Department of Internal Medicine and Clinical Immunology, University Hospital, Angers, France; MitoVasc unit, Inserm U1083, CNRS UMR6015, Angers University, France.
Laboratory of Immunology, University Hospital, Angers, France.
Am J Clin Nutr. 2024 Jul;120(1):217-224. doi: 10.1016/j.ajcnut.2024.05.019. Epub 2024 May 24.
The absorption of vitamin B12 is hindered in pernicious anemia (PA) owing to intrinsic factor deficiency. Traditionally, intramuscular vitamin B12 injections were the standard treatment, bypassing the impaired absorption. Although there is potential for oral vitamin B12 supplementation through passive enteral absorption, it is not commonly prescribed in PA owing to limited studies assessing its efficacy.
We aimed to assess the efficacy of oral vitamin B12 supplementation in PA.
We enrolled participants diagnosed with incident vitamin B12 deficiency related to PA. The diagnosis of PA was based on the presence of classical immune gastritis and of anti-intrinsic factor and/or antiparietal cell antibodies. To evaluate the vitamin B12 status, we measured total plasma vitamin B12, plasma homocysteine, and plasma methylmalonic acid (pMMA) concentration and urinary methylmalonic acid-to-creatinine ratio. Participants were treated with oral cyanocobalamin at a dosage of 1000 μg/d throughout the study duration. Clinical and biological vitamin B12 deficiency related features were prospectively and systematically assessed over the 1-y study duration.
We included 26 patients with vitamin B12 deficiency revealing PA. Following 1 mo of oral vitamin B12 supplementation, 88.5% of patients were no longer deficient in vitamin B12, with significant improvement of plasma vitamin B12 [407 (297-485) compared with 148 (116-213) pmol/L; P < 0.0001], plasma homocysteine [13.5 (10.9-29.8) compared with 18.6 (13.7-46.8) μmol/L; P < 0.0001], and pMMA [0.24 (0.16-0.38) compared with 0.56 (0.28-1.09) pmol/L; P < 0.0001] concentrations than those at baseline. The enhancement of these biological parameters persisted throughout the 12-month follow-up, with no patients showing vitamin B12 deficiency by the end of the follow-up period. The median time to reverse initial vitamin B12 deficiency abnormalities ranged from 1 mo for hemolysis to 4 mo for mucosal symptoms.
Oral supplementation with 1000 μg/d of cyanocobalamin has been shown to improve vitamin B12 deficiency in PA.
由于内因子缺乏，维生素 B12 在恶性贫血（PA）中吸收受阻。传统上，肌内注射维生素 B12 是标准治疗方法，可绕过受损的吸收。尽管通过被动肠内吸收补充口服维生素 B12 有一定的作用，但由于评估其疗效的研究有限，因此在 PA 中并不常用。
评估口服维生素 B12 补充剂在 PA 中的疗效。
我们招募了诊断为与 PA 相关的维生素 B12 缺乏症的参与者。PA 的诊断基于经典的免疫性胃炎和抗内因子和/或抗壁细胞抗体的存在。为了评估维生素 B12 状态，我们测量了总血浆维生素 B12、血浆同型半胱氨酸和血浆甲基丙二酸（pMMA）浓度以及尿甲基丙二酸与肌酐的比值。在整个研究期间，参与者接受 1000μg/d 的口服氰钴胺治疗。在 1 年的研究期间，前瞻性和系统地评估了与临床和生物学维生素 B12 缺乏相关的特征。
我们纳入了 26 名维生素 B12 缺乏症患者，这些患者均患有 PA。口服维生素 B12 补充 1 个月后，88.5%的患者不再缺乏维生素 B12，血浆维生素 B12 显著改善[407（297-485）与 148（116-213）pmol/L；P<0.0001]，血浆同型半胱氨酸[13.5（10.9-29.8）与 18.6（13.7-46.8）μmol/L；P<0.0001]和 pMMA[0.24（0.16-0.38）与 0.56（0.28-1.09）pmol/L；P<0.0001]的浓度也明显改善。这些生物学参数的改善一直持续到 12 个月的随访期，随访结束时没有患者出现维生素 B12 缺乏症。从溶血性贫血的 1 个月到黏膜症状的 4 个月，初始维生素 B12 缺乏异常逆转的中位时间范围。
每日口服 1000μg 的氰钴胺可改善 PA 中的维生素 B12 缺乏症。
