Similarly, the dose should be reduced by half in those taking strong CYP2D6 inhibitors. Vortioxetine can be discontinued abruptly without tapering, but it is recommended that at doses of 15 to 20 mg/day it be tapered first to 10 mg/day one week prior to full discontinuation if possible. Available forms
Vortioxetine is available in the form of 5, 10, and 20 mg immediate-release, film-coated oral tablets. Contraindications
Vortioxetine is contraindicated in those with hypersensitivity to vortioxetine or to any other components of vortioxetine tablets. It is also contraindicated in those taking monoamine oxidase inhibitors (MAOIs) due to the possibility of serotonin syndrome. Adverse effects
The most common side effects reported with vortioxetine are nausea, vomiting, constipation, and sexual dysfunction, among others. With the exceptions of nausea and sexual dysfunction, these side effects were reported by less than or equal to 10% of study participants given vortioxetine. Significant percentages of placebo-treated participants also report these side effects. Discontinuation of treatment due to adverse effects in clinical trials was 8% with vortioxetine versus 3% with placebo.Sexual dysfunction, such as decreased libido, abnormal orgasm, delayed ejaculation, and erectile dysfunction, are well-known side effects of SSRIs and serotonin–norepinephrine reuptake inhibitors (SNRIs). In clinical trials, sexual dysfunction occurred more often with vortioxetine than with placebo and appeared to be dose-dependent. The specific incidences of treatment-emergent sexual dysfunction as measured with the Arizona Sexual Experience Scale (ASEX) were 14 to 20% for placebo and 16 to 34% for vortioxetine over a dosage range of 5 to 20 mg/day.
Hence, there is no response to treatment with phenobarbital, which causes CYP450 enzyme induction. Most patients (type IA) have a mutation in one of the common exons (2 to 5), and have difficulties conjugating several additional substrates (several drugs and xenobiotics). A smaller percentage of patients (type IB) have mutations limited to the bilirubin-specific A1 exon; their conjugation defect is mostly restricted to bilirubin itself. Before the availability of phototherapy, these children died of kernicterus (bilirubin encephalopathy) or survived until early adulthood with clear neurological impairment. Today, therapy includes

exchange transfusions in the immediate neonatal period
12 hours/day phototherapy
heme oxygenase inhibitors to reduce transient worsening of hyperbilirubinemia (although the effect of the drug decreases over time)
oral calcium phosphate and carbonate to form complexes with bilirubin in the gut
liver transplantation before the onset of brain damage and before phototherapy becomes ineffective at later age

Type II
The inheritance patterns of both Crigler–Najjar syndrome types I and II are autosomal recessive.However, type II differs from type I in a number of different aspects:

Bilirubin levels are generally below 345 μmol/L [20 mg/dL] (range 100–430 μmol/L [6–24 mg/dL]; thus, overlap may sometimes occur), and some cases are only detected later in life. Because of lower serum bilirubin, kernicterus is rare in type II. Bile is pigmented, instead of pale in type I or dark as normal, and monoconjugates constitute the largest fraction of bile conjugates. UGT1A1 is present at reduced but detectable levels (typically <10% of normal), because of single base pair mutations.