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emedicine.medscape.com

Protein-Energy Malnutrition
Updated: Sep 14, 2016
Author: Noah S Scheinfeld, JD, MD, FAAD; Chief Editor: Romesh Khardori, MD, PhD, FACP

Overview

Background
The World Health Organization (WHO)[1] defines malnutrition as "the cellular imbalance between the supply of
nutrients and energy and the body's demand for them to ensure growth, maintenance, and specific functions." The
term protein-energy malnutrition (PEM) applies to a group of related disorders that include marasmus, kwashiorkor
(see the images below), and intermediate states of marasmus-kwashiorkor. The term marasmus is derived from the
Greek word marasmos, which means withering or wasting. Marasmus involves inadequate intake of protein and
calories and is characterized by emaciation. The term kwashiorkor is taken from the Ga language of Ghana and
means "the sickness of the weaning." Williams first used the term in 1933, and it refers to an inadequate protein intake
with reasonable caloric (energy) intake. Edema is characteristic of kwashiorkor but is absent in marasmus.

This photograph shows children and a nurse attendant at a Nigerian orphanage in the late 1960s. Notice four of the
children with gray-blond hair, a symptom of the protein-deficiency disease kwashiorkor. Image courtesy of Dr. Lyle
Conrad and the CDC Public Health Image Library.

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This late 1960s photograph shows a seated, listless child who was among many kwashiorkor cases found in Nigerian
relief camps during the Nigerian-Biafran war. Kwashiorkor is a disease brought on due to a severe dietary protein
deficiency, and this child, whose diet fit such a deficiency profile, presented with symptoms including edema of legs
and feet, light-colored, thinning hair, anemia, a pot-belly, and shiny skin. Image courtesy of Dr. Lyle Conrad and the
CDC Public Health Image Library.

Studies suggest that marasmus represents an adaptive response to starvation, whereas kwashiorkor represents a
maladaptive response to starvation. Children may present with a mixed picture of marasmus and kwashiorkor, and
children may present with milder forms of malnutrition. For this reason, Jelliffe suggested the term protein-calorie
(energy) malnutrition to include both entities.

Although protein-energy malnutrition affects virtually every organ system, this article primarily focuses on its cutaneous
manifestations. Patients with protein-energy malnutrition may also have deficiencies of vitamins, essential fatty acids,
and trace elements, all of which may contribute to their dermatosis.

Pathophysiology
In general, marasmus is an insufficient energy intake to match the body's requirements. As a result, the body draws on
its own stores, resulting in emaciation. In kwashiorkor, adequate carbohydrate consumption and decreased protein
intake lead to decreased synthesis of visceral proteins. The resulting hypoalbuminemia contributes to extravascular
fluid accumulation. Impaired synthesis of B-lipoprotein produces a fatty liver.

Protein-energy malnutrition also involves an inadequate intake of many essential nutrients. Low serum levels of zinc
have been implicated as the cause of skin ulceration in many patients. In a 1979 study of 42 children with marasmus,
investigators found that only those children with low serum levels of zinc developed skin ulceration. Serum levels of
zinc correlated closely with the presence of edema, stunting of growth, and severe wasting. The classic "mosaic skin"
and "flaky paint" dermatosis of kwashiorkor bears considerable resemblance to the skin changes of acrodermatitis
enteropathica, the dermatosis of zinc deficiency.

In 2007, Lin et al[2] stated that "a prospective assessment of food and nutrient intake in a population of Malawian

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children at risk for kwashiorkor" found "no association between the development of kwashiorkor and the consumption
of any food or nutrient."

