Nutritional Disorders

Published on 05/03/2015 by admin

Filed under Dermatology

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1995 times

43

Nutritional Disorders

Malnutrition

Poor nutrition resulting from an insufficient or poorly balanced diet or from defective digestion or utilization of foods.

Malnutrition encompasses both deficiencies and excesses (e.g. obesity) (Fig. 43.1; Tables 43.1 and 43.2).

Table 43.2

Malnutrition-excess syndromes with mucocutaneous manifestations.

Excess Syndrome Mucocutaneous Features Systemic Features
Obesity Plantar hyperkeratosis
Acanthosis nigricans
Acrochordons
Striae distensae
Intertrigo
Frictional hyperpigmentation
Hyperhidrosis
Stasis dermatitis
Leg ulcers, mostly venous > arterial
Lipodermatosclerosis, including the pannus
Stasis mucinosis
Body mass index >30
Hypertension
Diabetes and insulin resistance
Gastroesophageal reflux disease
Atherosclerotic cardiovascular disease
Steatorrhea
Vitamin A Mucocutaneous findings similar to patients on oral retinoids
Xerotic, rough, pruritic, and scaly skin
Xerotic cheilitis
Diffuse alopecia
Anorexia, weight loss, lethargy
Elevated liver enzymes
Painful swellings in limbs due to bony changes
Radiographic bone changes, e.g. skeletal hyperostosis, extraspinal tendon and ligament calcification
Beta carotene (the natural pro-vitamin of vitamin A)
Carotenemia
Carotenoderma (Fig. 43.11) – orange-yellow skin pigmentation primarily in sebaceous gland-rich areas (forehead, nasolabial fold) and in areas with a thicker stratum corneum (palms, soles)
Differentiated from jaundice, which has prominent yellow discoloration of the sclerae and mucosae
Copper
Acquired – rare
Genetic (Wilson’s disease) – autosomal recessive; mutation in gene that encodes a copper transporting P-type ATPase
Genetic
Kayser–Fleischer corneal rings
Genetic
Liver disease and cirrhosis
Dysarthria, dyspraxia, ataxia, and parkinsonian-like extrapyramidal signs
Iron
Acquired – numerous blood transfusions; excess intake
Genetic (type I hemochromatosis) – autosomal recessive; mutation in gene (HFE) that regulates absorption of iron; two most common mutations of HFE gene are C282Y and H63D
Generalized hyperpigmentation (bronzing) Chronic fatigue
Diabetes
Liver disease, cirrhosis
Arthritis
Cardiac disease
Impotence
Hypothyroidism

Primary or exogenous: related to the ingestion of food.

Secondary or endogenous: inadequate or faulty absorption and/or defective metabolism of food and nutrients.

In low-income populations, exogenous protein-energy malnutrition (marasmus), due to diminished or inadequate food ingestion, is often observed.

In high-income populations, obesity due to excessive food consumption and primary or secondary deficiencies due to psychiatric or medical conditions are more commonly seen.

Vitamins

Organic compounds that are biologically active and indispensable for normal physiologic functions.

Serve as coenzymes of cellular metabolic processes essential for the adequate functioning and growth of tissues.

Supplied exogenously.

Both vitamin deficiency (hypovitaminosis) and excess (hypervitaminosis) can cause dermatologic abnormalities (see Tables 43.1 and 43.2; Figs. 43.443.9).

Vitamin excess is more common with the fat-soluble vitamins (A, D, K, E).

Vitamin D

Fat-soluble vitamin that regulates calcium and phosphate homeostasis and bone metabolism; also involved in gene regulation, cell differentiation, and the normal functioning of the innate and adaptive immune system.

Initial step in synthetic pathway occurs in the skin (Fig. 43.10); many tissues, in addition to the kidney, have been shown to hydroxylate vitamin D precursors to produce the active form.

image

Fig. 43.10 Cutaneous production of vitamin D and its functional metabolism. During exposure to ultraviolet B radiation, 7-dehydrocholesterol within the skin is converted to previtamin D3, which is then immediately converted to vitamin D3 in a heat-dependent process. Of note, the heat from excessive sunlight exposure can degrade previtamin D3 and vitamin D3 into inactive photoproducts. Both forms of vitamin D (D3 and D2) are biologically inactive and they require activation in the liver and then the kidney. After binding to carrier proteins, vitamin D is transported to the liver, where it is enzymatically hydroxylated to 25-hydroxyvitamin D [25(OH)D], the major circulating form of vitamin D. 25-Hydroxyvitamin D is then converted into its active form, 1,25-dihydroxyvitamin D [1,25(OH)2D], within the kidney by the enzyme 1α-hydroxylase. Of interest, this final hydroxylation step can also occur in keratinocytes when the enzyme CYP27B1 is upregulated in response to wounding or by Toll-like receptor (TLR) activation from microbial-derived ligands. Serum levels of phosphate, calcium, and fibroblast growth factor 23 can either increase or decrease renal production of 1,25(OH)2D. 1,25(OH)2D decreases its own synthesis via feedback inhibition and decreases the synthesis and secretion of parathyroid hormone by the parathyroid glands. 1,25(OH)2D also enhances intestinal calcium absorption in the small intestine by interacting with the vitamin D receptor–retinoic acid X receptor complex (VDR-RXR) to enhance the expression of the epithelial calcium channel and calbindin-D 9K, a calcium-binding protein. In addition, 1,25(OH)2D is recognized by its receptor in osteoblasts, leading to a series of events that maintain calcium and phosphorus levels in the blood which in turn promotes mineralization of the skeleton. *Most effective wavelength = 300 ± 5 nm. **Measurement of this form most commonly done to assess vitamin D status.

Endogenous synthesis and exogenous sources (fortified foods and supplements) represent the major sources.

Individual vitamin D requirements vary depending on an individual’s age, skin pigmentation, underlying diseases, current medications, geographic location, and season of the year; vitamin D receptor polymorphisms may play an important role in disease risk.

Vitamin D body stores decline with age, during the winter months, and at higher latitudes.

Phototypes V and VI require about threefold more UVB exposure than phototypes I and II to maintain adequate vitamin D body stores.

Oral glucocorticoids inhibit the vitamin D-dependent intestinal absorption of calcium.

Vitamin D insufficiency is actually quite common and is thought to contribute to the development of osteoporosis; it has been associated with decreased immune function, bone pain, and possibly cardiovascular disease and certain malignancies.

True vitamin D deficiency is more rare and results in rickets in children and osteomalacia in adults.

Deficiency of vitamin D can result from inadequate dietary intake, fat malabsorption, lack of adequate UVB exposure, older age with its associated decrease in endogenous vitamin D production, impairment in liver and kidney hydroxylation of active vitamin D precursors, and end-organ resistance to vitamin D metabolites.

Excess vitamin D, typically resulting from prolonged and excessive intake of vitamin D supplements, can present with anorexia, vomiting, diarrhea, headaches, hypercalcemia, hypercalciuria, muscle weakness, and bone demineralization.

No specific cutaneous features have been described with vitamin D deficiency or excess.

The best indicator of vitamin D stores is a measurement of the serum 25-OH vitamin D3 level, and this laboratory value is frequently used to guide individual vitamin D requirements.

Guidelines for vitamin D supplementation have been in flux, but oral supplementation is generally recommended for exclusively breast-fed infants, children who drink less than a liter of fortified milk per day, pregnant women, the elderly, most adults for the prevention of osteoporosis, and individuals on long-term oral glucocorticoids.

Dermatologists recommend oral vitamin D supplementation over the practice of getting more UVB exposure to maintain adequate vitamin D stores.