Vitamins
2012; American Academy of Pediatrics; Volume: 33; Issue: 8 Linguagem: Inglês
10.1542/pir.33.8.339
ISSN1529-7233
AutoresBryon Lauer, Nancy D. Spector,
Tópico(s)Therapeutic Uses of Natural Elements
ResumoBecause vitamin D deficiency has been shown to increase the risk of autoimmune diseases, osteoarthritis, type 1 diabetes mellitus, cardiovascular disease, schizophrenia, depression, and wheezing, the Institute of Medicine recently made recommendations that adolescents and children age >1 year need 600 IU/day of vitamin D.After completing this article, readers should be able to:Vitamins are organic compounds that must be consumed in our diet because humans cannot synthesize them in adequate quantities. Each vitamin has unique functions in the body, including hormone regulation, cell proliferation, tissue growth and differentiation, and antioxidant effects; vitamins also serve as cofactors for multiple metabolic pathways. Vitamins A, D, E, and K are fat soluble, whereas vitamin B complexes and vitamin C are water soluble.A 3-year-old boy recently adopted from Ghana is brought in for his first well-child visit. His adoptive parents are concerned because he is skinny and runs into things, especially at night. On examination, the boy is below the 5th percentile for height and weight. The pediatrician notes foam-like patches on his bulbar conjunctiva and dry, scaly skin on his extensor surfaces.Vitamin A is found in green leafy vegetables, carrots, sweet potatoes, and liver in the form of carotenoids and retinals. Once ingested, vitamin A is absorbed in the terminal ileum and esterified by the enterocytes to retinyl esters, which are stored in the liver until being transported to target organs, bound by retinal-binding proteins. (1)The main function of vitamin A is to maintain the growth and functional integrity of epithelial cells, especially in the eyes and respiratory, urinary, and digestive tracts. (2) Vitamin A also plays a role in the function of the immune system. (3) Retinal is an essential component of retinal pigments and hence of normal vision. Retinoic acid is needed for synthesis of glycoproteins. (1)Worldwide, vitamin A deficiency is the most common cause of preventable blindness in children. Ophthalmologic disease is usually the first clinical sign of vitamin A deficiency. Night blindness (nyctalopia) is first noted as a result of delayed ability of rhodopsin to regenerate when bright light bleaches the retina. Goblet cells on the conjunctiva are then lost, leading to conjunctival xerosis. Foam-like patches called Bitot spots form from the accumulation of dead epithelial and microbial cells on the conjunctiva (Fig 1). Progression to corneal xerosis can lead to ulcerations (keratomalacia) and infections of the cornea, resulting in total or partial blindness. The ophthalmologic effects of vitamin A deficiency are reversible until the progression to keratomalacia. Once keratomalacia is present, the best hope is for a partial recovery of vision. (1)(2)(3) Children’s skin also may be affected, developing dry and scaly patches (follicular hyperkeratosis), especially on the extensor surfaces. (1)Failure to thrive and depressed immune function occur with subclinical vitamin A deficiency. The epithelial system is the body’s first line of defense from infection. With vitamin A deficiency, the integrity of epithelial cells is compromised, and there is depression of the systemic immunologic response, leading to increased susceptibility to and morbidity from infections. (3) In particular, there is increased risk of severe diarrheal illnesses, acute respiratory tract infections, and morbidity from measles. It is now recommended by the World Health Organization and the American Academy of Pediatrics (AAP) to supplement children’s diets with vitamin A if infected with measles. (2)(3)In developing countries, there are an estimated 70 to 80 million preschool-age children who have subclinical vitamin A deficiency and 3 million with clinical ophthalmologic disease. (3) The main cause is malnutrition in developing countries. Children who have malabsorption, as in Crohn disease, celiac disease, or hepatic failure, are similarly at risk and can develop vitamin A deficiency. (1)Vitamin A deficiency is diagnosed clinically if