Nutritional Dermatoses in the Hospitalized Patient

HOSPITAL CONSULT

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Cutaneous disease may be the first manifestation of an underlying nutri-tional deficiency, highlighting the importance of early recognition by der-matologists. Undernutrition occurs when there is an imbalance between nutrient intake and metabolic demand. Many hospitalized patients are in catabolic states due to chronic illness, infection, malabsorption, or medication. These patients are at an increased risk for undernutrition and therefore associated cutaneous disease. This review details the risk factors for nutritional deficiency, illustrates the presentations of cutane-ous disease, reviews diagnostic workups, and provides suggestions for supplementation in the undernourished patient.

Cutis. 2020;105:296-302, 308.

T he World Health Organization defines malnutri-tion as deficiencies, excesses, or imbalances in an individual’s intake of energy and/or nutrients.1

This review will focus on undernutrition, which may result from macronutrient or micronutrient deficiencies. Undernutrition in the hospitalized patient is a common yet underrecognized phenomenon, with an estimated prevalence of 20% to 50% worldwide.2 Malnutrition is an independent risk factor for patient morbidity and mortality and has been associated with increased health care costs.3

Nutritional deficiencies may arise from inadequate nutrient intake, abnormal nutrient absorption, or improper nutrient utilization.4 Unfortunately, no standardized algorithm for screening and diagnosing patients with malnutrition exists, making early physical examination findings of utmost importance. Herein, we present a review of acquired nutri-tional deficiency dermatoses in the inpatient setting.

Protein-Energy MalnutritionProtein-energy malnutrition (PEM) refers to a set of related disorders that include marasmus, kwashiorkor (KW), and marasmic KW. These conditions frequently are seen in developing countries but also have been reported in developed nations.5 Marasmus occurs from a chronic deficiency of protein and calories. Decreased insulin pro-duction and unopposed catabolism result in sarcopenia and loss of bone and subcutaneous fat.6 Affected patients include children who are less than 60% ideal body weight (IBW) without edema or hypoproteinemia.7 Kwashiorkor is the edematous form of PEM that develops from iso-lated protein deficiency, resulting in edema, diarrhea, and immunosuppression.6 Micronutrient deficiencies, oxida-tive stress, slow protein catabolism, and excess antidi-uretic hormone have been proposed as potential drivers of KW.8 Kwashiorkor affects children between 60% and 80% IBW. Marasmic KW has features of both diseases, including children who are less than 60% IBW but with associated edema and/or hypoproteinemia.9

Although PEM is uncommon in adults, hospitalized patients carry many predisposing risk factors, including infections, malabsorptive conditions, psychiatric disease, and chronic illness (eTable). Patients with chronic infec-tions present with findings consistent with marasmic KW due to lean body mass loss.

The cutaneous findings in PEM are related to dysmatu-ration of epidermal keratinocytes and resultant epidermal atrophy.10 Patients with marasmus exhibit dry, wrinkled, loose skin due to subcutaneous fat loss. Emaciated chil-dren often lose their buccal fat pads, and reduced perianal

Nutritional Dermatoses in the Hospitalized Patient

Melissa Hoffman, MS; Robert G. Micheletti, MD; Bridget E. Shields, MD

From the Department of Dermatology, University of Pennsylvania Perelman School of Medicine, Philadelphia.The authors report no conflict of interest.The eTable is available in the Appendix online at www.mdedge.com/dermatology.Correspondence: Bridget E. Shields, MD, 3400 Civic Center Blvd, Philadelphia, PA 19104 ([email protected]).

PRACTICE POINTS• Nutritional deficiencies are common in hospitalized

patients and often go unrecognized.• Awareness of the risk factors predisposing patients

to nutritional deficiencies and the cutaneous manifes-tations associated with undernutrition can promote early diagnosis.

• When investigating cutaneous findings, undernutri-tion should be considered in patients with chronic infections, malabsorptive states, psychiatric illness, and strict dietary practices, as well as in those using certain medications.

• Prompt nutritional supplementation can prevent patient morbidity and mortality and reverse skin disease.

Copyright Cutis 2020. No part of this publication may be reproduced, stored, or transmitted without the prior written permission of the Publisher.

