• Nutrition and cancer · Jan 2006

    Frequency of combined deficiencies of vitamin D and holotranscobalamin in cancer patients.

    • Ashley Serene Plant and Glenn Tisman.
    • Glenn Tisman, MD, Inc., Whittier, California 90601, USA.
    • Nutr Cancer. 2006 Jan 1;56(2):143-8.

    AbstractVitamin D and holotranscobalamin (HTCII) deficiencies have been seen to demonstrate an association with various types of cancers. The objective of this study is to determine the frequency of vitamin D and HTCII deficiency in cancer patients. Our study investigated vitamin D, total B12, and HTCII levels in 70 cancer patients. Vitamin D status was measured as serum 25-hydroxyvitamin D [25(OH)D, Nichols Advantage assay], and serum B12 was measured as both total B12 and as the metabolically active HTCII (Immulite B12 assay followed by glass adsorption). Insufficiency of serum 25(OH)D levels for this study is defined based on differing literature standards of insufficiency and was selected to be either <50 or <75 nmol/l. When 25(OH)D insufficiency is defined as serum level of <75 nmol/l, 43 of 60 (72%) of cancer patients were found to be insufficient. At the lower definition of insufficiency, <50 nmol/l, 24 of 60 patients (40%) were insufficient. Of 52 patients, only 3 (6%) were found to have insufficient serum levels of total B12 (normal = >300 pg/ml), whereas 17 of 52 (34%) were found to be HTCII insufficient (normal = >69 pg/ml). Of these 17 patients, 14 (84.4%) had normal total B12 levels. Low serum levels of 25(OH)D strongly correlated with low serum HTCII. All 12 HTCII-deficient patients were vitamin D insufficient at the <75-nmol/l standard. Six of 12 HTCII-deficient patients (50%) were vitamin D deficient at the <50-nmol/l cutoff. The standard measurement of total serum B12 alone is inadequate for identifying patients with insufficient levels of metabolically active B12. Deficiency of vitamin D (72%) and HTCII (34%) is prevalent among newly diagnosed patients with cancer and could play a role in cancer development and host response to tumor and therapy. Possible explanations for combined HTCII and 25(OH)D deficiencies include patient age, presence of atrophic gastritis, and lack of sun exposure.

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