8.12 Nutrition disorders of the skin

EB9Y / 5C3Y

Skin nutrition deficiency.

Skin disorders which include dermatoses resulting either from disturbed metabolic processes or from defective nutrition. Primary disorders of the skin which may be provoked or maintained by nutrition deficiencies.

Nutritional deficiency is a global problem not only in developing countries.  It belongs to the large group of non-communicable diseases (NCDs), also known as chronic diseases, which tend to have of long duration and are the result of a combination of genetic, physiological, environmental and behavioural factors.

• In developing countries, nutritional deficiency mainly result from insufficient food supply, 
• In industrialized countries alcoholism, gastrointestinal disorders and unhealthy and long-lasting diets, including anorexia nervosa are the main drivers of nutritional deficiencies. 
• Higher risk groups include infants, pregnant women, alcoholics, vegetarians,  and patients on dialysis, on certain medications, or with a history of malabsorption or gastrointestinal surgery.
• Poverty and low socioeconomic status are closely linked with nutritional deficiency.

Disorders of essential deficient supply of minerals of trace elements and / or vitamins or their metabolism affecting the skin. Early clinical signs of nutrition deficiency are often visible at the skin, nails and/or hairs first. Although some signs are characteristic for a specific nutrient deficiency, often an overlap of skin manifestations is observed in multiple deficiency states.

Vitamin deficiencies: 

Vitamin A is major factor in the maintenance of epithelial tissues. Deficiency occurs mainly from an inadequate intake, liver disorders and fat malabsorption. Disturbed keratinization of epidermis and follicles. Phrynoderma is a maximal clinical feature with follicular plugging.

Vitamin B3 (niacin) deficiency (pellagra) arises most commonly in areas where corn is a substantial part of the food intake. Cutaneous manifestations of pellagra include dermatitis, sunlight sensitivity and hair loss. Supplementation with niacin has a UV light damage protective effect.

Vitamin B6 (pyridoxine) plays a key role as a co-factor in many enzymatic reactions in different metabolic pathways. In the skin, vitamin B6 deficiency leads to seborrheic dermatitis-like eruptions, angular cheilitis, anemia and atrophic glossitis.

Vitamin B12 (cyanocobalmin) is involved in many metabolic pathways especially the development of red blood cells and function of the nervous system. Vitamin B12 deficiency has become an increasing problem in people having a strict vegan diet without supplemental vitamin B12 in Europe.

Vitamin C (ascorbic acid) is one of the major anti-oxidative factors and plays an important role in collagen synthesis. Skin manifestations of vitamin C deficiency includes rough skin, follicular hyperkeratosis, peri-follicular hemorrhage, petechial bleeding, coiled hair and impaired wound healing. Scurvy represents the extreme of the disease manifestation.

Vitamin D and its active metabolite 1,25(OH)2D3 are decreased when insufficient UVB exposure occurs. Skin types 5 and 6 living in northern European latitudes risk inadequate sun exposure for conversion of 7-dehydrocholesterol in the epidermis. Some evidence exists of low D3 levels aggravating skin aging and xerosis of the skin.

Vitamin H (Biotin) as a co-enzyme of carboxylases and acting in signal transduction can be reduced in pregnancy, long-term parenteral nutrition and biotinidase deficiency. Hair loss, brittle nails, periorificial dermatitis of mouth, nostrils, anus or vulva may appear.

Trace elements deficiency:

Iron deficiency resulting from reduced delivery via iron-containing food (meat, vegetables) can lead to pale skin due to anemia and via reduced oxygen supply causing disturbed skin, hair and nail growth (brittle nails). Itchy skin can be another symptom.

Selenium is present in various selenoproteins, including phospholipid hydroperoxide glutathionine peroxidase (PHGPx) and thioredoxin reductase (TDR). TDR is associated with keratinocyte cell membranes and its levels appear to correlate with susceptibility to UVB-induced damage (oxygen radical scavenger). Enzymes that convert the thyroid hormone thyroxine (T4) to triiodothyronine (T3) are selenium-dependent. Hair loss and some skin immune functions are disturbed in deficiency.

Zinc deficiency most commonly results from an inadequate dietary intake, imbalanced parenteral nutrition but also from a reduced absorption or increased loss. It is important  for protein synthesis and plays a role in wound healing and mucosal barrier. It is needed for constructing keratin and for the formation of structural protein – collagen. In acrodermatitis enteropathica, zinc cannot be absorbed and once breast-feeding stops, the first signs occur on the skin. Erosive inflammatory skin with elevated desquamative margins at the anogenital area, fingers,feet and perioral area may occur.

See symptoms.

Vitamins, trace elements and combinations.

Laboratory analysis of blood and urine vitamin and trace element levels can be misleading because of the poor correlation with tissue vitamin concentrations. Sometimes genetic counselling because of rare enzymatic deficiency disorders become necessary.

Depending on the individual nutritional disorder and symptoms.

Depending on type of vitamin or trace elements either alone or in combination.

Depending on severity of malnutrition. The most severe form  of protein-energy malnutrition (PEM) is Kwashiorkor.  Skin lesions usually first occur where friction or pressure takes place (groin, knees, buttocks and elbows). In advanced cases, the dermatosis may be almost anywhere on the body. Darkly pigmented patches with desquamation and feature like old painting paper are seen.

The dermatologist is often the first physician who recognize nutritional deficiencies because mucocutaneous changes are visible and can be diagnostic in malnutrition. However, it is frequently difficult to make a clear diagnosi in early stages of any nutritional disease.

Nutritional deficiency disorders of the skin can mimic several dermatoses.

Individual oral or parenteral supplementation depending on the type deficiency. Whereas substitution of water-soluble vitamins is not problematic, the treatment with fat-soluble vitamins (E-D-K-A) and zinc or selenium should be carefully controlled because of the risk of over-dosage.