Pantothenic acid

Coenzyme A

Transfer of acetyl groups

Cyanocobalamin (B12)

Nucleic acid synthesis


Fatty acid synthesis

Folic acid (folacin)

Pteroylglutamic acid-containing coenzymes

Nucleic acid synthesis, protein metabolism

signs include vascularization of the cornea and keratitis. This deficiency usually occurs in association with deficiency of other B complex vitamins.

Niacin or nicotinic acid deficiency produces the symptoms of pellagra. The clinical picture progresses from an initial phase of general malaise to symptoms including photosensitivity, sore and swollen tongue, gastritis, and diarrhea. Neurological disturbances, depression, and apathy also may occur. Both niacin and the amino acid tryptophan can be converted to diphospho-pyridine nucleotide and triphosphopyridine nucleotide. These reactions require the presence of thiamine, riboflavin, and pyridoxine. Therefore, treatment of the symptoms of pellagra should include, in addition to B complex vitamin supplementation, an intake of dietary proteins to provide adequate amounts of tryptophan.

Pyridoxine (vitamin B6) deficiency symptoms are generally expressed as alterations in the skin, blood, and central nervous system. Symptoms include sensory neuritis, mental depression, and convulsions. Hypochromic, sideroblastic anemia also may result. Since pyridoxine is required for the conversion of tryptophan to diphos-phopyridine and triphosphopyridine nucleotides, pellagralike symptoms can occur with vitamin B6 deficiency. This deficiency is found most often in conjunction with other B complex deficiencies.

The symptoms of pantothenic acid deficiency have not been clinically described. Since pantothenic acid is a ubiquitous vitamin, isolated deficiency is unlikely. However, marginal deficiency may exist in persons with general malnutrition.

Severe cyanocobalamin (vitamin B12) deficiency results in pernicious anemia that is characterized by megaloblastic anemia and neuropathies. The symptoms of this deficiency can be masked by high intake of fo-late. Vitamin B12 is recycled by an effective enterohep-atic circulation and thus has a very long half-life. Absorption of vitamin B12 from the gastrointestinal tract requires the presence of gastric intrinsic factor. This factor binds to the vitamin, forming a complex that can now be absorbed in the terminal ileum. Lack of this factor results in pernicious anemia. Following a gastrectomy, patients must be given vitamin B12 parenterally. There is no way to determine how many people have undiagnosed vitamin B12 deficiency. Since Vitamin B12 is found in almost all animal products, dietary deficiencies are rare except in some vegan vegetarians who consume no animal products and need to get their vitamin B12 from a supplement. However, marginal nutritional levels of Vitamin B12 have been observed in elderly persons, demented patients, AIDS patients, and patients with malignant diseases.

Biotin deficiency is characterized by anorexia, nausea, vomiting, glossitis, depression, and dry, scaly dermatitis. Biotin deficiency occurs when avidin, a biotin-binding glycoprotein, is present. Avidin, which is found in raw egg whites, binds the biotin, making it nutritionally unavailable.

Folic acid deficiency symptoms include megaloblas-tic anemia, glossitis, diarrhea, and weight loss. The requirement for this vitamin increases during pregnancy and lactation.

The effects of most vitamin B overdoses have not been documented, although large dosages of pyridoxine have been reported to cause peripheral neuropathies. Ataxia and numbness of the hands and feet and impairment of the senses of pain, touch, and temperature may result. Excessive niacin intake may result in flushing, pruritus, and gastrointestinal disturbances. These symptoms are due to niacin's ability to cause the release of histamine. Large dosages of niacin can result in hepatic toxicity.

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