Pediatric Annals

Special Issue Article 

The ABCs of Nutrient Deficiencies and Toxicities

Kristin Capone, MD; Timothy Sentongo, MD


Vitamins and minerals are part of a well-balanced diet. They are essential for normal growth and development, which is especially crucial for the pediatric population. Vitamins are divided based on their solubility into fat-soluble vitamins, which include vitamins A, D, E, and K and water-soluble vitamins, which include the B vitamins and vitamin C. Minerals include calcium, magnesium, and phosphorus. Trace minerals are micronutrients and include copper, zinc, selenium, chromium and manganese. The pediatrician is often the first health care provider to interface with patients, allowing them to pick up on nutritional derangements. This article reviews the basic sources, absorption, metabolism as well as the signs and symptoms that arise in deficient and toxic states of fat-soluble vitamins, water-soluble vitamins, minerals, and trace elements. [Pediatr Ann. 2019;48(11):e434–e440.]


Vitamins and minerals are part of a well-balanced diet. They are essential for normal growth and development, which is especially crucial for the pediatric population. Vitamins are divided based on their solubility into fat-soluble vitamins, which include vitamins A, D, E, and K and water-soluble vitamins, which include the B vitamins and vitamin C. Minerals include calcium, magnesium, and phosphorus. Trace minerals are micronutrients and include copper, zinc, selenium, chromium and manganese. The pediatrician is often the first health care provider to interface with patients, allowing them to pick up on nutritional derangements. This article reviews the basic sources, absorption, metabolism as well as the signs and symptoms that arise in deficient and toxic states of fat-soluble vitamins, water-soluble vitamins, minerals, and trace elements. [Pediatr Ann. 2019;48(11):e434–e440.]

Vitamins and minerals are essential components of a balanced diet. Nutritional status is especially important in children for appropriate growth and development. Pediatricians have the unique role of frequent contacts with pediatric patients allowing for nutritional counseling and recognition of nutritional derangements. In this article, we approach the sometimes daunting “alphabet soup” of vitamins and minerals to provide an overview of nutrient deficiencies and toxicities.

Fat-soluble vitamins include vitamins A, D, E, and K, which dissolve in fat and are dependent on bile acids for absorption.1,2 They can be stored for a long time in adipose tissue, and therefore have a higher potential for toxicity (Table 1).1 Water-soluble vitamins dissolve in water and include the B vitamins and vitamin C. The B vitamins include thiamine (B1), riboflavin (B2), niacin (B3), pantothenic acid (B5), pyridoxine (B6), biotin (B7), folic acid (B9), and cobalamin (B12) (Table 2). They are released with digestion of foods and absorbed mostly in the jejunum except for cobalamin (absorbed in the ileum), niacin (absorbed in the stomach), and riboflavin and biotin (absorbed in the proximal colon). The nonvitamin minerals include calcium, magnesium, and phosphorus and micronutrients include copper, zinc, selenium, chromium, and manganese.

Fat-Soluble Vitamins

Table 1:

Fat-Soluble Vitamins

Water-Soluble Vitamins

Table 2:

Water-Soluble Vitamins

Vitamin A

Vitamin A refers to retinol, retinal, retinoic acid, and retinyl esters, which differ in their terminal C-15 groups. Provitamin A carotenoids, or beta-carotenes, are precursors to retinol. Dietary sources of retinyl esters include liver, fish oils, dairy, kidney, milk, and eggs.1,2 Beta-carotene is found in green and yellow fruits, vegetables, and some oils. Dietary retinyl esters are freed by acidic digestion, emulsified by bile salts to form micelles, transported into intestinal cells where they are hydrolyzed, re-esterified and incorporated into chylomicrons, and then secreted into the lymphatic system.1 Retinyl esters are stored in hepatic stellate cells, also known as Ito cells, then hydrolyzed to retinol and circulate bound to retinol binding protein/ transthyretin for delivery to target tissues (eg, retina).1

