The important role of vitamin B12



Vitamin B12 benefits,Vitamin B12 deficiency, Oral therapy


   What is vitamin B-12?

Vitamin B-12 is an important vitamin that you should get their food. It is found primarily in fish, shellfish, meat and dairy products. Vitamin B-12 helps make red blood cells and DNA, and keeps your nervous system working properly.

Most people with low vitamin B-12 levels or not consume meat products and milk or who have trouble absorbing vitamin B-12 of the stomach or small intestine. Vegetarians, vegans (strict vegetarians who eat no animal products) and the elderly are most at risk of not getting enough vitamin B-12.

  What can cause problems with absorbing vitamin B-12?

The following are some things that can cause problems with absorbing vitamin B-12:

   ~  Having a disease called pernicious anemia that destroys the cells in your stomach that help you absorb vitamin B-12.
   ~  Having an intestinal condition that interferes with the way your body absorbs food, such as Crohn's disease or celiac disease.
   ~  Having abnormal bacterial growth in your stomach.
   ~  Taking certain medicines that are used to treat heartburn and ulcers for a long time.
   ~  Having had surgery on your stomach or your intestines, such as gastric bypass surgery.
Your doctor will find out why you have a low vitamin B-12 level by asking questions about your health, giving you a physical exam and checking your blood. He or she may need to do other tests to check for a low level of vitamin B-12.

   Vitamin B-12 Deficiency

Vitamin B12 (cobalamin) deficiency is a common cause of macrocytic anemia and has been involved in a spectrum of neuropsychiatric disorders. The role of vitamin B12 deficiency in hyperhomocysteinemia and the promotion of atherosclerosis is only now being studied. The diagnosis of vitamin B12 deficiency is typically based on measuring serum vitamin B12, however, about 50 percent of patients with subclinical disease have normal levels of vitamin B12. A more sensitive method of screening for vitamin B12 deficiency is a measure of serum methylmalonic acid and homocysteine levels, which rose in early vitamin B12 deficiency. Use of the Schilling test for the detection of pernicious anemia has been largely supplanted by serological tests for antibodies to parietal cells and intrinsic factor. Contrary to current medical practice, studies show that supplementation of vitamin B12 orally is a safe and effective treatment for the condition of vitamin B12. Even when intrinsic factor is not present to help the absorption of vitamin B12 (pernicious anemia) or other diseases that affect the usual absorption sites in the terminal ileum, oral therapy is effective.

Vitamin B12 (cobalamin) plays an important role in DNA synthesis and neurologic function. A deficiency can lead to a wide range of hematological and neuropsychiatric disorders can often be reversed by early diagnosis and prompt treatment.

The prevalence of vitamin B12 in the general population is unknown. The impact, however, seems to increase with age. In one study,  15 percent of adults over 65 had laboratory findings of vitamin B12. The use almost everywhere gastric acid inhibitors, which can lead to lower levels of vitamin B12. May play a role in the development of vitamin B12 undervalued. Noting the widespread use of these agents and the aging U.S. population into account, the true prevalence of vitamin B12 deficiency may be even higher than statistics indicate. Despite these facts, the need for universal screening in the elderly remains controversial.

   Clinical Manifestations

Vitamin B12 deficiency is associated with haematological, neurological and psychiatric disorders. It is a common cause of macrocytic (megaloblastic) anemia and, in advanced cases, pancytopenia. Neurologic sequelae of vitamin B12 deficiency include paresthesia, peripheral neuropathy, and demyelination of the corticospinal tract and dorsal columns (subacute combined systems disease). Vitamin B12 deficiency has also been linked to psychiatric disorders, including memory problems, irritability, depression, dementia and, more rarely, psychosis.

In addition to hematologic and neuropsychiatric manifestations, vitamin B12 deficiency may exert indirect cardiovascular effects. Similar to folic acid deficiency, vitamin B12-teinemia hyperhomocys product, which is an independent risk factor for atherosclerosis disease. Although the role of folic acid in reducing homocysteine levels as a method to prevent coronary heart disease and stroke continues to be a topic of great interest, it has little focus on the potential role of vitamin B12 deficiency as a factor contributing to the development of cardiovascular disease. This is particularly important when one considers the replacement therapy of vitamins. Folic acid supplementation may mask B12 deficiency and cause or exacerbate occult neurological disease. Therefore, physicians should consider excluding B12 deficiency before starting therapy with folic acid.

