8.12 Nutrition disorders of the skin

Nutritional deficiency is a global problem not only in developing countries or at war times and climate catastrophies. Despite being uncommon in developed areas of the world, it has become an increasing problem in these countries as well. 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. Whereas in developing countries, nutritional deficiency mainly results from insufficient food supply, in industrialized countries alcoholism, gastrointestinal disorders and unhealthy and long-duration weight loss diets are the main drivers of nutritional deficiencies. However, poverty and loss to access of food is closely linked with nutritional deficiency.

Disorders of essential deficient supply of minerals 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. Sandpaper comedo pattern in acne can be associated with disturbed retinol metabolism.

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 (prevention of actinic keratoses).

Vitamin B₆ (pyridoxine) plays a key role as a co-factor in many enzymatic reactions in different metabolic pathways. At 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 becomes an increasing problem in people under strict vegan diet without additional vitamin B12 substitution in Europe. Trichodynia may be associated with B12 deficiency.

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, perifollicular hemorrhagia, petechial bleeding, coiled hair and impaired wound healing. Scurvy represents the zenith of 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 North European latitudes are in danger of insufficient sun exposure for conversion of 7-dehydrocholesterol in the epidermis. Some evidence exists to link low D3 levels and skin aging and xerosis of the skin.

Vitamin H (Biotin) as a co-enzyme of carboxylases and acting in signal transduction can be found 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 disturbed skin and hair and nail growth (brittle nails). Itchy skin can be another symptom including urticaria.

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 tri-iodothyronine (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 the mucosal barrier. It is needed for constructing keratin and for the formation of the structural protein, collagen. In acrodermatitis enteropathica, zinc cannot be absorbed and after breast feeding is stopped, the first signs occur on the skin. Erosive inflammatory skin occurs with elevated desquamative margins in the anogenital area, fingers and feet and perioral areas.

Potassium deficiency (hypokalemia) most commonly results from an inadequate dietary intake, imbalanced parenteral nutrition but also from a reduced absorption or increased loss i.e. diuretics. It keeps cells in the epidermis hydrated and parallels skin dryness (xerosis) and reduced cell renewal. Foods high in potassium include all meats, potato skins, banana and broccoli.

The dermatologist is often the first physician who recognize nutritional deficiencies because mucocutaneous changes are visible and can be diagnostic in malnutrition. However, sometimes no clear diagnosis can be made in early stages of the deficiency. Although some signs are characteristic of a specific nutrient deficiency, an overlap of skin manifestations is observed in multiple deficiency states. Often, patients present with more than one deficiency. Fully developed clinical signs such as acrodermatitis in zinc deficiency, phrynoderma in vitamin A deficiency, vitamin H (biotin) and folic acid in seborrhoeic dermatitis or hair loss and brittle nails in iron deficiency, xeroderma in hypokalemia and combination of several vitamins and trace elements are diagnostic clues.

Although nutritional deficiencies are relatively uncommon in the general population, certain groups have a higher risk, including infants, pregnant women, alcoholics, vegetarians, persons of poor socio-economic status and war situations, poverty, and patients on dialysis, on certain medications (especially polypharmacy), or with a history of malabsorption or gastrointestinal surgery. Individual supplementation via the oral or parenteral route depending on the cause of deficiency has to be selected. 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 overdosage risk. Rapid clinical improvement following vitamin and trace element substitution frequently confirms the clinical diagnosis.