Vitamin A deficiency can be seen with fat malabsorption, veganism, fad diets, or alcoholism. The hallmark finding of severe deficiency is xeropthalmia or dry eyes.1 Earlier signs of deficiency include impaired dark adaptation and night blindness because retinol aids in rhodopsin formation, the visual pigment in dark adaptation. More severe deficiency manifests as xeropthalmia and Bitot's spots, ocular finding resulting from superficial conjunctival keratin buildup.3 Other manifestations of deficiency include impaired humoral and cellular mediated immunity, impaired bone growth, and follicular hyperkeratosis.1

Vitamin A toxicity can either be acute or chronic. Acute toxicity results from a single large ingestion of preformed vitamin A (>150,000 mcg in adults) leading to nausea, vomiting, headache, vertigo, blurred vision, and increased intracranial pressure.1 Chronic toxicity is more common resulting from prolonged, often under recognized, intake of supplements highly fortified with vitamin A.4 Chronic toxicity manifests as irritability, anorexia, skin desquamation, hepatomegaly, cirrhosis, and resultant portal hypertension.4 High vitamin A levels are also teratogenic in the first trimester, causing neural tube defects.1 Hypercarotenemia, although not a toxicity, results from increased beta-carotene consumption and presents as benign carotenodermia or orange/yellow skin discoloration.1

Biotin (Vitamin B7)

Biotin, or vitamin B7, is a coenzyme for many carboxylation reactions including the tricarboxylic acid cycle. It is absorbed in the small and large intestine, and it is found in liver, meats, egg yolks, milk, and fruits.1,5,6 Deficient states can result from parenteral nutrition (PN) therapy without supplementation or an adverse effect from chronic raw egg white consumption, which naturally contains avidin that strongly binds to biotin making it unavailable for digestion/absorption. Biotin deficiency causes atypical facies with dermatitis around the mouth, nose, and eyes.6,7 It can also cause alopecia, hypotonia, or ataxia.1

Vitamin C

Vitamin C, or ascorbic acid, is an antioxidant serving as an electron donor for redox reactions and regenerates other antioxidants like vitamin E and glutathione. It also allows for normal functioning of the eyes, neutrophils, sperm DNA, connective tissue, hormones, and amino acid biosynthesis.1

Dietary sources include citrus fruits, berries, and vegetables especially peppers, tomatoes, and potatoes.1,2 Vitamin C deficiency, also known as scurvy, results from elastic tissue deterioration and manifests with petechiae, ecchymosis, inflamed bleeding gums, brittle coiled hairs with perifollicular hemorrhages, fatigue, arthralgias, and edema.1,2


Calcium is a mineral that provides structural support for bones and teeth, which account for 99% of the body's calcium. An additional 1% is circulating, of which approximately 50% is ionized and functions in muscle contraction, nerve signaling, and hormone secretion.1 Dairy products are the main dietary source.1,2 Hypocalcemia can result in jitters, seizures, tetany, and osteopenia. It is associated with concomitant vitamin D or magnesium deficiency. Hypercalcemia can cause abdominal pain, polyuria, depression, confusion, and metastatic calcifications.1

Cobalamin (Vitamin B12)

Cobalamin, or vitamin B12, is a folate coenzyme that aids in synthesis of DNA from its precursors and methionine from homocysteine. Dietary sources include animal products like meat, fish, poultry, and eggs as well as fortified cereals and soymilk. Breast milk also contains cobalamin, dependent upon maternal diet.1,2,6

Absorption of cobalamin is highly specialized. It requires an intact stomach, gastric acidity, transport proteins, pancreatic sufficiency, and functioning terminal ileum. Cobalamin bound to food proteins is released by gastric hydrochloric acid then free cobalamin binds to R-binder from salivary glands. Pancreatic proteases split R-binder from cobalamin so it can bind intrinsic factor (IF) produced by gastric parietal cells. The cobalamin-IF complex is absorbed in the terminal ileum via endocytosis.1