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adipose may lead to rectal prolapse. Increased lanugo hair may be present on the face, and alopecia of the scalp may occur.6 In KW, cutaneous disease progresses from conflu-ent hyperkeratosis to a dry atrophic epidermis that erodes easily, leaving underlying pale erythema. The resultant pattern is one of hyperpigmented plaques with slightly raised borders, and hypopigmented patches and erosions described as flaky paint dermatitis (Figure 1).5 Lesions appear first in areas of friction. The hair often is dry and brittle; curly hair may straighten and scale.11 Red-yellow to gray-white hypopigmentation may develop, denoting periods of inadequate nutrition. The flag sign describes alternating horizontal bands of hypopigmentation inter-spersed with bands of pigmented hair. The nails usually are thin and soft and may exhibit the nail flag sign, char-acterized by horizontal bands of white and red.12 Cheilitis, angular stomatitis, and vulvovaginitis may be present.6

In adults, weight loss and body mass index can be used to assess nutritional status, along with a focused history and physical examination. Complete blood cell count, electrolyte levels, and blood urea nitrogen should be assessed, as hypoglycemia and anemia often accompany PEM.13 In KW, hypoalbuminemia and hypoproteinemia are invariably present. Although prealbumin may be a valid prognostic indicator of disease outcomes and mor-tality in patients at risk for malnutrition, checking other serum biomarkers remains controversial.14 Focused testing may be warranted in patients with risk factors for chronic infectious processes, such as human immunodeficiency virus or tuberculosis.6 Skin biopsy may solidify the diagno-sis of PEM. Hypertrophy of the stratum corneum, atrophy of the stratum spinosum and stratum granulosum, and increased basal layer melanin have been reported.15

Treatment involves initial fluid resuscitation and cor-rection of electrolyte imbalances, followed by nutritional replacement.13 Oral or enteral tube feedings are preferred over total parenteral nutrition (TPN), as they enhance recov-ery of the gastrointestinal tract.16 Refeeding should occur in

small amounts and frequent intervals.5 Skin-directed therapy is aimed at restoring epidermal function and hydration, with regular moisturization and application of barrier creams, such as zinc oxide ointment or petrolatum.10

Zinc DeficiencyZinc is an essential trace element that provides regulatory, structural, and catalytic functions across multiple bio-chemical pathways6 and serves as an enzymatic cofactor and key component for numerous transcription factors.17 Zinc is derived from food sources, and its concentration correlates with protein content.18 Zinc is found in both animal and plant-based proteins, albeit with a lower oral bioavailability in the latter. Zinc deficiency may be inher-ited or acquired. Primary acrodermatitis enteropathica is an autosomal-recessive disorder of the solute carrier fam-ily 39 member 4 gene, SLC39A4 (encodes zinc transporter ZIP4 on enterocytes); the result is abnormal zinc absorp-tion from the small intestine.18

Acquired zinc deficiency occurs from decreased dietary zinc intake, impaired intestinal zinc absorption, excessive zinc elimination, or systemic states of high catabolism or low albumin (eTable). Total parenteral nutrition–associated deficiency has arisen when nutritional formulations did not contain trace elements during national shortages or when prolonged TPN was not anticipated and trace elements were removed.19 Zinc levels may already be low in patients with chronic illness or inflammation, so even a short period on TPN can precipitate deficiency.18,19 Diets high in phytate may result in zinc deficiency, as phytate impairs intestinal zinc absorption.20 Approximately 15% of patients with inflamma-tory bowel disease experienced zinc deficiency worldwide.21 In Crohn disease, zinc deficiency has been associated with active intestinal inflammation, increased risk for hospitaliza-tion, surgeries, and disease-related complications.22,23

Medications such as antiepileptics, antimetabolites, or penicillamine may induce zinc deficiency, highlight-ing the importance of medication review for hospitalized patients (eTable). Catabolic states, frequently encoun-tered in hospitalized patients, increase the risk for zinc deficiency.24 Patients with necrolytic migratory erythema (associated with pancreatic glucagonomas) often experi-ence low serum zinc levels.25

The skin is the third most zinc-abundant tissue in the human body. Within keratinocytes, zinc is critical to normal proliferation and suppression of inflammation.17 Zinc also plays an important role in cutaneous immune function.26 Zinc deficiency presents with sharply demar-cated, flaccid pustules and bullae that erode into scaly, pink, eczematous or psoriasiform plaques. Lesions are found preferentially in acral and periorificial sites, often with crusting and exudate. The groin and flexural sur-faces may be affected. Erosions often become secondarily impetiginized. Other cutaneous findings include angular cheilitis, stomatitis, glossitis, paronychia, onychodys-trophy, generalized alopecia, and delayed wound heal-ing.26 Histopathology of skin lesions is characterized by

FIGURE 1. Dermatitis resembling flaky paint in a patient with protein-energy malnutrition (kwashiorkor).