ophthalmologic disease is present. Low plasma retinol acids help to support the diagnosis or to diagnose subclinical disease. (1)Breastfeeding, food diversification, fortified foods, and supplementation with vitamin A are key interventions in preventing vitamin A deficiency. Children age 9 years should receive 1,700 μg/day until they have recovered. (1)(3)Symptoms of hypervitaminosis A include drowsiness, painful joints, loss of hair, increased intracranial pressure, and carotenemia. (1)Thiamine is a water-soluble vitamin that serves as a coenzyme in decarboxylation and transketolation of α-ketoacids and is needed for the synthesis of acetylcholine. (1) Foods that contain thiamine include yeast, legumes, pork, rice, cereals, milk products, and vegetables. Cooking, baking, canning, and pasteurizing can destroy thiamine. (1)(2)Thiamine deficiency can lead to beriberi (infantile and adult) and Wernicke-Korsakoff syndrome. Infants afflicted with beriberi present with signs of cardiac failure, which include cardiomegaly, tachycardia, cyanosis, dyspnea, vomiting, and a loud piercing cry. Irritability, peripheral neuritis, decreased tendon reflexes, loss of vibration sense, aseptic meningitis, and ataxia also can be present. Wernicke encephalopathy presents with ophthalmoplegia, nystagmus, ataxia, intracranial hemorrhage, and confusion. Korsakoff psychosis results in short-term memory loss and confabulation with normal cognition. (1)(2)Beriberi can occur after weight loss surgery and with total parental nutrition if thiamine is not included. There are reports of thiamine deficiency with chronic loop diuretic use. (2)Beriberi is diagnosed clinically.Infantile beriberi treatment involves treating breastfed infants with 10 mg of thiamine per day and their mothers with 50 mg of thiamine per day. (1)Riboflavin serves as a catalyst for mitochondrial oxidative and reductive reactions and hydrogen transfer reactions, and is involved with tryptophan metabolism. Meats, fish, eggs, milk, green vegetables, yeast, and enriched foods contain riboflavin. (1)(2)Cheilosis, glossitis, keratitis, photophobia, seborrheic dermatitis, sore throat, edema, hyperemia of mucous membranes, and normocytic anemia all can occur with riboflavin deficiency. (1)(2)The main cause of riboflavin deficiency is lack of consumption of vitamin B2. Studies have shown a higher prevalence in adolescent females and those of a low socioeconomic status. (2)The diagnosis of riboflavin deficiency is made clinically and supported by decreased erythrocyte glutathione reductase activity. (2)Treatment consists of 3 to 10 mg of riboflavin daily. (1)Niacin is important in electron transport and glycolysis because it forms nicotinamide adenine dinucleotide (NAD) and NADPH (reduced form of nicotinamide adenine dinucleotide phosphate) and is an end-product in tryptophan metabolism. Niacin is found in large quantities in milk and eggs but is not found in cereals and corn. (1)(2)Pellagra is the result of niacin deficiency and is characterized by the three Ds: diarrhea, dementia, and dermatitis. The dermatitis looks like a sunburn on the photosensitive areas of the skin. (1)(2)Malnutrition and tryptophan-deficient corn diets are the main causes of niacin deficiency. However, pellagra can occur in association with alcoholism, anorexia nervosa, prolonged isoniazid therapy, and malabsorptive diseases. Pellagra has not been documented in normally growing children. (1)(2)The diagnosis of niacin deficiency is made clinically. (1)Treatment consists of 50 to 300 mg of niacin per day and supplementation with a multivitamin. (1)Pyridoxine is a coenzyme in the metabolism and transport of amino acids. Yeast, rice polishing, and cereals are the main dietary source of pyridoxine. (1)Refractory seizures, peripheral neuritis, dermatitis, and microcytic anemia are the main presenting signs of pyridoxine deficiency. (1)Pyridoxine deficiency is rare but can be seen in malabsorption, diarrhea, isoniazid treatment, and in exclusively breastfed infants older than 6 months if the mother is pyridoxine deficient. Pyridoxine-dependent seizures, vitamin B6 responsive anemia, xanthurenic acidemia, cystathioninuria, homocystinuria, and type 2 hyperprolinemia are pyridoxine dependent syndromes associated with pyridoxine