Abstract
Background
Vitamin B12, or cobalamin, is a nutrient that is vital for metabolic function. Absorption
of ingested B12 is dependent on intrinsic factor, which is secreted by parietal cells
within the stomach. Pernicious anemia is caused by an intrinsic factor deficiency
or autoantibodies against intrinsic factor. The presence of parietal cell antibodies
can destroy parietal cells, which can also lead to a deficiency in intrinsic factor.
Both lead to megaloblastic anemia caused by vitamin B12 deficiency. The typical presentation
of pernicious anemia includes fatigue, pale appearance, tingling sensation, depression,
alterations to vision and smell, urinary incontinence, psychotic episodes, and weakness.
The most effective treatment for pernicious anemia is intramuscular B12.
Case Report
A 27-year-old woman with a history of vitiligo presented to the emergency department
(ED) with bilateral lower extremity weakness, clumsiness, numbness, and tingling.
Physical examination revealed ataxia, no sensation below her umbilicus, decreased
strength, and hyperreflexia in both lower extremities. Complete blood count in the
ED revealed low hemoglobin and hematocrit and elevated mean corpuscular volume, concerning
for pernicious anemia. Further laboratory testing upon inpatient admission revealed
a low vitamin B12 level and parietal cell antibodies in the blood. The patient's pernicious
anemia was treated with intramuscular vitamin B12 injections, which led to near complete
resolution of her symptoms.
Why Should an Emergency Physician Be Aware of This?
Early suspicion and detection of pernicious anemia in the ED can prevent serious and
permanent hematologic and neurologic damage and the development of other autoimmune
disorders.
Keywords
To read this article in full you will need to make a payment
Purchase one-time access:
Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online accessOne-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:
Subscribe to Journal of Emergency MedicineAlready a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect
References
- Marks’ Basic Medical Biochemistry: A Clinical Approach.5th edn. Wolters Kluwer, 2018
- Autoimmune mechanisms in pernicious anaemia & thyroid disease.Autoimmun Rev. 2015; 14: 763-768
- Optimal management of pernicious anemia.J Blood Med. 2012; 3: 97-103
- Pernicious Anemia.StatPearls Publishing, 2022 (Accessed May 27, 2022)
- Comorbid autoimmune diseases in patients with vitiligo: a cross-sectional study.J Am Acad Dermatol. 2016; 74: 295-302
- Comorbidities associated with vitiligo: a ten-year retrospective study.Dermatology. 2013; 227: 311-315
- Epidemiology of vitiligo, associated autoimmune diseases and audiological abnormalities: Ankara study of 80 patients in Turkey: Clinical, laboratory and genetic aspects of vitiligo.J Eur Acad Dermatol Venereol. 2010; 24: 1144-1150
- Vitiligo and associated autoimmune disease: retrospective review of 300 patients.J Cutan Med Surg. 2012; 16: 261-266
- Vitiligo, hypothyroidism and cardiomyopathy.Indian J Endocr Metab. 2012; 16: 463
- Severe weight loss in a hypothyroid patient as an acute presentation of autoimmune polyglandular syndrome type II.Hormones. 2022; 21: 317-322
- Vitiligo and pernicious anemia.N Engl J Med. 2004; 350: 2698
- Prevalence of MR imaging abnormalities in vitamin B12 deficiency patients presenting with clinical features of subacute combined degeneration of the spinal cord.J Neurol Sci. 2014; 342: 162-166
- Neuroanatomy Atlas in Clinical Context: Structures, Sections, Systems, and Syndromes.10th edn. Wolters Kluwer, 2019
- Neurologic signs in Addison-Biermer disease (report of 3 cases)).Neurol Neurochir Pol. 1997; 31: 35-41
- Vitamin B 12 deficiency – A 21st century perspective.Clin Med. 2015; 15: 145-150
Article info
Publication history
Published online: October 28, 2022
Accepted:
October 21,
2022
Received in revised form:
October 6,
2022
Received:
July 7,
2022
Identification
Copyright
© 2022 Elsevier Inc. All rights reserved.