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granular layer loss, epidermal pallor, confluent parakera-tosis, spongiosis, dyskeratosis, and psoriasiform hyper-plasia.27 Acquired bullous acrodermatitis enteropathica has been reported as a histologic mimicker of pemphigus foliaceous in patients on TPN.28

Diagnosis of zinc deficiency is made by measuring plasma zinc levels. Fasting levels should be drawn in the morning, as they can fluctuate based on the time of day, stress levels, or inflammation.6 Sample hemolysis and anti-coagulants high in zinc may falsely elevate plasma zinc. A normal zinc level is greater than 70 µg/dL; however, normal levels do not rule out deficiency.18 Measurement of zinc-dependent enzymes, such as alkaline phospha-tase, can be a quick way to assess zinc status. Serum albumin also should be measured; because zinc is carried by albumin in the blood, hypoalbuminemia may result in secondary zinc deficiency.18

Zinc replacement therapy is largely through oral sup-plementation and should start at 0.5 to 2.0 mg/kg/d in adults with acquired disease.29,30 Zinc sulfate is the most affordable and is the supplement of choice, with 50 mg of elemental zinc per 220 mg of zinc sulfate (~23% elemen-tal zinc).31 Alternative zinc salts, such as zinc gluconate (13% elemental zinc), may be used. Patients with malab-sorptive disorders often require parenteral supplementa-tion.32 Clinical symptoms often will resolve within 1 to 2 weeks of supplementation.29 In patients with primary acrodermatitis enteropathica, lifelong supplementation with 3 mg/kg/d elemental zinc should occur.6 Calcium and folate may reduce zinc absorption, while zinc supplemen-tation can interfere with copper and iron absorption.33

Iron DeficiencyIron is an essential component of the hemoglobin mol-ecule. Iron homeostasis and metabolism are tightly regulated processes that drive erythropoiesis. Only 5% to 10% of dietary iron is absorbed through nutrition, while the remainder is recycled from red cell breakdown. Both normal iron levels and iron deficiency (ID) are defined by age and gender.34 Iron-deficiency anemia (IDA) is one of the most common cause-specific anemias worldwide.35

Fatigue is the most common and earliest symp-tom of ID. In a single study, pallor was predictive of anemia in hospitalized patients; however, absence of pallor did not rule out anemia.34 Dyspnea on exertion, tachycardia, dysphagia, and pica also may be reported. Cutaneous manifestations include koilonychia (Figure 2), glossitis, pruritus, angular cheilitis, and telogen effluvium. Plummer-Vinson syndrome is characterized by microcytic anemia, glossitis, and dysphagia.

Risk factors for ID include insufficient dietary consump-tion,36 blood loss, malabsorptive states,37,38 and increased iron requirements (eTable). Patient fragility (eg, elderly, chronic disease) is a newly described risk factor where correction of ID may impact morbidity, mortality, and quality of life.35

Iron deficiency can be present despite a normal hemo-globin level. Serum ferritin and percentage transferrin

saturation are key to early identification of IDA.35 Ferritin levels lower than 30 µg/L confirm the diagnosis. Decreased transferrin saturation and increased total iron binding capacity aid in the diagnosis of IDA. Serum ferritin is an acute-phase reactant, and levels may be falsely elevated in the setting of inflammation or infection.

Treatment includes reversing the cause of deficiency and supplementing iron. Calculation of the total iron deficit can help inform iron supplementation. First-line therapy for IDA is oral ferrous sulfate 325 mg (65 mg elemental iron) 3 times daily. Newer studies suggest 40 to 80 mg oral iron should be taken every other day to increase absorption.39 Other iron salts, such as ferrous gluconate (325 mg is equivalent to 38 mg elemental iron), have been used. Iron absorption is enhanced by an acidic environment. Parenteral iron is utilized in patients with uncorrectable blood loss, malabsorption, renal failure, intolerance to oral iron, and nonadherence in those who are unable to receive transfusions. Iron infusions are favored in frail patients, such as the elderly and those with chronic kidney disease or heart failure.35 Multiple parenteral iron formulations exist, and their use should be driven by underlying patient comorbidities and potential risks. Packed red blood cell transfusions should be considered in acute blood loss, hypoxia, or cardiac insufficiency.