Deficiency can occur with veganism, chronic acid suppression causing anchlorhydria, pancreatic insufficiency, inflamed or absent terminal ileum (eg, Crohn's disease, intestinal resection, and short bowel syndrome), and dietary competition from parasitic infestation with Diphyllobothrium latum (fish tapeworm).1,8 Deficiency results in megaloblastic anemia, hypersegmented neutrophils, and increased plasma methylmalonic acid. Clinical symptoms include weakness, impaired cognitive function, psychosis, neurologic deficits, and ataxia. Pernicious anemia, a specific form of deficiency, arises from autoimmune gastritis with antibodies against IF or hydrogen potassium ATPase (adenosine triphosphatase) causing loss of parietal cells. Clinical symptoms include glossitis, fatigue, and paresthesias.1,2,6,9

Repletion in patients with malabsorption is by 1,000 mcg intramuscular cobalamin administered in 100 to 200 mcg aliquots daily over 5 to 10 days.10 Larger doses are poorly retained due to rapid renal clearance. Oral or intranasal routes can be used in patients deficient in the vitamin who have an intact terminal ileum.1

Vitamin D

Vitamin D, also known as calciferol, is essential for calcium homeostasis, bone mineralization, immunomodulation, antimicrobial action, cell proliferation and apoptosis, insulin secretion, skin integrity, and beta-oxidation. It refers to two different fat-soluble sterols: cholecalciferol (D3) photosynthesized by ultraviolet light from a cholesterol precursor and ergocalciferol (D2) derived from yeast and plant sterols. Ergocalciferol and cholecalciferol are biologically inert prohormones requiring two hydroxylations to form the active 1,25-dihydroxyvitamin D.1,2

Only 10 to 15 minutes of whole-body summer sunlight exposure produces 20,000 IU of D3 in the circulation. Dietary vitamin D sources include fatty fish, fish liver oil, aquatic mammal liver, fortified milk, cheese, grains, and orange juice. Intestinal absorption is like vitamin A except vitamin D circulates bound to vitamin D binding protein or albumin to target tissues.1 Circulating vitamin D is either stored in fat tissue or hydroxylated by vitamin D 25-hydroxylase in hepatic mitochondria. The resultant 25-hydroxyvitamin D has a half-life of 10 to 20 days and is a reliable marker of vitamin D status because it reflects accumulation of both dietary and photosynthesized vitamin D. A second hydroxylation occurs in the proximal renal tubules by 1-alpha-hydroxylase in response to PTH to form 1,25-dihydroxyvitamin D, also known as calcitriol, which has a half-life of only 4 to 6 hours.1,2

Deficiency results from inadequate sun exposure, which occurs with higher latitudes, seasonal changes, sunscreen use, or increased melanin pigmentation. It can also result from decreased dietary D2 intake or drug interactions (eg, glucocorticoids decrease intestinal calcium absorption, phenobarbital and phenytoin decrease the half-life of circulating metabolites).1,2 Serum 25-hydroxyvitamin D levels <30 nmL/L (<12 ng/mL) indicate deficiency. Deficiency causes inadequate mineralization or demineralization of the skeleton. Ricketts occurs in the developing skeleton and manifests as metaphyseal widening, cupping and splaying, rachitic rosary, bowed legs or knock knees, and frontal bossing. Osteomalacia, alternatively, develops in the adult skeleton with decreased bone mineralization. Secondary hyperparathyroidism may develop with decreased serum 25-hydroxyvitamin D concentrations.1 Vitamin D toxicity can result from excessive ingestion but not from sunlight exposure. It presents with symptoms of hypercalcemia.1,2

Vitamin E

Vitamin E, or alpha-tocopherol, is a nonspecific chain-breaking antioxidant that sits within the cell membrane. It is a peroxyl radical scavenger that prevents propagation of free radical reaction and lipid peroxidation of cell membranes. When vitamin E intercepts a radical, alpha-tocopherol is oxidized to the tocopheryl radical, which can then be reduced back to alpha-tocopherol by other antioxidants like vitamin C or glutathione. It is also involved in cell proliferation, differentiation, and cell adhesion.1 Vitamin E is found in vegetable oils, avocado, nuts, and breast milk. Intestinal absorption is through mechanisms like the other fat-soluble vitamins.1,2 Vitamin E circulates in plasma with lipoproteins, mainly very low density lipoprotein, to target tissues where it rapidly transfers to cell membranes.1