deficiency. (1)(2)The diagnosis is made clinically and is confirmed by measuring large quantities of xanthurenic acid in the urine after administration of 100 mg of tryptophan. (1)Children with seizures secondary to pyridoxine deficiency should be given 100 mg of pyridoxine intramuscularly. Otherwise, children may require 10 to 100 mg of pyridoxine per day. (1)A 12-month-old boy presents for a well-child visit, and his mother is concerned because he is not developing like her other children. He has been breastfed exclusively, and his mother has been a strict vegetarian for a number of years. On examination, he is at the 5th percentile for weight and has mild conjunctival pallor. A complete blood cell count is ordered, which shows macrocytic anemia.Our dietary source of vitamin B12 is animal meat. Once ingested, vitamin B12 is bound to R protein in the stomach. Pancreatic proteases release vitamin B12 from the R proteins in the small intestine, where it binds to intrinsic factor (IF). Bound to IF, which is produced by gastric parietal cells, vitamin B12 is transported to the terminal ileum. Enterocytes in the terminal ileum absorb vitamin B12, break the vitamin B12-IF complex, and release vitamin B12 into the portal circulation bound to transcobalamin II. Vitamin B12 is then transported to different tissues throughout the body. Humans recycle vitamin B12 via the enterohepatic circulation; it is excreted in bile and reabsorbed in the terminal ileum. The liver stores 2 to 3 mg of vitamin B12. Because of large stores of vitamin B12 in the liver and active enterohepatic circulation, it takes several years of a deficient diet to become vitamin B12 deficient. (4)The primary role of vitamin B12 is serving as a cofactor for two major metabolic reactions (Fig 2). Vitamin B12 is required for methylation of homocysteine to methionine. During this reaction, methyltetrahydrofolate is demethylated to tetrahydrofolate, which is important in DNA synthesis. Vitamin B12 is also necessary for conversion of methylmalonyl coenzyme A to succinyl coenzyme A. (4)Vitamin B12 deficiency mainly affects the hematologic and neurologic systems. The hematopoietic cells are affected because they are rapidly dividing cells, and vitamin B12 deficiency slows DNA synthesis. Hematologic abnormalities include macrocytic anemia, hypersegmented neutrophils, leukopenia, thrombocytopenia, and pancytopenia. Vitamin B12 deficiency can have multiple effects on the neurologic system, including developmental delay or regression, paresthesias, impaired vibratory and proprioceptive sense, hypotonia, seizures, ataxia, dementia, paralysis, abnormal movements, memory loss, personality changes, depression, irritability, weakness, and poor school performance. The neurologic sequelae can occur without the hematologic sequelae, especially if there is adequate folate intake. Children also can present with failure to thrive, anorexia, fatigue, glossitis, skin hyperpigmentation, vomiting, diarrhea, and icterus. (4)Children can become deficient in vitamin B12 by three pathophysiologic mechanisms: decreased intake, abnormal absorption, or inborn errors of vitamin B12 transport and metabolism. Dietary deficiency of vitamin B12 rarely occurs in children adhering to a normal western diet. The daily requirement for children is only 0.4 to 2.4 μg. However, adolescents on strict vegetarian diets can become deficient over time. The most common scenario for infants who become vitamin B12 deficient is an exclusively breastfed infant by mothers who are vitamin B12 deficient. Much less commonly, vitamin B12 deficiency can occur in children who are on restricted diets, such as in poorly controlled phenylketonuria, or in children with glycogen storage disease type Ib. (4)Abnormal absorption can occur for multiple reasons. Gastric resection and autoimmune pernicious anemia, as part of autoimmune polyglandular syndrome, result in decreased IF. Long-term gastric acid suppression, as with proton pump inhibitors, results in decreased release of vitamin B12 from dietary proteins. Pancreatic insufficiency can result, although rarely, in malabsorption secondary to decreased proteases that degrade R proteins. Bacterial overgrowth and intestinal parasitic infections can act as competitors for vitamin B12 