  Normal Absorption of Vitamin B-12

In humans, only two enzymatic reactions are known to be dependent on vitamin B12. In the first reaction, methylmalonic acid is converted to succinyl-CoA with vitamin B12 as a cofactor. B12 deficiency can lead to serum levels of methylmalonic acid. In the second reaction, homocysteine is converted to methionine using vitamin B12 and folic acid as cofactors. In this reaction, a deficiency in vitamin B12 or folic acid may increase homocysteine levels.
Understanding the cycle of vitamin B12 helps to illuminate the potential causes of deficiency. The acidic environment of the stomach facilitates the distribution of vitamin B12 that is bound to food. Intrinsic factor, which is released by parietal cells of the stomach, binds vitamin B12 in the duodenum. This complex intrinsic factor-vitamin B12 aids subsequently the absorption of vitamin B12 in the terminal ileum.

In addition to the absorption method, the evidence supports the existence of an alternative system that is independent of intrinsic factor or even an intact terminal ileum. About 1 percent of a large dose of vitamin B12 orally is absorbed by this second mechanism. This route is important in relation to oral replacement. Once absorbed, vitamin B12 bound to transcobalamin II and is carried throughout the body. The interruption of one or any combination of these steps places a person at risk of developing deficits.



   Diagnosis of Vitamin B12 Deficiency

The diagnosis of vitamin B12 deficiency is traditionally based on serum vitamin B12 low, usually less than 200 pg / ml (150 pmol / L) with clinical signs of disease. However, studies indicate that older patients tend to have neuropsychiatric disorders, in the absence of hematological findings.5, 6 In addition, measurements of metabolites such as methylmalonic acid and homocysteine have been shown to be more sensitive in diagnosing deficiency Measurement of levels of vitamin B12 in serum B12 alone.

In a large study 10 of 406 patients with vitamin B12 deficiency is known, 98.4 percent had high levels of serum methylmalonic acid, and 95.9 percent had elevated serum homocysteine (defined as three standard deviations above average). Only one patient of 406 had normal levels of both metabolites, resulting in a sensitivity of 99.8 percent when methylmalonic acid and homocysteine are used for diagnosis. Interestingly, 28 percent of patients in this study had normal hematocrit levels, and 17 percent had normal mean corpuscular volumes.

In another study of patients with pernicious anemia who had not received maintenance injections of vitamin B12 for months or years, the increase of methylmalonic acid and homocysteine was found to precede the decrease of vitamin B12 in serum and decreased hematocrit. This finding suggests that methylmalonic acid and homocysteine levels may be early markers of vitamin B12 from tissues, even before hematologic manifestations occur.

The use of homocysteine and methylmalonic acid in diagnosing vitamin B12 deficiency has led to surprising results. If the rate of increase of methylmalonic acid and homocysteine levels or normalization of these metabolites in response to replacement therapy are used as diagnostic criteria for vitamin B12 deficiency, approximately 50 percent of these patients had levels vitamin B12 in serum above 200 pg / mL.1 This observation suggests that the use of a low level of vitamin B12 in serum as the only means of diagnosis may miss up to half of patients with deficiency Vitamin B12 of real fabric. Other studies have shown similar results, with the rate of misdiagnosis ranging from 10 to 26 percent when the diagnosis is based on low serum vitamin B12 alone.

There are, however, some caveats to keep in mind. Looking at the reactions that the use of vitamin B12, 3 high levels of methylmalonic acid is much more specific for vitamin B12 deficiency a high level of homocysteine. Vitamin B12 or folic acid can cause homocysteine levels to rise, so folic acid levels should be monitored in patients with isolated hyperhomocysteinemia.

In addition, folic acid deficiency can cause falsely low vitamin B12 serum. One study found that about one third of patients with folate deficiency had low levels of vitamin B12 in serum, less than 100 pg / ml (74 pmol / L) in some patients. In addition, methylmalonic acid levels may be elevated in patients with renal impairment (the result of the decrease in urinary excretion), and high levels must be interpreted with caution.

