The relationship between Vitamin B Complex and Neuropathic Pain: Case Report
In the present study, a case of a 28-year-old sub-Saharan female is presented with insidious onset of painful burning sensations on the upper trunk, symmetrical numbness and tingling sensation on the hands and feet, progressing over a 5 year period. These symptoms began as intermittent burning sensations on the scapulae and pectoral regions of the upper trunk, which progressed to numbness and paraesthesia of the upper and lower limbs respectively. These were associated with mild weakness of the hands and feet, insomnia, irritability and constipation. There were no urinary symptoms, paralysis, gait disturbances, tremors, jaundice, limb swelling, changes in skin colour, or delusion.
She had no known history of Human Immunodeficiency Virus (HIV) infection, diabetes, thyroid disease, syphilis, liver disease, renal disease, diphtheria, spinal cord injury or exposure to heavy metals. She had been on omeprazole for 4 years for recurrent dyspepsia. She neither smokes nor consumes alcohol. She consumes meat regularly on weekly basis. A review of her previous consultations and laboratory results showed the following results; Aspartate aminotransferase: 15 U/I, Alanine aminotransferase: 22 U/I, Haemoglobin: 11 g/dl, HIV test: negative, fasting blood sugar: 97 g/dl. Spinal x-ray done 1 month prior to the consultation was unremarkable. She had taken multivitamins, calcium and magnesium tablets, tramadol, prednisolone, and benzathine penicillin since the onset of illness. Despite these medications, there was no reduction in her symptoms.
Examination and Lab Investigations:
Vital signs were stable. There were no skin changes, cervical adenopathy, or thyroid mass. The cardio-respiratory examination was normal and no hepato-splenomegaly or symptoms of liver disease.
She had standard pupillary size, reflexes and cranial nerves. Her muscle tone and power on both upper and lower limbs were normal. In addition, she had the normal sensation to touch, pain and temperature. She had impaired proprioception in both upper limbs. Based on these examinations, she has speculated a peripheral neuropathy with HIV peripheral neuropathy, neurosyphilis, and vitamin B12 deficiency as differentials.
Her blood tests report showed Hemoglobin: 10.5 g/dl, Red blood cell count: 3 million/mcL, reticulocyte count: 0.3%, Mean Corpuscular Volume (MCV):110 fl, WBC: 8500 cells/μl, HIV test: negative, Treponema pallidum hemaglutinin assay (TPHA): negative, erythrocyte sedimentation rate (ESR): 10 mm/h, and peripheral blood smear analysis: ovalo-macrocytosis, and hypersegmented neutrophils. Based on her symptom, vitamin B12 deficiency related peripheral neuropathy was diagnosed.
She was treated with oral vitamin B12 tablets, at doses of 2 mg daily for three months. One month of therapy was marked with improvement in neurological symptoms and a follow-up MCV of 97 fl, red blood cell count of 4.1 million/µl, and reticulocyte count of 0.95%.
B-vitamins are essential water-soluble vitamins which are necessary for cellular metabolism and maintenance of the integrity of the nervous system . Its deficiency has numerous aetiologies, which include; lack of intrinsic factor, nutritional deficiency, malabsorption and competition for VB12 [2, 3].
The primary neurological symptoms associated with vitamin B12 deficiency includes: paraesthesia , ataxia , and limb weakness , delusions , irritability , and decreased interest . Other indications included depression and sleep disturbances . These symptoms are also associated with other common diseases like HIV infection, diabetes, syphilis, alcoholism, and some medications, thus posing a diagnostic challenge .
Necessary laboratory examinations like full blood count (FBC) and peripheral blood smear analysis are vital in the diagnosis of this pathology as evidenced by the present case . Ovalo-macrocytosis and hypersegmented neutrophils are essential judgments in VB12 deficiency , mainly in settings were serum cyanocobalamin, methylmalonic and homocysteine levels cannot be assessed. However, studies have designated that serum levels of VB12 can be unpredictable for the assessment of VB12 deficiency . Levels of serum transcobalamin II and methylmalonic acid are considered the most specific laboratory indications. Nonetheless, Hyper-segmented neutrophils are 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.
Anti-intrinsic factor and anti-parietal cell antibodies are also essential factors for the diagnosis of VB12 deficiency. Conversely, mal-absorption from probable pernicious anaemia or omeprazole use was the most likely aetiologies considered in this case.
The various parenteral and oral methods of VB12 replacement therapy are available. The patient in the present study was controlled 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).
The present case study highlights the role of Vitamin B12 deficiency in patients with peripheral neuropathic symptoms. It also marks the role of basic examinations like peripheral blood smear and the vitality of therapeutic trials, which are crucial to the timely detection, and management of vitamin B12 associated neurological disease in resource-limited settings.
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