Successful Sublingual Cobalamin Treatment in a Child with Short-Bowel Syndrome

Abstract

Vitamin B12 (B12) is essential for deoxyribonucleic acid synthesis, to maintain normal hematologic and neurologic functions. Studies suggest that cobalamin deficiency in children is more common than previously recognized. Main causes are decreased intake, abnormal absorption, and inborn errors of metabolism. The classic treatment for cobalamin deficiency is intramuscular administration of B12. There are no data concerning the use of alternative routes of cobalamin administration in children. This report shares the experience of sublingual administration of B12 to a patient with short-bowel syndrome and B12 malabsorption. We report the case of successful treatment of cobalamin deficiency by sublingual administration in a 9-year-old patient who had undergone intestinal resection and jejunum-colon, with anastomosis of 32 cm of residual small intestine and absence of distal jejunum and ileocecal junction. We determined a B12 deficiency because low serum cobalamin levels (<200 pg/mL) were shown in 2 consecutive tests (130 pg/mL and 170 pg/mL). The patient presented with neither clinical nor hematological manifestations. He received sublingual cobalamin preparation, 1000-mcg sublingual nuggets per day for 1 month. Normalization of serum cobalamin was obtained (790 pg/mL) after 1 month of treatment. The sublingual route of administration not only improved the quality of life of this patient by avoiding monthly painful injections but also reduced the cost of treatment and the number of hospital visits.

Gradual onset of psychotic symptoms in an adolescent

“…The most common causes of B12 deficiency are abnormal absorption or restrictive diets that exclude animal‐derived protein. Malabsorption can be due to gastric bypass or the loss of the terminal ileum, the site of maximal B12 absorption, in short bowel syndrome . Malabsorption can also be due to low intrinsic factor, a protein necessary for B12 absorption, by autoimmune‐mediated or congenital mechanisms .…”

“…For those who receive early treatment, full recovery is possible, with neurologic symptoms often improving within a day and resolving within 3 months . Lifelong therapy is required if patients are unable to supplement though dietary changes, have antibodies to intrinsic factor, or have significant malabsorption due to short bowel syndrome or gastric bypass surgery …”

“…Malabsorption can be due to gastric bypass or the loss of the terminal ileum, the site of maximal B12 absorption, in short bowel syndrome. [4][5][6][7][8] Malabsorption can also be due to low…”

“…1 Lifelong therapy is required if patients are unable to supplement though dietary changes, have antibodies to intrinsic factor, or have significant malabsorption due to short bowel syndrome or gastric bypass surgery. [5][6][7][8] Paediatric providers should consider B12 deficiency in the differential for patients presenting with neurologic or psychiatric symptoms, particularly if they have risk factors. Patients must be closely monitored to identify the need for early supplementation so as to prevent neuropsychiatric complications.…”

Clinical case and short review of extreme short bowel syndrome: an update 21 years after

“…It has been reported that extended resection of small intestine, particularly the ones involving the last ileal loop, may determine a vitamin B12 absorption deficit and a consequential megaloblastic anemia. [43][44][45] As well, the prolonged use of loperamide, to reduce the speed of intestinal transit and, therefore, to increase the absorption capacity of the residual loops, should not be underestimated. 43,46,47 Finally, it is noteworthy the development, after 21 years, of an oxalate-related bilateral nephrocalcinosis, a condition, which led to CKD, successively worsened by several episodes of ureteral lithiasis, up to the development of a III degree hydronephrosis which required the placement of bilateral ureteral stents.…”