Download Protein-energy malnutrition

Definition
Protein-energy malnutrition (PEM) is a potentially fatal0ody-depletion disorder. It is the leading cause of death in
children in developing countries.
-The World Health Organization (WHO) 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 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-calori 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 .....
Internationally
: In 2000, the WHO estimated that malnourished children
Numbered 181.9 million (32%) in developing countries. Also, an estimated
measured in terms of 149.6 children younger than 5 years are malnourished when
Africa, about one half of children weight for age. In south central Asia and eastern
This figure is 5 times the prevalence in the .have growth retardation due to PEM
western world
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Description
PEM is also referred to as protein-calorie malnutrition. It develops in children and
adults whose consumption of protein and energy (measured by calories) is
insufficient to satisfy the body's nutritional needs. While pure protein deficiency
can occur when a person's diet provides enough energy but lacks the protein
minimum, in most cases the deficiency will be dual. PEM may also occur in persons
who are unable to absorb vital nutrients or convert them to energy essential for
healthy tissue formation and organ function.
Although PEM is not prevalent among the general population of the United States,
it is often seen in elderly people who live in nursing homes and in children whose
parents are poor. PEM occurs in one of every two surgical patients and in 48% of
all other hospital patients.
Although PEM is not prevalent among the general population of the United
States, it is often seen in elderly people who live in nursing homes and in
children whose parents are poor. PEM occurs in one of every two surgical
patients and in 48% of all other hospital patients.
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Kwashiorkor
also called wet protein-energy malnutrition, is a form of PEM
characterized primarily by protein deficiency. This condition usually
appears at the age of about 12 months when breastfeeding is
discontinued, but it can develop at any time during a child's formative
years. It causes fluid retention (edema); dry, peeling skin; and hair
Discoloration******People who have kwashiorkor often have extremely thin arms and
legs, but liver enlargement and ascites (abnormal accumulation of fluid) can
distend the abdomen and disguise weight loss. Hair may turn red or yellow.
Anemia, diarrhea, and fluid and electrolyte disorders are common. The
body's immune system is often weakened, behavioral development is slow,
and mental retardation may occur. Children may grow to normal height but
are abnormally thin.
******Kwashiorkor-like secondary PEM usually develops in patients who
have been severely burned, suffered trauma, or had sepsis (tissue-destroying
infection) or another life-threatening illness. The condition's onset is so
sudden that body fat and muscle mass of normal-weight people may not
change. Some obese patients even gain weight
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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 darkerskinned 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.
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History
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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.
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Kwashiorkor characteristically affects children who are being weaned. Signs
include diarrhea and psychomotor changes.
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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.
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Patients with PEM can also present with nonhealing wounds. This may signify
a catabolic process that requires nutritional intervention.
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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 sunexposed 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.
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.
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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 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.
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.
Complications
Hypoglycemia
Hypothermia
Hypokalemia
Hyponatremia
Heart failure
Infections (bacterial, viral & thrush)
Dehydration & shock
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Causes &symptoms
Primary PEM results from a diet that lacks sufficient sources of protein and/or energy. Secondary
PEM is more common in the United States, where it usually occurs as a complication of AIDS,
cancer, chronic kidney failure, inflammatory bowel disease, and other illnesses that impair the body's
ability to absorb or use nutrients or to compensate for nutrient losses. PEM can develop gradually in
a patient who has a chronic illness or experiences chronic semi-starvation. It may appear suddenly in
a patient who has an acute illness
***Secondary PEM symptoms range from mild to severe, and can alter the form or function of
almost every organ in the body. The type and intensity of symptoms depend on the patient's prior
nutritional status and on the nature of the underlying disease and the speed at which it is
progressing.
Mild, moderate, and severe classifications have not been precisely defined, but patients who lose 1020% of their body weight without trying are usually said to have moderate PEM. This condition is
also characterized by a weakened grip and inability to perform high-energy tasks.
**Losing 20% of body weight or more is generally classified as severe PEM. People with this
condition can't eat normal-sized meals. They have slow heart rates and low blood pressure and body
temperatures. Other symptoms of severe secondary PEM include baggy, wrinkled skin; constipation;
dry, thin, brittle hair; lethargy; pressure sores and other skin lesions.
Values Commonly Used to Grade the Severity of Protein-Energy
Malnutrition
Measurement
Mild
Moderate
Severe
Malnutrition
Malnutrition
Malnutrition
90–110
85–90
75–85
< 75
Body mass index
19–24*
18–18.9
16–17.9
< 16
Serum albumin
3.5–5.0
3.1–3.4
2.4–3.0
< 2.4
220–400
201–219
150–200
< 150
Total lymphocyte
2000–
1501–1999
800–1500
< 800
count (per mm3)
3500
Delayed
2
2
1
0
Normal weight
Normal
(%)
(g/dL)
Serum transferrin
(mg/dL)
hypersensitivity
index†
*In the elderly, BMI < 21 may increase mortality risk.
