Overview of eating disorders
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OVERVIEW OF EATING DISORDERS. Dr. Gillian Baksh Monday Meeting February 2011. USE OF TERMS. EATING DIFFICULTY. FEEDING DISORDER. EATING DISTRESS. EATING DISTURBANCE. EATING DISTURBANCE. FEEDING PROBLEM. EATING PROBLEM. FEEDING DIFFICULTY. FEEDING DISTURBANCE. EATING

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Overview of eating disorders

OVERVIEW OF EATING DISORDERS

Dr. Gillian Baksh

Monday Meeting

February 2011


Use of terms

USE OF TERMS

EATING

DIFFICULTY

FEEDING

DISORDER

EATING

DISTRESS

EATING

DISTURBANCE

EATING

DISTURBANCE

FEEDING

PROBLEM

EATING

PROBLEM

FEEDING

DIFFICULTY

FEEDING

DISTURBANCE

EATING

DISORDER


Diagnosis and classification

DIAGNOSIS AND CLASSIFICATION

  • ‘True Eating Disorder’ – grossly disordered or chaotic eating behaviour associated with morbid preoccupation with body weight and shape (irrespective of weight)

  • Eating difficulty / problem – not associated with clinically significant functional or developmental impairment


True eating disorders

TRUE EATING DISORDERS

  • AN

    ▪ Restricting or binge-purge subtypes (DSM 1V)

  • BN

    ▪ Purging and non-purging subtypes (DSM 1V)

  • Related atypical or not otherwise specified forms

    ▪ EDNOS (DSM 1V)

    ▪ Atypical AN and atypical BN (ICD 10)


Other eating disorders

OTHER EATING DISORDERS

  • Selective eating

  • Restricted / minimal eating

  • Phobia associated with limited intake

  • Functional dysphagia

  • Food avoidance emotional disorder (FAED)

  • Food refusal

  • ?Pervasive food refusal syndrome

  • Overeating associated with obesity


Eating disorders in children

EATING DISORDERS IN CHILDREN

  • Not developmentally sensitive

  • Do not consider parental observed behaviours

  • FAED = Non-fat phobic ED – not classifiable in DSM as an ED

  • Mismatch between diagnostic categories and clinical presentations

  • DSM V and ICD 11

EDNOS or

ATYPICAL

FAED

AN

BN


Dsm v vs icd10 clinical eating disorders

DSM ΙV (Amer Psych Assoc1994)

AN restricting and binge-purge subtypes

BN purging and non-purging subtypes

EDNOS (clinically severe but does not meet criteria for AN, BN)

Feeding disorder of infancy or early childhood (onset before 6 years)

Pica

Rumination disorder

ICD 10 (WHO 1992)

AN

BN

Atypical AN and atypical BN

Other :

- Overeating associated with other psychological disturbances

- Vomiting associated with other psychological disturbances

- Other eating disorders

- Eating disorder, unspecified

Feeding disorder of infancy and childhood

Pica of infancy and childhood

DSM ΙV vs ICD10 CLINICAL EATING DISORDERS


Anorexia nervosa in children

ANOREXIA NERVOSA IN CHILDREN

  • First described in late 19th century

  • Defined from (6 –) 8 years

  • Weight loss at least 15% below normal weight for age and height

  • Weight control behaviours mainly dietary restriction and exercise, laxatives, vomiting

  • Older patients binge-purge (20-30% BN past history of AN)

  • Abnormal cognitions regarding weight and / or shape

  • Sometimes difficult to elicit explicit weight / shape psychopathology

  • Food preoccupations, guilt around eating, concern about eating with others, low self esteem common

  • In boys (10-25%) often concern around fitness and health – shape more than weight – excessive exercise more common - OCD commonly associated


Bulimia nervosa

BULIMIA NERVOSA

  • Requires degree of psychological maturation including capacity for self evaluation often manifest as shame or guilt

  • Rare under 13 years

  • Abnormal cognitions regarding weight and / or shape

  • Can arise out of anorexia or secondary to repeated dieting behaviour

  • Recurrent binging and inappropriate compensatory behaviours occur at least x2 per week for 3 months

  • Compensatory behaviours- purges, food restriction, excessive exercise– laxative/enema/appetite suppressant misuse more common in older adolescents

