Malnutrition and obesity

CONF.DR.INGRITH MIRONDR. MOCANU ADRIANA

What is malnutrition?

World Health Organization definition:

The term is used to refer to a number of diseases, each with a specific cause related to one or more nutrients (for example, protein, iodine or iron) and each characterized by cellular imbalance between the supply of nutrients and energy on the one hand, and the body's demand for them to ensure growth, maintenance, and specific functions, on the other.

HUMAN NUTRITION

• Obesity & under-nutrition are the 2 ends of the spectrum of malnutrition.

• A healthy diet provides a balanced nutrients that satisfy the metabolic needs of the body without excess or shortage.

• Dietary requirements of children vary according to age, sex & development.

Macro and micro nutrients

• Macro-nutrients– Protein (amino acids)– Energy (carbohydrates)– Fat (fatty acids)

• Micro-nutrients– Water soluble vitamins (assist in energy-release of

carbohydrates and red blood cell formation)– Fat soluble vitamins (development & metabolism)– Minerals

Malnutrition: definition• Malnutrition : chronic state of nutrition due to insufficient food

intake (caloric and / or protein) specific for infants and small child.

• Along with major deficits of nutrients occur also deficiencies in vitamins and minerals (deficiency anemia, rickets, avitaminoses).

• Depression of cellular immunity caused by malnutrition favors increased susceptibility to infection, which worsens the initial deficit, the infection is often the one that causes death.

• Half of the states of malnutrition : first 6 months of life, overlapping maximum period of CNS development (neuronal proliferation - to a maximum of 18 months).

Types of malnutrition• Severe Protein-Energy Malnutrition (>3 S.D.)– Kwashiorkor (low protein)– Marasmus (low calories)

• Mild/moderate undernutrition (>2 S.D.)– Stunting– Underweight– Wasting

• Micro-nutrient deficiency– Iodine– Iron– Vitamin A– Vitamin D

OVERVIEW OF MALNUTRITION• The majority of world’s children live in

developing countries• Lack of food & clean water, poor sanitation,

infection & social unrest lead to LBW & PEM• Malnutrition is implicated in >50% of deaths

of children <5years (5 million/yr).

OVERVIEW OF MALNUTRITION

• WHO estimated that 32% of children in developing countries are underweight (182 million).

• 78% of these children live in South-east Asia & 15% in Sub-Saharian Africa.

• The reciprocal interaction between PEM & infection is the major cause of death & morbidity in young children.

EPIDEMIOLOGY

• The term protein energy malnutrition has been adopted by WHO in 1976.

• Highly prevalent in developing countries among children <5 years; severe forms 1-10% & underweight 20-40%.

• All children with PEM have micronutrient deficiency.

Classification/Terminololgy

The term malnutrition (Anglo-Saxon School) or dystrophy (French School) define the states of malnutrition through food intake deficiency- qualitatively and/or quantitatively.

• Protein energy malnutrition (PEM); • Protein malnutrition (PM).

Classification/Terminololgy

WHO proposes 2 terms (referring to states of severe malnutrition)

• Marasmus - severe PEM; • Kwashiorkor - severe PM.

These terms are unsatisfactory for practice - do not include light and intermediate states of malnutrition→ new terminology.

WHO - classification of malnutrition • Primary malnutrition • Secondary malnutrition.

Primary Malnutrition :ETIOLOGYPrimary malnutrition

• correct food intake;• negativ prognosis due to disturbed growth that can not be

influenced therapeutically (frequent association with mental deficiency);

• commonly associated with: fetal malnutrition, low birth weight and small height sometimes.

The causes of primary malnutrition: organics (severe malformations: renal, digestive, cardiac) genetically conditioned diseases (chromosomal, metabolic) fetal infections (toxoplasmosis, syphilis, cytomegalovirus).

Etiology of Primary Malnutrition• Failure of lactation.• Improper weaning practices• Poverty• Food taboos• 2 or more children under 5 years of age in same

household• Death of mother• Incompetent/ ignorant mother.• Lack of family planning

SECONDARY MALNUTRITION

Secondary malnutrition (exogenous):

- deficiency due to dietary intake qualitatively or quantitatively,

- prognosis is generally good by correcting the cause and food intake ,

- usually no mental deficits.