Marasmus and kwashiorkor can both be associated with impaired glucose clearance that relates to dysfunction of
pancreatic beta-cells.[3] In utero, plastic mechanisms appear to operate, adjusting metabolic physiology and adapting
postnatal undernutrition and malnutrition to define whether marasmus and kwashiorkor will develop.[4]

In 2012, a report from Texas noted an 18-month-old infant with type 1 glutaric acidemia who had extensive
desquamative plaques, generalized nonpitting edema, and red-tinged sparse hair, with low levels of zinc, alkaline
phosphatase, albumin, and iron. This patient has a variation on kwashiorkor, and the authors suggest that it be termed
acrodermatitis dysmetabolica.[5] On the same note, a boy aged 18 months with type 1 glutaric academia suffered from
zinc deficiency and acquired protein energy malnutrition.[6]

For complex reasons, sickle cell anemia can predispose sufferers to protein malnutrition.[7]

Protein energy malnutrition ramps up arginase activity in macrophages and monocytes.[8]

Epidemiology
Frequency
United States

Protein-energy malnutrition is the most common form of nutritional deficiency among patients who are hospitalized in
the United States. As many as half of all patients admitted to the hospital have malnutrition to some degree. In a
recent survey in a large children's hospital, the prevalence of acute and chronic protein-energy malnutrition was more
than one half. This is very much a disease that occurs in 21st century America, and a case in an 8-month-old child in
suburban Detroit, Mich, was reported in 2010.[9] Additional cases of kwashiorkor have been noted to occur in the
United States. An interesting report of a baby with a clinical picture imitating Stevens-Johnson syndrome but who in
fact had kwashiorkor has been noted.[10] Babies solely fed on rice milk can develop kwashiorkor even in the United
States.

In a survey focusing on low-income areas of the United States, 22-35% of children aged 2-6 years were below the
15th percentile for weight. Another survey showed that 11% of children in low-income areas had height-for-age
measurements below the 5th percentile. Poor growth is seen in 10% of children in rural populations.

In hospitalized elderly persons, up to 55% are undernourished. Up to 85% of institutionalized elderly persons are
undernourished. Studies have shown that up to 50% have vitamin and mineral intake that is less than the
recommended dietary allowance and up to 30% of elderly persons have below-normal levels of vitamins and minerals.

International

In 2000, the WHO[11] estimated that malnourished children numbered 181.9 million (32%) in developing countries. In
addition, an estimated 149.6 million children younger than 5 years are malnourished when measured in terms of
weight for age. In south central Asia and eastern Africa, about half the children have growth retardation due to protein-
energy malnutrition. This figure is 5 times the prevalence in the western world.

A cross-sectional study of Palestinian adolescents found that 55.66% of boys and 64.81% of girls had inadequate
energy intake, with inadequate protein intake in 15.07% of boys and 43.08% of girls. The recommended daily
allowance for micronutrients was met by less than 80% of the study subjects.[12]

Mortality/Morbidity
Approximately 50% of the 10 million deaths each year in developing countries occur because of malnutrition in
children younger than 5 years. In kwashiorkor, mortality tends to decrease as the age of onset increases.

Race

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Dermatologic findings appear more significant and occur more frequently among darker-skinned peoples. This finding
is likely explained by the greater prevalence and the increased severity of protein-energy malnutrition in developing
countries and not to a difference in racial susceptibility.

Age
Marasmus most commonly occurs in children younger than 5 years. This period is characterized by increased energy
requirements and increased susceptibility to viral and bacterial infections. Weaning (the deprivation of breast milk and
the commencement of nourishment with other food) occurs during this high-risk period. Weaning is often complicated
by geography, economy, hygiene, public health, culture, and dietetics. It can be ineffective when the foods introduced
provide inadequate nutrients, when the food and water are contaminated, when the access to health care is
inadequate, and/or when the patient cannot access or purchase proper nourishment.

In some studies, the protein-energy malnutrition prevalence among elderly persons is estimated to be as high as 4%
for those living in the community, 50% for those hospitalized in acute care units or geriatric rehabilitation units, and 30-
40% for those in long-term care facilities. Protein-energy malnutrition has also been found to be a primary factor of
poor prognosis in elderly persons.

