Spinel Damage in Middle of Back From B12 Denficiencey

Dietary vitamin B12 deficiency usually results from inadequate absorption, but deficiency can develop in vegans who do not take vitamin supplements. Deficiency causes megaloblastic anemia, damage to the white matter of the spinal cord and brain, and peripheral neuropathy. Diagnosis is usually made by measuring serum vitamin B12 levels. The Schilling test helps determine etiology. Treatment consists of oral or parenteral vitamin B12. Folate (folic acid) should not be used instead of vitamin B12 because folate may alleviate the anemia but allow neurologic deficits to progress.

Cobalamin is a general term for compounds with biologic vitamin B12 activity. These compounds are involved in nucleic acid metabolism, methyl transfer, and myelin synthesis and repair. They are necessary for the formation of normal red blood cells and normal neural function (see table Sources, Functions, and Effects of Vitamins Sources, Functions, and Effects of Vitamins Vitamins may be Fat soluble (vitamins A, D, E, and K) Water soluble (B vitamins and vitamin C) The B vitamins include biotin, folate, niacin, pantothenic acid, riboflavin (B2), thiamin (B1)... read more ).

Dietary sources of vitamin B12 include meats (especially beef, pork, and organ meats [eg, liver]), poultry, eggs, fortified cereals, milk and milk products, and seafood such as clams, oysters, mackerel, and salmon. Food-bound vitamin B12 is released in the stomach's acid environment and is bound to R protein (haptocorrin). Pancreatic enzymes cleave this B12 complex (B12-R protein) in the small intestine. After cleavage, intrinsic factor, secreted by parietal cells in the gastric mucosa, binds with vitamin B12. Intrinsic factor is required for absorption of vitamin B12, which takes place in the terminal ileum.

Vitamin B12 in plasma is bound to transcobalamins I and II. Transcobalamin II is responsible for delivering vitamin B12 to tissues. The liver stores large amounts of vitamin B12. Enterohepatic reabsorption helps retain vitamin B12. Liver vitamin B12 stores can normally sustain physiologic needs for 3 to 5 years if B12 intake stops (eg, in people who become vegans) and for months to 1 year if enterohepatic reabsorption capacity is absent.

Large amounts of vitamin B12 seem to be nontoxic but are not recommended for regular use (ie, as a general tonic).

Vitamin B12 deficiency can result from

• Inadequate intake

• Inadequate absorption

• Decreased utilization

• Use of certain drugs

Inadequate vitamin B12 intake is possible in vegans but is otherwise unlikely. Breastfed babies of vegan mothers may develop vitamin B12 deficiency by age 4 to 6 months because in these babies, liver stores (which are normally extensive in other babies) are limited and their rapid growth rate results in high demand.

Less common causes of inadequate vitamin B12 absorption include chronic pancreatitis, gastric or bariatric surgery, malabsorption syndromes, AIDS, use of certain drugs (eg, antacids, metformin), repeated exposure to nitrous oxide, and a genetic disorder causing malabsorption in the ileum (Imerslund-Graesbeck syndrome).

Symptoms and Signs of Vitamin B12 Deficiency

Occasionally, splenomegaly and hepatomegaly occur. Various gastrointestinal symptoms, including weight loss and poorly localized abdominal pain, may occur. Glossitis, usually described as burning of the tongue, is uncommon.

Neurologic symptoms develop independently from and often without hematologic abnormalities.

Subacute combined degeneration refers to degenerative changes in the nervous system due to vitamin B12 deficiency; they affect mostly brain and spinal cord white matter. Demyelinating or axonal peripheral neuropathies can occur.

In early stages, decreased position and vibratory sensation in the extremities is accompanied by mild to moderate weakness and hyporeflexia. In later stages, spasticity, extensor plantar responses, greater loss of position and vibratory sensation in the lower extremities, and ataxia emerge. These deficits may develop in a stocking-glove distribution. Tactile, pain, and temperature sensations are usually spared but may be difficult to assess in the elderly.

Some patients are also irritable and mildly depressed. Paranoia (megaloblastic madness), delirium, confusion, and, at times, postural hypotension may occur in advanced cases. The confusion may be difficult to differentiate from age-related dementias, such as Alzheimer disease.

• Complete blood count (CBC) and vitamin B12 and folate levels

• Sometimes methylmalonic acid levels or Schilling test

It is important to remember that severe neurologic disease may occur without anemia or macrocytosis.