  • Sense of lack of control & chaos

  • May be associated with other teenage problem behaviours – drinking, self harm, casual sex, drugs


Differential diagnosis

DIFFERENTIAL DIAGNOSIS


Epidemiology

EPIDEMIOLOGY

AN

  • Incidence

    - 4.2 – 8.3 / 100 000 (Currin et al,Hoek et al)

    - 40% between 14 – 19 years

    - 1.2/ 100 000 hospitalised

  • Stable over time ? except young

  • Prevalence

    - average 0.3% ( 0-0.9%)

    - 0.4 % adolescent girls

    - lifetime 1.4 – 2.2 %

3-12% of adolescents experience some form of eating disorder – most EDNOS (Machado 2007; Slice et al 2009)

-

BN

  • Incidence

    - 6.6 – 13.5 / 100 000

  • More sensitive to global environmental changes - possibly decreasing from peak in 1990’s (Currin et al, BJ Psych 2005)

  • Prevalence

    - average 1% (similar to schizophrenia)

    - lifetime 4 -7%


Prognosis and outcome

PROGNOSIS AND OUTCOME

  • Predictors of outcome of EDs – mixed results

  • Fair degree of association of morbid family functioning and poor prognosis in AN regardless of age

  • At 2 years – 33% fully recovered, 27% still full AN (Toucan study)

  • Adolescents do slightly better than adults – 75% or more fully recover

  • Children < 11years may do worse – only 2 studies


Recovery an

RECOVERY AN

? 30 %

11 – 27 %

ADOLESCENT ONSET

ED

ADULT ONSET

ED

CHILDHOOD

ONSET ED

Depression / OCD/

Other axis 1

diagnosis

Halvorsen et al 2003

Raastam et al 2003

Patton et al 2003


Mortality

MORTALITY

  • Mortality AN 0% – 22 % depending on follow up period

  • Crude mortality: 4% AN, 3.9% BN, 5.2% EDNOS

  • 3x more likely to die of a childhood or adolescent ED than any other causes

  • AN – 12x annual death rate from all causes in 15 – 24 year females (physical complications &suicide)

  • Highest mortality (2%) in the first year after presentation in females and in the first 2 years (5%) after presentation in males


Overview of eating disorders

EATING DISORDERS ARE SERIOUS

AND NEED TO BE TAKEN SERIOUSLY


Helpful sites

HELPFUL SITES

  • B-EAT

  • http://www.youtube.com/watch?v=K5WZv8PrTRo

  • http://sites.google.com/site/marsipannini

  • www.rcpsych.ac.uk/files/pdfversion/CR162.pdf


Genes

GENES

  • Family studies- female relatives of someone with an ED are >x4 risk of BN and >x11 risk AN than someone with no family history (probably higher for subclinical and partial syndromes)

  • Twin studies – (MZ:DZ concordance) – AN has estimated heritability of 58 -76 %, BN from 31 – 83%

  • Puberty may activate some aspect of genetic heritability (Klump et al)

  • A 7% increased incidence in first degree relatives may be related to area on chromosome 1p at the DF1153721 locus (Grice et al 2002)


Biopsychosocial models of risk and maintenance

BIOPSYCHOSOCIAL MODELS OF RISK AND MAINTENANCE

  • Physical and nutritional status

  • Temperament

  • Self esteem,values,personal identity

  • Emotional processing and literacy

SOCIAL

INDIVIDUAL

  • Life events

  • Peer relationships

  • Media influence

SYSTEMIC

Predisposing

Precipitating

Perpetuating

  • Genetic

  • Family beliefs re weight,shape,

  • eating


Overview of eating disorders

MALNUTRITION IS A MEDICAL EMERGENCY


Medical complications

MEDICAL COMPLICATIONS

Underweight

  • CVS: ECG (low voltage;sinus bradycardia;T wave inversions:ST depression-electrolyte imbalance:prolonged QTc), dysrhythmias(SV ectopics, VT), pericardial effusions – all reversible except following ipecac use

  • Growth and development: pubertal and growth delay, 1˚ amenorrhoea, delayed bone mineral accretion

  • Dietary deficiencies: calcium, vit D , folate, B12

  • GIT: delayed gastric emptying, ↓gastric motility, constipation, bloating, fullness, abnormal LFTs, hypercholesterolaemia, pancreatitis,abnormal LFTs(fatty infiltration):superior mesenteric artery syndrome– all reversible

