Managing B12 deficiency in the time of coronavirus.
For managing pernicious anaemia at this time, there are several options:
Ask the patient if there is a nurse among their family or friends who might give them the injections. Then a prescription for B12, needles and syringes suffices.
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Ask the patient if they are happy to self-inject subcutaneously. There is no reason vitamin B12 should work any differently when diffusing into the blood from the subcutaneous fat than from muscle.
Prescribe 1,000 mcg cyanocobalamin tablets, to take 1-2 tablets daily. In patients with Pernicious Anaemia, oral B12 cannot get absorbed through the intrinsic factor route, because they do not have any. However, there is a second, much more limited route of absorption, passively through the intestinal mucosa. If symptoms return on oral medication, either the dose needs to be increased to 2,000 mcg daily, or they need to be restarted on parenteral B12.Please note: oral medication is not suitable for initial loading after diagnosis. On 1,000 mcg daily it takes c. three months for B12-deplete patients to become replete again. During this time further neurological damage can occur.
Stopping vitamin B12 treatment is dangerous for patients
For people with B12 deficiency, whether due to Pernicious Anaemia, doing without their regular treatment is simply not an option.
Irreversible neurological damage. The whole of the nervous system absolutely depends on sufficient supply of vitamin B12.
Severe loss of quality of life – debilitating fatigue, insomnia (B12 is required for synthesis of melatonin), mental illness, and neurological symptoms.
It seems reasonable to assume that patients who feel unwell due to lack of B12 will be less able to fight the coronavirus, should they get infected.
Stopping vitamin B12 treatment is as dangerous.
Some clinicians assume (incorrectly) that 1000 mcg of B12 should last patients at least 200 days, calculating from a 5 mcg daily requirement for the vitamin. Research indicates that the daily requirement may be closer to 10 mcg daily. Unfortunately, B12 is not stored in the body. After an injection, as much B12 as possible is captured by the transport protein in the blood (Transcobalamin II) and delivered to the cells. All non-protein-bound B12 is quickly excreted by the kidneys. One product leaflet for B12 states 50-98% of injected B12 is excreted with the urine. This explains why patients may experience relapse as early as 4 weeks after their last injection. When I ask patients, about 80% of them report that their symptoms return weeks or months before the next injection is due. It makes them feel unwell and puts them at risk of neurological damage.
Many patients don’t feel well on three-monthly injections. If anything, we should be shortening the interval between injections. Any excess B12 is eliminated by the kidneys.
Guidance for the frequency of injections of hydroxocobalamin:
The symptoms of B12 deficiency follow from the metabolic functions of vitamin B12. It is needed for:
Methylation – B12 is cofactor in the process that synthesises the nearly universal methyldonor in the body: S-adenosyl-methionine. Methylation is needed for synthesis of myelin, neurotransmitters (including adrenalin and melatonin), epigenetics, protein repair and much more.
Cell multiplication – While B12 is cofactor, methylfolate is the methyldonor in the above process. As a result, methylfolate is converted to tetrahydrofolate, which is required for purine synthesis – which in turn is required for DNA synthesis. Therefore both B12 and folate deficiency can result in anaemia and intestinal atrophy. However, not all patients with vitamin B12 deficiency develop anaemia.
My mnemonic for the symptoms of B12 deficiency is:
A. Any neurological symptoms:
Mind: ‘brain fog’, poor memory, poor concentration, word finding difficulties, dementia, parkinsonism, insomnia. In about 1% of patients with deficiency, optic neuropathy.
Mood: anxiety, depression – sometimes to the point of suicidality. Some even experience hallucinations and psychosis.
Sensory: pins and needles or numbness in feet and/or hands, or sometimes increased sensitivity to pain.
Motor: muscle weakness, ataxia, reduced reflexes (if peripheral neuropathy) or increased reflexes and/or upgoing plantars (if central neuropathy).
Autonomic: postural hypotension, incontinence (which often seems to be urgency incontinence).
B. Problems due to lack of cell division in fast dividing tissues:
Anaemia, or any cytopaenia (including leucocytes, lymphocytes, platelets)
Mouth ulcers, malabsorption, diarrhoea due to macrocytosis and atrophy of the intestinal mucosa.
The debilitating fatigue which seems to be the most common symtpom of B12 deficiency may be due to a combination of neurological factors, anaemia, and the role of B12 in the mitochondria.
