Clinical and laboratory features and response to treatment in patients presenting with vitamin B12 deficiency-related neurological syndromes

Abstract

Aims and objectives: To study the clinical and laboratory features of patients admitted with vitamin B 12 deficiency-related (B 12 def) neurological syndromes. Settings and Design: A hospital-based retrospective and prospective study conducted at a referral teaching hospital. Materials and Methods: Consecutive patients admitted with vitamin B 12 deficiency-related neurological disorders during a three-year period from June 2000 to May 2003 were included. Data regarding clinical and laboratory features were obtained. Follow-up was done at least six months following treatment with parenteral vitamin B 12. Chi-square test was used for statistical analysis. Results: A total of 63 patients (52 males) with a mean age of 46.2 years were studied. The mean duration of symptoms at presentation was 10.3 months. Myeloneuropathy (54%) was the commonest neurological manifestation, followed by myeloneuropathy with cognitive dysfunction (34%), and peripheral neuropathy (9%). Neuropsychiatric manifestations and dementia were observed in 38% and 19% of patients respectively. All the patients had megaloblastic changes in the bone marrow smear. Eleven (17.5%) patients had both hemoglobin and the mean corpuscular volume (MCV) within the normal range. Follow-up after at least six months of therapy with parenteral B12 showed improvement in 54% patients. Conclusions: A high index of suspicion of B 12 def is required in patients presenting with myelopathy, cognitive decline, or neuropathy. A normal hemoglobin or MCV does not exclude B 12 def; therefore, other tests such as bone marrow smear and serum vitamin B 12 assay are essential, as the condition is often reversible with treatment.

Reversible ecchymosis and hyperpigmented lesions: A rare presentation of dietary Vitamin B12 deficiency

“…These manifestations are reversible after the Vitamin B12 supplementation. [23] A hypothesis explained hyperpigmentation in Vitamin B12 deficiency due to increase synthesis of melanin with increased melanosomes in the basal layer of skin by decreasing the level of reduced glutathione, which activates tyrosinase and thus leads to transfer to melanosomes; a defect is also described in the melanin transfer between melanocytes and keratinocytes, resulting in pigmentary incontinence. [45] The patients with nutritional Vitamin B12 deficiency also had bleeding manifestations and qualitative abnormalities of platelets, i.e., abnormal aggregation to adenosine diphosphate, collagen, epinephrine, and ristocetin.…”

“…The cutaneous symptoms of disease are rare, these include vitiligo, angular glossitis, hyperpigmented lesions of the skin, sparse hypopigmented hairs, and hemorrhages. [12] The hyperpigmentation in Vitamin B12 deficiency is explained because of increased melanin synthesis. The presence of thrombocytopenia in Vitamin B12 deficiency is common finding because of dyshemopoietic in the bone marrow.…”

Mild Cognitive Impairment: Clinical and Imaging Profile in a Memory Clinic Setting in India

“…One third had vascular aetiology, reflecting the high prevalence of cardiovascular disease in India [20 ]and consistent with studies that have demonstrated the association between vascular disease and cognitive impairment [40]. Vitamin B 12 deficiency was an important reversible cause of cognitive dysfunction, a reflection of the frequent occurrence of vitamin B 12 deficiency-related dementia in India [41]. …”

Reversible Vitamin B12 Deficiency Presenting with Acute Dementia, Paraparesis, and Normal Hemoglobin

“…At the same time, serum vitamin B12 levels need not to be very low in order to produce psychiatric symptoms [10]. It has been shown that vitamin B12 levels become deficient in neuronal tissue before deficiency is evident in the serum [11]. In such cases, homocysteine and methylmalonic acid assays increase the specificity of the diagnosis of B12 deficiency [12].…”