Vitamin [Bsub12] (cobalamin) plays ...

Vitamin [Bsub12] (cobalamin) plays an important character in DNA synthesis and neurologic function. Deficiency can lead to a wide image of hematologic and neuropsychiatric disorders that can many times be reversed by early diagnosis and ready treatment.

The veritable prevalence of vitamin [B.sub.12] deficiency in the general population is unknown. The incidence, however, appears to increase with age. In the same study, (1) 15 percent of adults older than 65 years had laboratory evidence of vitamin [Bsub12] deficiency. The nearly ubiquitous use of gastric acid-blocking agents, which can lead to decreased vitamin [Bsub12] flats (2) may have an underappreciated part in the development of vitamin [Bsub12] deficiency. Taking the widespread use of these agents and the aging of the U population into consideration, the actual prevalence of vitamin [Bsub12] deficiency may be unruffled higher than statistics indicate. Despite these facts, the ne for universal screening in older adults remains a matter of discussion (3,4)

Clinical Manifestations

Vitamin [Bsub12] deficiency is associated with hematologic, neurologic, and psychiatric manifestations (Table 1) It is a customary cause of macrocytic (megaloblastic) anemia and, in advanced cases, pancytopenia. Neurologic sequelae from vitamin [Bsub12] deficiency include paresthesias, peripheral neuropathy, and demyelination of the corticospinal tract and dorsal lines (subacute combined systems disease). Vitamin [Bsub12] deficiency also has been linked to psychiatric disorders, including impaired memory, irritability, depression, dementia and, rarely, psychosis. (56)

In addition to hematologic and neuropsychiatric manifestations, vitamin [Bsub12] deficiency may use indirect cardiovascular effects. Similar to folic acid deficiency, vitamin [Bsub12] deficiency creates hyperhomocysteinemia, which is an independent risk factor for atherosclerotic disease. (7) Although the part of folic acid supplementation in reducing homocysteine flushs as a method for preventing coronary artery disease and affliction continues to be a expose of great interest, there has been little emphasis onward the potential role of vitamin [Bsub12] deficiency as a contributing factor in the progressive growth of cardiovascular disease. This possibility becomes especially important when considering vitamin replacement therapy. Folic acid supplementation may mask an latent vitamin [B.sub.12] deficiency and further exacerbate or initiate neurologic disease. Therefore, clinicians should consider ruling abroad vitamin [B.sub.12] deficiency before initiating folic acid therapy. (8)

Normal Absorption of Vitamin [Bsub12]

In humans, barely two enzymatic reactions are known to be unable to exist without on vitamin [B.sub.12]. In the first reaction, methylmalonic acid is create anewed to succinyl-CoA using vitamin [Bsub12] as a cofactor (Figure 1) Vitamin [Bsub12] deficiency, therefore, can lead to increased plains of serum methylmalonic acid. In the inferior reaction, homocysteine is converted to methionine by the agency of using vitamin [B.sub.12] and folic acid as cofactors. In this reaction, a deficiency of vitamin [Bsub12] or folic acid may lead to increased homocysteine levels

[FIGURE 1 OMITTED]

An understanding of the vitamin [Bsub12] absorption period helps illuminate the potential causes of deficiency. The acidic environment of the stomach facilitates the breakdown of vitamin [Bsub12] that is border to food. Intrinsic factor, which is released on parietal cells in the stomach, binds to vitamin [Bsub12] in the duodenum This vitamin [B.sub.12]-intrinsic factor composed of several elements subsequently aids in the absorption of vitamin [Bsub12] in the terminal ileum.

In addition to this course of absorption, evidence supports the existence of an alternate regularity that is independent of intrinsic factor or uniform an intact terminal ileum. Approximately 1 percent of a large oral dose of vitamin [Bsub12] is absorbed at this second mechanism. (9) This pathway is important in relation to oral replacement. one time absorbed, vitamin [B.sub.12] binds to transcobalamin II and is transported from end to end the body. The interruption of individual or any combination of these paces places a person at risk of developing deficiency (Figure 2)

Diagnosis of Vitamin [Bsub12] Deficiency

The diagnosis of vitamin [Bsub12] deficiency has traditionally been based forward low serum vitamin [B.sub.12] of the same heights usually less than 200 pg by means of mL (150 pmol per L) along with clinical evidence of disease. However, studies indicate that older patients look after to present with neuropsychiatric disease in the absence of hematologic findings. (56) Furthermore, measurements of metabolites as it is as methylmalonic acid and homocysteine have been shown to be more sensitive in the diagnosis of vitamin [Bsub12] deficiency than measurement of serum [Bsub12] flushs alone. (3,10-14)

In a large close attention (10) of 406 patients with known vitamin [Bsub12] deficiency, 984 percent had elevated serum methylmalonic acid flats and 95.9 percent had elevated serum homocysteine flats (defined as three standard deviations above the mean). solely one patient out of 406 had normal evens of both metabolites, resulting in a sensitivity of 998 percent when methylmalonic acid and homocysteine horizontals are used for diagnosis. Interestingly, 28 percent of the patients in this investigation had normal hematocrit levels, and 17 percent had normal mean corpuscular volumes