Deficiency is seen with fat malabsorption or abetalipoproteinemia. Vitamin E requirements are increased in people with increased physical activity, high polyunsaturated fatty acid intake, and smokers. Increased plasma lipid concentrations lead to increased plasma carriers for alpha-tocopherol but not necessarily increased tissue delivery.1 With elevated serum lipids, a serum alpha-tocopherol to lipid ratio <0.6 mg/g indicates vitamin E deficiency regardless of serum alpha-tocopherol level. Deficiency is defined as alpha-tocopherol levels <12 mcmol/L and is associated with increased infections, anemia due to increased erythrocyte fragility, stunted growth, axonal degeneration, posterior column and spinocerebellar symptoms, peripheral neuropathy, and ophthalmoplegia. Neurological symptoms can progress if untreated but normally reverse with adequate supplementation.1,2

Toxicity leads to hemorrhagic complications especially with vitamin K deficiency or anticoagulation therapy. Adults can tolerate up to 800 mg/day of supplemental vitamin E.1 In premature infants, elevated serum alpha-tocopherol is associated with increased risk of necrotizing enterocolitis and sepsis.11

Folate (Vitamin B9)

Folate, or vitamin B9, plays a role in nucleic acid and amino acid metabolism, cellular growth, and erythrocyte maturation. Dietary sources include green vegetables, liver, yeast, fruits, and fortified cereals.1,2

Folate deficiency can result from a low-folate diet (eg, infants fed primarily goats milk), and prolonged therapy with medications that interfere with folate absorption, metabolism, or bioavailability (eg, cholestyramine, phenytoin, sulfasalazine, methotrexate, pyrimethamine, pentamidine, and triamterene).1,12 Deficiency results in megaloblastic anemia, weakness, behavior disorders, and increased risk of neural tube defects in infants born to mothers who are deficient.1,6 In 1998, the US Food and Drug Administration mandated folic acid fortification of all enriched grain products, which has corresponded to a decline in the prevalence of folate deficiency anemia and incidence of infants born with neural tube defects.13,14

Vitamin K

Vitamin K is essential for coagulation. It is a cofactor for gamma-glutamyl carboxylase enzymes, which perform post-translational carboxylation of proteins known as vitamin K-dependent proteins. These include coagulation proteins (eg, prothrombin, proteins C and S, and factors II, VII, IX, X), and proteins in mineralized tissues (eg, osteocalcin, matrix gla-protein).1,2 There are two naturally occurring vitamin K compounds: phylloquinone (K1) from plant sources and long-chain menaquinones (K2) synthesized by gut flora. Menadione (K3) is a chemically synthesized compound.1,2

Dietary sources include green leafy vegetables and vegetable oils (eg, soybean, cottonseed, canola, olive). It is found in low concentrations in breast milk, but infant formulas are fortified. Absorption is low from food sources (<20%), but free phylloquinone is almost completely absorbed.1,2

Vitamin K deficiency occurs with severe fat malabsorption (eg, pancreatic insufficiency, biliary obstruction/cholestasis, bariatric surgery), severely restricted diets, prolonged therapy with broad-spectrum antibiotics, which alter gut flora, and elevated vitamin E intake, which antagonizes vitamin K absorption.1 Clinical manifestations include increased prothrombin time and international normalized ratio, bleeding, and easy bruising.1,2

Hemorrhagic disease of the newborn results from poor placental vitamin K transfer, immature liver function, which inefficiently uses vitamin K, and a sterile gut at birth. Infants who are exclusively breast-fed and do not receive vitamin K prophylaxis at birth are at the highest risk.15

