Avoiding rabeprazole during breastfeeding confers to lowest possible risk. Geriatrics
Advanced age does not appear to clinically impact rabeprazoles metabolism. However, elevations in the maximum plasma concentration and the total drug exposure (area under the curve, AUC) have occurred. Japanese ancestry
In a study on rabeprazoles pharmacokinetics, the AUC was elevated by approximately 50–60% in men of Japanese ancestry compared to men in the United States. See the pharmacogenetics section below for a pharmacogenetic explanation of these findings. Kidney or liver problems
In people that have kidney or liver problems, these problems do not appear to affect rabeprazoles metabolism in a clinically meaningful way. This includes individuals on dialysis for kidney problems. Severe liver problems like cirrhosis of the liver do affect rabeprazoles elimination half-life, but not to a degree of dangerous accumulation. In a review of patients taking rabeprazole while having end-stage kidney disease and mild-to-moderate severity, chronic compensated cirrhosis of the liver, the alteration in rabeprazoles metabolism was not clinically meaningful. Contraindications
Rabeprazole is contraindicated in the following populations and situations:
people with a known hypersensitivity to rabeprazole, substituted benzimidazoles (which are chemically similar to rabeprazole, like omeprazole), or any other component of the capsule formulation (e.g. certain dyes)
concurrent use of rilpivirine, a medication used to treat HIV infection

Hypersensitivity
Syndrome
An allergy to a PPI like rabeprazole may take the form of type I hypersensitivity or delayed hypersensitivity reactions. A selective (pattern C—see below for a discussion of cross-reactivity patterns) type I hypersensitivity reaction to rabeprazole resulting in anaphylaxis has been reported, as well as several whole group hypersentivities.
Sorsbys fundus dystrophy (SFD) is a very rare genetic disorder characterized by the loss of central vision. It was first described by Sorsby and Mason in 1949. Signs and symptoms
Patients typically become symptomatic in their 40s due to loss of central vision. However, tests of rod photoreceptor function (i.e., night vision tests) show dysfunction at an earlier age. One of the most sensitive visual function parameters for early SFD is a prolongation of rod-mediated dark adaptation. High-resolution structural imaging of the Bruchs membrane and of the underlying choriocapillaris – the capillary plexus nourishing the outer retina – also shows early alterations. Genetics
The inheritance pattern is autosomal dominant. It is related to a mutation in the TIMP3 gene. Diagnosis
Treatment
References
External links

Sorsbys fundus dystrophy at OMIM
Sorsbys fundus dystrophy at Orpha.net