†Delayed hypersensitivity index quantitates the amount of induration elicited by skin testing
using a common antigen, such as those derived from Candida sp or Trichophyton sp.
Induration grade 0 = < 0.5 cm, 1 = 0.5–0.9 cm, 2 = ≥ 1.0 cm.
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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 (1025 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
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Treatment
Treatment is designed to provide adequate nutrition, restore normal body
composition, and cure the condition that caused the deficiency. Tube feeding or
intravenous feeding is used to supply nutrients to patients who can't or won't eat
protein-rich foods.
In patients with severe PEM, the first stage of treatment consists of correcting fluid
and electrolyte imbalances, treating infection with antibiotics that don't affect
protein synthesis, and addressing related medical problems. The second phase
involves replenishing essential nutrients slowly to prevent taxing the patient's
weakened system with more food than it can handle. Physical therapy may be
beneficial to patients whose muscles have deteriorated significantly.
Prevention
Breastfeeding a baby for at least six months is considered the best way to prevent
early-childhood malnutrition. Preventing malnutrition in developing countries is a
complicated and challenging problem. Providing food directly during famine can
help in the short-term, but more long-term solutions are needed, including
agricultural development, public health programs (especially programs that
monitor growth and development, as well as programs that provide nutritional
information and supplements), and improved food distribution systems. Programs
that distribute infant formula and discourage breastfeeding should be discontinued,
except in areas where many mothers are infected with HIV.
Every patient being admitted to a hospital should be screened for the presence of
illnesses and conditions that could lead to PEM. The nutritional status of patients
at higher-than-average risk should be more thoroughly assessed and periodically
reevaluated during extended hospital stays or nursing home residence.
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Marasmus
Primarily caused by energy deficiency, marasmus is characterized by stunted
growth and wasting of muscle and tissue. Marasmus usually develops between the
ages of six months and one year in children who have been weaned from breast
milk or who suffer from weakening conditions like chronic diarrhea.
Profound weakness accompanies severe marasmus. Since the body breaks
down its own tissue to use as calories, people with this condition
lose all their body fat and muscle strength, and acquire a skeletal
appearance most noticeable in the hands and in the temporal muscle
in front of and above each ear. Children with marasmus are small for
their age. Since their immune systems are weakened, they suffer from
,frequent infections. Other symptoms include loss of appetite
diarrhea, skin that is dry and baggy, sparse hair that is dull brown
or reddish yellow, mental retardation, behavioral retardation, low
.body temperature (hypothermia), and slow pulse and breathing rates
The absence of edema distinguishes marasmus-like secondary PEM, a
gradual wasting process that begins with weight loss and progresses
to mild, moderate, or severe malnutrition (cachexia). It is usually
associated with cancer, chronic obstructive pulmonary disease
COPD), or another chronic disease that is inactive or progressing(
Some individuals have both kwashiorkor and marasmus at the same.very slowly
,time. This most often occurs when a person who has a chronic
inactive condition develops symptoms of an acute illness
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*Metabolic adaptation in protein-energy malnutrition
***The metabolic response to chronic undernutrition covers a wide spectrum that ranges from decreased growth
velocity in mild cases to profound distortion of body silhouette and composition and functional derangements in
advanced stages of the protein-energy malnutrition-infection complex. A wide gamut of molecular, enzymatic,
and hormonal processes assure a temporary availability of endogenous nutrients and the maintenance of vital
functions.
Skin in protein energy malnutrition
D. S. McLaren Department of Medicine, University of Edinburgh, Royal
Infirmary, Scotland.
**Protein energy malnutrition (PEM), the most widespread nutritional deficiency disorder of mankind, is a
group of related disorders, with a more complex and still incompletely understood etiologic basis than
its name suggests. Dermatologic and other clinical manifestations are more florid and characteristic
in kwashiorkor than in marasmus. The complex of clinical syndromes that constitute PEM is best
considered when using a three-dimensional model to illustrate its varying degrees (ie, mild, moderate,
or severe) and the spectrumlike nature of the forms of the severe degree (ie, kwashiorkor, marasmickwashiorkor, or marasmus). Protein energy malnutrition is not confined to children in the Third
*******World and is the most common form of undernutrition in hospitalized patients in Western
countries. Marasmus is by far the most prevalent form. Much of the nutritional support given in
hospitals is not based on an assessment of nutritional status, and little attention is paid to the
different forms PEM might take. Even those who do consider this last point confuse
hypoalbuminemia in patients acutely stressed or infected with kwashiorkor. Recent evidence suggests
that the skin changes of kwashiorkor may be caused by zinc deficiency. Almost nothing is known
about the histopathology of the skin per se in PEM but studies of the hair bulb have shown important
differences among patients with kwashiorkor, marasmus, and normal skin.