Essential Fatty Acid Deficiency Essential fatty acids (EFAs) including linoleic and α-linolenic acid cannot be synthesized by the human body and must be obtained through diet (mostly plant oils). Essential fatty acids have various functions, includ-ing maintaining phospholipid membrane integrity, form-ing prostaglandins and leukotrienes, and storing energy.40 Essential fatty acids are important in the structure and function of the stratum corneum and are crucial in main-taining epidermal barrier function.41 Increased epidermal permeability and transepidermal water loss may be the first signs of EFA deficiency (EFAD).42

The cutaneous manifestations of EFAD include xero-sis, weeping eczematous plaques, and erosions in inter-triginous sites. The lesions may progress to widespread desquamation and erythema. With time, the skin can become thick and leathery. Alopecia may occur, and hair

FIGURE 2. Koilonychia in a patient with iron-deficiency anemia.


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may depigment.7 Additional findings include poor wound healing and increased susceptibility to infections.43,44

Essential fatty acid deficiency may occur when dietary fat intake is severely restricted or in malabsorptive states.45,46 It develops in patients on prolonged TPN, typi-cally when receiving fat-restricted nutrition,47,48 as occurs in hypertriglyceridemia.47 Essential fatty acid deficiency has developed in patients on TPN containing EFAs,47 as the introduction of novel intravenous lipid emulsions has resulted in varying proportions of EFA.40 Premature neo-nates are particularly at risk for EFAD.49

The diagnosis of EFAD involves the measurement of the triene to tetraene ratio. A ratio of more than 0.2 sug-gests EFAD, but the clinical signs are not seen until the ratio is over 0.4.40 Low plasma levels of linoleic, linolenic, and arachidonic acids also are seen. Elevated liver function tests are supportive of the diagnosis. Biochemical findings typically are seen before cutaneous manifestations.40

Treatment of EFAD includes topical, oral, or intrave-nous replacement of EFAs. Improvement of EFAD with the application of topical linoleic acid to the skin has been reported.50 Patients receiving TPN should undergo assess-ment of parenteral lipid emulsion to ensure adequate fatty acid composition.

Vitamin A DeficiencyVitamin A (retinol) is a fat-soluble vitamin that plays a criti-cal role in keratinization, epithelial proliferation, and cellular differentiation.6 Vitamin A is found in animal products as retinyl esters and in plants as beta-carotene. Vitamin A has 2 clinically important forms: all-trans retinoic acid and 11-cis-retinal. All-trans retinoic acid is involved in cellular differen-tiation and regulating gene transcription, while 11-cis-retinal is key to rhodopsin generation required for vision. Vitamin A deficiency presents with early ophthalmologic findings, spe-cifically nyctalopia, or delayed adaptation to the dark.51 Xerophthalmia, abnormal conjunctival keratinization, and Bitot spots subsequently develop and may progress to corneal ulceration and blindness.6

Vitamin A deficiency manifests in the skin as follicu-lar hyperkeratosis, or phrynoderma. Notably, numerous other micronutrient deficiencies may result in phrynoderma. Clinically, multiple pigmented keratotic papules of various sizes, many with a central keratinous plug, are distrib-uted symmetrically on the extensor elbows, knees, shoul-ders, buttocks, and extremities. The skin surrounding these lesions may be scaly and hyperpigmented.52 Generalized xerosis without preceding nyctalopia has been reported.53 Accompanying pityriasis alba may develop.52 Lesions on the face may mimic acne, while lesions on the extremities may simulate a perforating disorder. Histopathology of phryno-derma reveals epidermal hyperkeratosis, follicular hyperkera-tosis, and follicular plugging.52

Patients at risk for vitamin A deficiency include those with conditions that affect intestinal fat absorption, underlying psychiatric illness, or chronic disease (eTable). Chronic alco-hol use predisposes patients to a multitude of micronutrient

deficiencies, including vitamin A deficiency.54 In chronic alco-hol use, even mild cutaneous changes may be the first clue to low serum retinol.55