  • Renal: dehydration, ↓GFR, stones, polyuria, total body Na and K depletion; peripheral edema with refeeding

  • Haematologic: leukopoenia, anaemia, thrombocytopoenia, iron deficiency

  • Endocrine: sick euthyroid syndrome, amenorrhoea, osteopoenia

  • Neurologic: cortical atrophy, seizures


Medical complications1

MEDICAL COMPLICATIONS

Purging / Binging

  • Fluid and electrolyte imbalance: ↓K and Na, hypochloremic alkalosis

  • Use of ipecac: irreversible myocardial damage and diffuse myositis

  • Chronic vomiting: esophagitis, dental erosions, parotitis, Mallory-Weiss tears, oesophageal or gastric rupture, aspiration pneumonia

  • Use of laxatives: dehydration, renal stones, metabolic acidosis, ↓Ca and Mg, ↑uric acid – withdrawal may get fluid retention (up to 4 kg in 24 hours)

  • Amenorrhoea (may see in normal or overweight with BN): menstrual irregularities, osteopoenia


Cardiovascular

CARDIOVASCULAR

  • Cardiac death – 1/3 all deaths in adults

  • Cardiac deaths unknown in paediatrics

  • ↓ PR- ↓ vagal tone, ↓ BMR- aim to ↓cardiac output and preserve energy and reduce demand on malnourished heart

  • ↓ BP –myocardial atrophy

  • Orthostatic changes – leg and heart muscles

  • ECG – electrolytes

  • Changes reversible with weight restoration

  • Caution with fluids – boluses often unnecessary and can be dangerous


History

HISTORY

  • Detailed feeding history

  • Duration eating concerns

  • Rapidity weight loss - > 1 kg/week serious risk

  • Current intake & pattern including fluids

  • Use laxatives, diuretics etc

  • Weight / shape cognitions

  • Sleep pattern

  • Menstrual history / pubertal progression

  • Co-morbid mental illness (anxiety, phobia, OCD, depression)

  • Personality description from relatives

  • Suicidal ideation, DSH, overdose

  • Symptoms of hyperthyroidism, diabetes, malignancy, IBD, tumour etc

  • Symptoms related to complications – acute and chronic


History1

HISTORY

  • Family and social history – ED , mental illness

  • Female relative of someone with an ED is > x4 likely to have BN and > x11 likely to have AN than someone with no family history

  • Activities / exercise

  • School attendance

  • Relationships


Medical assessment

MEDICAL ASSESSMENT

  • History

  • WFH / BMI

  • Temp

  • Urine

  • Examination:

    -haemodynamic stability – lying / standing BP & PR

    -pubertal status

    -signs of malnutrition

    -signs of possible underlying medical condition

  • SUSS Test – stand up sit up test

  • Investigations


Examination

EXAMINATION

  • Oversized clothes

  • Muscle wasting / lack subcutaneous fat

  • Cold extremities, cyanosis

  • Anaemia

  • Dehydration

  • Murmurs, arrythmias, weak pulse

  • Lanugo, dull thin scalp hair

  • Signs binging / purging: Russell’s sign, palatal scratches / petechiae, dental erosions, parotitis

  • Signs of vitamin and mineral deficiency: anaemia, dry/sallow skin, carotenaemia , glossitis, lip fissures, bleeding gums, brittle nails, Chvostek’s sign, Trousseau’s sign

  • Look for signs to help rule out possible underlying medical condition


Bmi and weight for height

BMI AND WEIGHT FOR HEIGHT

  • Weight loss – loss fat and muscle

  • A low BMI more strongly correlated with lean muscle mass than fat mass (Cole et al BMJ 2007)

  • BMI:

    - Adults concern if BMI < 17.5

    - Adults severe malnutrition cut off BMI =13

  • WFH : % Median BMI= Actual BMI / Median BMI (50th percentile for age & sex) x 100

  • WFH 100% = BMI 50th centile


Overview of eating disorders

WFH

  • Be concerned if WFH < 90% = BMI < 9th centile – stop exercise

  • Be very concerned WFH 80% = BMI < 2nd centile (definition of underweight) – stop school