Prognosis
The extent of growth failure and the severity of hypoproteinemia, hypoalbuminemia, and electrolyte imbalances are
predictors of a poorer prognosis. Additionally, underlying HIV infection is associated with a poor prognosis.

Presentation

History
Low intake of calories or an inability to absorb calories is the key factor in the development of kwashiorkor. A variety of
syndromes can be associated with kwashiorkor.[13] This can include a rice milk diet used to treat atopic dermatitis.
[14]

In children, the findings of poor weight gain or weight loss; slowing of linear growth; and behavioral changes, such as
irritability, apathy, decreased social responsiveness, anxiety, and attention deficit may indicate protein-energy
malnutrition. In particular, the child is apathetic when undisturbed but irritable when picked up. Kwashiorkor
characteristically affects children who are being weaned. Signs include diarrhea and psychomotor changes.

Adults generally lose weight, although, in some cases, edema can mask weight loss. Patients may describe
listlessness, easy fatigue, and a sensation of coldness. Global impairment of system function is present.

Patients with protein-energy malnutrition can also present with nonhealing wounds. This may signify a catabolic
process that requires nutritional intervention. Lewandowski et al[15] reported kwashiorkor and an acrodermatitis
enteropathica–like eruption after a distal gastric bypass surgical procedure. Kwashiorkor was reported in an infant
presenting with diarrhea and dermatitis, due to infantile Crohn disease.[16] The diarrhea and dermatitis improved in 2
weeks with treatment.

A 3-year-old child with coexisting celiac and Hartnup disease that resulted in kwashiorkor, anemia, hepatitis,
hypoalbuminia, angular cheilitis, glossitis, conjunctivitis and diffuse alopecia, erythematous skin, desquamation,
erosions, and diffuse hyperpigmentation was reported by Sander et al in 2009.[17] With the proper nutritional
supplementation, these findings resolved.

"Cupping" (placing suction cups on the body to cure disease) on the abdomen in patients with diseases resulting in
abdominal swelling (eg, kwashiorkor) can give interesting clinical presentations.[18]

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Maintenance hemodialysis can result in protein-energy-malnutrition and relates strongly with mortality with serum
albumin being the only predictor of death.[19]

Physical
In marasmus, the child appears emaciated with marked loss of subcutaneous fat and muscle wasting. The skin is
xerotic, wrinkled, and loose. Monkey facies secondary to a loss of buccal fat pads is characteristic of this disorder.
Marasmus may have no clinical dermatosis. However, inconsistent cutaneous findings include fine, brittle hair;
alopecia; impaired growth; and fissuring of the nails. In protein-energy malnutrition, more hairs are in the telogen
(resting) phase than in the anagen (active) phase, a reverse of normal. Occasionally, as in anorexia nervosa, marked
growth of lanugo hair is noted.

Kwashiorkor typically presents with a failure to thrive, edema, moon facies, a swollen abdomen (potbelly), and a fatty
liver. When present, skin changes are characteristic and progress over a few days. The skin becomes dark, dry, and
then splits open when stretched, revealing pale areas between the cracks (ie, crazy pavement dermatosis, enamel
paint skin). This feature is seen especially over pressure areas. In contrast to pellagra, these changes seldom occur
on sun-exposed skin.

Depigmentation of hair causes it to be reddish yellow to white. Curly hair becomes straightened. If periods of poor
nutrition are interspersed with good nutrition, alternating bands of pale and dark hair, respectively, called the flag sign,
may occur. Also, hairs become dry, lusterless, sparse, and brittle; they can be pulled out easily. Temporal recession
and hair loss from the back of the head occur, likely secondary to pressure when the child lies down. In some cases,
loss of hair can be extreme. Hair can also become softer and finer and appear unruly. The eyelashes can undergo the
same change, having a so-called broomstick appearance.

Nail plates are thin and soft and may be fissured or ridged. Atrophy of the papillae on the tongue, angular stomatitis,
xerophthalmia, and cheilosis can occur.

