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

Thiamine Deficiency: TreatmentIn 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.ToxicityAlthough 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...
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Chapter 071. Vitamin and Trace Mineral Deficiency and Excess (Part 4) 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 10mg/d orally until there is complete recovery. Cardiovascular improvement occurswithin 24 h, and ophthalmoplegic improvement occurs within 24 h. Othermanifestations gradually clear, although psychosis in Wernicke-Korsakoffsyndrome may be permanent or persist for several months. Toxicity Although anaphylaxis has been reported after high doses of thiamine, noadverse 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, andprotein, 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 (e.g., succinic aciddehydrogenase, monoamine oxidase, glutathione reductase). FAD is a cofactor formethyltetrahydrofolate reductase and therefore modulates homocysteinemetabolism. The vitamin also plays a role in drug and steroid metabolism,including detoxification reactions. Although much is known about the chemical and enzymatic reactions ofriboflavin, the clinical manifestations of riboflavin deficiency are nonspecific andsimilar to those of other B vitamin deficiencies. Riboflavin deficiency ismanifested principally by lesions of the mucocutaneous surfaces of the mouth andskin (Table 71-1). In addition to the mucocutaneous lesions, cornealvascularization, anemia, and personality changes have been described withriboflavin 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 importantdietary sources of riboflavin in the United States, although lean meat, fish, eggs,broccoli, and legumes are also good sources. Riboflavin is extremely sensitive tolight, and milk should be stored in containers that protect againstphotodegradation. Laboratory diagnosis of riboflavin deficiency can be made bymeasurement of red blood cell or urinary riboflavin concentrations or bymeasurement of erythrocyte glutathione reductase activity, with and without addedFAD. Because the capacity of the gastrointestinal tract to absorb riboflavin islimited (~20 mg if given in one oral dose), riboflavin toxicity has not beendescribed. Niacin (Vitamin B3) The term niacin refers to nicotinic acid and nicotinamide and theirbiologically active derivatives. Nicotinic acid and nicotinamide serve as precursorsof two coenzymes, nicotinamide adenine dinucleotide (NAD) and NAD phosphate(NADP), which are important in numerous oxidation and reduction reactions inthe body. In addition, NAD and NADP are active in adenine diphosphate–ribosetransfer reactions involved in DNA repair and calcium mobilization. Metabolism and Requirements Nicotinic acid and nicotinamide are absorbed well from the stomach andsmall intestine. Niacin bioavailability is high from beans, milk, meat, and eggs;bioavailability from cereal grains is lower. Since flour is enriched with the freeniacin (i.e., non-coenzyme form), bioavailability is excellent. Median intakes ofniacin in the United States considerably exceed the recommended dietaryallowance (RDA). The amino acid tryptophan can be converted to niacin with an efficiency of60:1 by weight. Thus, the RDA for niacin is expressed in niacin equivalents. Alower conversion of tryptophan to niacin occurs in vitamin B 6 and/or riboflavindeficiencies, or in the presence of isoniazid. The urinary excretion products ofniacin include 2-pyridone and 2-methyl nicotinamide, measurements of which areused in diagnosis of niacin deficiency. Deficiency Niacin deficiency causes pellagra, which is mostly found among peopleeating corn-based diets in parts of China, Africa, and India. Pellagra in NorthAmerica is found mainly among alcoholics; in patients with congenital defects ofintestinal and kidney absorption of tryptophan (Hartnup disease; Chap. 358); andin patients with carcinoid syndrome (Chap. 344), where there is increasedconversion of tryptophan to serotonin. In the setting of famine or populationdisplacement, the occurrence of pellagra results from the absolute lack of niacinbut also the deficiency of micronutrients required for the convers ...