Reading Part B33

B33. The drug which is administered at bedtime to reduce further flushing is:

Niacin-Induced flushing:

This comprehensive review of the mechanism of action of niacin-induced flushing critically evaluates research regarding flushing mitigating formulations and agents. Niacin induces flushing through dermal Langerhans cells where the activation of G protein-coupled receptor 109A (GPR109A) increases arachidonic acid and prostaglandins, such as prostaglandin D 2 (PGD 2) and prostaglandin E 2 (PGE 2), subsequently activating prostaglandin D 2 receptor (DP I), prostaglandin E 2 receptor (EP 2) and prostaglandin E receptor 4 (EP 4) in capillaries and causing cutaneous vasodilatation. Controlling niacin absorption rates, inhibiting prostaglandin production, or blocking DP I, EP 2 and EP 4 receptors can inhibit flushing. Niacin extended-release (NER) formulations have reduced flushing incidence, duration and severity relative to crystalline immediate-release niacin with similar lipid efficacy. Non- steroidal anti-inflammatory drugs (NSAlDs), notably aspirin given 30 min before NER at bedtime, further reduce flushing. An antagonist to the DP 1 receptor (laropiprant) combined with an ER niacin formulation can reduce flushing; however, significant residual flushing occurs with clinically-relevant dosages. Niacin is an attractive option for treating dyslipidemic patients, and tolerance to niacin-induced flushing develops rapidly. Healthcare professionals should particularly address flushing during niacin dose titration.