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MYELOPATHY INDUCED BY VITAMIN B12 DEFICIENCY IN THE PRESENCE OF PERNICIOUS ANEMIA: CASE REPORT

RESUMO

CASE PRESENTATION:
I.F.W, female, 65 years old, with diabetes mellitus and hypothyroidism, with no history of alcoholism or gastrointestinal complaint. She started a progressive picture of paraparesis, hypoesthesia below T10, urinary and fecal retention more than 30 days ago. On physical examination, she was lethargic, a force preserved in the upper limbs and reduced in the lower limbs. Hypoesthesia at T10 level, paresthesia and dysesthesia in feet and hands bilaterally, in addition to hypopalestinian and proprioception abolished in lower limbs.
Normal CSF, serological tests for syphilis, HIV, HTLV and normal liver function, blood count with pancytopenia, normal iron and folic acid profile, and vitamin B12 < 50 mg/dL. High digestive endoscopy with biopsy confirming pernicious anemia. Normal magnetic resonance imaging (MR) of the skull and cervical spine, and in the dorsal column, the presence of hypersignal in the posterior portion of the spinal cord at T10 and T11 levels, considering subacute degeneration due to vitamin B12 deficiency.
In view of the predominant clinical picture of a posterior cord, the diagnosis of myelopathy due to vitamin B12 deficiency was established. Parenteral replacement was initiated with a slight improvement up to discharge, considering the time of evolution and involvement of nervous fibers.
DISCUSSION:
Vitamin B12 deficiency is caused by bad gastrointestinal absorption, insufficient diet or genetic defects, and anemia is pernicious due to the absence of intrinsic factors. There are several neurological manifestations, including myelopathy, neuropathy, cognitive alterations and others. The motor deficit results from involvement of pyramidal pathways associating the hypoPalestinian and batiesthesia due to posterior twonal involvement, and the paresthesias due to polyneuropathy, usually axonal pattern.
Such a vitamin is a coenzyme in metabolic functions, and neuronal damage occurs by accumulation of methylmalonyl coenzyme A and increase of methylmalonic acid (MMA) and homocysteine, compromising normal myelin synthesis. The diagnosis is made by the clinic, imaging examination and vitamin B12 and/or homocysteine or urinary MMA dosage.
FINAL COMMENTS:
Neurological clinical presentation with definition of sensitive level of B12 deficiency is rare and of worse prognosis, and it is essential to suspect myelopathy cases, since early identification with immediate treatment may result in better outcomes for the patient.