Inflammatory bowel diseases, such as Crohn disease and ulcerative colitis, may also produce skin manifestations
secondary to malnutrition.[20]

In elderly persons, an indicative sign of malnutrition is delayed healing and an increased presence of decubitus ulcers
of stage III or higher.

Vitamin C deficiency commonly manifests in elderly persons as perifollicular hemorrhages, petechiae, gingival
bleeding, and splinter hemorrhages, in addition to hemarthroses and subperiosteal hemorrhages. Anemia may result,
and wound healing may be impaired. Niacin deficiency clinically manifests as pellagra (ie, dermatitis, dementia,
diarrhea) in advanced cases. The dermatitis manifests in sun-exposed areas, including the back, neck (Casal
necklace), face, and dorsum of the hands (gauntlet of pellagra) initially as painful erythema and itching. Subsequently,
vesicles and bullae may develop and erupt, creating crusted, scaly lesions. Finally, the skin becomes rough and
covered by dark scales and crusts. Striking demarcation of affected areas from normal skin is noted.

Protein-energy malnutrition is also associated with an increased likelihood of calciphylaxis, a small vessel
vasculopathy involving mural calcification with intimal proliferation, fibrosis, and thrombosis. As a result, ischemia and
necrosis of skin occurs. Other tissues affected include subcutaneous fat, visceral organs, and skeletal muscle.

A study by Harima et al reported on the effects of an evening snack in patients receiving chemotherapy for
hepatocellular carcinoma. They reported a lower nonprotein respiratory quotient in patients with advanced
hepatocellular carcinoma compared with patients with cirrhosis who did not have hepatocellular carcinoma and in
patients with early-stage hepatocellular carcinoma. Patients with cirrhosis and advanced hepatocellular carcinoma
who were receiving chemotherapy and who received the late-evening snack had an improved nonprotein respiratory
quotient, branched-chain amino acid/tyrosine ratio, alanine aminotransferase level, and prealbumin level compared
with controls.[21]

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Causes
Worldwide, the most common cause of malnutrition is inadequate food intake. Preschool-aged children in developing
countries are often at risk for malnutrition because of their dependence on others for food, increased protein and
energy requirements, immature immune systems causing a greater susceptibility to infection, and exposure to
nonhygienic conditions.

Another significant factor is ineffective weaning secondary to ignorance, poor hygiene, economic factors, and cultural
factors. The prognosis is worse when protein-energy malnutrition occurs with HIV infection. Gastrointestinal infections
can and often do precipitate clinical protein-energy malnutrition because of associated diarrhea, anorexia, vomiting,
increased metabolic needs, and decreased intestinal absorption. Parasitic infections play a major role in many parts of
the world.

In developed countries, inadequate food intake is a less common cause of malnutrition; protein-energy malnutrition is
more often caused by decreased absorption or abnormal metabolism. Thus, in developed countries, diseases, such as
cystic fibrosis, chronic renal failure, childhood malignancies, congenital heart disease, and neuromuscular diseases,
contribute to malnutrition. Fad diets, inappropriate management of food allergies, and psychiatric diseases, such as
anorexia nervosa, can also lead to severe protein-energy malnutrition.

Populations in both acute-care and long-term facilities are at risk for clinically significant involuntary weight loss (IWL)
that can result in protein-energy malnutrition. IWL is defined as a loss of 4.5 kg or greater than 5% of the usual body
weight over a period of 6-12 months. Protein-energy malnutrition occurs when weight loss of greater than 10% of
normal body weight occurs.

Elderly persons often develop malnutrition, common causes of which include decreased appetite, dependency on help
for eating, impaired cognition and/or communication, poor positioning, frequent acute illnesses with gastrointestinal
losses, medications that decrease appetite or increase nutrient losses, polypharmacy, decreased thirst response,
decreased ability to concentrate urine, intentional fluid restriction due to fear of incontinence or choking if dysphagic,
psychosocial factors such as isolation and depression, monotony of diet, higher nutrient density requirements, and
other demands of age, illness, and disease on the body.

