I am concerned about a man with neuropathy for several years. In addition, he now has diabetes type II (diabetes of adults). His neuropathy started prior to any laboratory signs of cobalamin deficiency. After confirmed diagnosis of cobalamin deficiency, treatment modes have varied. The clinical response and the laboratory response on treatment are difficult to evaluate. How do you tackle problems of this sort?

Dear Sven Axel,

I prefer to avoid sophisticated investigations and evaluations by regarding such a patient as a patient with a new diagnosis of cobalamin deficiency. Since much of the ordinary investigations are veiled by previous treatment, a stringent test treatment with cobalamin is crucial.

One problem with patients of this sort is that an incipient deficiency of other nutrients may block the effect of cobalamin (cf 1,2). Consequently, the patient should be provided with a broad spectrum of nutrients in order to avoid unpleasant surprises and misinterpretations.

During remission treatment, the patient should have oral cobalamin, 2-4 mg daily. The oral folic acid supplementation should be about 5mg daily, the oral pyridoxin supplementation 10-40 mg daily. Remission treatment should continue for 3-5 months on an average.

The maintenance therapy may be performed with oral cobalamin, 1 mg daily. Some patients need 2 mg daily in order to achieve serum levels between 500 and 1,000 pmol/L, a classical therapeutic range. In oral cobalamin therapy, the serum levels are thought to reflect body stores of cobalamin. Conversely, in parenteral therapy serum levels of cobalamin reflect transportation from injection site to body tissues.

During maintenance therapy, the patient should be supplemented with at least 0.4 mg of folic acid and two or three mg of pyridoxin. Usually, some combined vitamin preparation may be found, which meets these minimum demands. The rule of thumb is that about 50-100% of daily requirements of vitamins should be administered as tablets or capsules. Especially in elderly, cobalamin deficiency is seldom an isolated phenomenon.

I would like to emphasize some mementos. Not all neeuropathies are due to cobalamin deficiency. The patient response to oral cobalamin therapy is sometimes swift, within days or weeks, but usually slow, within months and years. Test treatment for three years is advised in order to exclude cobalamin deficiency as cause of a neuropathy. Furthermore, serum levels of cobalamin rise slowly during oral cobalamin treatment, within months. This phenomenon in thought to reflect swift transportation to the tissues. The half-time of serum transcobalamin is about four hours.

It is not wrong to choose parenteral cobalamin therapy. In fact, it is still predominant in all countries except Sweden, where approximately two out of three patients were treated with oral high-dose cyanocobalamin by 1998 (3). The guidelines above only reflect my personal preferences at present. With kind regards! Yours sincerely!/Bo Norberg