  • Consider hospitalisation if WFH < 75%


Diagnostic decision tree

DIAGNOSTIC DECISION TREE

YES

NO

YES

YES

NO

NO

NO

YES

NO

YES

YES


Investigations

INVESTIGATIONS

  • Baseline bloods including clotting, Ca, PO4, Mg, HCO3, iron studies, folate, B12, Vit D, amylase, ESR, CRP,TFTs, lipids, glucose

  • ECG

  • Urinalysis

  • Wrist Xray - Bone age and density

  • Pelvic USS

    Consider:

  • DEXA scan

  • CXR

  • Abdominal Xray

  • MRI / CT scan

  • Autoimmune, coeliac screen

  • Cardiac ECHO

    DON’T BE FALSELY REASSURED BY NORMAL BLOOD RESULTS


Medical treatment

MEDICAL TREATMENT

  • When to hospitalise / inpatient treatment?

  • Weight recovery usually 2 – 3 kg per month

  • Target weight : WFH 95 – 110%

  • Resumption of growth and / or menses are better indicators of recovery than targets


Eds and guidelines evidence base

EDs and GUIDELINES/ EVIDENCE BASE

  • Clinical guidelines (e.g. NICE 2004) mostly based on consensus views

  • NICE guidelines developed to advise on the identification, treatment and management of AN, BN, and related conditions in those 8 years and over

  • EDNOS may not be same as in adults

  • Guidelines do not cover other eating disturbances

  • Evidence for effectiveness of treatments weak across age range (5RCT : 3 AN, 2 BN)

  • No large scale randomised controlled drug trials for AN

  • MARSIPAN (2010) and Junior MARSIPAN(2011)

    http://www.rcpsych.ac.uk/files/pdfversion/CR162.pdf

    Nicholls D, Hudson L, Mohamed f. Arch Dis Child. 2010 Oct 7. (Epub) Managing anorexia nervosa


Inpatient treatmant

INPATIENT TREATMANT

  • 1 in 4 AN will be hospitalised

  • The need for inpatient treatment for AN and the need for urgent weight restoration should be balanced alongside the educational and social needs of the young person (NICE)

  • Admit locally and in age appropriate setting (NICE)

  • Do not isolate

  • Attend school


Overview of eating disorders

INDICATIONS FOR HOSPITALISATION IN AN ADOLESCENT WITH AN EATING DISORDER(Society for Adolescent Medicine position paper Dec 2003)

One or more of the following:

  • Wt for ht ≤ 75%

  • Dehydration

  • Electrolyte disturbance (hypokalaemia, hyponatremia, hypophosphataemia, hypomagnesemia)

  • Cardiac dysrhythmia

  • Physiological instability

  • Severe bradycardia (< 50 b/min day; < 45 b/min night)

  • Hypotension (< 80/50 mm Hg)

  • Hypothermia (< 35 ˚C)


Overview of eating disorders

INDICATIONS FOR HOSPITALISATION IN AN ADOLESCENT WITH AN EATING DISORDER(Society for Adolescent Medicine position paper Dec 2003)

  • Orthostatic changes in pulse (↑> 20 b/min) or ↓ BP (> 10 mm Hg systolic) from lying to standing

  • Arrested growth and development

  • Failure of outpatient treatment

  • Acute food refusal

  • Uncontrollable binging and purging

  • Acute medical complications of malnutrition ( e.g. syncope, seizures, cardiac failure, pancreatitis etc.)

  • Acute psychiatric emergencies (e.g. suicidal ideation, acute psychosis)

  • Co-morbid diagnosis that interferes with the treatment of the eating disorder (e.g. severe depression, OCD, severe family dysfunction)


Medical inpatient treatment

MEDICAL INPATIENT TREATMENT

  • Difference between stabilisation and refeeding

  • Food= medicine therefore need to be helped to eat

  • Support for nurses

  • Admission may give the wrong message to patient and family

  • Autistic spectrum disorder patients fare badly when admitted

  • Studies on outcome following admission – patients admitted are very ill or don’t do very well


Refeeding

REFEEDING

  • Parents helped to take responsibility

  • Establish parental control of food and fluid intake

  • Patient encouraged to negotiate the “how” of food intake and not the “whether”

