![]() In a clinical pharmacokinetic study that evaluated concomitant use of WAKIX with modafinil or sodium oxybate, WAKIX had no effect on the pharmacokinetics (PK) of either modafinil or sodium oxybate and these agents had no clinically relevant effect on the PK of WAKIX. WAKIX is contraindicated in patients with severe hepatic impairment and not recommended in patients with end-stage renal disease. The maximum recommended dosage of WAKIX is 35.6 mg once daily.ĭose modifications are recommended for patients with moderate hepatic impairment, moderate or severe renal impairment, concomitant use of strong CYP2D6 inhibitors or strong CYP3A4 inducers, and for those known to be poor CYP2D6 metabolizers. WAKIX is initiated 8.9 mg once daily and is titrated at weekly intervals. ![]() WAKIX offers once-daily morning oral dosing and has a recommended dosage range of 17.8 mg to 35.6 mg daily. WAKIX is not a stimulant and not a controlled substance. 13-16 WAKIX is the first and only histaminergic treatment for EDS or cataplexy in narcolepsy. 11,12 Originating in the hypothalamus, hypocretin and histamine neurons play complementary roles in promoting and stabilizing wakefulness by activating the cortex and other wake-promoting neurons and inhibiting both non-REM and REM sleep-promoting neurons. The mechanism of action of WAKIX in EDS or cataplexy in adult patients with narcolepsy is unclear however, its efficacy could be mediated through its activity as an antagonist/inverse agonist at H 3 receptors, which results in increased levels of histamine in the brain. In this article, we will review the safety and efficacy data for WAKIX from clinical studies, as well as a clinical case study of a patient with type 1 narcolepsy who started treatment with WAKIX. It is the first and only FDA-approved non-scheduled therapeutic option for this patient group. WAKIX ® (pitolisant) is a histamine 3 (H 3) receptor antagonist/inverse agonist indicated for the treatment of EDS or cataplexy in adult patients with narcolepsy. 4įalse Please click here after selecting answerįor those diagnosed with narcolepsy, identifying appropriate interventions for the treatment of EDS and/or cataplexy is important. 4,5 Identification of EDS can be a challenge. 5 Additionally, EDS can manifest in ways that are not obvious, such as lapses in vigilance or concentration. 4,5 Lapses into sleep may occur several times each day, although episode frequency and duration can vary considerably across different individuals and environments. 3,5 EDS involves an overwhelming need to sleep throughout the day and lapses into sleep-typically during sedentary activities but sometimes may occur during active activities. 4 The reduced or inconsistent activation of histamine and other wake-promoting neurons is the cause of EDS. 1,3 The hallmark narcolepsy symptom is excessive daytime sleepiness (EDS), which is defined as daily episodes of an irrepressible need to sleep or unintended lapses into sleep. 1-3 The cause of narcolepsy in most patients is the loss of hypocretin (orexin) neurons in the brain that leads to reduced or inconsistent activation of histamine and other wake-promoting neurons, resulting in sleep-wake state instability. Because narcolepsy is an under-recognised disease, it is important that general practitioners and other primary health-care workers identify abnormal daytime sleepiness early.Narcolepsy is a rare, chronic, debilitating neurological disorder of sleep-wake state instability that affects approximately 165,000 individuals in the United States. Treatment is with stimulant drugs to suppress daytime sleepiness, antidepressants for cataplexy, and gamma hydroxybutyrate for both symptoms. The cause of neural loss could be autoimmune since most patients have the HLA DQB1*0602 allele that predisposes individuals to the disorder. ![]() Pathophysiological studies have shown that the disease is caused by the early loss of neurons in the hypothalamus that produce hypocretin, a wakefulness-associated neurotransmitter present in cerebrospinal fluid. The onset of narcolepsy with cataplexy is usually during teenage and young adulthood and persists throughout the lifetime. Sleep monitoring during night and day shows rapid sleep onset and abnormal, shortened rapid-eye-movement sleep latencies. It is characterised by severe, irresistible daytime sleepiness and sudden loss of muscle tone (cataplexy), and can be associated with sleep-onset or sleep-offset paralysis and hallucinations, frequent movement and awakening during sleep, and weight gain. Narcolepsy with cataplexy is a disabling sleep disorder affecting 0.02% of adults worldwide.
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