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Dermatology > METABOLIC DISEASES
Protein-Energy Malnutrition
Article Last Updated: Feb 18, 2008
AUTHOR AND EDITOR INFORMATION
Section 1 of 9
Author: Noah S Scheinfeld, MD, JD, FAAD, Assistant Clinical Professor, Department of Dermatology, Columbia University; Consulting Staff, Department of Dermatology, St Luke's Roosevelt Hospital Center, Beth Israel Medical Center, New York Eye and Ear Infirmary; Private Practice
Noah S Scheinfeld is a member of the following medical societies: American Academy of Dermatology
Coauthor(s):
Anusuya Mokashi, MS, Medical Student, New York Medical College;
Andrew Lin, MD, FRCPC, Associate Professor, Department of Internal Medicine, Division of Dermatology, University of Alberta
Editors: Michelle Pelle, MD, Clinical Assistant Professor, Division of Dermatology, Department of Medicine, University of California at San Diego; David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Director, Division of Dermatology, Scott and White Clinic; Director Dermatology Residency Training Program, Scott and White Clinic; Jeffrey J Miller, MD, Associate Professor, Department of Dermatology, Penn State University, Milton S Hershey Medical Center; Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University; William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System
Author and Editor Disclosure
Synonyms and related keywords:
PEM, kwashiorkor, malignant malnutrition and infantile pellagra, marasmus
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, 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. 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 PEM affects virtually every organ system, this article primarily focuses on its cutaneous manifestations. Patients with PEM 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. PEM 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 al2 stated that "a prospective assessment of food and nutrient intake in a population of Malawian children at risk for kwashiorkor" found "no association between the development of kwashiorkor and the consumption of any food or nutrient."
Frequency
United States
PEM 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 PEM was more than one half.
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 WHO3 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 PEM. This figure is 5 times the prevalence in the western world.
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
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 PEM in Third World 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 PEM 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. PEM has also been found to be a primary factor of poor prognosis in elderly persons.
History
- 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 PEM. 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 PEM can also present with nonhealing wounds. This may signify a catabolic process that requires nutritional intervention.
- Lewandowski et al4 reported kwashiorkor and an acrodermatitis enteropathica–like eruption after a distal gastric bypass surgical procedure.
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 PEM, 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.5 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. PEM 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.
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 PEM occurs with HIV infection. Gastrointestinal infections can and often do precipitate clinical PEM 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; PEM 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 PEM. Populations in both acute-care and long-term facilities are at risk for clinically significant involuntary weight loss (IWL) that can result in PEM. 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. PEM 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 PEM because of inadequate nutrition, which has been determined to be a common comorbid factor for increased morbidity and mortality in elderly burn victims.6 Patients with liver cirrhosis are also at risk for PEM, 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 PEM being more severe in persons with alcoholic cirrhosis than in those with nonalcoholic cirrhosis. Patients on long-term hemodialysis also may develop PEM; this is associated with increased morbidity and mortality. Patients with squamous cell carcinoma of the esophagus are at risk for PEM.
Actinic Prurigo
Other Problems to be Considered
Riboflavin deficiency
Any vitamin, fatty acid, or trace mineral deficiency may coexist with PEM.
Lab 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 PEM 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).
Histologic Findings
In a 1989 study,7 skin biopsy samples taken from 20 children with PEM 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 al8 found that childhood malnutrition correlates with a reduction in the total melanin content of scalp hair.
Medical Care
In both children and adults, the first step in the treatment of 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 PEM (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.
Chung et al,9 in discussing that PEM 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 PEM.
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 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.
Diet
See Medical Care.
Further Outpatient Care
- Patients should receive follow-up care with nutrition professionals and social services.
Prognosis
- The extent of growth failure and the severity of hypoproteinemia, hypoalbuminemia, and electrolyte imbalances are predictors of a poorer prognosis.
- Underlying HIV infection is associated with a poor prognosis.
The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Dr. Dino Santoro, to the development and writing of this article.
- Onis M de, Monteiro C, Clugston G. The worldwide magnitude of protein-energy malnutrition: an overview from the WHO Global Database on Child Growth. Bulletin of the World Health Organization. 1993;71(6).