Erythrocyte membrane (Ca2+ + Mg2+)-ATPase in human protein-energy
malnutrition.
Calmodulin-free ghost membranes were prepared from erythrocytes of kwashiorkor children and
from healthy children in the same age bracket. In the absence of calmodulin, the specific activity of
Mg2+-dependent Ca2+-pumping ATPase (Ca2+ + Mg2+-ATPase) of kwashiorkor membranes was
more than 40 percent lower than the specific activity of the normal enzymes, whose maximum
velocity was increased by at least four-fold by the modulator protein. In contrast, the maximum
velocity of the enzymes of kwashiorkor membranes was enhanced by calmodulin by about 1 1/2 times
the basal activity of the normal enzymes and by 2 times the basal activity of the kwashiorkor enzymes.
The affinity of the pump for ATP was lower in the membranes of kwashiorkor children (Km for ATP
= 30.6 +/- 2.8 microM ATP) in comparison to normal membranes (Km for ATP = 21.7 +/- 2.0
microM ATP). Similarly, calmodulin-affinity of the enzymes, was lower in kwashiorkor membranes
than in the normal membranes irrespective of source of calmodulin. Calmodulin from haemolysates
of kwashiorkor red cells activated the enzymes of normal and kwashiorkor membranes to the same
degree as calmodulin partially purified from the haemolysate of healthy children. A determination of
the dependence of the activity of the pump on calcium in the absence and presence of calmodulin
reveals that the affinity of the kwashiorkor enzymes for Ca2+ is at least 70 percent lower than that of
enzymes of normal membranes. Altogether, these findings suggest that the Ca2+-pumping ATPase of
kwashiorkor membranes is less functional than the enzymes of healthy erythrocytes
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Effects of Malnutrition on the Gastrointestinal Tract
and Pancreas
******Protein-energy malnutrition may produce major structural and
functional changes in the gastrointestinal tract and pancreas, which, in
turn, may aggravate the underlying poor nutritional condition. In severe
protein-energy malnutrition, for example, acinar cell atrophy occurs and
exocrine cells have decreased numbers of zymogen granules. Pancreatic
secretion may be reduced following stimulation with cholecystokinin and/or
secretin. With malnutrition, the activities of enzymes contained in
pancreatic juice (i.e., trypsin, chymotrypsin, lipase, amylase) are reduced.
With reversal of malnutrition these can return to normal levels, but this
may require several weeks.
In addition to pancreatic exocrine changes, the entire wall and
mucosal lining of the stomach and intestine may be reduced in thickness.
This change appears to be reversible, as a more normal macroscopic
appearance can follow nutritional repletion. Microscopically, marked
changes may develop, including severe "flattening" of the small intestinal
mucosa,
similar to celiac disease. In contrast to celiac disease, however, reduced
numbers of crypt mitoses are seen; the mucosa is hypoplastic rather than
hyperplastic. In this setting, correction of the nutritional state per se
can produce a complete reversion to normal. Nonspecific ultrastructural
changes also occur, including epithelial cell lipid droplets. Changes may be
present throughout the small intestine in an irregular patchy distribution,
although the jejunum appears to be most severely affected. Qualitative and
quantitative changes in the intestinal microflora, particularly anaerobes,
also occur in protein-energy malnutrition. However, their role in altering
mucosal structure and function requires definition. Some brush-border
enzymes (i.e., disaccharidases) may be reduced; as a result, malabsorption
of a variety of substances (e.g., lactose) may be observed. Altered uptake
of glucose and D-xylose has also been reported, and steatorrhea may be
present with impaired absorption of fat and some fat-soluble vitamins. In
addition, there may be increased protein loss from the gut, leading to
increased fecal nitrogen loss. Finally, specific nutrients may be deficient
and cause alterations in certain tissues. For example, folic acid and
vitamin B12 deficiencies have well-recognized effects on rapidly dividing
hematopoietic precursor cells in the bone marrow; for similar reasons, as
shown in Table 5, analogous changes may be anticipated in the small
intestinal epithelium.
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SOURCES
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INDEX
Definition00000000000000000000000000001
Discribition0000000000000000000000000002
Kwashiorkor0000000000000000000000000
Mortality\Morbidity& History000000000000000
CAUSES& Complications000000000000000
Causes &symptoms00000000000000000
Lab Studies00000000000000000
Prevention& Treatment000000000000000000000000
Marasmus000000000000000000000000
Effects of PEM0000000000000000000000
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