Elderly patients are often at risk for protein-energy malnutrition because of inadequate nutrition, which has been
determined to be a common comorbid factor for increased morbidity and mortality in elderly burn victims.[22]

Patients with liver cirrhosis are also at risk for protein-energy malnutrition, which is a risk factor that portends a poor
prognosis for survival. This risk correlates with the degree of liver injury and the etiology of liver injury, with the risk of
protein-energy malnutrition being more severe in persons with alcoholic cirrhosis than in those with nonalcoholic
cirrhosis.

Patients on long-term hemodialysis also may develop protein-energy malnutrition; this is associated with increased
morbidity and mortality.

Patients with squamous cell carcinoma of the esophagus are at risk for protein-energy malnutrition.

Bariatric surgery can be associated with iatrogenic kwashiorkor.[23, 24]

DDx

Differential Diagnoses
Actinic Prurigo

Workup

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Workup

Laboratory Studies
The WHO recommends the following laboratory tests:

Blood glucose

Examination of blood smears by microscopy or direct detection testing

Hemoglobin

Urine examination and culture

Stool examination by microscopy for ova and parasites

Serum albumin

HIV test (This test must be accompanied by counseling of the child's parents, and strict confidentiality should be
maintained.)

Electrolytes

Significant findings in kwashiorkor include hypoalbuminemia (10-25 g/L), hypoproteinemia (transferrin, essential amino
acids, lipoprotein), and hypoglycemia. Plasma cortisol and growth hormone levels are high, but insulin secretion and
insulinlike growth factor levels are decreased. The percentage of body water and extracellular water is increased.
Electrolytes, especially potassium and magnesium, are depleted. Levels of some enzymes (including lactase) are
decreased, and circulating lipid levels (especially cholesterol) are low. Ketonuria occurs, and protein-energy
malnutrition may cause a decrease in the urinary excretion of urea because of decreased protein intake. In both
kwashiorkor and marasmus, iron deficiency anemia and metabolic acidosis are present. Urinary excretion of
hydroxyproline is diminished, reflecting impaired growth and wound healing. Increased urinary 3-methylhistidine is a
reflection of muscle breakdown and can be seen in marasmus.

Malnutrition also causes immunosuppression, which may result in false-negative tuberculin skin test results and the
subsequent failure to accurately assess for tuberculosis.

Other Tests
Detailed dietary history, growth measurements, body mass index (BMI), and a complete physical examination are
indicated.

Sensitive measures of nutritional deficiency in children include height-for-age or weight-for-height measurements less
than 95% and 90% of expected, respectively, or greater than 2 standard deviations below the mean for age. In children
older than 2 years, growth of less than 5 cm/y may also be an indication of deficiency.

Procedures
Skin biopsy and hair-pull analysis may be performed (see Histologic Findings below).

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Histologic Findings
In a 1989 study,[25] skin biopsy samples taken from 20 children with protein-energy malnutrition were examined with
hematoxylin and eosin and stained for collagen, elastic fibers, mucopolysaccharides, and melanin. Findings included
variable degrees of hypertrophy of the stratum corneum with atrophy of both the stratum granulosum and the prickle
cell layers. A large amount of melanin was found in the basal layer in all samples. Also, the amount of collagen and
associated crowding of elastic fibers was reduced.

In kwashiorkor, microscopic studies of hair have revealed a decrease in the proportion of anagen follicles. The anagen
hairs were usually abnormal, exhibiting severe atrophy and shaft constriction. Most of the hairs examined were in the
telogen phase, and the loss of pigment was consistent with the lack of melanin production during the telogen cycle.

In patients with marasmus, essentially no hairs were in the anagen phase, with a shift to the telogen phase. Many
more broken hairs were found in patients with marasmus when compared with patients with kwashiorkor. Hair analysis
has been advocated as a useful diagnostic procedure for both conditions.