Vitamin K toxicity is rare but can result from ingestion of large amounts of water-soluble synthetic vitamin K and is associated with hemolytic anemia, hyperbilirubinemia, and kernicterus.1,2 Additionally, high dietary or supplemental vitamin K can antagonize anticoagulation effects of warfarin.1


Magnesium is essential for skeletal and cardiac muscle and is a cofactor in more than 300 enzymatic processes.1,2 Magnesium is found in green leafy vegetables, grains, and nuts. Hypomagnesemia leads to tremors, muscle twitches, muscle cramps, or seizures. It is associated with malabsorption states and use of tacrolimus or loop diuretics.2 Hypermagnesemia from pharmacologic excess leads to diarrhea, hyporeflexia, hypotonia, and respiratory depression.1

Niacin (Vitamin B3)

Niacin, or vitamin B3, refers to nicotinamide and nicotinic acid, which are converted to the two coenzymes, nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP), that are essential in more than 200 different redox reactions.1,2,6 Endogenous niacin synthesis occurs in the liver and kidney from tryptophan. Dietary sources include yeast, meats, poultry, fish, fortified cereals, legumes, and seeds. Niacin is absorbed in the stomach and small intestine.1,2

Niacin deficiency can be seen in carcinoid syndrome where tryptophan is preferentially oxidized to serotonin and with medications (eg, isoniazid, 5-fluorouracil) that compete with the pyridoxine-derived coenzyme required in the tryptophan-niacin pathway.1 Hartnup's disease is a genetic disorder leading to impaired absorption of neutral amino acids including tryptophan.2 Niacin deficiency manifests as pellagra, meaning “rough skin,” and is comprised of the three D's: diarrhea, dermatitis, dementia (and fourth D for death). Glossitis or angular stomatitis may also occur. Serum NAD/NADP levels or 24-hour urine niacin and derivatives can diagnose deficiencies.1,2

Pantothenic Acid (Vitamin B5)

Pantothenic acid, or vitamin B5, is a cofactor in many acetylation reactions including the tricarboxylic acid cycle and fatty acid metabolism. It functions as part of coenzyme A.6 It is found ubiquitously in food but more concentrated in egg yolk, broccoli, liver, yeast, and milk.2,6 It is also synthesized by colonic bacteria. Deficiency is rare but can cause weakness, fatigue, irritability, and paresthesias referred to as “burning feet syndrome.”6


Phosphorus plays a role in acid-base balance, transfer of energy, and phosphorylation. About 85% is in skeletal support, 14% is intracellular, and only 1% is circulating.1 Dietary sources include dairy, meats, nuts and plants. Hypophosphatemia manifests as anorexia, anemia, muscle weakness, and bone pain. It can result from refeeding syndrome or PN with inadequate supplementation. Hyperphosphatemia can be seen with renal disease and cause hypocalcemia.1

Pyridoxine (Vitamin B6)

Pyridoxine, or vitamin B6, is composed of six compounds including pyridoxine (Pn), pyridoxal (PL), pyridoxamine (PM), and their pentophosphates: PnP, PLP, PMP. Pyridoxine is a coenzyme for metabolism of many amino acids (eg, conversion of tryptophan to niacin or serotonin, homocysteine to cysteine, dopa to dopamine) and synthesis of gamma-aminobutyric acid and heme.1,2,6 PLP and PMP are derived from animal sources, whereas pyridoxine and PnP come from plants. Dietary sources include bananas, cantaloupe, walnuts, green leafy vegetables, peas, carrots, brown rice, yeast, eggs, meats, fish, and fortified cereals.2 Some microbial synthesis also occurs.1

Deficiency can result from medications that lower plasma PLP (eg, isoniazid, hydralazine, oral contraceptives, penicillamine, theophylline, L-dopa).2 PLP is a negative acute-phase reactant and, therefore, inversely associated with markers of inflammation.1 Additionally, deficiency can be seen with genetic mutations affecting pyridoxine metabolism. Clinical manifestations include microcytic anemia, glossitis, seborrheic dermatitis, depression, and neurologic manifestations including seizures or abnormal electroencephalograms.1,2,6 Plasma PLP is the best marker of pyridoxine status.1