absorption. Decreased absorption in the ileum can occur in Crohn disease, celiac disease, and surgical resection of the ileum. Imerslund-Grasbeck disease, an autosomal recessive syndrome in which there are abnormal ileal receptors for vitamin B12, also leads to malabsorption of vitamin B12. (4)The diagnosis of vitamin B12 deficiency is not straightforward. Measuring levels of vitamin B12, total homocysteine, and methylmalonic acid (MMA) is the current strategy. Normal vitamin B12 levels vary according to laboratory, with the normal range being 200 to 900 pg/mL. Serum levels of vitamin B12 <80 pg/mL are considered low. Vitamin B12 levels can be normal, however, and a patient may still be deficient. MMA and homocysteine are precursors to the vitamin B12 pathway and are elevated when a patient is vitamin B12 deficient. MMA levels are more specific than homocysteine levels in determining vitamin B12 deficiency because homocysteine levels may be affected by folate and vitamin B6. Once the diagnosis is suspected, further testing is necessary to help determine the cause. This evaluation includes a detailed diet history, a Schilling test, evaluation for parasite infections, amino acid analysis, transcobalamin II levels, measurement of the unsaturated vitamin B12–binding capacity, genetic testing, and testing for antibodies to parietal cells and IF. The Schilling test assesses if vitamin B12 is absorbed adequately via the gut by orally administering food-bound radioactive vitamin B12 and measuring urinary vitamin B12 levels. (4)The treatment for vitamin B12 deficiency depends on the underlying cause. Most patients will require subcutaneous correction of vitamin B12 deficiency. Treatment starts with low-dose injections of cyanocobalamin (0.2 μg/kg) for 2 days because of the risk of hypokalemia with this initial treatment, followed by 1,000 μg/day of subcutaneous cyanocobalamin on days 2 through 7, and then 100 μg/week for 1 month. Children with vitamin B12 deficiency as a result of malabsorption may require chronic monthly injections. (1)(4)A 5-month-old boy is brought in because of pallor. He stayed with his grandparents over the weekend, who first noticed his pallor. During the last week, he has been eating less and sleeping more. Thus far in his life, he has been fed only a homemade goat milk–based formula. On examination, he was observed to be mildly tachycardic, and pallor is noted. The pediatrician checks a complete blood cell count, which shows macrocytic anemia.The main dietary sources of folic acid for humans are animal products, leafy vegetables, and fortified foods. Folic acid is absorbed into target tissues by binding to folate receptors. Folic acid plays a role in red blood cell maturation and synthesis of nucleic acid. The body stores only 5 to 10 mg of folic acid, so effects of folate deficiency can occur in ∼4 to 5 months of a diet deficient in folic acid. The daily requirement of folic acid is ∼200 to 400 μg. However, pregnant and lactating women require approximately double that amount. (2)(4)Folate deficiency manifests as macrocytic anemia with hypersegmented neutrophils. Other laboratory abnormalities include decreased reticulocytes, elevated iron levels, thrombocytopenia, and neutropenia. Unlike with vitamin B12 deficiency, neurologic complications are not seen. (2) Patients also may present with irritability, chronic diarrhea, and failure to thrive. (1) Data have shown that 50% to 75% of neural tube defects may be prevented by maternal folic acid supplementation. (2)Lack of dietary intake, malabsorption, increased demand, or medication that interferes with folate metabolism are the main causes of folate deficiency. Starting in 1998, the US Food and Drug Administration required that cereal-grain products be fortified with folic acid because inadequate dietary intake of folic acid is the most common cause of folate deficiency.Malabsorption of folate can occur with Crohn disease, celiac disease, and small bowel resection. Individuals with hemolytic anemia or exfoliative skin diseases have increased requirements for folate. Medications such as methotrexate and pyrimethamine disrupt folic acid metabolism, and phenytoin blocks folate absorption, potentially leading to folate deficiency. (2) Infants also can develop folate