SECONDARY MALNUTRITIONClassification of secondary malnutrition (WHO):

I. Moderate malnutrition: - mild (grade I dystrophy, hypotrophy, "poor child"); - medium (grade II dystrophy);

II. Severe malnutrition (grade III dystrophy): - energy-protein malnutrition (PEM) :marasmus, atrepsia; - protein malnutrition (PM)

• acute form (kwashiorkor); • chronic form (marasmic kwashiorkor ).

Etiology of secondary malnutrition

A)Dietary deficiency • quantitatively: native hipogalactia; late diversification

over 6 months of age; improper dilution of milk, restrictive diets, taboos related to food, family, religious, ethnic;

• quality: carbohydrate deficiency ( cow’s milk distrofy ), protein deficiency (edematous dystrophy by excess flour, using vegetable protein low biological value), lipid deficiency ( regimes without lipids)

• lead to imbalance by decreasing caloric intake.

Etiology of secondary malnutrition

B) infections:enteric infection;bronchopneumonia, otomastoidite, chronic urinary tract infection, bacterial or parasitic diarrhea, syphilis, tuberculosis- poor appetite, digestive losses, increased catabolism.

c) psychosocial events:maternal deprivation, neglect of physiological rhythm of alimentation, lack of hygiene, pollution, cold, hospitalism;

Etiology of secondary malnutrition

D) psychosomatic disorders : - anorexia ,- organic disease (hypertrophic pyloric stenosis,

congenital malformations that cause repeated vomiting, cystic fibrosis, celiac disease, congenital intolerance to disaccharides, labio-maxillo-palatine cleft) ,

- infantile cerebral palsy with impaired swallowing, pharyngeal incoordination.

Etiology of secondary malnutrition

Chronic illnesses that commonly are associated with nutritional deficiencies include the following:– Cystic fibrosis– Chronic renal failure– Childhood malignancies– Congenital heart disease– Neuromuscular diseases– Chronic inflammatory bowel diseases

Etiology of secondary malnutrition• In addition, the following conditions place children at

significant risk for the development of nutritional deficiencies:– Prematurity– Developmental delay– In utero toxin exposure (ie, fetal alcohol exposure)

• Children with multiple food allergies present a special nutritional challenge because of severe dietary restrictions. Patients with active allergic symptoms may have increased caloric and protein needs.

Protein-energy malnutrition pathogenesis

In severe forms when nutritional deficit exceeds a certain limit, the consequences are severe:

• regression of all metabolic activities (decreased basal metabolism, decreased intracellular water, decreasing opportunities to retain water and salt);

• low digestive tolerance (decreased activity of disaccharideses, pancreatic secretion, bile acids);

• loss of defense to infection. Very low digestive tolerance and dietary intake can not maintenance energy needs lead to autophagic processes (the metabolism of starvation).

Protein-energy malnutrition pathogenesis

Severe lack of calorie and protein → hypoglycemia, decreased serum amino acids in pancreatic reaction → → hipoinsulinism (main endocrine changes in starvation) → decrease peripheral insulin and the appearance adaptive responses:

• mobilization of fatty acids from adipose tissue (lipolysis) to the liver to be an energy source;

• decrease in muscle glucose utilization and incorporation of amino acids that are directed to the liver, where they are used for protein synthesis and neoglucogeneză (the exhausted body fat);

• hepatic protein synthesis is achieved by sacrificing muscle proteins.

Protein-energy malnutrition pathogenesis

Infection - is the vicious circle in severe malnutrition, worsening starvation and being the main cause of death by:

• loss of appetite; • digestive losses (diarrhea); • increased catabolism (febrile illness); • disorders of intermediary metabolism by reducing

metabolic efficiency of nutrients; • increased urinary nitrogen loss, K, Mg, Zn, P, vitamin A,

C, B2.

Pathogenesis of protein malnutrition

The acute form (typical Kwashiorkor) • occurs after 6-8 months; • diversification normal calorie but devoid of protein; • deposits of fat are consumed, stature is normal and

causes severe loss of protein (proteins from the liver, muscle, pancreatic proteins, serum albumins deficiency) and loss of intracellular K (preservation mitosis), hepatic fatty infiltration if infection occurs - marked reduction albumin (hepatic synthesis deficient) → fluid retention (decrease in colloid osmotic pressure capillary) → edema.

Pathogenesis of protein malnutrition

Chronic form (Marasmic Kwashiorkor) - secondary selective protein intake deficiency is characterized by:

- sufficient caloric intake;- normal secretion of insulin: favors lipogenesis (fatty acids are not available in place of

amino acid oxidation - fatty tissue is preserved); reduced level of plasma amino acids by three mechanisms:

• reduce the release of amino acids from muscle;• stimulates the passage of serum amino acids in muscle;• favors the the incorporation of amino acids into the muscle.