Vitamin A deficiency can be diagnosed by measur-ing 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 dis-order 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 manu-facturers 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 (defi-ciency 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 pap-ules 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 glutathi-one 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 can-not 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


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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

Causes of niacin deficiency include malabsorptive conditions, malignancy (including carcinoid tumors), parenteral nutrition, psychiatric disease,74,75 and restric-tive diets (eTable).76 Carcinoid tumors divert tryptophan to serotonin resulting in niacin deficiency.77

The diagnosis of niacin deficiency is based on clinical findings and response to supplementation.75 Low niacin urinary metabolites (N-methylnicotinamide and 2-pyridone) may aid in diagnosis.6 Treatment generally includes oral nicotinamide 100 mg every 6 hours; the dose can then be tapered to 50 mg every 8 to 12 hours until symptoms resolve. Severe deficiency may require parenteral nicotinamide 1 g 3 to 4 times daily.75

Vitamin B6

Vitamin B6 (pyridoxine, pyridoxamine, pyridoxal) is found in whole grains and plant and animal products. Vitamin B6 functions as a coenzyme in many metabolic pathways and is involved in the conversion of tryptophan to niacin.44 Absorption requires hydrolysis by intestinal phos-phates and transport to the liver for rephosphorylation prior to release in active form.6

Cutaneous findings associated with vitamin B6 deficiency include periorificial and perineal seborrheic dermatitis,78 angular stomatitis, and cheilitis, with associated burning, redness, and tongue edema.6 Vitamin B6 deficiency is a rarely reported cause of burning mouth syndrome.79 Because vitamin B6 is involved in the conversion of tryptophan to nia-cin, deficiency also may present with pellagralike findings.70 Other clinical symptoms are outlined in the eTable.80,81

Conditions that increase risk for vitamin B6 deficiency are highlighted in the eTable and include malabsorp-tive disorders; psychiatric illness82; and chronic disease, especially end-stage renal disease.83 Vitamin B6 deficiency associated with chronic alcohol use is due to both inad-equate vitamin B6 intake as well as reduced hepatic stor-age.78 Medications such as isoniazid, hydralazine, and oral contraceptives may decrease vitamin B6 levels (eTable).82

Vitamin B6 can be measured in the plasma as pyri-doxal 5′-phosphate. Plasma concentrations of less than 20 nmol/L are suggestive of deficiency.82 Indirect tests include tryptophan and methionine loading.6 The treat-ment of vitamin B6 deficiency is determined by symp-tom severity. Recommendations for oral supplementation range from 25 to 600 mg daily.82 Symptoms typically improve on 100 mg daily.6

Vitamins B9 and B12

Deficiencies of vitamins B9 (folic acid, folate) and B12 (cobalamin) have similar clinical presentations. Folate is essential in the metabolism of amino acids, purines, and pyrimidines.6 Cobalamin, found in animal products, is a cofactor for methionine synthase and methylmalonyl-CoA mutase.84 Megaloblastic anemia is the main finding in folate or cobalamin deficiency. Neurologic findings only accompany cobalamin deficiency. Risk factors for folate deficiency include malabsorptive conditions,6 chronic alcohol use,85 and antifolate medication use (eTable).6

Cobalamin absorption requires gastric acid and intrin-sic factor binding in the duodenum. Deficiency may occur from strict diets, psychiatric illness, old age,86 decreased gastric acid secretion,87 abnormal intrinsic factor function, or intestinal infections.6

Generalized cutaneous hyperpigmentation may be the first manifestation of vitamins B9 and B12 deficiency.88 Typically accentuated in acral creases and the oral cavity, pigmentation may mimic Addison disease. Hair depig-mentation and linear streaking of the nails are reported.84 The tongue becomes painful and red with atrophy of the filiform papillae (Hunter glossitis).78 Linear lesions on the tongue and hard palate may serve as an early sign of cobalamin deficiency.89

Folate deficiency is diagnosed by measuring the plasma folate level; coincidental cobalamin deficiency should be excluded. Deficiency is managed with oral supplementation (when possible) with 1 to 5 mg of folate daily.6 Cobalamin deficiency is based on low serum levels (<150 pg/mL is diagnostic).86 Cobalamin defi-ciency may take years to develop, as vitamin B12 exists in large body stores.6 Serum methylmalonic acid may be elevated in patients with clinical features but normal-low serum vitamin B12 level.86 Treatment of vitamin B12 deficiency is with oral (2 mg once daily) or parenteral (1 mg every 4 weeks then maintained at once monthly) cyanocobalamin. For patients with neurologic symptoms, intramuscular injection should be given.86 The underlying cause of deficiency must be elucidated and treated.