deficiency if their primary source of nutrition is fresh goat milk.Folate deficiency is defined by folate levels <4 μg/mL. Homocysteine levels typically are elevated; however, MMA levels remain normal. (1)The treatment of folate deficiency depends on the cause. To replete body stores and correct the deficiency, folate 1 to 5 mg/d should be given either orally or parentally. (1)An 8-month-old girl presents to the clinic because of irritability, bleeding gums, and not moving her legs. Her diet consists only of evaporated boiled milk, but she has been taking less over the last 2 to 3 days. On physical examination, she is in the 5th percentile for weight and 10th percentile for height. She is fussy and lying in a frog-legged position. Her gums are bleeding and necrotic.Humans lack the ability to convert glucose to vitamin C (ascorbic acid); we therefore consume the vitamin through our diet in citrus fruits, green leafy vegetables, raw meat, and human and cow milk. Vitamin C is absorbed in the intestine via active transport. The largest stores of vitamin C in the body are found in the pituitary and adrenal glands. (5) Vitamin C is involved in many enzymatic reactions in the body. It is a cofactor for hydroxylation of proline to lysine as well as a reducing agent in hydroxylation reactions catalyzed by dopamine β-monooxygenase and peptidyl glycine α-amidating monooxygenase. Vitamin C is essential also for collagen synthesis; connective tissue integrity; metabolism of tyrosine, folate, and xenobiotics; and synthesis of carnitine, histamine, adrenal steroids, and nitric oxide synthase. (6) In addition, vitamin C plays a role in promoting iron absorption, serving as an antioxidant, and protecting against diphtheria, tetanus, and typhoid toxins. (5)Scurvy, or Barlow disease, occurs after ∼1 to 3 months of a diet deficient in vitamin C. The typical age of presentation in children is between 6 months and 2 years. Newborns are protected because human milk and infant formulas contain adequate amounts of vitamin C. Poor wound healing and bleeding secondary to poor collagen formation and damage to coagulation factors are the main clinical manifestations of scurvy. Bleeding may occur in the skin, mucous membranes, joints, muscle, or gastrointestinal tract. Hemorrhagic skin lesions present early in the course and may be ecchymotic, petechial, or purpuric.Muscle pain, pseudoparalysis, or holding legs in a frog-leg position may develop as a result of subperiosteal hemorrhage, hemarthrosis, and soft tissue and muscle bleeding. Before developing signs of bleeding, children generally are irritable and manifest developmental delay, decreased appetite, and fatigue. They also may develop dystrophic hair and follicular keratosis on their buttocks and legs.Gingival disease begins as swollen, red, and shiny gums and progresses into black or necrotic gums. Minimal trauma leads to bleeding gums. With advanced disease, teeth may loosen and be lost secondary to collagen damage of the periodontal ligaments. Children with scurvy almost invariably have a mild anemia secondary to iron deficiency, folate deficiency, bleeding, and hemolysis. Children also may have weakness, cardiac hypertrophy, alopecia, diminished adrenal and bone marrow function, and edema. In many cases of scurvy, there are other coexisting nutritional deficiencies. (5)(7)Osteopenia is common in vitamin C deficiency. Other radiographic changes are more specific but less frequent: rachitic rosary; Frankel line, a white dense line of provisional calcification at the metaphysis; Wimberger ring, central rarefaction on the epiphyseal centers surrounded by a thickened white line of calcification; scurvy lines, less dense transverse bands adjacent to Frankel lines; and corner sign, lateral metaphyseal spurs, which are pathognomonic for scurvy. (5)(7)Scurvy develops as a result of lack of vitamin C in the diet. Overheating foods rich in vitamin C can inactivate the vitamins. Infants receiving evaporated boiled milk are at particular risk. Alcoholism, diabetes, smoking, AIDS, short gut syndrome, and chronic diarrhea can lead to vitamin C deficiency, even if the individual is receiving an adequate oral intake of vitamin C. (5)(7)The diagnosis of scurvy is a clinical one supported by laboratory and