Vitamin B12 deficiency in patients after enterocystoplasty. Issue 5 (October 2015) - Keenan, Alison
Summary: Introduction: Serum B12 deficiency is a known sequlae of enterocystoplasty. The complications of B12 deficiency include megaloblastic anemia, neuropsychiatric disease, and demyelinating diseases such as peripheral neuropathy. Some studies have suggested that underlying disease states may be more important than enteric absorptive capacity in predicting acquired B12 deficiency. A 38% incidence of low or low-normal serum B12 in patients who have undergone enterocystoplasty has previously been reported, and oral B12 supplementation has been demonstrated to be an effective short-term therapy; however, the long-term results remain unclear. Aims: This study hypothesized that oral vitamin B12 supplementation in patients with B12 deficiency following enterocystoplasty is an effective long-term treatment. Additionally, it sought to determine if underlying disease state predicts B12 deficiency following enterocystoplasty. Design: Children who underwent enterocystoplasty at the present institution prior to August 2007 were reviewed. Patients with non-ileal augment, insufficient follow-up or hematologic disorders were excluded. Patients with low or low-normal B12 levels were included. Treatment consisted of daily oral therapy of 250 mcg or monthly parenteral therapy of 1000 mcg IM. Separately, the institutional database of 898 patients who underwent enterocystoplasty was searched and patients with at least one post-operative B12 level were highlighted. The indication for enterocystoplasty was classified as neuropathic or non-neuropathic. Results: Twenty-three patients met inclusion criteria. The mean follow-up was 49 months (range 5–85) following initial abnormal B12 level. On the last follow-up, 4/23 (17%) patients had normal serum B12 levels. No patients reported sequelae of long-term B12 deficiency. In the secondary investigation, 113 patients met inclusion criteria. A total of 101 had neuropathic indications for enterocystoplasty, and 12 had non-neuropathic indications. At any time during follow-up, 48/101 (47.5%) neuropathic patients had low or low-normal B12 levels, and 4/12 (33.3%) non-neuropathic patients had low or low-normal B12 levels during follow-up ( P = 0.54) (Figure). Discussion: The initial success of oral B12 deficiency treatment following enterocystoplasty does not persist over time. This contradicts previous results with short duration follow-up. Underlying disease as the indication for enterocystoplasty did not predict B12 deficiency risk. The study was limited by the small number of patients with B12 deficiency who were started on treatment, as well as by the small number of patients with non-neuropathic indications for enterocystoplasty. Conclusion: The aims of the study were met. Further investigation is required to assess predictors of B12 deficiency following enterocystoplasty. Figure Underlying indication for enterocystoplasty does not predict B12 deficiency.