FIGURE 3. Photosensitive dermatitis of the neck and upper chest (Casal necklace) seen in vitamin B3 deficiency (pellagra).


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Vitamin C DeficiencyVitamin C (ascorbic acid) is an essential cofactor for the hydroxylation of proline and lysine residues in collagen synthesis. Plant-based foods are the main dietary source of vitamin C, and deficiency presents clinically as scurvy. Cutaneous findings include follicular hyperkeratosis, perifollicular petechiae, and curled hair shafts (corkscrew hairs)(Figure 4). Ecchymoses of the lower extremities, forearms, and abdomen may be seen. Nodules represent-ing intramuscular and subcutaneous hemorrhage can be present.90 Woody edema may mimic cellulitis, while lower extremity hemorrhage may mimic vasculitis. Gingival hyperplasia, hemorrhage, and edema may occur,90 along with linear splinter hemorrhages.91

Hypovitaminosis C has been routinely demonstrated in hospitalized patients.92 Scurvy may occur in patients on strict diets,93 chronic alcohol use,94 psychiatric ill-ness,95 or gastrointestinal tract disease (eTable).96-99 Those with low socioeconomic status70 or dementia100 as well as the elderly also are at risk.101 Scurvy has developed in patients with iron overload and those who are on hemo-dialysis44 as well as in association with nilotinib use.102 Patients with chronic mucous membrane graft-vs-host disease may exhibit vitamin C deficiency.103

Scurvy is a clinical diagnosis. Vitamin C levels normal-ize quickly with supplementation. Cutaneous biopsy will exhibit follicular hyperkeratosis, perifollicular hemor-rhage, and fibrosis.91

Oral ascorbic acid supplementation should be initiated at 500 to 1000 mg daily in adults.104 The cause of deficiency should be identified, and further supplementation should be decided based on patient risk factors. Lifestyle modifi-cations, such as cessation of smoking and chronic alcohol use, is recommended. The diagnosis of scurvy should prompt workup for additional nutrient deficiencies.

Final ThoughtsDermatologists play an important role in the early recognition of nutritional deficiencies, as cutaneous manifestations often are the first clue to diagnosis. Nutritional deficiencies are

common yet underrecognized in the hospitalized patient and serve as an independent risk factor for patient morbidity and mortality.3 Awareness of the cutaneous manifestations of undernutrition as well as the risk factors for nutritional defi-ciency may expedite diagnosis and supplementation, thereby improving outcomes for hospitalized patients.

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FIGURE 4. Perifollicular hemorrhage and corkscrew hairs in a patient with vitamin C deficiency (scurvy).


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HOSPITAL CONSULT

WWW.MDEDGE.COM/DERMATOLOGYE2 I CUTIS®

Co

nditi

on

Ris

k F

acto

rs

Cut

aneo

us M

anife

stat

ions

Sys

tem

ic M

anife

stat

ions

Vita

min

B2

defic

ienc

y•

Dec

reas

ed in

take

: str

ict d

iets

(veg

an/v

eget

aria

n),84

•

Mal

abso

rptio

n: in

test

inal

sur

gery

, int

estin

al b

ypas

s su

rger

y85

• C

hron

ic il

lnes

s: h

ypot

hyro

idis

m86

•

Psy

chia

tric

illn

ess:

chr

onic

alc

ohol

use

, eat

ing

diso

rder

s76

• M

edic

atio

ns: a

ntie

pile

ptic

s38

• O

ther

: eld

erly,

87 p

regn

ant o

r la

ctat

ing

wom

en,88

pho

toth

erap

y,89

bo

ric a

cid

inge

stio

n90

Seb

orrh

eicl

ike

derm

atiti

s,75

inte

rtrig

olik

e de

rmat

itis,

91 o

ral-o

cula

r-ge

nita

l sy

ndro

me

(che

ilitis

; ang

ular

sto

mat

itis;