Toxicity can result in peripheral sensory neuropathy with high-dose pyridoxine that can improve with withdrawal of supplementation.1

Riboflavin (Vitamin B2)

Riboflavin, or vitamin B2, is a fluorescent yellow compound comprised of flavin mononucleotide (FMN) and flavine adenine nucleotide (FAV). It is involved in oxidation-reduction reactions integral in carbohydrate, fat, and protein metabolism.1,6 It can be used for migraine headache prophylaxis.1 It is involved in niacin, pyridoxine, and folate metabolism, and is also essential for optimized iron absorption and utilization.16 Riboflavin is found in animal proteins like meat, dairy, and eggs, and green vegetables and fortified grains. FMN and FAV are released from dietary protein by gastric acid then hydrolyzed to riboflavin in the jejunum where it is absorbed. An additional small amount is absorbed in the colon. It circulates bound to albumin or immunoglobulins and very little is stored in the body.1,6

Deficiency can result from prolonged low meat or dairy intake. It is seen with severe protein calorie malnutrition (eg, kwashiorkor, anorexia nervosa) and often associated with other vitamin deficiencies. Deficiency can be measured through erythrocyte riboflavin levels or 24-hour urinary excretion. Ariboflavinosis manifests as glossitis, angular stomatitis, pharyngitis, or atopic dermatitis of the nasolabial folds.1,6

Thiamin (Vitamin B1)

Thiamin, or vitamin B1, exists as thiamin monophosphate, triphosphate, and approximately 80% as pyrophosphate (TPP). TPP is a coenzyme for decarboxylation of alpha-keto acids and transketolation, important steps in carbohydrate and branched-chain amino acid metabolism. Dietary sources include fortified whole grains and cereals, pork, eggs, legumes, and nuts.1,6

Deficient states can occur in less than 3 weeks with a strict thiamin deficient diet, which can occur with PN support without supplementation, malabsorption, alcoholism, and rapid weight loss.1 During thiamin deficiency, oxidative decarboxylation of pyruvate does not occur; thus, it cannot enter the Krebs cycle preventing the synthesis of ATP. Pyruvate is instead metabolized to lactic acid leading to metabolic acidosis.10 Clinically, the patient presents with beriberi, a life-threatening acute septic shock-like state characterized by high output heart failure, opthalmoplegia, altered mental status, and severe metabolic acidosis with a high risk for death if thiamin is not urgently administered.1,6 The diagnosis is confirmed by clinical improvement after intramuscular or intravenous thiamin repletion of 10 to 25 mg.2,10 Wernicke's encephalopathy is usually seen in the setting of alcoholism and malnutrition with altered consciousness plus a triad of ophthalmoplegia, nystagmus, and ataxia.1

Trace Minerals

Trace minerals are essential nutritional components required in small amounts in the diet. They include, among others, copper, chromium, selenium, zinc, and manganese. Trace element deficiencies most often occur in children requiring PN support with inadequate supplementation or severe malnutrition.10 Copper plays a role in energy metabolism, iron metabolism, and antioxidation. Deficiency results in anemia, neutropenia, decreased pigmentation, and poor growth.2,10 Chromium potentiates the action of insulin and deficiency can cause glucose intolerance.17 Selenium aids in antioxidation and thyroid function. Deficiency results in hair and skin depigmentation, macrocytosis, muscle weakness, and cardiomyopathy.2 Zinc is an essential cofactor for numerous enzymatic reactions. Deficiency manifests with decreased alkaline phosphatase levels, poor growth, diarrhea, impaired wound healing, immune dysfunction, and a characteristic acro-orificial rash known as acrodermatitis enterohepatica.2,10 Manganese is a cofactor for enzymes including arginase and pyruvate decarboxylase. Deficiency is not well-documented in humans; however, toxicity from excessive parenteral manganese or inhaled manganese in industrial settings causes ataxia, confusion, and lack of coordination.2


Vitamins and minerals are essential for growth and development in children. Pediatricians play a vital role in identifying nutritional deficiencies and toxicities through clinical signs and symptoms. Recognition of these abnormalities can allow for prompt investigation and correction of derangements to optimize the health of their patients.