MARASMUS/KWASHIORKOR

• Marasmus represents an adaptive response to starvation, whereas kwashiorkor represents a maladaptive response to starvation

• In Marasmus the body utilizes all fat stores before using muscles.

Assessment of Nutrition Status

–Clinical–Anthropometric–Dietary– Laboratory

Investigations for PEM• Full blood counts, inflammatory markers;• Blood glucose profile, lipidic profile• Iron, vitamin levels;• Microbiology: septic screening,stool & urine for parasites &

germs;• Electrolytes, Ca, Ph & Mg;• Serum proteins, protein electrophoresis;• immunological status: cellular immunity - decreased T cell,

interferon, IDR lack of response to tuberculin; humoral immunity - low IgA (secretory IgA), IgM - high, low IgG.

• Decrease complement C3;• Exclude HIV & malabsorption.

Investigations for PEMIn essence:

• decrease serum albumins → edema; • decrease apoproteins (lipoproteins carrier); • storage of fat in the liver (fatty infiltration);

Clinical outcomes: oedema, hepatomegaly (fatty liver), changes in hair growth and skin (areas of hypo-or hyperpigmentation, fissures), diarrhea (villous atrophy), predisposition to infection (humoral and cellular immunity disturbed).

Anthropometric assessment of malnutrition

anthropometric criteria : percentiles method (normal 10-90). standard derivations method (normal + / - 2 SD). ponderal index (PI) PI = actual weight of the child / ideal weight (W of child of the

same age located on the 50th percentile of the growth curve). After the PI values : 3 degrees of PEM(Gomez) degree I (PI = 0.89 to 0.76); degree II (PI = 0.75 to 0.60); degree III ( PI = 0.60). PI = 0.90- underweight or child at risk of malnutrition.

Anthropometric assessment of malnutrition

The protein malnutrition are two degrees: degree I PI = 0.8-0.6 - KWASHIORKOR; degree II PI= 0.6 – MARASMIC KWASHIORKOR

Nutritional index (NI) - index diets. • NI = actual weight / weight appropriate waist. After this indicator there are 3 degrees of malnutrition: • grade I (NI= 0.89 to 0.81); • grade II (NI= 0.80 to 0.71); • grade III (NI= 0.70).

Head circumference (HC) - highlights the true growth in the first two years. Midarm circumference (measured at the ½ distance between the acromion and

olecranon) pathological - under 13 cm - available in children over 2 years.

Assessment of malnutrition- functional criteria

Appreciation of the digestive tolerance:• paradoxical reaction to hunger (disproportionate weight loss);• food paradoxical reaction (weight loss to increased food

intake, sometimes diarrhea);• sensitivity to fasts - by spacing meals: hypoglycaemia,

especially nocturnal → apnea, sudden death.• immunological reactivity :

- increased responsiveness to infection;- reactivity collapsed (serious infection without fever, leukocytosis, sometimes opportunistic).

Assessment of malnutrition

Neuropsychological development:• Archaic reflexes;• Muscle tone;• Posture;• Mobility;• Development of language;• Affection.They are affected differently depending on the severity

of malnutrition .

Clinical features in marasmus

• Marked muscle wasting and loss of subcutaneous fat;

• Monkey facies;• Skin becomes loose and hangs in folds;• Abdomen protuberant due to hypotonic

muscles;• Temperature is usually sub-normal;• Child is alert.

Clinical features of kwashiorkor• Generalized edema more marked in lower

extremeties, muscle wasting; • Growth retardation;• Psychomotor changes;• Apathy and irritability;• Fine and discoloured hair;• Anemia;• Usually flaky paint dermatitis;• Enlarged liver due to fatty changes.

Complications of PEM• Hypoglycemia• Hypothermia• Hypokalemia• Hyponatremia• Heart failure• Dehydration & shock• Infections (bacterial, viral & thrush)

TREATMENT: Prevention of Malnutrition• Primary Prevention– Health Education to mothers about good nutrition and

food hygiene – Immunization of children.– Growth monitoring on Growth Charts specially of all

children under 3 years of age• Secondary Prevention– Mass Screening of high risk populations, using simple

tools like Weight for age .• Tertiary Prevention– Good Nutritional Care, supplementary feedings and

rehabilitation, counselling of mothers.

