Vitamin B deficiencies
Vitamin B deficiencies: Excerpt from Professional Guide to Diseases (Eighth Edition)
Vitamin B complex is a group of water-soluble vitamins essential to normal metabolism, cell growth, and blood formation. (See Recommended daily allowance of B-complex vitamins.) The most common deficiencies involve thiamine (B1), riboflavin (B2), niacin, pyridoxine (B6), and cobalamin (B12).
Causes and incidence
Thiamine deficiency results from malabsorption or inadequate dietary intake of vitamin B1. It also results from alcoholism, prolonged diarrhea, or from increased requirement, which can occur in pregnancy, lactation, and hyperthyroidism. Beriberi, a serious thiamine-deficiency disease, is most prevalent in Asians, who subsist mainly on diets of unenriched rice and wheat. Although this disease is uncommon in the United States, alcoholics may develop cardiac (wet) beriberi with high-output heart failure, neuropathy, and cerebral disturbances. In times of stress (pregnancy, for example), malnourished young adults may develop beriberi; infantile beriberi may appear in infants on low-protein diets or in those breast-fed by thiamine-deficient mothers.
Riboflavin deficiency (ariboflavinosis) results from a diet deficient in milk, meat, fish, legumes, and green, leafy vegetables. Alcoholism or prolonged diarrhea may also induce riboflavin deficiency. Exposure of milk to sunlight or treatment of legumes with baking soda can destroy riboflavin.
Niacin deficiency, in its advanced form, produces pellagra, which affects the skin, central nervous system (CNS), and GI tract. (See Recognizing pellagra.) Although this deficiency is now seldom found in the United States, it was once common among Southerners who subsisted mainly on corn and consumed minimal animal protein. (Corn is low in niacin and in available tryptophan, the amino acid from which the body synthesizes niacin.) Niacin deficiency is still common in parts of Egypt, Romania, Africa, Serbia, and Montenegro, where corn is the dominant staple food. Niacin deficiency can also occur secondary to carcinoid syndrome or Hartnup disease.
Pyridoxine deficiency usually results from destruction of pyridoxine in infant formulas by autoclaving. A frank deficiency is uncommon in adults, except in patients taking pyridoxine antagonists, such as isoniazid and penicillamine.
Cobalamin deficiency most commonly results from an absence of intrinsic factor in gastric secretions, or an absence of receptor sites after ileal resection. Other causes include malabsorption syndromes associated with sprue, intestinal worm infestation, regional ileitis, and gluten enteropathy, and a diet low in animal protein.
Signs and symptoms
Thiamine deficiency causes polyneuritis and, possibly, Wernicke’s encephalopathy and Korsakoff’s psychosis. In infants (infantile beriberi), this deficiency produces edema, irritability, abdominal pain, pallor, vomiting, loss of voice and, possibly, seizures. In wet beriberi, severe edema starts in the legs and moves up through the body; dry beriberi causes multiple neurologic symptoms and an emaciated appearance. Thiamine deficiency may also cause cardiomegaly, palpitations, tachycardia, dyspnea, and circulatory collapse. Constipation and indigestion are common; ataxia, nystagmus, and ophthalmoplegia are also possible.
Riboflavin deficiency characteristically causes cheilosis (cracking of the lips and corners of the mouth), sore throat, and glossitis. It may also cause seborrheic dermatitis in the nasolabial folds, scrotum, and vulva and, possibly, generalized dermatitis involving the arms, legs, and trunk. This deficiency can also affect the eyes, producing burning, itching, light sensitivity, tearing, and vascularization of the corneas. Late-stage riboflavin deficiency causes neuropathy, mild anemia and, in children, growth retardation.
Niacin deficiency in its early stages produces fatigue, anorexia, muscle weakness, headache, indigestion, mild skin eruptions, weight loss, and backache. In advanced stages (pellagra), it produces dark, scaly dermatitis, especially on exposed body parts, that makes the patient appear to be severely sunburned. The mouth, tongue, and lips become red and sore, which may interfere with eating. Common GI symptoms include nausea, vomiting, and diarrhea. Associated CNS aberrations — confusion, disorientation, and neuritis — may become severe enough to induce hallucinations and paranoia. Because of this triad of symptoms, pellagra is sometimes called a “3-D” syndrome — dementia, dermatitis, and diarrhea. If not reversed by therapeutic doses of niacin, pellagra can be fatal.
Pyridoxine deficiency in infants causes a wide range of symptoms: dermatitis, occasional cheilosis or glossitis unresponsive to riboflavin therapy, abdominal pain, vomiting, ataxia, and seizures. This deficiency can also lead to CNS disturbances.
