SEnterocystoplasty is a widely accepted treatment modality
for medically refractory neuropathic bladder dysfunction.
The metabolic consequences of enteric bladder augmentation
are well described and should be regularly monitored
in all patients [1]. Serum B12 deficiency is a particularly
fearsome sequlae of enterocystoplasty; this is due to the
potentially irreversible neurologic changes associated with
long-term deficiency. Reported complications of B12 defi-
ciency include: megaloblastic anemia, neuropsychiatric
disease, and demyelinating diseases such as peripheral
neuropathy, which may not improve with appropriate
replacement therapy [2]. More recently, some studies have
suggested that underlying disease states may be more
important that enteric absorptive capacity in predicting
acquired B12 deficiency [3