Mielopatia por deficiência de vitamina B12 apresentando-se como mielite transversa

Vasconcellos, Luiz Felipe Rocha; Corrêa, Rosalie Branco; Chimelli, Leila; Nascimento, Fernanda Amorim de Morais; Fonseca, Adriane Baptista; Nagel, Janaina; Novis, Sérgio A. P.; Vincent, Maurice

doi:10.1590/s0004-282x2002000100028

Cited by 7 publications

(6 citation statements)

References 13 publications

(16 reference statements)

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“…Neuropathy associated with PA classically involves disease progression, beginning in the cervicothoracic region of the spine,202,441 with upper extremity findings classically occurring before lower extremity findings, followed by peripheral nerve involvement, and lastly, if at all, brain involvement 23,200,203. Dementia is believed to be a late and rare finding of neuropathy associated with PA 19,25,48,203,290.…”

Section: Discussionmentioning

confidence: 99%

Cobalamin deficiency, hyperhomocysteinemia, and dementia

Werder¹

2010

NDT

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IntroductionAlthough consensus guidelines recommend checking serum B12 in patients with dementia, clinicians are often faced with various questions: (1) Which patients should be tested? (2) What test should be ordered? (3) How are inferences made from such testing? (4) In addition to serum B12, should other tests be ordered? (5) Is B12 deficiency compatible with dementia of the Alzheimer’s type? (6) What is to be expected from treatment? (7) How is B12 deficiency treated?MethodsOn January 31st, 2009, a Medline search was performed revealing 1,627 citations related to cobalamin deficiency, hyperhomocysteinemia, and dementia. After limiting the search terms, all abstracts and/or articles and other references were categorized into six major groups (general, biochemistry, manifestations, associations and risks, evaluation, and treatment) and then reviewed in answering the above questions.ResultsThe six major groups above are described in detail. Seventy-five key studies, series, and clinical trials were identified. Evidence-based suggestions for patient management were developed.DiscussionEvidence is convincing that hyperhomocysteinemia, with or without hypovitaminosis B12, is a risk factor for dementia. In the absence of hyperhomocysteinemia, evidence is less convincing that hypovitaminosis B12 is a risk factor for dementia. B12 deficiency manifestations are variable and include abnormal psychiatric, neurological, gastrointestinal, and hematological findings. Radiological images of individuals with hyperhomocysteinemia frequently demonstrate leukoaraiosis. Assessing serum B12 and treatment of B12 deficiency is crucial for those cases in which pernicious anemia is suspected and may be useful for mild cognitive impairment and mild to moderate dementia. The serum B12 level is the standard initial test: 200 picograms per milliliter or less is low, and 201 to 350 picograms per milliliter is borderline low. Other tests may be indicated, including plasma homocysteine, serum methylmalonic acid, antiparietal cell and anti-intrinsic factor antibodies, and serum gastrin level. In B12 deficiency dementia with versus without pernicious anemia, there appear to be different manifestations, need for further workup, and responses to treatment. Dementia of the Alzheimer’s type is a compatible diagnosis when B12 deficiency is found, unless it is caused by pernicious anemia. Patients with pernicious anemia generally respond favorably to supplemental B12 treatment, especially if pernicious anemia is diagnosed early in the course of the disease. Some patients without pernicious anemia, but with B12 deficiency and either mild cognitive impairment or mild to moderate dementia, might show some degree of cognitive improvement with supplemental B12 treatment. Evidence that supplemental B12 treatment is beneficial for patients without pernicious anemia, but with B12 deficiency and moderately-severe to severe dementia is scarce. Oral cyanocobalamin is generally favored over intramuscular cyanocobalamin.

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Section: Discussionmentioning

confidence: 99%

Cobalamin deficiency, hyperhomocysteinemia, and dementia

Werder¹

2010

NDT

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“…Megaloblastic anemia is present in most cases and in 1/3 of the cases may be absent. 13 Healton et al 10 in a study on 143 patients, who had a vitamin B12 deficiency, observed that 27.4% had normal hematocrit and 23% had a normal MCV. A bone marrow biopsy is usually hyperplastic, with a predominance of red cell precursors.…”

Section: Discussionmentioning

confidence: 97%

“…Kosik et al 12 reported the framework of a young patient with a diagnosis of pernicious anemia with acute transverse myelitis and level at T10 due to vitamin B12 deficiency. Vasconcellos et al 13 in turn, described a severe and fatal reports of transverse myelitis with sensory level, which did not respond to replacement therapy. According to Vasconcellos, the presence of sensory level denotes severe case of vitamin B12 deficiency and may be considered a finding associated with a bad prognosis.…”

Section: Discussionmentioning

confidence: 99%

“…Laboratory diagnosis of vitamin B12 deficiency can be accomplished through the dosage of cyanocobalamin or homocysteine and methylmalonic acid in the urine. 13 However, the dosage of homocysteine and methylmalonic acid have better sensitivity and specificity than cyanocobalamin, which has limited sensitivity and specificity. 14 Though infrequent, deficiency of vitamin B12 may present with normal or even increased serum level.…”

Section: Discussionmentioning

confidence: 99%

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Polyglandular Syndrome Type III and Severe Peripheral Neuropathy: An Unusual Association

Sousa

Silva

Fernandes

et al. 2015

GE Portuguese Journal of Gastroenterology

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IntroductionPolyglandular syndrome is characterized by the association of autoimmune, organ-specific, endocrine and non-endocrine diseases.ObjectiveTo present a case of polyglandular syndrome type III (b) accompanied by pernicious anemia and autoimmune thyroiditis.MethodReport the clinical case of a young patient that developed progressive and disabling peripheral neuropathy framework, triggered by vitamin B12 deficiency.DiscussionIt was proven that atrophic gastritis with positive intrinsic anti-factor was responsible for the framework of pernicious anemia, which in turn dangerously reduced the serum levels of vitamin B12, leading to myelopathy. There was a progressive neurological improvement after parenteral cyanocobalamin replacement, keeping the patient at ambulatory, under maintenance therapy.ConclusionThe importance of suspecting on polyglandular syndrome in the presence of autoimmune frameworks is important, especially those involving diabetes, thyroiditis, atrophic gastritis, pernicious anemia, vitiligo, among others.

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“…Um fator genético tem sido implicado em alguns casos de anemia perniciosa com várias gerações acometidas. Trata-se de uma doença tratável que, se diagnosticada precocemente, apresenta bom prognóstico 20 .…”

Section: Constatou-se Também No Estudo Realizado Naunclassified

Efeitos da deficiência de vitamina B12 no cérebro

Streck

Martins

Carvalho-Silva

2017

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A vitamina B12 desempenha importante papel no funcionamento das células. Sua deficiência pode levar a doenças hematológicas e neurológicas. A deficiência origina-se principalmente da dieta pobre de alimentos de origem animal e também de fatores intrínsecos, como a má absorção. Esse artigo de revisão bibliográfica aborda os principais efeitos da deficiência da vitamina B12 sobre o cérebro.

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Mielopatia por deficiência de vitamina B12 apresentando-se como mielite transversa

Cited by 7 publications

References 13 publications

Cobalamin deficiency, hyperhomocysteinemia, and dementia

Cobalamin deficiency, hyperhomocysteinemia, and dementia

Polyglandular Syndrome Type III and Severe Peripheral Neuropathy: An Unusual Association

Efeitos da deficiência de vitamina B12 no cérebro

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