radiologic studies. Plasma levels of vitamin C vary by dietary intake and are not a true measure of the body’s stores. Therefore, low levels of vitamin C in platelets, leukocytes, or buffy coat layers are a better indicator. Another way to make the diagnosis is by administering vitamin C parentally and measuring urinary excretion. In individuals with a normal vitamin C level, ∼80% of the dose will be present in the urine in 3 to 5 hours. In scurvy, the urinary excretion of vitamin C is reduced. The best way to confirm the diagnosis is by seeing improvement in symptoms after initiating treatment. Muscle pain and spontaneous bleeding will improve in 2 to 3 days, gum disease improves in 2 to 3 weeks, and bone disease and ecchymosis resolve over several weeks. The only permanent damage that occurs after scurvy is treated is tooth loss. (5)(7)Administering 100 to 300 mg daily of vitamin C in children and 500 to 1,000 mg in adults for 1 month or until symptoms resolve is the recommended treatment for scurvy. (7)Oxaluria can result from excess vitamin C. (1)A 15-month-old African American toddler presents to his pediatrician for a routine well-child visit. His mother is concerned because his legs are bowed and wants to know if he will need braces. She is concerned also because he has not yet developed any teeth. He was a full-term infant who was exclusively breastfed and was not given any vitamin D supplementation. On physical examination, he is just below the 5th percentile for weight and height. His head circumference is at the 25th percentile. Abnormalities noted on examination include absent teeth, bony protuberances along the anterior lateral chest wall, widened wrist, and bowed legs.Cod liver oil, liver, organ meats, egg yolk, and oily fish such as salmon, mackerel, and sardines are the most common natural sources of vitamin D. Unfortunately, many children do not consume sufficient natural sources of vitamin D. Thus, fortified foods and exposure to sunlight are the two main sources of vitamin D. (8) Vitamin D2 (ergocalciferol) and D3 (cholecalciferol) are prohormones that are derived from UV irradiation of ergosterol in yeast and 7-dehydrocholesterol in animals, respectively. In the intestine, vitamin D2 and vitamin D3 are absorbed readily and therefore used in supplements. Vitamin D3 may be as much as three times as potent as vitamin D2. (8)(9)Figure 3 reviews the metabolism of vitamin D. UV irradiation converts 7-dehydrocholesterol, which is found in its highest concentration in the stratum basale and stratum spinosum in the epidermis, to vitamin D3. Vitamin D3 enters the circulation and is hydroxylated by vitamin D-25 hydroxylase to 25-hydroxyvitamin D (25[OH]-D) while passing through the liver. The vitamin D status of a patient is determined by measuring the 25(OH)-D plasma level. From the liver, 25(OH)-D is transported to the kidneys and converted to its active form, 1,25-dihydroxyvitamin D (1,25[OH]-D), by 1-α-hydroxylase.The major role of 1,25(OH)-D is to increase plasma concentrations of calcium and phosphorus. This reaction is accomplished by acting on receptors in the gut and bones. 1,25(OH)-D increases renal calcium reabsorption and increases intestinal absorption of calcium and phosphorus. In fact, 1,25(OH)-D can increase intestinal calcium absorption by 30% to 40% and phosphorus absorption by ∼80%. (9) In bones, 1,25(OH)-D and parathyroid hormone (PTH) stimulate osteoblasts to become osteoclasts, which release calcium and phosphorus into the blood. This process dissolves the mineralized collagen matrix in bones and over time results in osteopenia and osteoporosis. (9)PTH, calcium, and phosphorus plasma levels tightly regulate the production of 1,25(OH)-D. Hypocalcemic states trigger the release of PTH, which upregulates 1,25(OH)-D formation. Hypophosphatemia directly stimulates 1-α-hydroxylase to form 1,25(OH)-D, and fibroblast growth factor 23, produced in bones, inhibits 1,25(OH)-D formation. (1)(9)Vitamin D deficiency presents differently at different ages. Infants and children may be asymptomatic or can present with seizures and tetany as a result of hypocalcemia. They also may have failure to thrive, hypotonia, widened cranial sutures, and frontal bossing. Craniotabes (thinning of the skull) also may be