People may have differences in their capacity to metabolize rabeprazole to an inactive metabolite. This may be mediated through genetic differences in the gene that encodes for the metabolic enzyme CYP2C19. For example, people that are poor CYP2C19 metabolizers (i.e. their version of CYP2C19 is less effective than average) will have trouble metabolizing rabeprazole, allowing the active rabeprazole to stay in the body, where it can exert its effect, longer than intended. Conversely, extensive CYP2C19 metabolizers (i.e. the average metabolic capacity of CYP2C19) will extensively metabolize rabeprazole, as expected. The poor metabolizing CYP2C19 phenotype is found in roughly 3–5% of Caucasian people, and in 17–20% of people of Asian ancestry. In a study on men of Japanese ancestry, this has translated to an average increase of total drug exposure by 50–60% compared to men in the United States.However, rabeprazoles metabolism is primarily non-enzymatic (it is often inactivated chemically, without the participation of the bodys natural drug metabolizing enzymes). Therefore, while a persons CYP2C19 phenotype will affect rabeprazoles metabolism, it is not expected to dramatically affect the efficacy of the medication. Chemistry
Rabeprazole is classified as a substituted benzimidazole, like omeprazole, lansoprazole, and pantoprazole. Rabeprazole possess properties of both acids and bases, making it an amphotere. The acid dissociation constant (pKa) of the pyridine nitrogen is about equal to 5. Synthesis
The above synthesis pathway begins with 2,3-dimethypyridine N-oxide (1).
In cases of saccular type of cyst, excision and placement of T-shaped tube is done.Currently, there is no accepted indication for fetal intervention in the management of prenatally suspected choledochal cysts. References


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