When clinical judgment suggests vitamin B12 deficiency but the vitamin B12 level is low-normal (200 to 350 pg/mL [145 to 260 pmol/L]) or hematologic indexes are normal, other tests can be done. They include measuring the following:

• Serum methylmalonic acid (MMA) levels: An elevated MMA level supports vitamin B12 deficiency but may be due to renal failure. MMA levels can also be used to monitor the response to treatment. MMA levels remain normal in folate deficiency.

• Homocysteine levels: Levels may be elevated with either vitamin B12 or folate deficiency.

• Less commonly, holotranscobalamin II (transcobalamin II–B12 complex) content: When holotranscobalamin II is < 40 pg/mL (< 30 pmol/L), vitamin B12 is deficient.

After vitamin B12 deficiency is diagnosed, additional tests (eg, Schilling test) may be indicated for younger adults but usually not for the elderly. Unless dietary vitamin B12 is obviously inadequate, serum gastrin levels or autoantibodies to intrinsic factor may be measured; sensitivity and specificity of these tests may be poor.

The Schilling test is useful only if diagnosing intrinsic factor deficiency is important, as in classic pernicious anemia. This test is not necessary for most elderly patients. The Schilling test measures absorption of free radiolabeled vitamin B12. Radiolabeled vitamin B12 is given orally, followed in 1 to 6 hours by 1000 mcg (1 mg) of parenteral vitamin B12, which reduces uptake of radiolabeled vitamin B12 by the liver. Absorbed radiolabeled vitamin B12 is excreted in urine, which is collected for 24 hours. The amount excreted is measured, and the percentage of total radiolabeled vitamin B12 is determined. If absorption is normal, ≥ 9% of the dose given appears in the urine. Reduced urinary excretion (< 5% if kidney function is normal) indicates inadequate vitamin B12 absorption. Improved absorption with the subsequent addition of intrinsic factor to radiolabeled vitamin B12 confirms the diagnosis of pernicious anemia.

The test is often difficult to do or interpret because of incomplete urine collection or renal insufficiency. In addition, because the Schilling test does not measure absorption of protein-bound vitamin B12, the test does not detect defective liberation of vitamin B12 from foods, which is common among the elderly. The Schilling test repletes vitamin B12 and can mask deficiency, so it should be done only after all other diagnostic tests and therapeutic trials.

If malabsorption is identified, the Schilling test can be repeated after a 2-week trial of an oral antibiotic. If antibiotic therapy corrects malabsorption, the likely cause is intestinal overgrowth of bacteria (eg, blind-loop syndrome).

• Supplemental vitamin B12

Vitamin B12 1000 to 2000 mcg orally can be given once a day to patients who do not have severe deficiency or neurologic symptoms or signs. A nasal gel preparation of vitamin B12 is available at a higher price. Large oral doses can be absorbed by mass action, even when intrinsic factor is absent. If the methylmalonic acid (MMA) level (sometimes used to monitor treatment) does not decrease, patients may not be taking vitamin B12.

For more severe deficiency, vitamin B12 1 mg IM is usually given 1 to 4 times a week for several weeks until hematologic abnormalities are corrected; then it is given once a month.

Although hematologic abnormalities are usually corrected within 6 weeks (reticulocyte count should improve within 1 week), resolution of neurologic symptoms may take much longer. Neurologic symptoms that persist for months or years become irreversible. In most elderly people with vitamin B12 deficiency and dementia, cognition does not improve after treatment.

Vitamin B12 treatment must be continued for life unless the pathophysiologic mechanism for the deficiency is corrected.

Infants of vegan mothers should receive supplemental vitamin B12 from birth.

• Common causes of vitamin B12 deficiency include inadequate dietary amounts (eg, in vegans), impaired absorption, age-related decreased acid secretion, and autoimmune metaplastic atrophic gastritis (which causes pernicious anemia).

• The deficiency commonly causes megaloblastic anemia, loss of position and vibration sensation (which occurs early and progresses), and, when advanced, paranoia, delirium, and confusion.

• Do a complete blood count and measure vitamin B12 and folate levels.

• Do a Schilling test in young and middle-aged adults with vitamin B12 deficiency.

• Treat with supplemental vitamin B12.

Spinel Damage in Middle of Back From B12 Denficiencey

Source: https://www.msdmanuals.com/professional/nutritional-disorders/vitamin-deficiency,-dependency,-and-toxicity/vitamin-b12-deficiency

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