By Domenic A. Ciraulo MD, Richard I. Shader, David J. Greenblatt MD, Wayne L. Creelman MD
Thoroughly up to date for its 3rd variation, this instruction manual presents entire, present, and simply obtainable details on how psychotropic medicines engage with each other and with compounds used to regard non-psychiatric health conditions. The e-book is equipped for quick reference, contains quite a few tables, and gives guidance for dealing with adversarial effects.
The 3rd variation comprises an hostile drug results desk within the appendix part, tables on receptor binding and dosing, and the most recent details on medicines of abuse and chemical dependence. This variation additionally comprises drug-food interactions for every drug type and interactions of psychotropic medications with HIV medications.
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Extra resources for Drug Interactions in Psychiatry
Clinically significant CYP1A2 inhibitors include the SSRI antidepressant fluvoxamine and the fluoroquinolone antibiotics ciprofloxacin and enoxacin. CYP2A6 CYP2A6 has a relatively minor role in the biotransformation of drugs and accounts for only ϳ4% of total immunoquantified levels of human hepatic CYP. This enzyme has been characterized as a coumarin 7-hydroxylase; it is an important molecular determinant of nicotine metabolism in humans, and it plays a role in the reductive metabolism of the anesthetic halothane.
Enzymes of the UGT2 family include UGT2A1, UGT2B4, UGT2B7, UGT2B15, and UGT2B17. Several of the UGTs are expressed extrahepatically in tissues such as the esophagus (1A7, 1A8, 1A10, 2B7, 2B10, 2B15), intestine (1A8, 1A10, 2B7) and brain (1A6, 2A1, 2B7). , UGTs 1A7, 1A8, and 1A10 are expressed primarily in the gastrointestinal tract, including the esophagus; UGT2A1 is expressed primarily in olfactory epithelium and the brain; and UGT2B17 appears to be a prostate-specific enzyme). Although UGTs have been shown to metabolize therapeutic agents, their significance to drug clearance remains to be systematically evaluated.
9 for both drugs). Paroxetine at usual clinical doses produces a six- to sevenfold increase in the exposure of both drugs. Despite similar pharmacokinetic consequences, the clinical consequences of these two interactions are strikingly different.