McKenzie et al[26] found that childhood malnutrition correlates with a reduction in the total melanin content of scalp
hair.

Treatment

Medical Care
In both children and adults, the first step in the treatment of protein-energy malnutrition (PEM) is to correct fluid and
electrolyte abnormalities and to treat any infections. The most common electrolyte abnormalities are hypokalemia,
hypocalcemia, hypophosphatemia, and hypomagnesemia. Macronutrient repletion should be commenced within 48
hours under the supervision of nutrition specialists.

A 1980 double-blind study of 8 children with kwashiorkor and skin ulceration found that topical zinc paste was more
effective than placebo in healing areas of skin breakdown. Oral zinc supplements were also found to be effective.

The second step in the treatment of protein-energy malnutrition (which may be delayed 24-48 h in children) is to
supply macronutrients by dietary therapy. Milk-based formulas are the treatment of choice. At the beginning of dietary
treatment, patients should be fed ad libitum. After 1 week, intake rates should approach 175 kcal/kg and 4 g/kg of
protein for children and 60 kcal/kg and 2 g/kg of protein for adults. A daily multivitamin should also be added.

For most of the cutaneous manifestations of inflammatory bowel disease, the primary therapy remains treatment of the
bowel.

In one study, patients who were undergoing chemotherapy for advanced hepatic cancer who received a late-evening
snack enhanced with branched-chain amino acids had improvements in energy metabolism parameters compared
with controls.[21]

Chung et al,[27] in discussing that protein-energy malnutrition is highly prevalent among peritoneal dialysis patients,
noted that although nutritional status assessments are better now than they were a decade ago, no definitive single
test is available to assess nutritional status. Instead, they propose that several different markers of nutrition must be
used to understand nutritional status. Thus, the treatment for peritoneal dialysis patients with malnutrition must be
multifaceted, and they suggest using nontraditional strategies such as appetite stimulants, anti-inflammatory diets, and
anti-inflammatory pharmacologic agents combined with more traditional forms of nutritional support to abate the
protein-energy malnutrition.

An intervention that brought buddies to the homes of the elderly who were at risk for protein malnutrition was
successful at decreasing such malnutrition.[28]

Nutritional support guidelines are available in the National Institute for Health and Clinical Excellence Nutrition Support

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in Adults quick reference guide.

The clinical guideline summary, Dietary guidelines for Americans, 2010, from the US Department of Health and Human
Services and US Department of Agriculture, may also be helpful.[29]

In the setting of malnutrition, risk of refeeding syndrome represents an additional clinical challenge.

Prolonged starvation followed by rapid feeding leads to refeeding syndrome (RS).[30] RS involves resultant
biochemical disturbance, physical symptoms, and physical signs. Insulin release leading to anabolic activity underlies
the pathophysiology of RS. Feeding overwhelms the dearth of electrolytes and micronutrients. This effect disrupts
cellular function. Tissue edema, hypophosphatemia and pathological fluid shifts define RS. RS was identified in 4% of
cases of parenteral nutrition (PN) in a UK study while physicians only recognized it half the time. A study in New
Zealand also shows similar data. RS remains underrecognized. PN patients are considered to be at high risk and
using protocols with slower and lower rates of refeeding reduces deaths attributable to RS.[30]

Using guidelines when treating children at risk for RS saves lives. Al Sharkawy et al in 2010 notes a Kuwaiti male
aged 13 months who presented with marasmic Kwashiorkor. Blood sugar and serum electrolytes were normal initially.
However, RS occurred by day 3 with severe hypomagnesemia, hypokalemia, hypophosphatemia, and hypocalcemia.
The child then was given a lower calorie intake. Caloric intake was increased gradually with vitamins, thiamine, and
electrolyte supplementation and survived.[31] This shows that death can be avoided if RS is recognized and treated
with diet adjustments.