TREATMENT: Prevention of Malnutrition

- Natural nutrition - first 4-6 months;- Artificial nutrition - milk type, dilution,

enrichment rice mucilage; - Compliance with immunization schedule, the

correct treatment of infections; - Inadequate conditions and social

environment.

TREATMENT

OBJECTIVES:• accurate assessment of the form and degree of

malnutrition;• pointing out the main deficiencies (protein, fat,

carbohydrates, fluid and electrolyte minerals and vitamins), immune status and the possibility of co-infection;

• finding the cause which produced malnutrition;• recovery plan individualized for the nutritional

deficiency as quickly as possible.

TREATMENTGeneral principles:The recovery of PEM (II and III degree) :

I. The initial phase •Correction of water & electrolyte imbalance; • Treatment of infectious complications. II. Repair phase • Dietary therapy; • Correction of deficiencies (anemia, rickets, hypovitaminosis, etc). III. Convalescence phase• Restoration of body composition; • Enhancing healing. Optimal objective is to resume growth after 2-3 weeks of starting the diet and

clinical recovery in 6-8 weeks.

TREATMENTI)Parenteral nutrition for 2-3 days → enteral nutrition with flow probe using hyperproteic and hypercaloric solutions ; II) Early initiation of oral nutrition : hypoallergenic preparations rich in proteins and calories, low osmolarity: Alfare, PeptiJunior, Pregestimil, Nutramigen, Pregomin or amino acid formulas, such as Neocate .

• Keep in parallel parenteral intake of carbohydrates, amino acids, lipids.

• Simultaneously treating infections, hypoproteinemia, anemia, multivitamins deficiencies .

• This variant is also little used because it requires specials dietetics and carefully monitorization of nutritional therapy .

TREATMENT III) after fluid replacement and electrolyte - digestive tolerance :- with carrot soup or rice mucilage (in various concentrations ) in a dose of

150-200 ml / kg ( not exceeding 1000 ml / day)- carbohydrates were obtained from glucose 5%, 7 %, 10 % and chicken

mixed proteins ( hypoallergenic, 100g , 17g protein). - after normalization of the stools ( 7 days) :oil gradually (3-4 ml / day ) and

after 10 days from the beginning of enteral diet →hypoallergenic preparation can be inserted (!preparations lactose free- can induce cow's milk protein intolerance ) .

- week 4 :sugar (restoring lactose tolerance is difficult , 3-4 months); - flour products containing gluten will not enter until full recovery;- increases in protein - calorie intake by parenteral administration of

carbohydrates , amino acids and proteins;- treat the infection , iron or vitamin deficiencies .

TREATMENTMalnutrition has its weight age. • correct food intake : 8-10% protein, 54-50% fat, 50-60%

carbohydrates: 1 g lipid - 9 kcal; 1 g protein - 4.1 kcal; 1 g carbohydrate - 4.1 kcal.

• complete metabolism of 1 g of protein are required 35-40 kcal. • a protein intake ˃ 5 g / kg / day is dangerous, resulting

hyperammonemia, increased blood urea nitrogen ;• Increasing K intake to 4-5 mEq / l .

TREATMENTRecovery of PEM degree II(advenced) and III (Suskie) contains: calorie - 175 kcal / kg / day; protein - 4 g / kg / day; lipid - 9.59 g / kg / day; carbohydrate - 18.3 g / kg / day.• Research and treating infection with antibiotics (ideally etiologic)

is mandatory. • In severe malnutrition ↓ IgG: iv administration of gamma globulin • protein malnutrition (low albuminand proteinemia ): human

albumin administered iv (1 g / kg / day). • basal energy needs - 70 kcal / kg / day.

TREATMENT

Mild forms of MPC • Treat at home by correcting the diet (food ration

for age - increasing protein intake to 0.5-1 g / kg / day→ 20 to 30 kcal / kg / day).

• correction of the causes: maternal hipogalactia, hypocaloriec diet with incorrect mixed or artificial nutrition, extending over six months natural nutrition with delayed/incorrect diversification.

• Quick recovery in 1-2 weeks.

TREATMENT

PEM (severe forms degree II-III , III) • Treat only in hospital. • The first 24 hours - fluid replacement and

electrolyte and acid-base fluid resuscitation. • The following 48-72 hours (sometimes more)

partial or total parenteral nutrition, reaching 80-90 kcal / kg / day.

