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Thursday, 11 August 2011

What Happens When You Have Vitamin B-12 Deficiency

Vitamin B-12 or cobalamin plays a vital role in DNA synthesis and neurological function. Deficiency can lead to a wide range of hematological and neuropsychiatric disorders that can often be cured provided treatment is given during early stages of diagnosis.

It is an important vitamin that is acquired by the body through various kinds of food items.

It is more often found in meat as well as diary products like milk, cheese, curd, butter, etc. and its helps in producing red blood cells and ensures smooth functioning of the nervous system. Usually individuals who do not eat meat or have adequate amount of dairy products tend to have low vitamin B-12, however, it is not always the case. In some cases, Vitamin B-12 deficiency is seen in people owing to their inability to absorb the vitamin through their stomach or small intestines.

Among humans, only two enzymatic reactions are found to be based on vitamin B-12. In the first reaction, methylmalonic acid is converted to succinyl-CoA using vitamin B-12 as a cofactor. In individuals with vitamin B-12 deficiency, there is an increased level of serum methylmalonic acid.

In the second reaction, homocysteine is converted to methionine by using vitamin B-12 and folic acid as cofactors. In this reaction, a deficiency of vitamin B-12 or folic acid may lead to increased homocysteine levels.

The true cause of vitamin B-12 deficiency in the general population is unknown, however, the number of cases is comparatively higher among middle as well as old aged. This condition is evident mainly due to increased intake of gastric acid-blocking agents used predominantly for ulcers and heartburns, which can lead to decreased vitamin B-12 levels.

The actual causes of vitamin B12 deficiency can be divided into three classes: nutritional deficiency owing to lack of nutrition in the diet; mal absorption syndromes by certain parts of the body and other gastrointestinal causes. Vitamin B-12 deficiency is a common cause of macrocytic anemia. The role of B-12 deficiency in hyperhomocysteinemia and the promotion of arteriosclerosis are only now being explored.

Diagnosis of vitamin B-12 deficiency is based on calculating the serum vitamin B-12 levels in the blood.

Apart from nutritional deficiency or mal absorption syndromes, vitamin B-12 deficiency can also be due to chronic gastrointestinal symptoms such as dyspepsia, recurrent peptic ulcer disease, or diarrhea.

Apart from these, in rare cases, the deficiency could be due to Whipple's disease which is a rare bacterial infection that impairs absorption; Zollinger-Ellison syndrome which is gastrinoma causing peptic ulcer and diarrhea or Crohn's disease.

Patients with a history of intestinal surgery, strictures, or blind loops may have bacterial overgrowth which might take away all the dietary vitamin B-12 in the small bowel. Same is the case when a person is infested with tapeworms or other intestinal parasites. Congenital transport-protein deficiencies, including transcobalamin II deficiency, are some of the other rare causes of vitamin B12 deficiency.

If the level of vitamin B-12 goes much below normal, then the individual may suffer from anemia, depression, dementia or a serious problem with the nervous system. In some severe cases, people have high levels of homocysteine owing to the presence of an amino acid in the blood.

These symptoms would make the individual more susceptible to heart diseases or strokes. Some of the main causes of this disorder wherein there is reduced absorption of vitamin B-12 are pernicious anemia wherein the cells in the stomach with the ability to absorb vitamin B-12 are destroyed; excessive usage of medication for heartburn and ulcers and/or surgery of the stomach or intestine resulting in an inability to absorb vitamin B-12.

Treatment for Vitamin B-12 deficiency cannot be done by taking over-the-counter vitamin tablets but through special vitamin B-12 pills or injections.

During the beginning of the treatment, the injections are administered more frequently which is 1 to 2 days for about 2 weeks and then once every month which needs to be taken usually rest of their lives.

Once a person has been diagnosed to have vitamin B-12 deficiency, a treatment plan needs to be put together which should have adequate follow-ups to ensure that the patient is responding favorably to therapy.

If vitamin B-12 deficiency is associated with severe anemia, correction of the deficiency state should lead to a marked reticulocytosis in one to two weeks. In mild vitamin B-12 deficiency, repeat tests of the serum vitamin B-12, homocysteine, and methylmalonic acid levels over two to three months after initiating treatment should be undertaken.

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