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Fat-Soluble Vitamins

Vitamin Name Alternative Name Sources Risk Factors for Deficiency Manifestations of Deficiency Manifestations of Toxicity
Vitamin A Retinol Liver, vegetables, dairy, kidney, eggs Fat malabsorption, vegan diet, alcoholism Xeropthalmia, night blindness, Bitot's spots, follicular hyperkeratosis Increased intracranial pressure, headache, nausea/vomiting, hepatotoxicity
Vitamin D Calciferol Sunlight, fatty fish, fortified dairy Fat malabsorption, low sun exposure, glucocorticoid use Rickets, hypocalcemia, hypophosphatemia, osteomalacia Hypercalcemia
Vitamin E Alpha-tocopherol Vegetable oils, avocados, nuts Fat malabsorption, abetalipoproteinemia Neuropathy, ataxia Bleeding, necrotizing enterocolitis, sepsis
Vitamin K Phytonadione Intestinal flora, green leafy vegetables, vegetable oils Fat malabsorption, antibiotic use, vitamin K refusal at birth Bleeding, bruising Hemolytic anemia, hyperbilirubinemia, kernicterus

Water-Soluble Vitamins

Vitamin Name Alternative Name Sources Risk Factors for Deficiency Manifestations of Deficiency
Vitamin B1 Thiamin Fortified grains, pork, eggs, legumes, nuts Alcoholism, rapid weight loss Beriberi, high output cardiac failure, ophthalmoplegia, altered mental status, metabolic acidosis
Vitamin B2 Riboflavin Animal proteins, green vegetables, fortified grains Severe malnutrition Glossitis, angular stomatitis, pharyngitis, nasolabial atopic dermatitis
Vitamin B3 Niacin Yeast, meats, fish, fortified cereals, legumes Carcinoid syndrome, isoniazid use, 5-fluorouracil use, Hartnup's disease Pellagra, diarrhea, dermatitis, dementia
Vitamin B6 Pyridoxine Fruits, vegetables, animal proteins, fish, fortified grains Isoniazid use, hydralazine use, oral contraceptives use, penicillamine use, L-dopa use Anemia, glossitis, depression, seizures/electroencephalogram abnormalities
Vitamin B7 Biotin Liver, egg yolks, meat High egg-white consumption, parenteral nutrition dependence Dermatitis, alopecia, hypotonia
Vitamin B9 Folate Green vegetables, liver, yeast, fruits, fortified grains Infants fed goat's milk, methotrexate use, cholestyramine use, phenytoin use, sulfasalazine use, pentamidine use Megaloblastic anemia, behavior disorder, neural tube defects
Vitamin B12 Cobalamin Animal products, fish, fortified grains, soymilk Veganism, absent terminal ileum, pancreatic insufficiency, anchlorhydria Megaloblastic anemia, hypersegmented neutrophils, glossitis, neurologic deficits
Vitamin C Ascorbic acid Citrus fruits, peppers, tomatoes Severely restricted diet, unsupplemented parenteral nutrition Scurvy, petechia, bleeding gums, perifollicular hemorrhages

Kristin Capone, MD, is an Assistant Professor, Department of Pediatrics, Section of Gastroenterology, Rutgers University-Robert Wood Johnson Medical School. Timothy Sentongo, MD, is an Associate Professor of Pediatric Gastroenterology; the Director, Pediatric Nutrition Support; and the Director, Pediatric Gastrointestinal Endoscopy, Section of Gastroenterology, Hepatology and Nutrition, The University of Chicago Medical Center.

Address correspondence to Kristin Capone, MD, Department of Pediatrics, Section of Gastroenterology, Rutgers University-Robert Wood Johnson Medical School, 89 French Street, 2nd Floor, New Brunswick, NJ, 08901; email:

Disclosure: The authors have no relevant financial relationships to disclose.


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