Deficiency dermatitis

The deleterious effects of pyridoxine deficiency have been observed by experimentation on animals, by observations of people with deficient diets, and by experimentation with antivitamins in humans. Depending upon the animals used in the experiments, at least four major groups of lesions have been attributed to pyridoxine deficiency dermatitis involving the extremities, microcytic hypochromic anemia, nervous injuries associated with convulsions, and vascular lesions resembling those of arteriosclerosis. 

Goldberger and Lillie in 1926 found that rats fed certain nutritionally deficient diets developed dermatitis acrodynia, a skin disorder characterized by edema and lesions of the ears, paws, nose, and tail. Szent-Gyorgyi later found that a factor he had isolated prevented these skin lesions in the rat. He proposed the name vitamin Bg for his factor. Pyridoxine, a form of this vitamin found in plants (and the form of Bg sold commercially), was isolated in 1938 by three research groups working independendy. Pyridoxal and pyridoxamine, the forms that predominate in animals, were... 

Although riboflavin is fundamentally involved in metabolism, and deficiencies are found in most countries, it is not fatal as there is very efficient conservation of tissue riboflavin. Riboflavin deficiency is characterized by cheilosis, lingual desquamation and a seborrheic dermatitis. Riboflavin nutritional status is assessed by measurement of the activation of erythrocyte glutathione reductase by FAD added in vitro. 

Connective tissue disease Substance abuse Stevens-Johnson syndrome Immunocompromised Atopic dermatitis Gonococcal infection Vitamin A deficiency... 

The answers are 404-e, 405-c. (Hardman, pp 1555-1557, 1559-1561.) Angular stomatitis, dermatitis, and corneal vascularization are considered classic signs of human riboflavin deficiency, although multiple B vitamins may be involved. 

Zinc deficiency in domestic pig (Sus spp.) is associated with a condition known as porcine parakeratosis, characterized by dermatitis, diarrhea, vomiting, anorexia, severe weight loss, and eventually death. The condition is exacerbated by high calcium levels (Vallee 1959). 

The physiologic sequelae of biotin deficiency are almost unexplored. Severe skin lesions, especially seborrheic dermatitis and Leiner s disease (Erythroderma desquamativum or exfoliative dermatitis), were increased in young infants bom of mothers on a restricted diet low in eggs, livers, and other biotin-rich foods. After biotin administration the lesions healed. There are claims that excess biotin produces a fatty liver characterized by heightened cholesterol content. Choline has no effect in the prevention of biotin-fatty livers (G2, M2). In mice with transplanted tumors, both the tumors and the blood levels of biotin are below normal (R8). More recent studies established a protection with avidin, the biotin-binding fraction of egg white, against tumor formation (K4). More data along these lines are still needed for confirmation. 

The last essential dietary components to which we will refer and which were also discovered through feeding experiments with rats, are certain unsaturated fatty acids identified as linoleic, linolenic, and arachidonic acids by Burr and Burr in 1930. The acids are required for the formation of complex lipids which are essential in membranes for the maintenance of their fluidity (Chapter 9). Deficiencies lead to a dermatitis which does not respond to additional B vitamin supplements or to oleic acid. 

Howell MD, Boguniewicz M, Pastore S, Novak N, Bieber T, Girolomoni G, Leung DY Mechanism of HBD-3 deficiency in atopic dermatitis. Clin Immunol 2006 121 332-338. 

Schittek B Deficiency of dermcidin-derived antimicrobial peptides in sweat of patients with atopic dermatitis correlates with an impaired innate defense of human skin in vivo. J Immunol 2005 174 8003-8010. 

A deficiency of niacin in the diet results in the disease known as pellagra, characterized by the four D s diarrhea, dermatitis, dementia, and death. In the early years of the twentieth century in the United States, pellagra was common among poor tenant farmers and mill workers in the rural South. The diet there at that time was rich in com that contained little niacin and little available tryptophan from which to synthesize it. 

Oxidation of nicotine with chromic acid led to the isolation of pyridine-3-carboxylic acid, which was given the trivial name nicotinic acid. We now find that nicotinic acid derivatives, especially nicotinamide, are biochemically important. Nicotinic acid (niacin) is termed vitamin B3, though nicotinamide is also included under the umbrella term vitamin B3 and is the preferred material for dietary supplements. It is common practice to enrich many foodstuffs, including bread, flour, corn, and rice products. Deficiency in nicotinamide leads to pellagra, which manifests itself in diarrhoea, dermatitis, and dementia. 

Deficiency - Pellagra is a state of niacin deficiency characterized by dermatitis, diarrhea, and dementia (manifestations of mucous membranes, Gl system, and CNS). In severe cases, confusion, delusions, disorientation, and hallucinations may occur. 

Hartnup disorder exhibits symptoms similar to pellagra (niacin deficiency), characterized by three of the "four D s" diarrhea, dermatitis (a red, scaly rash), dementia (intermittent ataxia), and death... 

Biotin (vitamin B ) is widespread in foods and is also synthesized by intestinal bacteria. It is a coenzyme for the carboxylation of pyruvate, acetyl-coenzyme-A (CoA), propionyl CoA, and /1-methyl-crotonyl CoA and is involved in fatty acid formation and in energy release from carbohydrates. In humans deficiencies only occur in patients with an abnormal gut flora and manifests itself as exfoliative dermatitis and alopecia. 

Riboflavin vitamin Bf) deficiency results in local seborrheic dermatitis that may be limited to the face and scrotum. Other symptoms of ariboflavinosis include angular stomatitis, cheilitis, and glossitis. Specific ocular... 

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

Vitamin Bj deficiency, known as beriberi, was historically seen primarily in people of southeast Asia, for dietary reasons. The symptoms of beriberi are neurological disorders (weakness, paralysis, painful neuritis), diarrhea, loss of appetite, dermatitis, and anemia. These symptoms are due mainly to the accumulation of pyruvate and lactate. 

Nicotinamide deficiency leads to pellagra [pelle agra (Italian) = rough skin], which manifests itself in dermatitis (skin rash), pigmentation, a red and inflamed tongue, diarrhea, and weakness. People who consume large amounts of corn in an unbalanced diet are prone to develop the disease. 

---