  • Consistency of approach


Refeeding1

REFEEDING

  • Aim for 0.5 -1.0 kg weight gain per week

  • At least 500 – 1000 Kcals above basic requirement

  • Inpatients may need 3000 Kcals /d

  • Start at 15 – 20 Kcal/kg/d

  • Avoid underfeeding syndrome

  • NICE: refeeding is a necessary component but is not sufficient

    - refeeding against the will of a patient is a highly specialised procedure requiring expertise – Mental Health Act 1983, Children Act 1989, (Mental Capacity Act 2007)


Refeeding syndrome

REFEEDING SYNDROME

  • Oral, enteral, parenteral route

  • Refeeding: → insulin surge → extracellular to intracellular phosphate, magnesium, potassium, glucose, water

  • Cardiovascular, neurologic, haematologic complications

  • Can cause prolonged QTc or variable QTc

  • Can be associated with significant morbidity and mortality

  • Usuallly 4-6 days after refeeding started

  • Highest risk : WfH <75%, BMI < 13,laxative use, diabetics, too rapid feeding, abnormal electrolytes (Glucose, Na, K, PO4, Ca at start)

  • Start Thiamine 50 – 200mg bd (necessary for utilisation glucose in Krebs cycle)

  • Daily bloods and ECG for 1 week then alternate days for 1 week

  • Daily physical assessments and weights


Inpatient treatment an

Short term

Physical evaluation and stabilisation

Reestablishment of food intake

Risk assessment

Relief of patient, parent, professional anxiety

Assessment of treatment needs

Long term

Establish healthy body weight

Identify and manage emotions

Develop new coping skills

Develop communication skills

Develop peer relationships

Learn to use help

Reintegrate to home or other environment

INPATIENT TREATMENT - AN


Inpatient treatment bn

INPATIENT TREATMENT - BN

  • Not used in adults as a rule

  • Means of breaking cycles of binge / purge and establishing regular eating patterns

  • Related to risks of other self-harming behaviours

  • Related to severity of other co-morbid illness


Psychology

AN

Avoidance, anxiety, obsessionality

Vicious circle of restraint

Need for control is central

Egosyntonic – rarely seek voluntary treatment

BN

Impulsivity, emotionality, chaos

Vicious circle of failed restraint

Need for control is central

Depressed by behaviour

Egodystonic – more motivated but ambivalent about weight gain

PSYCHOLOGY


Physical effects of an on brain

PHYSICAL EFFECTS OF AN ON BRAIN

  • Cortical atrophy and ventricular enlargement

  • Secondary to starvation

  • Reverse with restoration of adequate nutrition


Functional effects of an on brain

FUNCTIONAL EFFECTS OF AN ON BRAIN

  • Significantly reduced activity in antero-medial temporal region (insula)

  • Correlates with neuropsychological findings

  • Does not correlate with BMI, mood, length of illness nor cerebral dominance

  • No reversal with nutritional restoration

    Gordon et al 1997, Chowdhury et al 2003, Key et al 2004, Lask et al 2005, Agrawal and Lask 2009, Brewerton et al 2009, Frampton et al 2010


Functions of the insula

FUNCTIONS OF THE INSULA

  • Regulates the ANS (anxiety)

  • Regulates appetite and eating

  • Monitors the gut (sense of fullness / emptiness)

  • Monitors body image

  • Reception, perception and integration of taste

  • Perception and integration of disgust

  • Perception of pain

  • Integrates thoughts and feelings

  • Awarenass of illness

  • Social awarenaee

  • Global processing

  • Motivation


Overview of eating disorders

BRAIN FUNCTION

IN AN

UNLIKELY THAT EACH OF THESE IS NOT FUNCTIONING CORRECTLY


Therapy

THERAPY

  • Family therapy

    - family members including siblings should normally be included in the treatment of children and adolescents with EDs (NICE)

  • Multi- family therapy

  • Individual therapy

    - child should be offered individual sessions with professional separate from family worker (NICE)

  • Adolescent focussed therapy

  • Interpersonal therapy

  • Directed behaviour therapy

  • Group therapy

  • CBT –

    - adolescents with BN may be treated with CBT, adapted as needed to suit their age, circumstances and level of development (NICE)

    - some suggest if WFH < 80% should avoid

  • Motivational enhancement therapy

  • Cognitive remediation therapy – focuses on the process (how) rather than the content (what) of thought and perception


