Patients at risk for vitamin A deficiency include those with conditions that affect intestinal fat absorption, underlying psychiatric illness, or chronic disease (eTable). Chronic alcohol use predisposes patients to a multitude of micronutrient deficiencies, including vitamin A deficiency.54 In chronic alcohol use, even mild cutaneous changes may be the first clue to low serum retinol.55
Vitamin A deficiency can be diagnosed by measuring serum retinol levels, with levels lower than 20 µg/dL being diagnostic of deficiency.56 Decreased serum retinol in patients hospitalized with flaring irritable bowel disorder has been repeatedly reported.57-59 Notably, serum retinol concentration does not decline until liver reserves of vitamin A are nearing exhaustion.33
The US Food and Drug Administration requires manufacturers to list retinol activity equivalents on labels. One international unit of retinol is equivalent to 0.3 µg of retinol activity equivalents.60 The treatment of vitamin A deficiency involves high-dose oral supplementation when possible.61 Although dependent on age, the treatment dose for most adults with vitamin A deficiency is 3000 µg (10,000 IU) once daily.
Phrynoderma has been specifically treated with salicylic acid ointment 3% and intramuscular vitamin A.62 Topical urea cream also may treat phrynoderma.63
Vitamin B2
Vitamin B2 (riboflavin) is absorbed in the small intestine and converted into 2 biologically active forms—flavin adenine dinucleotide and flavin mononucleotide—which serve as cofactors in metabolic and oxidation-reduction reactions. Malabsorptive disorders and bowel resection can lead to riboflavin deficiency.64 Other at-risk populations include those with restrictive diets,65 psychiatric illness, or systemic illness (eTable). Riboflavin can be degraded by light (deficiency has been reported after phototherapy for neonatal jaundice66) and following boric acid ingestion.67 Medications, including long-term treatment with antiepileptics, may lead to riboflavin deficiency.68
Riboflavin is critical to maintaining collagen production. Riboflavin deficiency may manifest clinically with extensive seborrheiclike dermatitis,44 intertrigolike dermatitis,69 or oral-ocular-genital syndrome.70 Angular cheilitis may accompany an atrophic tongue that is deep red in color. The scrotum is characteristically involved in men, with confluent dermatitis extending onto the thighs and sparing the midline. Red papules and painful fissures may develop. Balanitis and phimosis have been reported. Testing for riboflavin deficiency should be considered in patients with refractory seborrheic dermatitis.
Riboflavin stores are assessed by the erythrocyte glutathione reductase activity coefficient.44 A level of 1.4 or higher is consistent with deficiency. Serum riboflavin levels, performed after a 12-hour fast, may support the diagnosis but are less sensitive. Patients with glucose-6-phosphate deficiency cannot be assessed via the erythrocyte glutathione reductase activity coefficient and may instead require evaluation of 24-hour urine riboflavin level.44
Vitamin B3
Vitamin B3 (niacin, nicotinamide, nicotinic acid) is found in plant and animal products or can be derived from its amino acid precursor tryptophan. Niacin deficiency results in pellagra, characterized by dermatitis, dementia, and diarrhea.71 The most prominent feature is a symmetrically distributed photosensitive dermatitis of the face, neck (called Casal necklace)(Figure 3), chest, dorsal hands, and extensor arms. The eruption may begin with erythema, vesicles, or bullae (wet pellagra) and evolve into thick, hyperpigmented, scaling plaques.71 The skin may take on a copper tone and become atrophic.72 Dull erythema with overlying yellow powdery scale (called sulfur flakes) at follicular orifices has been described on the nasal bridge.73
Figure 3. Photosensitive dermatitis of the neck and upper chest (Casal necklace) seen in vitamin B3 deficiency (pellagra).