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Neuropathy caused by B12 deficiency in a patient with ileal tuberculosis: A case report
INTRODUCTION: Vitamin B12 deficiency can result in macrocytic anemia. Neurologic abnormalities of B12 deficiency include sensory deficits, loss of deep tendon reflexes, movement disorders, neuropsychiatric changes and seizures. Segmental involvement of the distal ileum, such as in tuberculosis, can...
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2008
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2329654/ https://www.ncbi.nlm.nih.gov/pubmed/18355418 http://dx.doi.org/10.1186/1752-1947-2-90 |
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author | Toosi, Taraneh Dormohammadi Shahi, Farhad Afshari, Ali Roushan, Nader Kermanshahi, Marjan |
author_facet | Toosi, Taraneh Dormohammadi Shahi, Farhad Afshari, Ali Roushan, Nader Kermanshahi, Marjan |
author_sort | Toosi, Taraneh Dormohammadi |
collection | PubMed |
description | INTRODUCTION: Vitamin B12 deficiency can result in macrocytic anemia. Neurologic abnormalities of B12 deficiency include sensory deficits, loss of deep tendon reflexes, movement disorders, neuropsychiatric changes and seizures. Segmental involvement of the distal ileum, such as in tuberculosis, can cause vitamin B12 deficiency. To our knowledge, macrocytic anemia with unusual manifestations such as brain atrophy and seizures due to intestinal tuberculosis has not been reported in the literature. CASE PRESENTATION: A 14-year-old girl presented with complaints of paraplegia, ataxia, fever and fatigue that had started a few months earlier and which had been getting worse in the last three weeks. Her laboratory results were indicative of macrocytic anemia with a serum B12 level <100 (normal, 160–970) pg/ml and hypersegmented neutrophils. Her MRI findings showed brain atrophy. Her fever workup eventually led to the diagnosis of tuberculosis which was documented by bone marrow aspiration smear & culture. A small bowel series showed that tuberculosis had typically involved the terminal ileum which had resulted in vitamin B12 deficiency. She was treated for vitamin B12 deficiency and tuberculosis. Her fever ceased and her hemoglobin level returned to normal. At present, she can eat, write, and speak normally as well as walk and ride a bicycle. CONCLUSION: Vitamin B12 deficiency should be considered in patients with neurologic features such as paresthesia, sensory deficits, urinary incontinence, dysarthria, and ataxia. The underlying cause of B12 deficiency should be determined and treated to obviate the patients' need for long term vitamin B12 therapy. |
format | Text |
id | pubmed-2329654 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-23296542008-04-23 Neuropathy caused by B12 deficiency in a patient with ileal tuberculosis: A case report Toosi, Taraneh Dormohammadi Shahi, Farhad Afshari, Ali Roushan, Nader Kermanshahi, Marjan J Med Case Reports Case Report INTRODUCTION: Vitamin B12 deficiency can result in macrocytic anemia. Neurologic abnormalities of B12 deficiency include sensory deficits, loss of deep tendon reflexes, movement disorders, neuropsychiatric changes and seizures. Segmental involvement of the distal ileum, such as in tuberculosis, can cause vitamin B12 deficiency. To our knowledge, macrocytic anemia with unusual manifestations such as brain atrophy and seizures due to intestinal tuberculosis has not been reported in the literature. CASE PRESENTATION: A 14-year-old girl presented with complaints of paraplegia, ataxia, fever and fatigue that had started a few months earlier and which had been getting worse in the last three weeks. Her laboratory results were indicative of macrocytic anemia with a serum B12 level <100 (normal, 160–970) pg/ml and hypersegmented neutrophils. Her MRI findings showed brain atrophy. Her fever workup eventually led to the diagnosis of tuberculosis which was documented by bone marrow aspiration smear & culture. A small bowel series showed that tuberculosis had typically involved the terminal ileum which had resulted in vitamin B12 deficiency. She was treated for vitamin B12 deficiency and tuberculosis. Her fever ceased and her hemoglobin level returned to normal. At present, she can eat, write, and speak normally as well as walk and ride a bicycle. CONCLUSION: Vitamin B12 deficiency should be considered in patients with neurologic features such as paresthesia, sensory deficits, urinary incontinence, dysarthria, and ataxia. The underlying cause of B12 deficiency should be determined and treated to obviate the patients' need for long term vitamin B12 therapy. BioMed Central 2008-03-21 /pmc/articles/PMC2329654/ /pubmed/18355418 http://dx.doi.org/10.1186/1752-1947-2-90 Text en Copyright © 2008 Toosi et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Case Report Toosi, Taraneh Dormohammadi Shahi, Farhad Afshari, Ali Roushan, Nader Kermanshahi, Marjan Neuropathy caused by B12 deficiency in a patient with ileal tuberculosis: A case report |
title | Neuropathy caused by B12 deficiency in a patient with ileal tuberculosis: A case report |
title_full | Neuropathy caused by B12 deficiency in a patient with ileal tuberculosis: A case report |
title_fullStr | Neuropathy caused by B12 deficiency in a patient with ileal tuberculosis: A case report |
title_full_unstemmed | Neuropathy caused by B12 deficiency in a patient with ileal tuberculosis: A case report |
title_short | Neuropathy caused by B12 deficiency in a patient with ileal tuberculosis: A case report |
title_sort | neuropathy caused by b12 deficiency in a patient with ileal tuberculosis: a case report |
topic | Case Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2329654/ https://www.ncbi.nlm.nih.gov/pubmed/18355418 http://dx.doi.org/10.1186/1752-1947-2-90 |
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