ReviewFrontiers in nutrition2026
Revisiting the hematological manifestations of vitamin B12 deficiency.
Review in Frontiers in nutrition, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vitamin B12 (cobalamin) deficiency remains a significant problem affecting both children and adults and is associated with a wide range of hematological manifestations that are largely preventable with timely diagnosis and treatment. Vitamin B12 deficiency can present with variable hematological, neuropsychiatric, and mucocutaneous changes. Hematological abnormalities are among the most common presentations. The classical peripheral blood smear shows macrocytosis with oval macrocytes, anisopoikilocytosis, and hypersegmented neutrophils. Anemia may be accompanied by leukopenia and thrombocytopenia due to ineffective hematopoiesis. Bone marrow examination typically reveals hypercellularity with erythroid hyperplasia and large megaloblasts exhibiting open chromatin and nuclear-cytoplasmic asynchrony as a result of defective DNA synthesis. Ineffective erythropoiesis leads to intramedullary destruction of hematopoietic precursors, resulting in elevated lactate dehydrogenase, indirect hyperbilirubinemia, and reduced haptoglobin, thereby mimicking hemolytic anemias. Abnormal red cells and megaloblasts that enter the circulation have a shortened lifespan, leading to megaloblastic anemia, with reticulocyte counts that are inappropriately low for the degree of anemia. In pediatric patients, manifestations may be severe, particularly in infants born to cobalamin-deficient mothers. Presentations include profound anemia, pancytopenia, failure to thrive, recurrent infections, and bleeding manifestations due to thrombocytopenia, often misdiagnosed as aplastic anemia or myelodysplasias. Pigmentary changes in the form of hyperpigmentation of knuckles, oral mucosa and rarely Addisonian pigmentation have been described. In older children, isolated anemia or bicytopenia with subtle macrocytosis may delay diagnosis. Severe presentations, seen in approximately 10% of cases, include pancytopenia, hemolytic anemia, and pseudothrombotic microangiopathy, which may mimic hematological malignancies or thrombotic microangiopathies. Early recognition is crucial, as vitamin B12 replacement leads to rapid and often complete hematological recovery.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.