- Lin CA, Boslaugh S, Ciliberto HM, Maleta K, Ashorn P, Briend A, et al. A prospective assessment of food and nutrient intake in a population of Malawian children at risk for kwashiorkor. J Pediatr Gastroenterol Nutr. Apr 2007;44(4):487-93. [Medline].
- World Health Organization, Dept of Nutrition for Health and Development. Nutrition for health and development: a global agenda for combating malnutrition. World Health Organization. Available at http://whqlibdoc.who.int/hq/2000/WHO_NHD_00.6.pdf.
- Lewandowski H, Breen TL, Huang EY. Kwashiorkor and an acrodermatitis enteropathica-like eruption after a distal gastric bypass surgical procedure. Endocr Pract. May-Jun 2007;13(3):277-82. [Medline].
- Tavarela Veloso F. Review article: skin complications associated with inflammatory bowel disease. Aliment Pharmacol Ther. Oct 2004;20 Suppl 4:50-3. [Medline].
- Demling RH. The incidence and impact of pre-existing protein energy malnutrition on outcome in the elderly burn patient population. J Burn Care Rehabil. 2005;Jan-Feb;26(1):94-100. [Medline].
- Thavaraj V, Sesikeran B. Histopathological changes in skin of children with clinical protein energy malnutrition before and after recovery. J Trop Pediatr. Jun 1989;35(3):105-8. [Medline].
- McKenzie CA, Wakamatsu K, Hanchard NA, Forrester T, Ito S. Childhood malnutrition is associated with a reduction in the total melanin content of scalp hair. Br J Nutr. Jul 2007;98(1):159-64. [Medline].
- Chung SH, Stenvinkel P, Lindholm B, Avesani CM. Identifying and managing malnutrition stemming from different causes. Perit Dial Int. Jun 2007;27 Suppl 2:S239-44. [Medline].
- Balint JP. Physical findings in nutritional deficiencies. Pediatr Clin North Am. Feb 1998;45(1):245-60. [Medline].
- Beers MH, Berkow R, eds. Nutritional Disorders: Malnutrition. In: The Merck Manual. 17th ed. Merck; 1999:28-32.
- Caksen H, Kendirci M, Kandemir O, Patiroglu T. A case of malignant histiocytosis associated with skin involvement mimicking kwashiorkor. Pediatr Dermatol. Nov-Dec 2001;18(6):545-6. [Medline].
- Collins N. Protein-energy malnutrition and involuntary weight loss: nutritional and pharmacological strategies to enhance wound healing. Expert Opin Pharmacother. Jul 2003;4(7):1121-40. [Medline].
- Constans T, Alix E, Dardaine V. [Protein-energy malnutrition. Diagnostic methods and epidemiology]. Presse Med. Dec 16 2000;29(39):2171-6. [Medline].
- De Caprio C, Alfano A, Senatore I, Zarrella L, Pasanisi F, Contaldo F. Severe acute liver damage in anorexia nervosa: two case reports. Nutrition. May 2006;22(5):572-5. [Medline].
- Delahoussaye AR, Jorizzo JL. Cutaneous manifestations of nutritional disorders. Dermatol Clin. Jul 1989;7(3):559-70. [Medline].
- Gehri M, Stettler N, Di Paolo ER. Marasmus. eMedicine from WebMD [serial online]. May 22, 2006;Available at http://www.emedicine.com/ped/topic164.htm.
- Glaser, KL. Pediatrics: Malnutrition. Medstudents. Available at http://www.medstudents.com.br/pedia/pedia1.htm.
- Golden MHN. Severe malnutrition. In: Weatherall DJ, Ledingham JGG, Warrell DA, eds. Oxford Textbook of Medicine. 3rd ed. 1996:1278-96.
- Goskowicz M, Eichenfield LF. Cutaneous findings of nutritional deficiencies in children. Curr Opin Pediatr. Aug 1993;5(4):441-5. [Medline].
- Grigsby DG. Malnutrition. eMedicine from WebMD [serial online]. June 30, 2006;Available at http://www.emedicine.com/ped/topic1360.htm.