Cobalamin deficiency causes pernicious anemia, which produces anorexia, weight loss, abdominal discomfort, constipation, diarrhea, and glossitis; peripheral neuropathy; and, possibly, ataxia, spasticity, and hyperreflexia.
Diagnosis
The following values confirm vitamin B deficiency:
❑ Thiamine deficiency: commonly measured as micrograms per deciliter in a 24-hour urine collection. Deficiency levels are age-related: 1 to 3 years, less than 120; 4 to 6 years, less than 85; 7 to 9 years, less than 70; 10 to12 years, less than 60; 13 to 15 years, less than 50; adults, less than 27; pregnant women, less than 23 (second trimester), less than 21 (third trimester).
❑ Riboflavin deficiency: measured as micrograms per gram of creatinine in a 24-hour urine collection. Deficiency levels are age-related: 1 to 3 years, less than 150; 4 to 6 years, less than 100; 7 to 9 years, less than 85; 10 to 15 years, less than 70; adults, less than 27; pregnant women, less than 39 (second trimester); less than 30 (third trimester).
❑ Niacin deficiency: measured by N-methyl nicotinamide in a 24-hour urine collection as micrograms per gram of creatinine. Deficiency levels are: adults, less than 0.5; first trimester of pregnancy, less than 0.5; second trimester, less than 0.6; third trimester, less than 0.8.
❑ Pyridoxine deficiency: xanthurenic acid more than 50 mg/day in 24-hour urine collection after administration of 10 g of L-tryptophan; decreased levels of serum and red blood cell transaminases; reduced excretion of pyridoxic acid in urine.
❑ Cobalamin deficiency: cobalamin serum levels less than 150 pg/ml. Tests to discover the deficiency’s cause include gastric analysis and hemoglobin studies. In addition, the Schilling test measures absorption of radioactive cobalamin with and without intrinsic factor.
Treatment
Diet and supplementary vitamins can correct or prevent vitamin B deficiencies, as follows:
❑ Thiamine deficiency: a high-protein diet, with adequate calorie intake, possibly supplemented by B-complex vitamins for early symptoms. Thiamine-rich foods include pork, peas, wheat bran, oatmeal, and liver. Alcoholic beriberi may require thiamine supplements or thiamine hydrochloride as part of a B-complex concentrate.
❑ Riboflavin deficiency: supplemental riboflavin in patients with intractable diarrhea or increased need for riboflavin related to growth, pregnancy, lactation, or wound healing. Good sources of riboflavin are meats, enriched flour, milk and dairy products, green, leafy vegetables, eggs, and cereal. Acute riboflavin deficiency requires daily oral doses of riboflavin alone or with other B-complex vitamins. Riboflavin phosphate can also be administered I.V. or I.M.
❑ Niacin deficiency: supplemental B-complex vitamins and dietary enrichment in patients at risk because of marginal diets or alcoholism. Meats, fish, peanuts, brewer’s yeast, enriched breads, and cereals are rich in niacin; milk and eggs, in tryptophan. Confirmed niacin deficiency requires daily doses of niacinamide orally or I.V.
❑ Pyridoxine deficiency: prophylactic pyridoxine therapy in infants and in children with a seizure disorder; supplemental B-complex vitamins in patients with anorexia, malabsorption, or those taking isoniazid or penicillamine. Some women who take hormonal contraceptives may have to supplement their diets with pyridoxine. Confirmed pyridoxine deficiencies require oral or parenteral pyridoxine. Children with convulsive seizures stemming from metabolic dysfunction may require daily doses of 200 to 600 mg pyridoxine.
❑ Cobalamin deficiency: parenteral cobalamin in patients with reduced gastric secretion of hydrochloric acid, lack of intrinsic factor, some malabsorption syndromes, or ileum resections. Strict vegetarians may have to supplement their diets with oral vitamin B12. Depending on the deficiency’s severity, supplementary cyanocobalamin is usually given parenterally for 5 to 10 days, followed by monthly or daily vitamin B12 supplements.
Special considerations
An accurate dietary history provides a baseline for effective dietary counseling.
❑ Identify and observe patients who are at risk for vitamin B deficiencies — alcoholics, the elderly, pregnant women, and people on limited diets.
❑ Administer prescribed supplements. Make sure patients understand how important it is that they adhere strictly to their prescribed treatment for the rest of their lives. Watch for adverse effects from large doses of niacinamide, such as a flushed sensation or hot flashes, in patients with niacin deficiency. Remember, prolonged intake of niacin can cause hepatic dysfunction. Caution patients with Parkinson’s disease receiving pyridoxine that this drug can impair response to levodopa therapy.
❑ Explain all tests and procedures. Reassure patients that, with treatment, the prognosis is good. Refer patients to appropriate assistance agencies if their diets are inadequate due to adverse socioeconomic conditions.
Pictures
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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