tailieunhanh - Chapter 071. Vitamin and Trace Mineral Deficiency and Excess (Part 4)

Thiamine Deficiency: Treatment In acute thiamine deficiency with either cardiovascular or neurologic signs, 100 mg/d of thiamine should be given parenterally for 7 days, followed by 10 mg/d orally until there is complete recovery. Cardiovascular improvement occurs within 24 h, and ophthalmoplegic improvement occurs within 24 h. Other manifestations gradually clear, although psychosis in Wernicke-Korsakoff syndrome may be permanent or persist for several months. Toxicity Although anaphylaxis has been reported after high doses of thiamine, no adverse effects have been recorded from either food or supplements at high doses. Thiamine supplements may be bought over the counter in doses of up to. | Chapter 071. Vitamin and Trace Mineral Deficiency and Excess Part 4 Thiamine Deficiency Treatment In acute thiamine deficiency with either cardiovascular or neurologic signs 100 mg d of thiamine should be given parenterally for 7 days followed by 10 mg d orally until there is complete recovery. Cardiovascular improvement occurs within 24 h and ophthalmoplegic improvement occurs within 24 h. Other manifestations gradually clear although psychosis in Wernicke-Korsakoff syndrome may be permanent or persist for several months. Toxicity Although anaphylaxis has been reported after high doses of thiamine no adverse effects have been recorded from either food or supplements at high doses. Thiamine supplements may be bought over the counter in doses of up to 50 mg d. Riboflavin Vitamin B2 Riboflavin is important for the metabolism of fat carbohydrate and protein reflecting its role as a respiratory coenzyme and an electron donor. Enzymes that contain flavin adenine dinucleotide FAD or flavin-mononucleotide FMN as prosthetic groups are known as flavoenzymes . succinic acid dehydrogenase monoamine oxidase glutathione reductase . FAD is a cofactor for methyltetrahydrofolate reductase and therefore modulates homocysteine metabolism. The vitamin also plays a role in drug and steroid metabolism including detoxification reactions. Although much is known about the chemical and enzymatic reactions of riboflavin the clinical manifestations of riboflavin deficiency are nonspecific and similar to those of other B vitamin deficiencies. Riboflavin deficiency is manifested principally by lesions of the mucocutaneous surfaces of the mouth and skin Table 71-1 . In addition to the mucocutaneous lesions corneal vascularization anemia and personality changes have been described with riboflavin deficiency. Deficiency and Excess Riboflavin deficiency is almost always due to dietary deficiency. Milk other dairy products and enriched breads and cereals are the most important dietary sources of