Parents

PARENTS

  • Sense of guilt, self-blame

  • Sense of failure

  • Mistrust for professionals

  • May reject child in response to ED

  • View ED as a personal attack on them as parents

  • No empirical evidence to suggest that families cause EDs, but no doubt that families becomes dysfunctional in response to ED

  • Engaging parents as important as engaging child


Therapy1

THERAPY

DOCTOR

Parent & patient relieved

of anxiety

Patient relieved of internal conflict

Reinforces parents’ sense of failure

PARENT

PATIENT


Long term physical sequelae

LONG TERM PHYSICAL SEQUELAE

  • Growth

  • Bone density

  • Puberty


Growth

GROWTH

  • Important in boys and prepubertal girls

  • Slows / stops in starvation

  • No weight gain = weight loss

  • ‘Catch-up growth’- may be first sign of a healthy weight

  • The ‘dose’ of starvation needed to have a permanent effect on height is 4 years before completion of growth


Linear growth

LINEAR GROWTH

  • Retardation may be related to –

    - ↓ T4, T3

    - ↑ cortisol

    - ↓ sex hormones

    - relative resistance to GH

  • Catch up growth with weight restoration

  • Variable reports of effect on final height versus height potential


Bone mineral density

BONE MINERAL DENSITY

  • Changes start early in disease

  • Impaired bone formation and increased absorption

  • Factors:low oestrogen & IGF1

    high cortisol

    poor nutrition, low BMI

    low Ca and Vit D

  • Greatest risk:> 12 months onset AN

    > 6months amenorrhoea

    low BMI

    low Ca intake

    low physical activity (Castro et al 2000)


Bone density

BONE DENSITY

  • Mainstay treatment – weight gain, nutritional rehabilitation, spontaneous resumption menses

  • Oestrogen administration should not be used to treat bone density problems in children and adolescents as this may lead to premature fusion of the epiphyses (NICE)

  • Ca and Vit D supplements may be prescribed

  • Full recovery unlikely – osteopoenia in 1/3 recovered AN

  • Long term fracture risk around x3 –x7 of general population


Puberty

PUBERTY

Menses:

  • Clearest marker of adequate endocrine function

  • Pubertal delay / arrest almost inevitable with WFH < 90%

  • Pelvic USS more sensitive than other hormone markers and not susceptible to diurnal variation

    - regression in size uterus and ovarian activity

    - experienced ultrasonographer

    - can be used to guide weight restoration and determine onset of menses

  • No use in boys!

  • May not return until 6 months after achieving appropriate weight (about 95% WFH)


Outcome

OUTCOME

  • Response to treatment – difficult to distinguish from natural course as treatment almost invariably ensues and limited on untreated cases

  • Remission

  • Recovery

    Remission and recovery similar for AN since relapse rare


Prognosis and outcome1

PROGNOSIS AND OUTCOME

  • Predictors of outcome of EDs – mixed results

  • Fair degree of association of morbid family functioning and poor prognosis in AN regardless of age

  • At 2 years – 33% fully recovered, 27% still full AN (Toucan study)

  • Adolescents do slightly better than adults – 75% or more fully recover

  • Children < 11years may do worse – only 2 studies


Poor outcome

POOR OUTCOME

  • Continuing illness associated with functional impairment or death

  • Lower body fat at presentation (Mayer et al. Am J Psych 2007)

  • Longer duration illness

  • Hospitalised (Gowers et al. B J Psych 2007)

  • Readmitted (up to 45%) (Steinhausen 2007)


Mortality1

MORTALITY

  • Mortality AN 0% – 22 % depending on follow up period

  • Crude mortality: 4% AN, 3.9% BN, 5.2% EDNOS

  • 3x more likely to die of a childhood or adolescent ED than any other causes

  • AN – 12x annual death rate from all causes in 15 – 24 year females (physical complications &suicide)

  • Highest mortality (2%) in the first year after presentation in females and in the first 2 years (5%) after presentation in males


Helpful sites1

HELPFUL SITES

  • B-EAT

  • http://www.youtube.com/watch?v=K5WZv8PrTRo

  • http://sites.google.com/site/marsipannini

  • www.rcpsych.ac.uk/files/pdfversion/CR162.pdf


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