Association between 8 P‐glycoprotein (MDR1/ABCB1) gene polymorphisms and antipsychotic drug‐induced hyperprolactinaemia; British Journal of Clinical Pharmacology; Vol. 86, iss. 9

Association between 8 P‐glycoprotein (MDR1/ABCB1) gene polymorphisms and antipsychotic drug‐induced hyperprolactinaemia; British Journal of Clinical Pharmacology; Vol. 86, iss. 9

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Parent link:British Journal of Clinical Pharmacology
Vol. 86, iss. 9.— 2020.— [P. 1827-1835]
Korporativní autor: Национальный исследовательский Томский политехнический университет Инженерная школа неразрушающего контроля и безопасности Отделение контроля и диагностики
Další autoři: Geers L. M., Pozhidaev I. V. Ivan, Ivanova S. A. Svetlana Aleksandrovna, Freydin M. B. Maksim Borisovich, Schmidt A. F. Amand, Cohen D., Boyko A. S., Paderina D. Z. Diana, Fedorenko O. Yu. Olga Yurievna, Semke A. V., Bokhan N. A. Nikolay Aleksandrovich, Wilffert B. Bob, Kosterink J. G.W. Jos, Touw D. J., Loonen A. J. M Anton
Shrnutí:Title screen
Hyperprolactinaemia, a common adverse effect of antipsychotic drugs, is primarily linked to blockade of dopamine D2 receptors in the pituitary gland. Certain antipsychotic drugs, such as, for example risperidone and paliperidone, are more likely to induce hyperprolactinaemia compared to others. This effect is probably caused by a relatively high blood/brain concentration ratio, a consequence of being a substrate of P‐glycoprotein. Genetic variants of P‐glycoprotein with changed functional activity might influence the potential of risperidone and paliperidone to cause hyperprolactinaemia as the altered blood/brain concentration ratio would lead to a reduced therapeutic drug level within essential brain areas making dose adaptations necessary. This increases exposure of dopamine D2 receptors within the pituitary gland.
Режим доступа: по договору с организацией-держателем ресурса
Jazyk:angličtina
Vydáno: 2020
Témata:
электронный ресурс
труды учёных ТПУ
antipsychotics
hyperprolactinaemia
MDR1/ABCB1 gene
P-glycoprotein
polymorphisms
On-line přístup:https://doi.org/10.1111/bcpt.13173
Médium: Elektronický zdroj Kapitola
KOHA link:https://koha.lib.tpu.ru/cgi-bin/koha/opac-detail.pl?biblionumber=664042

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