glo

ssiti

s; d

eep

red,

atr

ophi

c to

ngue

; scr

otal

der

mat

itis

exte

ndin

g on

to th

e th

ighs

),18,7

6 re

d pa

pule

s an

d fis

sure

s, b

alan

itis,

phi

mos

is

Rar

e, p

redo

min

antly

m

ucoc

utan

eous

sym

ptom

s se

en

Vita

min

B3

defic

ienc

y•

Dec

reas

ed in

take

: str

ict d

iets

,92 T

PN

93

• M

alab

sorp

tion:

car

cino

id tu

mor

s,94

Har

tnup

dis

ease

,95 in

test

inal

by

pass

sur

gery

,96 IB

D97

•

Psy

chia

tric

illn

ess:

eat

ing

diso

rder

s,98

chr

onic

alc

ohol

use

99

Pel

lagr

a (p

hoto

sens

itive

der

mat

itis

of th

e fa

ce, n

eck

[Cas

al n

eckl

ace]

, ch

est,

dors

al h

ands

, and

ext

enso

r ar

ms;

ves

icle

s or

bul

lae

(wet

pe

llagr

a); t

hick

, hyp

erpi

gmen

ted,

sca

ling

plaq

ues)

,18 c

oppe

r to

ne to

sk

in,10

0 du

ll er

ythe

ma

with

yel

low

pow

dery

sca

le o

ver

follic

ular

orifi

ces

(sul

fur

flake

s),10

1 ch

eilit

is, g

loss

itis,

per

inea

l eru

ptio

n102

Psy

chia

tric

sym

ptom

s,

dem

entia

, dia

rrhe

a102

Vita

min

B6

defic

ienc

y•

Mal

abso

rptio

n: c

elia

c di

seas

e103

• P

sych

iatr

ic il

lnes

s: c

hron

ic a

lcoh

ol u

se,10

4 ea

ting

diso

rder

s103

• M

edic

atio

n in

duce

d: is

onia

zid,

hyd

rala

zine

, the

ophy

lline,

cyc

lose

rine,

pe

nici

llam

ine,

ora

l con

trac

eptiv

es10

3 •

Chr

onic

illn

ess:

hep

atic

dis

ease

, hep

atoc

ellu

lar

carc

inom

a,10

5 di

alys

is10

6 •

Oth

er: e

lder

ly10

7

Ang

ular

sto

mat

itis,

che

ilitis

, glo

ssiti

s, b

urni

ng to

ngue

, pel

lagr

alik

e de

rmat

itis,

inte

rtrig

o,18

seb

orrh

eicl

ike

derm

atiti

s104

Sid

erob

last

ic m

icro

cytic

ane

mia

, pe

riphe

ral n

euro

path

y,10

8 ne

urol

ogic

sym

ptom

s,10

9

depr

essi

on, i

rrita

bilit

y, in

crea

sed

infe

ctio

ns10

8

Vita

min

B9

defic

ienc

y•

Dec

reas

ed in

take

: str

ict v

egan

die

t110

• M

alab

sorp

tion:

IBD

,111

inte

stin

al b

ypas

s su

rger

y, c

elia

c di

seas

e,

chro

nic

diar

rhea

16

• P

sych

iatr

ic il

lnes

s: c

hron

ic a

lcoh

ol u

se11

2 •

Med

icat

ions

: trim

etho

prim

, met

hotr

exat

e, o

ral c

ontr

acep

tives

, an

tiepi

lept

ics,

pyr

imet

ham

ine16

Gen

eral

ized

cut

aneo

us h

yper

pigm

enta

tion

(acc

entu

ated

in a

cral

cr

ease

s, in

tert

rigin

ous

site

s, o

ral c

avity

),16 g

loss

itis,

ang

ular

che

ilitis

, de

pigm

ente

d ha

ir, li

near

str

eaki

ng o

f nai

ls,11

3 lin

ear

lesi

ons

on th

e to

ngue

and

har

d pa

late

114

Meg

alob

last

ic a

nem

ia, p

allo

r, irr

itabi

lity,

fatig

ue

Vita

min

B12

de

ficie

ncy

• D

ecre

ased

inta

ke: s

tric

t die

ts (v

egan

/veg

etar

ian)

