Abstract
Cobalamin-deficient (Cbl-D) central neuropathy in the rat is associated with a locally increased expression of neurotoxic tumour necrosis factor-alpha (TNF-alpha) and a locally decreased expression of neurotrophic epidermal growth factor (EGF). These recent findings suggest that cobalamin oppositely regulates the expression of TNF-alpha and EGF, and raise the possibility that these effects might be independent of its coenzyme function. Furthermore, adult Cbl-D patients have high levels of TNF-alpha and low levels of EGF in the serum and cerebrospinal fluid. Serum levels of TNF-alpha and EGF of cobalamin-treated patients normalize concomitantly with haematological disease remission. These observations suggest that cobalamin deficiency induces an imbalance in TNF-alpha and EGF levels in biological fluids that might have a role in the pathogenesis of the damage caused by pernicious anaemia.
MeSH terms
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Anemia, Pernicious / blood
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Anemia, Pernicious / cerebrospinal fluid
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Anemia, Pernicious / drug therapy
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Anemia, Pernicious / metabolism*
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Animals
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Central Nervous System / drug effects
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Central Nervous System / metabolism*
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Disease Models, Animal
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Epidermal Growth Factor / blood
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Epidermal Growth Factor / cerebrospinal fluid
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Epidermal Growth Factor / metabolism
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Gastrectomy
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Humans
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Nerve Degeneration / blood
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Nerve Degeneration / cerebrospinal fluid
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Nerve Degeneration / drug therapy
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Nerve Degeneration / metabolism*
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Nerve Growth Factor / blood
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Nerve Growth Factor / cerebrospinal fluid
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Nerve Growth Factor / metabolism
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Rats
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Tumor Necrosis Factor-alpha / cerebrospinal fluid
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Tumor Necrosis Factor-alpha / metabolism
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Vitamin B 12 / pharmacology
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Vitamin B 12 / therapeutic use
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Vitamin B 12 Deficiency / blood
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Vitamin B 12 Deficiency / cerebrospinal fluid
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Vitamin B 12 Deficiency / drug therapy
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Vitamin B 12 Deficiency / metabolism*
Substances
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Tumor Necrosis Factor-alpha
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Epidermal Growth Factor
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Nerve Growth Factor
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Vitamin B 12