Clinicopathologic Correlations

Healthy Tongue Secrets Revealed

Treating Geographic Tongue

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There are myriad vitamin and trace element deficiencies, and it is beyond the scope of this book to describe them. There are, however, several worth considering.

Vitamin A, a fat-soluble vitamin, is an integral component of rhodopsin and iodopsin, the light-sensitive proteins in the rods and cones of the retina. A deficiency of vitamin A is associated with follicular hyperkeratosis and night blindness. Figure 5-6 illustrates a patient with vitamin A deficiency and follicular hyperkeratosis.

Vitamin C, or ascorbic acid, is a biologic antioxidant and free radical scavenger. The biosynthesis of bile acids, collagen, and norepinephrine, as well as the normal functioning of the hepatic oxygenase system, depends on these antioxidant properties. Vitamin C deficiency is rarely found in the United States. The classic deficiency state is known as scurvy. It is characterized by depression, fatigue, and widespread abnormalities in connective tissue. Oral lesions (including inflamed gingiva), petechiae, hemorrhage, impaired wound healing, hyperkeratosis, and bleeding into body cavities are commonly seen. Figure 5-7 depicts marked periodontal disease in two patients with scurvy. Figure 5-8 illustrates perifollicular purpura and ecchymoses in a patient with vitamin C deficiency.

Figure 5—6 Effects of vitamin A deficiency.

Vitamin Defecencies

Folate is required for the synthesis of nucleotides and the metabolism of several amino acids. The inhibition of folate metabolism in bacteria and in cancer cell growth is the mechanism of action of the sulfonamide antibiotics and chemotherapeutic agents such as methotrexate and 5-fluorouracil. Folate deficiency is seen in women of childbearing age and in alcoholic patients. It manifests with a megaloblastic anemia reflecting ineffective DNA synthesis. Depapillation of the tongue and diarrhea are common findings. Figure 5-9A depicts the classic glossitis of folate deficiency in an alcoholic patient;Figure 5-9B illustrates the patient's tongue after folate replacement.

Niacin, a B-complex vitamin, is required as a coenzyme to form nicotinamide adenine dinucleotide or nicotinamide adenine dinucleotide phosphate. There are more than 200 enzymes that require the active coenzyme forms of niacin as electron acceptors or hydrogen donors. The classic deficiency of niacin is pellagra. It is seen in populations in China, Africa, and India,

Deficiency Vitamin DiseasesGlossitis Before And After

Figure 5—9 Tongue of a patient with folate deficiency. A, Before folate therapy. B, After folate therapy.

Figure 5—9 Tongue of a patient with folate deficiency. A, Before folate therapy. B, After folate therapy.

Figure 5—10 Legs and feet of a patient with niacin deficiency. A, Before niacin therapy. B, After A niacin therapy.

Tinea Cruris
Zinc Deficiency Skin
Figure 5—11 Legs of a patient with zinc deficiency. A, Before zinc therapy. B, After zinc therapy.

where rice is the major source of energy. The most common symptoms are diarrhea, dementia, and pigmented dermatitis in sun-exposed areas. Glossitis, stomatitis, vertigo, and burning paresthesias are also common. Figure 5-10A illustrates marked pigmented dermatitis secondary to niacin deficiency in an alcoholic patient; Figure 5-10B depicts the skin of the same patient after replacement therapy.

Zinc is a trace element needed for a variety of metabolic processes. It is a component of more than 100 enzymes, including DNA polymerase, RNA polymerase, and transfer RNA syn-thetase. Zinc deficiency is associated with growth retardation and hypogonadism in children. In adults, infertility, poor wound healing, diarrhea, and dermatitis are frequent symptoms. Figure 5-11A illustrates a widespread scaling dermatitis secondary to zinc deficiency in a patient with fat malabsorption;Figure 5-11B illustrates the patient's skin after treatment with zinc.

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