- Gupta MA, Gupta AK, Haberman HF. Dermatologic signs in anorexia nervosa and bulimia nervosa. Arch Dermatol. Oct 1987;123(10):1386-90. [Medline].
- Gurski RR, Schirmer CC, Rosa AR, Brentano L. Nutritional assessment in patients with squamous cell carcinoma of the esophagus. Hepatogastroenterology. Nov-Dec 2003;50(54):1943-7. [Medline].
- Harris CL, Fraser C. Malnutrition in the institutionalized elderly: the effects on wound healing. Ostomy Wound Manage. Oct 2004;50(10):54-63. [Medline].
- Hendricks KM, Duggan C, Gallagher L, Carlin AC, Richardson DS, Collier SB, et al. Malnutrition in hospitalized pediatric patients. Current prevalence. Arch Pediatr Adolesc Med. Oct 1995;149(10):1118-22. [Medline].
- Jilcott SB, Masso KL, Ickes SB, Myhre SD, Myhre JA. Surviving but not quite thriving: anthropometric survey of children aged 6 to 59 months in a rural Western Uganda district. J Am Diet Assoc. Nov 2007;107(11):1983-8. [Medline].
- Kuhl J, Davis MD, Kalaaji AN, Kamath PS, Hand JL, Peine CJ. Skin signs as the presenting manifestation of severe nutritional deficiency: report of 2 cases. Arch Dermatol. May 2004;140(5):521-4. [Medline].
- Lyder CH. Assessing risk and preventing pressure ulcers in patients with cancer. Semin Oncol Nurs. Aug 2006;22(3):178-84. [Medline].
- Manguso F, D'Ambra G, Menchise A, et al. Effects of an appropriate oral diet on the nutritional status of patients with HCV-related liver cirrhosis: a prospective study. Clin Nutr. Oct 2005;24(5):751-9. [Medline].
- McLaren DS. Skin in protein energy malnutrition. Arch Dermatol. Dec 1987;123(12):1674-1676a. [Medline].
- Miller SJ. Nutritional deficiency and the skin. J Am Acad Dermatol. Jul 1989;21(1):1-30. [Medline].
- Neldner KH. Nutrition, aging and the skin. Geriatrics. Feb 1984;39(2):69-82, 87-8. [Medline].
- Pelly TF, Santillan CF, Gilman RH, Cabrera LZ, Garcia E, Vidal C, et al. Tuberculosis skin testing, anergy and protein malnutrition in Peru. Int J Tuberc Lung Dis. Sep 2005;9(9):977-84. [Medline].
- Prendiville JS, Manfredi LN. Skin signs of nutritional disorders. Semin Dermatol. Mar 1992;11(1):88-97. [Medline].
- Roongpisuthipong C, Sobhonslidsuk A, Nantiruj K, Songchitsomboon S. Nutritional assessment in various stages of liver cirrhosis. Nutrition. Sep 2001;17(9):761-5. [Medline].
- Ryan AS, Goldsmith LA. Nutrition and the skin. Clin Dermatol. Jul-Aug 1996;14(4):389-406. [Medline].
- Schneider JB, Norman RA. Cutaneous manifestations of endocrine-metabolic disease and nutritional deficiency in the elderly. Dermatol Clin. Jan 2004;22(1):23-31, vi. [Medline].
- Shah S, Kannikeswaran N, Kamat D. A rash. Clin Pediatr (Phila). Sep 2007;46(7):650-4. [Medline].
- Soni BP, McLaren DS, Sherertz EF. Skin lesions in nutritional, metabolic and heritable disorders: cutaneous changes in nutritional disease. In: Fitzpatrick's Dermatology in General Medicine. Vol 2. 1999:1725-37.
- Tirmentajn-Jankovic B, Dimkovic N. [Simple methods for nutritional status assessment in patients treated with repeated hemodialysis]. Med Pregl. Sep-Oct 2004;57(9-10):439-44. [Medline].
- Wilmer WA, Magro CM. Calciphylaxis: emerging concepts in prevention, diagnosis, and treatment. Semin Dial. May-Jun 2002;15(3):172-86. [Medline].
Protein-Energy Malnutrition excerpt Article Last Updated: Feb 18, 2008
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