TREATMENT the rate of protein :4-5 g / kg / day (increasing protein is

progressively 1-1.5 g / kg / day, reaching in 4-5 days at this rate)

180-160 kcal / kg to 180-200 kcal / kg / day from day 3-4 start exploratory digestive maintaining iv

administration sugars, amino acids ; Diet exploratory :rice mucilage 3%, 5%, 8%; carrot soup 300

‰ or 500 ‰, sweetener - glucose 5%, 7%, 10% (even 15%). 7-8 lunches, from 30-50 ml ground in 2-3 days, if tolerance is

good - 140-150 kcal / kg.

TREATMENTCriteria to follow:

• normalization of the stools ;• growth rate - slow resume after 2-3 weeks to restore digestive

tolerance and achieve optimum value caloric and protein intake (early treatment can decrease the growth rate - restore electrolyte balance, after the disappearance of edema).

• avoid prolonged fasts - risk of hypoglycaemia.• immune recovery 25-30 days after initiation of dietary therapy.• histochemical normalization of intestinal mucosa after 3-4

months.

OBESITYObesity - chronic disorder of the nutrition in infants, children and adolescents characterized by the accumulation of fat in adipose tissue and other tissues and organs as a result of energy imbalance. The prevalence of the disease is on the rise: according to WHO 22 million children under 5 years are obese, the prevalence becoming triple in the past 30 years and overcoming the prevalence of malnutrition.For children who have an overweight or obese parent, the risk of becoming obese adults is higher than in normal weight children. If both parents are obese, a child's risk of becoming obese is 80%. 80% of obese adolescents become obese adults.

OBESITY

Obesity is a plurifactorial disease, favorable factors being:

• prenatal factors: maternal caloric intake, maternal diabetes, dismaturity, small size and small head circumference at birth;

• perinatal factors: cold climate at birth. • post-natal factors: the intensity of the increase in

body fat by the age of 1 year, artificial feeding from birth, adolescence weight.

OBESITY - pathophysiological mechanisms and clinical features

The major disturbances encountered in obesity are insulin and glucose homeostasis, dyslipidemia and hypercortisolemia.CLINICAL PICTURE a) Characteristic anthropometric data of obesity are: -excessive weight according to height, excessive weight in relation to the ideal weight for age; -normal-sized or even increased height compared to the average age; -increased upper-arm circumference comparing to age values ; -subcutaneous fat thickness increased compared to normal age; -sexual maturation and somatic maturation(bone age) normal or accelerated.b) somatic appearance: generalized symmetrically increased fat deposits, breast enlargement and distension of the abdomen.

OBESITY : Symptoms

-psychological problems: bad image of oneself, feelings of inferiority and rejection from the same aged children community, depression, frustration, tendency to antisocial behavior, difficult family relationships and social immaturity, increased dependence to the family.-mechanical overload-related symptoms represented by the excess weight: cardio-circulatory inadequacy, fatigue, polipnea and dyspnea on moderate effort, lower limb orthostatic edema, joint pain. -skin changes: intertrigo, skin folds irritation, itching, abcesses, acne. -nonspecific disorders: headache, vertigo, dizziness, fatigue, flatulence, constipation, difficult digestion, menstrual disorders in adolescents.

OBESITY: LABORATORY DATA

• carbohydrate metabolism: over 50% of obese children have impaired glucose tolerance. • lipid metabolism: hypercholesterolemia, hypertriglyceridemia, elevated levels of LDL and apolipoprotein B, decreased HDL and apolipoprotein AI. • protein metabolism: moderate increase in serum protein, the α2-and β-globulins.

• hormonal profile: elevated levels of insulin and cortisol; thyroid function is generally normal. • fluid and electrolyte balance : sodium retention and potassium excretion are elevated;aldosterone excretion is significantly increased.

OBESITY: POSITIVE DIAGNOSIS

- clinical appearance ;-anthropometric data : body mass index(BMI), size of skin fold. WHO recommendations :- overweight : BMI ˃ 1 SD or between 95-99 percentile; - obesity :BMI ˃2 SD or above the 99th percentile ;

- by the age of 2 years , overweight : reporting the actual weight to ideal weight for height , age and sex. The correct definition of obesity in children is given by the content of body fat mass measured by bioelectric impedance . Up to age 16 years:obesity →fat mass ˃ 20 % reference values for age and sex ;Over 16 years : obesity → fat mass ˃ 25 % of body weight in boys and ˃ 32 % for girls.

