2, CDK2, Neurotensin 2, DOPAMINE D2 Short, Multidrug Resistance Transporter MDR 1, GABA A Benzodiazepine, VEGF-R2, OPIATE Mu 2, Angiotensin II AT1, HISTAMINE H2, Angiotensin-converting enzyme, ACE, Sigma, beta-amyloid, ADENOSINE, ADENOSINE A2B, Adrenaline, Neurotensin 1
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