present. Classically, craniotabes is described as feeling like a ping-pong ball when the skull is depressed.Older infants and children present with bony changes and may have developmental delay, delayed tooth eruption, bowed legs, kyphosis, pelvic abnormalities, and potbellies. (1) Bony changes that occur in rickets are a result of delay in or failure of the cartilaginous growth plate to calcify before fusing of epiphyses. The clinical and radiologic findings that occur are secondary to a widening or deformity of the metaphyseal regions of the long bones (Figs 4, 5, and 6). Hence, children can have a widened wrist (Fig 7) or a rachitic rosary (Fig 8), an enlarged costochondral junction along the anterior lateral aspects of the chest wall. A Harrison groove, a horizontal depression across the chest, may be seen where the diaphragm pulls on the weakened chest wall. Adults generally present with osteomalacia. (1)(10)Over the years, it has been discovered that many tissues in the body, in addition to bone, have 1,25(OH)-D receptors. Vitamin D plays a role in cellular proliferation, differentiation, apoptosis, angiogenesis, and immunomodulation. The vitamin also inhibits renin synthesis, increases insulin production, and increases myocardial contractility. Studies have demonstrated that there is an increased incidence of Hodgkin lymphomas and colonic, pancreatic, prostate, ovarian, and breast cancers when 25(OH)-D levels are <20 ng/mL. Vitamin D deficiency has been shown to increase the risk of autoimmune diseases, osteoarthritis, type I diabetes mellitus, cardiovascular disease, schizophrenia, depression, and wheezing illnesses. (9)Vitamin D deficiency can occur because of decreased synthesis, decreased nutritional intake, decreased maternal vitamin D stores, malabsorption, and decreased synthesis or increased degradation of 25(OH)-D. There has been a resurgence of vitamin D deficiency in North America and northern Europe. Dark-skinned children on strict vegetarian diets or cult or fad diets, dark-skinned infants exclusively breastfed beyond age 3 to 6 months, premature infants, adolescents, and infants born to vitamin D–deficient mothers are all at increased risk. (8)Decreased UV-B exposure to the skin can result in decreased synthesis of vitamin D3. Darker-skinned individuals require greater UV-B exposure to maintain equal concentrations of vitamin D compared with lighter-skinned individuals. In fact, Asians may require 3 times and African Americans may require 6 to 10 times the exposure of UV-B as white individuals to synthesize equivalent amounts of vitamin D.The amount of an individual’s skin exposed to UV-B also plays a role in the synthesis of vitamin D. As an example, Middle Eastern women wearing traditional clothes are at greater risk for vitamin D deficiency. Sunscreen, increased time spent in the shade or indoors, air pollution, cloud cover, higher latitude (especially higher than 37.5°), and winter season all result in decreased UV radiation and, hence, decreased vitamin D levels. Higher altitudes and the summer season are protective against vitamin D deficiency. (1)(2)(8)Nutritional deficiency of vitamin D is more likely to occur if there are certain risk factors. Infants can be born deficient if there is maternal vitamin D deficiency. Transplacental transfer of vitamin D occurs throughout pregnancy. Thus, infants who are born prematurely can be deficient because there is less time to build up stores. Exclusively breastfed infants are at risk, especially if there is limited sun exposure, because human milk only provides 11 to 38 IU/day of vitamin D, assuming consumption of 750 mL/day of human milk. This lack of dietary vitamin D is exacerbated by the current AAP recommendation to limit sun exposure for infants younger than 6 months because of the harmful effects of UV radiation. Formula-fed infants also can be vitamin D deficient if other risk factors are present. (1)(2)(8)Any condition that leads to impaired fat absorption has the potential to result in vitamin D deficiency. Celiac disease, food allergies, gastric and small bowel resection, cystic fibrosis, and Crohn disease are a few of the disorders that can impair vitamin D absorption. (1)(2)(8)The diagnosis of vitamin D deficiency is based on clinical, r
Referência(s)