The patient has no previous history of HIV, diabetes, thyroid disease, syphilis, liver, kidney, diphtheria, spinal cord injuries, or exposure to heavy metals. She received omeprazole for 4 years due to recurrent dyspepsia. The patient does not smoke or drink alcohol. She regularly eats meat (weekly). An examination of her previous consultations and laboratory findings revealed the following information; Aspartate aminotransferase: 15 units / liter, alanine aminotransferase: 22 units / liter, hemoglobin: 11 g / dl, HIV test: negative, fasting blood sugar: 97 g / dl. An X-ray of the spine, performed one month before the consultation, was unremarkable. The patient took multivitamins, calcium and magnesium tablets, tramadol, prednisone and penicillin benzathine since the onset of the disease.

Physical examination:
Vital indicators are stable. Skin changes, cervical lymphadenopathy, or thyroid gland formation. Examination of the cardiovascular and respiratory systems did not reveal abnormalities, hepatomegaly or symptoms of liver disease.
Neurological examination:
Pupil size is standard, reflexes and cranial nerves are normal. Muscle tone and strength of the upper and lower extremities are normal. In addition, she has not impaired touch, perception of pain and temperature. The patient had a violation of proprioception on both upper limbs. Based on the survey data, a presumptive diagnosis of peripheral neuropathy was established, the differential diagnosis of which includes HIV-associated peripheral neuropathy, neurosyphilis and vitamin B12 deficiency.

Blood tests:
Blood tests revealed hemoglobin: 10.5 g / dl, red blood cells: 3 million / μl, reticulocytes: 0.3%, average red blood cell (MCV): 110 fl, white blood cells: 8,500 cells / μl, studies on HIV: negative, pale treponema hemagglutination test (TPHA): negative, erythrocyte sedimentation rate (ESR): 10 mm / h, peripheral blood smear: oval-macrocytosis and hyper-segmented neutrophils. Based on the symptoms, peripheral neuropathy associated with vitamin B12 deficiency was diagnosed.

The patient received oral vitamin B12 tablets in a daily dose of 2 mg for three months. One month after the start of therapy, the patient showed a decrease in the severity of neurological symptoms, and in the subsequent results of a blood test, the following result was obtained: MCV 97 fl, red blood cells 4.1 million / μl and the number of reticulocytes 0.95%.

Mandatory laboratory tests, such as a general blood test (OAC) and a smear analysis of peripheral blood are extremely important for the diagnosis of this pathology in the present case [12]. Oval macrocytes, as well as hypersegmented neutrophils, are the most important arguments in favor of vitamin B12 deficiency [13], mainly in conditions of the inaccessibility of determining serum cyanocobalamin, methylmalonic acid, and homocysteine. However, studies have shown that serum vitamin B12 levels are unpredictable in assessing vitamin B12 deficiency [5]. Serum transcobalamin II and methylmalonic acid levels are considered the most specific laboratory parameters. However, hypersegmented neutrophils, according to literature, have a sensitivity of 98% compared with serum cyanocobalamin with a sensitivity of 90–95%. Thus, a peripheral blood smear test is a cost-effective tool in diagnosing vitamin B12 deficiency.
Antibodies against Castle's intrinsic factor and gastric parietal cells also play a very important role in the diagnosis of vitamin B12 deficiency. Conversely, malabsorption due to possible pernicious anemia or the use of omeprazole were the most likely causes in the present case [12].
Various parenteral and oral vitamin B12 replacement therapy methods are currently available. The patient from the presented case received therapy with vitamin B12 tablets orally due to the inaccessibility of parenteral forms. Vitamin B12 is known to be actively absorbed by combining it with Castle's intrinsic factor. However, 1-2% of vitamin B12 is absorbed passively [14], and therefore oral replacement therapy can be as effective as parenteral therapy if large doses are given orally (2 mg per day).

The case presented highlights the role of vitamin B12 deficiency in patients with symptoms of peripheral neuropathy. He also draws attention to the role in the basic examination played by a peripheral blood smear and trial therapy, which are critical for the timely diagnosis and treatment of vitamin B12-related neurological disease in conditions of limited resources.

1. Rusher DR, Pawlak R. A review of 89 published case studies of vitamin B12 deficiency. J Hum Nutr Food Sci. 2013;1(2):1008.

2. Stabler Sally P. Vitamin B12 deficiency. N Engl J Med. 2013;368:149–160.

3. Lindenbaum J, Healton EB, Savage DG, et al. Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis. N Engl J Med. 1988;318:1720–1728.

4. Green R, Kara N, Cocks H. Vitamin B, deficiency: an unusual cause of vocal fold palsy. J Laryngol Otol. 2011;125:1309–1311.

5. Wong CL, Van Spall HG, Hassan KA, Coret-Simon J, Sahlas DJ, Shumak SL. A young man with deep vein thrombosis, hyperhomocysteinemia and cobalamin deficiency. Can Med Assoc J. 2008;178:279–281.

6. Molloy A, Cawley N, Ali E, Connolly S, Tubridy N, Hutchinson M. A pernicious leucoencephalopathy. Ir Med J. 2009;102:292–294.

7. Srikanth SG, Jayakumar PN, Vasudev MK, Taly AB, Chandrashekar HS. MRI in subacute combined degeneration of spinal cord: a case report and review of literature. Neurol India. 2002;50:310–312

8. Goebels N, Soyka M. Dementia associated with vitamin B12 deficiency: presentation of two cases and review of the literature. J Neuropsychiatry Clin Neurosci. 2000;12:389–394.

9. Sahoo MK, Avasthi A, Singh P. Negative symptoms presenting as neuropsychiatric manifestation of vitamin B12 deficiency. Indian J Psychiatry. 2011;53:370–371.

10. Milanlioglu A. Vitamin B12 deficiency and depression. J Clin Exp Investig. 2011;2:455–456.

11. Wilkinson Iain, Lennox Graham. Essential Neurology. 4. Oxford: Blackwell; 2005. p. p161.

12. Snow FC. Laboratory diagnosis of vitamin B12 and folate deficiency. Arch Intern Med. 1999;159:1289–1298.

13. Lindebaum J, Nath BJ. Megaloblastic anaemia and neutrophil hypersegmentation. Br J Haematol. 1980;44:511–513.

14. Berlin H, Berlin R, Brante G, Pilbrant A. Vitamin B12 body stores during oral and parenteral treatment of pernicious anaemia. Acta. Med. Scand. 1978;204(1–2):81–84.