Vitamin B12 is an essential water soluble vitamin which is important in cellular metabolism and maintenance of the integrity of the nervous system . VB12 deficiency has numerous aetiologies which include; lack of intrinsic factor, nutritional deficiency, malabsorption and competition for VB12 [1, 4, 5].
The main neurological symptoms include: paraesthesia [8,9,10,11,12], ataxia [9,10,11,12], and limb weakness [9, 11]. The most prevalent psychiatric symptoms associated with B12 deficiency include, delusions [12, 13], irritability [13, 14], and decreased interest [15, 16]. Other manifestations included depression [12, 16] and sleep disturbances [12, 16]. These neurological symptoms are associated with other common illnesses like HIV infection, diabetes, syphilis, alcoholism, and some medications, thus posing a diagnostic challenge .
Basic laboratory investigations like full blood count (FBC) and peripheral blood smear analysis are vital in the diagnosis of this pathology  as evidenced by our case. Ovalo-macrocytosis and hyper-segmented neutrophils are important findings in VB12 deficiency , especially in settings were serum cyanocobalamin, methylmalonic and homocystein levels cannot be assessed. However, studies have designated that serum levels of VB12 can be unreliable for the assessment of VB12 deficiency . Serum Transcobalamin II and methylmalonic acid levels are at present considered the most specific laboratory indices . Nonetheless, Hyper-segmented neutrophils is reported to have a sensitivity of 98% , compared to serum cyanocobalamin with a sensitivity of 90–95% . Thus, making peripheral blood smear analysis a cost effective tool in the diagnosis of VB12 deficiency, especially in settings like ours.
Anti-intrinsic factor and anti-parietal cell antibodies are important in diagnosing pernicious anaemia; a major aetiology of VB12 deficiency . Conversely, mal-absorption from probable pernicious anaemia or chronic omeprazole use was the most likely aetiologies considered in this case. The response to oral VB12 supplement therefore pointed to chronic omeprazole use because intrinsic factor is needed for oral absorption.
The various methods of VB12 replacement therapy includes parenteral and oral . Our patient was managed with oral VB12 tablets due to unavailability of the parenteral forms. It is known that VB12 is absorbed actively through its association with intrinsic factor. However, 1–2% of VB12 absorption occurs passively , thus oral replacement therapy can be as effective as parenteral therapy provided they are administered at high doses (2 mg daily) .
Therapeutic trials have also played vital roles in confirming VB12 deficiency, especially with follow up increases in MCV, RBC and Reticulocyte count [7, 24]. Follow up analysis of our case showed normalization of MCV, RBC and reticulocyte counts, which are important indices to assess therapeutic diagnosis and response in patients with VB12 deficiency.
This case emphasizes the importance of increased index of suspicion of Vitamin B12 deficiency in patients presenting with peripheral neuropathic symptoms. It also underscores the invaluable role of basic investigations like peripheral blood smear and the vitality of therapeutic trials which are pivotal to the timely detection and management of vitamin B12 associated neurological disease in resource-limited settings. Although this pathology is common in the old, young patients should be considered.