Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cobalamin-deficient (Cbl-D) central neuropathy is a pure myelinolytic disease, in which gliosis is also observed. Iron is abundant in the mammalian central nervous system, where it is required for various essential functions including myelinogenesis. It is predominantly located in the white matter and oligodendrocytes, which also actively synthesize the major iron proteins (e.g., ferritin, transferrin). We investigated the expression of the main proteins of iron metabolism in the spinal cord (SC) of totally gastrectomized Cbl-D rats 2 months after surgery (i.e., when the Cbl-D status has become severe). There were no significant changes in iron content, the activity of iron regulatory proteins, or the expression of transferrin or its receptor in the SC. We observed a significant decrease in the levels of both H and L ferritin subunits, with a more marked reduction in the latter. Post-operative cobalamin replacement therapy normalized only the H-ferritin subunits, and only in the SC. Our results therefore suggest that permanent cobalamin deficiency affects iron metabolism in the rat SC preferentially from a functional point of view, because H-ferritin is known to be involved in the uptake and release of iron.
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PMID:Regulation of the ferritin H subunit by vitamin B12 (cobalamin) in rat spinal cord. 1211 23

Cobalamin (vitamin B12) deficiency could be masked by lack of hematological abnormalities or by concomitant conditions associated with microcytosis such as iron deficiency and thalassemia traits. We examined blood and bone marrow morphology, serum ferritin and vitamin B12 levels and fasting gastric pH in nine patients who were suspected to have vitamin B12 deficiency with unusual manifestations. Two patients had neurological symptoms without any hematological abnormalities, two had thalassemia traits, and five had achlorhydria with severe iron and B12 deficiencies. Serum B12 was low in all cases, bone marrow was diagnostic in seven cases and peripheral blood showed hypersegmentation of neutrophils only in five cases. We conclude that vitamin B12 deficiency could be masked by lack of hematological changes or by concomitant causes of microcytosis and that serum vitamin B12 levels as well as other ancillary tests should be considered in all suspected cases.
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PMID:Unusual presentation of vitamin B12 deficiency. 1759 Jun 66