血液疾患と輸血ジャーナル

概要

Persistently High Plasma Vitamin B12 and the Risks of Malignancies

Makki H Fayadh*

A female patient was presented with features suggestive of neuropathy secondary to atrophic gastritis and raised serum gastrin but the surprising findings was the finding of very high Vitamin B12 despite severe gastric atrophy. Her investigations showed multiple small bowel erosions seen by colonoscopy and ileoscopy and confirmed by video capsule.
She has latent Celiac disease with positive Human Leukocyte Antigen HLA DQ2 but poor response to gluten free diet. To our knowledge this is the first case report in our area of very high Vitamin B12 with atrophic gastritis probably attributed to blocking antibodies to the vitamin B12 receptors or associated with hidden hematological or solid cancers.
Her sister developed colon cancer that raises great concerns about possible future development of cancers in this patient. This case study of high vitamin B12 associated with ileal ulceration and chronic auto immune gastritis with latent celiac disease is a new entity that needs further evaluations and awareness is needed to study high level of vitamin B12 and to our knowledge this is the first case of high B12 reported in our area.
Unusually high level of serum vitamin B12 levels is an underestimated entity; it can be paradoxically accompanied by signs of deficiency, reflecting a functional deficiency linked to qualitative abnormalities, which are related to defects in tissue uptake and action of vitamin B12. It can occur with solid neoplasms, hematological malignancies, and liver and kidney diseases. High serum vitamin B12 is defined by a rate above 950 pg/ml (701 pmol/l), which corresponds by biological standards, to the upper limit of biological normality, in the absence of any sign and/or clinical anomaly. A study of more than 80,000 cancer patients demonstrated that those with elevated plasma vitamin B12 levels prior to diagnosis had higher mortality, indicating more advanced and aggressive cancers. These results could not be explained by cancer type, sex, age, comorbidity or presence of non-localized disease suggesting that these associations reflect underlying alterations in the metabolism caused by the cancer.