Refeeding syndrome guidelines are available in the National Institute for Health and Clinical Excellence Nutrition
Support in Adults quick reference guide.

RS can also occur in patients who are replenished with food, vitamins and electrolytes after suffering from anorexia
nervosa (AN),[32] although some have argued that hypophosphatemia is not a problem in refeeding patients with AN.
[33]

Protein in 1 gram of food provides approximately 15 mg of phosphorus.[34] Marasmic Kwashiorkor is marked by

phosphorus deficiency. Chronic phosphorus deficiency in humans causes proximal myopathy. Hypophosphatemia can
precipitate rhabdomyolysis. Low blood phosphorus impedes concentration of red blood synthesis. Low blood
phosphorus depletes stored levels. 2,3-diphosphoglycerate affects affinity of oxygen for hemoglobin. Nervous system
dysfunction (eg, apathy, weakness, intention tremors, a bedridden state), are also characteristic of RS.[34]

Other groups at risk for RS include alcoholics undergoing detoxification, extremely-low-birth-weight neonates who
were intrauterine growth-restricted, cancer patients who have suffered from cachexia, and adults with kwashiorkor who
get enteral rather than parenteral feeding.

Consultations
Any patient at risk for nutritional deficiency should be referred to a registered dietitian or other nutritional professional
for a complete nutritional assessment and dietary counseling.

Other subspecialty referrals should be considered if findings from the initial evaluation indicate that the underlying
cause is not poor nutritional intake. If signs indicate malabsorption, a gastroenterologist should be consulted. Further,
in pediatric cases, a pediatrician, preferably one with experience in the management of protein-energy malnutrition
(PEM), should oversee care of the patient. Any patient with significant laboratory abnormalities, as discussed above,
may benefit from consultation with the appropriate subspecialty (eg, endocrinology, hematology).

Children with poor nutrition secondary to inadequate intake and/or neglect should be referred to the appropriate social
agencies to assist the family in obtaining resources and providing ongoing care for the child.

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Diet
See Medical Care.

Long-Term Monitoring
Patients should receive follow-up care with nutrition professionals and social services. Patients should have their
growth and development monitored as well.

Contributor Information and Disclosures

Author

Noah S Scheinfeld, JD, MD, FAAD Assistant Clinical Professor, Department of Dermatology, Weil Cornell Medical
College; Consulting Staff, Department of Dermatology, St Luke's Roosevelt Hospital Center, Beth Israel Medical
Center, New York Eye and Ear Infirmary; Assistant Attending Dermatologist, New York Presbyterian Hospital; Assistant
Attending Dermatologist, Lenox Hill Hospital, North Shore-LIJ Health System; Private Practice

Noah S Scheinfeld, JD, MD, FAAD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Abbvie<br/>Received income in an amount
equal to or greater than $250 from: Optigenex<br/>Received salary from Optigenex for employment.

Coauthor(s)

Anusuya Mokashi, MD, MS Resident Physician, Department of Radiology, Staten Island University Hospital

Disclosure: Nothing to disclose.

Andrew Lin, MD, FRCPC &#0134; Associate Professor, Department of Internal Medicine, Division of Dermatology,
University of Alberta

Andrew Lin, MD, FRCPC is a member of the following medical societies: American Academy of Dermatology, Royal
College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of
Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and
White Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, Association of Military
Dermatologists, American Academy of Dermatology, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

Jeffrey J Miller, MD Associate Professor of Dermatology, Pennsylvania State University College of Medicine; Staff
Dermatologist, Pennsylvania State Milton S Hershey Medical Center

Jeffrey J Miller, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of
Dermatology, Society for Investigative Dermatology, Association of Professors of Dermatology, North American Hair
Research Society

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Disclosure: Nothing to disclose.

Chief Editor

Romesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of
Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal
Medicine, Eastern Virginia Medical School

Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical
Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Dr. Dino
Santoro, to the development and writing of this article.

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