Maternal Crohn's disease-related vitamin B<sub>12</sub> deficient megaloblastic anemia in an infant

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  • OHYAMA Wataru
    Department of Pediatrics, The Jikei University School of Medicine
  • YAMAOKA Masayoshi
    Department of Pediatrics, The Jikei University School of Medicine
  • YOKOI Kentaro
    Department of Pediatrics, The Jikei University School of Medicine
  • IWAHASHI Megumi
    Department of Pediatrics, The Jikei University School of Medicine
  • INAGE Yuka
    Department of Pediatrics, The Jikei University School of Medicine
  • ARIHIRO Seiji
    Department of Gastroenterology and Hepatology, The Jikei University School of Medicine
  • KOGANEI Kazutaka
    Division of Inflammatory Bowel Disease (IBD), Yokohama Municipal Hospital
  • SUGITA Akira
    Division of Inflammatory Bowel Disease (IBD), Yokohama Municipal Hospital
  • IDA Hiroyuki
    Department of Pediatrics, The Jikei University School of Medicine
  • AKIYAMA Masaharu
    Department of Pediatrics, The Jikei University School of Medicine

Bibliographic Information

Other Title
  • 母親のクローン病に関連した乳児ビタミンB<sub>12</sub>欠乏性巨赤芽球性貧血
  • 症例報告 母親のクローン病に関連した乳児ビタミンB₁₂欠乏性巨赤芽球性貧血
  • ショウレイ ホウコク ハハオヤ ノ クローンビョウ ニ カンレン シタ ニュウジ ビタミン B ₁ ₂ ケツボウセイキョセキ ガキュウセイ ヒンケツ

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Abstract

We report an 11-month-old breast-fed boy with feeding difficulties, lethargy, and developmental delay. Blood examination showed pancytopenia and decreased serum levels of vitamin B12. Anisocytosis and poikilocytes were detected in his peripheral blood, and increased megaloblastosis without leukemic cells was detected in his bone marrow. After the diagnosis of megaloblastic anemia due to vitamin B12 deficiency, symptoms were improved by vitamin B12 administration. Further investigation of the mother identified Crohn's disease and suggested that the supply of vitamin B12 from the mother to the infant, via the placenta during pregnancy and via breast milk after birth, was decreased due to impaired absorption of vitamin B12 in the mother's small intestine. Magnetic resonance imaging of the boy's brain on admission showed cerebral cortex atrophy which had improved by the age of 1 year and 10 months after vitamin B12 treatment, though developmental delay was still evident at the age of 3 years. Infantile vitamin B12 deficiency often presents with nonspecific manifestations, such as developmental delay and failure to thrive, in addition to anemia and is thus not easily diagnosed. To prevent severe neurological sequelae, this condition must be rapidly diagnosed, because a prolonged duration increases the risk of permanent disabilities.

Journal

  • Rinsho Ketsueki

    Rinsho Ketsueki 57 (1), 15-19, 2016

    The Japanese Society of Hematology

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