Vitamin B12 Deficiency: What are the consequences?

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Pernicious Anaemia Background 

Pernicious anaemia , often seen with extreme vitamin B12 deficiency, is a chronic illness caused by impaired absorption of vitamin B12 from the intestine due to a lack of intrinsic factor (IF) (a specific transport protein require for vitamin B12 uptake) in gastric secretions. It occurs as a relatively common adult form of anaemia that is associated with gastric atrophy and a loss of IF production and as a rare congenital anaemia recessive form in which IF production is lacking without gastric atrophy. There may be a genetic link to the conditions as often more than one person in a family will have the condition. The condition may also be the result of antibodies to the parietal cells in the stomach, which leads to loss of production of both gastric acid and intrinsic factor..

General Symptoms

Pernicious anaemia may often be associated with unexplained weight loss of around 10-15 lb (4-7 kg) occurs in about 50% of patients possibly due to anorexia, which is observed in most patients. Low-grade fever occurs in one third of newly diagnosed patients and promptly disappears with treatment. The anaemia may also be accompanied by pallor, lesions of the spinal chord, weakness, sore tongue, numbness in the arm and legs, diarrhoea, sleeplessness, itchy skin,  and other symptoms, such as poorly controlled heart beat and respiratory rate..

Cardiac Symptoms

Tiredness and fatigue is associated with the anaemia (reduced red cell numbers), which is gradually restored during treatment. However, the cardiac output is usually increased with haematocrit values less than 20%, and the heart rate accelerates. This may in turn lead to congestive heart failure and coronary insufficiency particularly in patients with pre-existing heart disease.

Gastrointestinal Symptoms 

Approximately 50% of patients have a smooth tongue with loss of papillae, particularly along the edges of the tongue. The tongue may be painful and beefy red.  Many patients experience burning or soreness, most particularly on the anterior third of the tongue, and may lead to changes in taste and loss of appetite.
Altered bowel movements are common and include constipation or having several semisolid bowel movements daily. These symptoms have been attributed to megaloblastic changes of the cells of the intestinal mucosa. These changes can also be associated with altered uptake of essential nutrients such as B group vitamins.
Non-specific gastrointestinal (GI) symptoms include anorexia, heartburn, nausea, vomiting, heart burn, flatulence, and a sense of fullness.

Neurological Symptoms 

Neurologic symptoms typical of prolonged vitamin B12 deficiency can be elicited in patients with pernicious anemia. The most common of these are parasthesiae (feeling of pins and needles), weakness, clumsiness, and an unsteady gait. Impaired proprioception is worse in the dark as patients are unable to rely upon vision for compensation. These neurologic symptoms are due to myelin degeneration and loss of nerve fibres in the dorsal and lateral columns of the spinal cord and cerebral cortex.
Symptoms of long term VB12 deficiency can be seen in older patients such as senile dementia, peripheral neuropathy, and psychosis Alzheimer disease; memory loss, irritability, and personality changes delusions, hallucinations, outbursts, and paranoid schizophrenic ideation.

Genitourinary Symptoms 

Vitamin B12 deficiency can per se lead to urinary and fecal incontinence due to the neuronal consequences of inadequate VB12. The impaired micturition can predispose patients to urinary tract infections.


Typically patients who are eventually diagnosed with PA are treated by injection with cyanocobalamin or more recently hydroxycobalamin every 4 to 6 weeks. During that time they go through "overdose" initially (but without side effects), sufficiency and then deficiency. They are then re-injected and the cycle starts again. The tissues of the body have a limited ability to take up VB12 and so the majority of injected doses above 50 ug are rapidly excreted in the urine and hence the depleted stores in the liver and particularly the brain are not replenished. The continual need for re-injection of VB12 is testament to the lack of replenishment throughout the body, as in fully replete individuals, VB12 deficiency normally takes 2-5 years to manifest itself. Whilst hydroxycobalamin has been shown to be more efficient at uptake than cyanocobalamin, several studies have shown that many individuals who are severely deficient in VB12 have limited capacity to fully convert the OHCbl to Methyl and adenosylcobalamin. Whichever form of B12 provitamin (CN-Cbl or OH-Cbl)  is used, two thirds of pernicious anemia patients are unhappy with the current mode of treatment (according to a recent study in the UK). Furthermore persons with mutations in the MTRR gene have limited ability to reduce the Co(III) in CN-Cbl or OH-Cbl to Co(II) or Co(I), which is a requirement for the synthesis of the two active forms of vitamin B12, methylcobalamin and adenosylcobalamin.
Recently, a transdermal mode of vitamin B12 delivery has been developed with the distinct purpose of over-coming the "peak and trough" disadvantage of current injections> In addition this form of delivery avoids the pain and discomfort experienced during injection. Using this form of delivery of vitamin B12 the transdermal route allows a continuous release of low doses of vitamin B12 into the body. The continual trickle of vitamin B12 via the transdermal route greatly reduces the rapid loss of VB12 from the body, which occurs with injectable forms of vitamin B12 and in addition allows for greater priming of the VB12 transport protein, transcobalamin II. This in turn can potentially lead to more efficient replenishment of the liver, tissues and in particular the central nervous system. See 

Further Information on Vitamin B12 and Pernicious Anaemia

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