OBESITY: DIFFERENTIAL DIAGNOSIS

In case of suspected genetic or endocrine obesity, differential diagnosis should be done with:

- Laurence-Moon- Bardet-Biedl syndrome,- Prader-Willi syndrome,- Albright (pseudohypoparathyroidism), - Cushing's syndrome, - Stein-Leventhal syndrome (or Policystic ovarian syndrome)- Frolich syndrome ( or Adiposogenital Distrophy)- Mauriac syndrome (complication of diabet mellitus type I)- Von Gierke glycogenosis (storage disease).

OBESITY: TREATMENT

Treatment protocol includes: - dietary treatment, - physical activity program,- behavioral therapy, - drug therapy, -surgery, - treatment of complications,- family nutrition education. Dietary treatment remains a therapeutic basis.

OBESITY: TREATMENT

a)Dietary treatment during growth and development needs to ensure their normal ongoing, so that can not be overcome certain minimum amounts of caloric intake and dietary protein:

-110 calories / kg / day in infants < 6 months; - 90 calories / kg / day in infants 6-12 months;

- 60 calories / kg / day of ideal weight under 12 years; - 850 Calories / day in teenager during the weightloss period,1000 calories / day after the initial period of minimum one month.

OBESITY: TREATMENTIn most obese children good results are obtained by decreasing initial caloric intake with 30%. Nutritional content of the diet:

- 20% proteins,- 40% carbohydrates, - 40% fats,- 5-6 meals / day, with the following distribution of calories: 20% at

breakfast, 30% at lunch, 20% at dinner and two snacks by 15% in 5 meals / day version and by 10% in snacks in the 6 meals / day version. Diet is suitable for inducing a weight loss of 0.5-2 kg / week.In obese infants, the treatment goal is not to reduce weight, but slowing down the rate of weight gain in relation to increasing waistline.

OBESITY: TREATMENT

b) physical activity: important role in weight loss programs (discrepancy between caloric intake and physical energy expenditure). Activitaty will be chosen according to the personality, preferences and abilities of the child. c) behavioral therapy: to correct the habits that caused weight excess and promote a healthy lifestyle. d) drug treatment: minor role. e) surgery: surgical techniques recommended for adult are not appropriate for child.

OBESITY:EVOLUTION AND PROGNOSIS

Prophylaxis should start from prenatal period by identifying parents with increased familial risk for obesity.

Factors that may influence the evolution and prognosis of obesity are: -etiology of obesity: endocrine obesity is refractory to dietary therapy versus exogenous obesity;-severity: more severe degrees respond poorly to therapy and have higher risk of complications; -during evolution: as the disease is aging, eating habits are harder to be influenced by therapeutic measures; -age: critical periods in the development of obesity are infancy, preschool and adolescent; -the response to dietary treatment.

OBESITY: EVOLUTION AND PROGNOSIS

Slimming regime favorable results are:- acquiring a feeling of well being, - lowering blood pressure,- improving heart function,- reducing the number of apneas / hour, increase

blood oxygen saturation and lung capacity, - decreased basal hyperglycemia and

hyperinsulinemia and reduced postprandial insulin resistance, relieving joints symptoms.

OBESITY: COMPLICATIONS

Complications of obesity: orthopedic complications: genu valgum, flat feet,

Blount disease, coxa vara, epiphysitis of femoral head, aseptic necrosis of the femoral head, hyperlordosis, leg pain after prolonged standing.

metabolic complications: dyslipidemia, hyperinsulinemia, insulin resistance, type II diabetes, hyperuricemia (rare).

OBESITY: COMPLICATIONShormonal complications: hiperandrogenemy,

menstrual cycle disorders, hypercortisolism reagent. respiratory complications: hypoventilation

syndrome, obstructive apnea during sleep, asthma. The extreme manifestation of alveolar hypoventilation is Pickwick syndrome.

cardiovascular complications: hypertension, right ventricular hypertrophy, coronary atherosclerosis or generalized atherosclerosis.

OBESITY: COMPLICATIONSdigestive complications: hepatic steatosis,

cholelithiasis, cholecystitis.psychological complications: neuro-cognitive deficits,

feelings of inferiority, family conflict, social isolation, school problems, truancy, emotional and mental immaturity.

endocrine complications: polycystic ovary disease. skin complications: fungal and bacterial skin

infections, trophic disorders of the lower limbs, nail dysplasia.