115

• M

alab

sorp

tion:

dec

reas

ed g

astr

ic a

cid

secr

etio

n (p

roto

n pu

mp

inhi

bito

rs,

H2

antih

ista

min

es),11

6 de

crea

sed

intr

insi

c fa

ctor

(per

nici

ous

anem

ia),

inte

stin

al

infe

ctio

n (b

acte

rial o

verg

row

th, g

iard

iasi

s, D

iphy

llobo

thriu

m la

tum

),16 IB

D,

celia

c di

seas

e, W

hipp

le d

isea

se, Z

ollin

ger-

Ellis

on s

yndr

ome11

7

• P

sych

iatr

ic il

lnes

s: c

hron

ic a

lcoh

ol u

se,11

8 ob

sess

ive-

com

puls

ive

diso

rder

119

• M

edic

atio

n in

duce

d: m

etfo

rmin

120

• O

ther

: eld

erly,

110

inbo

rn e

rror

s of

met

abol

ism

110

Gen

eral

ized

cut

aneo

us h

yper

pigm

enta

tion

(acc

entu

ated

in a

cral

cr

ease

s, in

tert

rigin

ous

site

s, o

ral c

avity

),16 g

loss

itis,

ang

ular

che

ilitis

, de

pigm

ente

d ha

ir, li

near

str

eaki

ng o

f nai

ls,11

3 lin

ear

lesi

ons

on th

e to

ngue

and

har

d pa

late

114

Meg

alob

last

ic a

nem

ia,

pallo

r irr

itabi

lity,

fatig

ue,

neur

olog

ic s

eque

lae11

0

Vita

min

C

defic

ienc

y•

Dec

reas

ed in

take

: str

ict d

iets

121

• M

alab

sorp

tion:

Whi

pple

dis

ease

,122

IBD

,123

celia

c di

seas

e,12

4 in

test

inal

by

pass

sur

gery

125

• P

sych

iatr

ic il

lnes

s: c

hron

ic a

lcoh

ol u

se,12

6 an

orex

ia n

ervo

sa,12

7

psyc

hiat

ric d

isor

ders

128

• M

edic

atio

n in

duce

d: v

emur

afen

ib,12

9 ni

lotin

ib13

0

• C

hron

ic il

lnes

s: ir

on o

verlo

ad,13

1 di

alys

is,13

2 ch

roni

c G

VH

D,13

3 ho

spita

lizat

ion13

4 •

Oth

er: a

utis

m,13

5 lo

w s

ocio

econ

omic

sta

tus,

136 de

men

tia,13

7 el

derly

138

Follic

ular

hyp

erke

rato

sis,

per

ifollic

ular

pet

echi

ae, c

urle

d ha

ir sh

afts

(c

orks

crew

hai

rs),

ecch

ymos

es, n

odul

es (i

ntra

mus

cula

r an

d su

bcut

aneo

us h

emor

rhag

e), w

oody

ede

ma,

gin

giva

l hyp

erpl

asia

, lin

ear

splin

ter

hem

orrh

ages

139

Fatig

ue, e

pist

axis

, loo

se te

eth,

m

ood

chan

ges,

bon

y ch

ange

s,

depr

essi

on76

Abb

revi

atio

ns: H

IV, h

uman

imm

unod

efic

ienc

y vi

rus;

IBD

, irr

itabl

e bo

wel

dis

ease

; CK

D, c

hron

ic k

idne

y di

seas

e; S

LC39

A4,

sol

ute

carr

ier

fam

ily 3

9 m

embe

r 4;

TP

N, t

otal

par

ente

ral n

utrit

ion;

ED

TA, e

thyl

ened

iam

inet

etra

acet

ic a

cid;

AC

E, a

ngio

tens

in-c

onve

rtin

g en

zym

e; G

VHD

, gra

ft-vs

-hos

t dis

ease

.

cont

inue

d


CUTIS

Do no

t cop

y

HOSPITAL CONSULT


RE

FE

RE

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EP, S

age

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Shw

ayde

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was

hior

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rom

a s

ever

e di

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y re

stri

ctio

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an

8-m

onth

infa

nt in

su

burb

an D

etro

it, M

ichi

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27.

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met

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, K

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P.

Mal

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Mub

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L, A

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Cut

aneo

us p

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of k

was

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due

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fant

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Cro

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. Eur

J Pe

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, Had

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D, M

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the

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gro

wth

di

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and

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ater

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R. T

he n

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lag

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iam

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ee E

U, e

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CUTIS

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