   Nutritional Deficiency

Dietary sources of vitamin B12 are primarily meats and dairy products. In a typical Western diet, a person obtains approximately 5 to 15 mcg of vitamin B12 daily, much more than the recommended daily allowance of 2 mcg. Normally, humans maintain a large vitamin B12 reserve, which can last two to five years even in the presence of severe malab-sorption. Nevertheless, nutritional deficiency can occur in specific populations. Elderly patients with “tea and toast” diets and chronic alcoholics are at especially high risk. The dietary limitations of strict vegans make them another, less common at-risk population. 

   Malabsorption Syndromes

The classic disorder of malabsorption is pernicious anemia, an autoimmune disease that affects the gastric parietal cells. Destruction of these cells curtails the production of intrinsic factor and subsequently limits vitamin B12 absorption. Laboratory evidence of parietal cell antibodies is approximately 85 to 90 percent sensitive for the diagnosis of pernicious anemia. However, the presence of parietal cell antibodies is nonspecific and occurs in other autoimmune states. Intrinsic factor antibody is only 50 percent sensitive, but it is far more specific for the diagnosis of pernicious anemia.

A Schilling test, which distinguishes intrinsic factor-related malabsorption, can be used to diagnose pernicious anemia. Specifically, Schilling test results were once used to determine whether a patient required parenteral or oral vitamin B12 supplementation. This distinction is now unnecessary, because evidence points to a B12 absorption pathway independent of intrinsic factor, and studies have proved that oral replacement is equal in efficacy to intramuscular therapy. Regardless of the test result, successful treatment can still be achieved with oral replacement therapy.

   Oral vs. Parenteral Therapy

Because most clinicians are generally unaware that oral vitamin B12 therapy is effective, the traditional treatment for B12 deficiency has been intramuscular injections. However, since as early as 1968, oral vitamin B12 has been shown to have an efficacy equal to that of injections in the treatment of pernicious anemia and other B12 deficiency states. Although the majority of dietary vitamin B12 is absorbed in the terminal ileum through a complex with intrinsic factor, evidence for the previously mentioned alternate transport system is mounting.

In one study, patients with vitamin B12 deficiency were randomized to receive oral or parenteral therapy. Patients in the parenteral therapy group received 1,000 mcg of vitamin B12 intramuscularly on days 1, 3, 7, 10, 14, 21, 30, 60, and 90, while those in the oral treatment group received 2,000 mcg daily for 120 days. At the end of 120 days, patients who received oral therapy had significantly higher serum vitamin B12 levels and lower methyl-malonic acid levels than those in the parenteral therapy group. The actual transport mechanism used in this pathway remains unproved, but vitamin B12 is thought to be absorbed “en masse” in high doses. Surprisingly, one study showed that even in patients who had undergone gastrectomy, vitamin B12 deficiency could be easily reversed with oral supplementation.

Intramuscular injections, although safe and inexpensive, have several drawbacks. Injections are painful, medical personnel giving the injections are placed at risk of needlestick injuries, and administration of intramuscular injections often adds to the cost of therapy. Treatment schedules for intramuscular administration vary widely but usually consist of initial loading doses followed by monthly maintenance injections. One regimen consists of daily injections of 1,000 mcg for one to two weeks, then a maintenance dose of 1,000 mcg every one to three months.

Although the daily requirement of vitamin B12 is approximately 2 mcg, the initial oral replacement dosage consists of a single daily dose of 1,000 to 2,000 mcg. This high dose is required because of the variable absorption of oral vitamin B12 in doses of 500 mcg or less. This regimen has been shown to be safe, cost-effective, and well tolerated by patients.





    
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1 comment:

Anonymous said...

Thus, if biotin in the body is insufficient, the growth of these fast-growing
cells will not be as strong and healthy as those of a well-biotin-supplemented body.
Vitamin B6 (Pyridoxine): This one helps to convert proteins into energy and in
turn produce essential proteins for your body to use as building blocks.
Vitamin B12 (Diverse Cobalamins):
Benefits: Making red-colored blood cells, maintaining the nervous
technique healthy, releasing strength from foods people
consume and processing folic acid.

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