OBESITY AND OVERWEIGHT DR. MD ABU SAYEED MULLICK - PowerPoint Presentation

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OBESITY AND OVERWEIGHT

DR. MD ABU SAYEED MULLICK

MBBS. MD(PEDIATRICS)

Slide2

DEFINITIONS

Diagnostic criteria to classify overweight and obesity

AGE

0-2 YEARS

2-5 YEARS

>5 YEARS

INDEX

WEIGHT FOR LENGTH

WEIGHT FOR HEIGHT

BMI

REFERENCE

WHO

WHO

IAP

OVERWEIGHT

> +2 SD and =< +3 SD

>+2 SD and =< +3 SD

>23 Adult equivalent

OBESITY

> +3 SD

> +3 SD

>27 Adult equivalent

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ETIOLOGY

Slide4

History

Slide5

ENDOCRINE CAUSES

Slide6

GENETIC CAUSES

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PRADER WILLI SYNDROME

Rawat Ankur, Shaw Subhash Chandra, Kalra

Suprita

, Gupta Rakesh;

Prader–Willi syndrome: A syndromic cause of morbid obesity; Journal of maritime medical society;

Year : 2018 | Volume:  20 | Issue Number:  1 | Page: 76-78

A Rare Association of Obesity, Diabetes Mellitus and Bilateral Cryptorchidism: Prader - Willi Syndrome

Journal of Association of Physicians of India,

November 2016 

•

 Vol. 64 

  

Sridhar Subbiah1, Rakesh Chinnathurai2,

Jeyaraman

Sangumani2, S Somasundaram1

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BARDET-BIEDL SYNDROME ()

REF:

Kalathia

, Parikh, Parmar, Verma. (2014). Rare cause of

pediatric

obesity: Bardet - Biedl Syndrome. Medical Journal of Dr. D.Y. Patil University. 7. 198. 10.4103/0975-2870.126341.

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CARPENTER SYNDROME

CLOVER LEAF SKULL

Flattened nasal bridge , proptosis

Hypertelorism, cleft lip/palate

polydactyly

syndactyly

Absence of corpus callosum

consanguineous marriage, genu

valgum

, facial hypoplasia,

mental retardation,

congenital heart disease, obesity, bilateral cryptorchidism,

hearing loss,

o

mphalocele or umbilical hernia

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COHEN SYNDROME

1.M

icrocephaly 2.

O

pen mouth 3.Prominent central

incisors

4.T

hick pouting lower lip

5. High nasal bridge

6.

Malar hypoplasia – prominent nose

5.Truncal

obesity

S

lender fingers tapering from PIP.

E

xaggerated gap between first and second toes ; bulbous big toe.

Neonatal hypotonia with feeding difficulties; failure to thrive in infancy and childhood; truncal obesity

during puberty

; developmental delays and learning difficulties; microcephaly from the first year of life; psychomotor retardation; early onset myopia and a progressive pigmentary retinopathy; neutropenia with recurrent infections.

Ref: Chandler KE

, et al

;

Diagnostic criteria, clinical characteristics, and natural history of Cohen syndrome;

Journal of Medical Genetics 

2003;

40:

233-241.

Ref:

sathish

kt,

xavier

sj

,

Cohen syndrome

Indian Journal of Human Genetics, Vol. 11, No. 1, January-June, 2005, pp. 49-50

Ref: Said

Alavi

, A.

Kher

, A. Kumar, M.

Muranjan

and B.

Bharucha

;

Cohen syndrome

 

-

Indian Pediatrics - May 1993, Vol. 30, Number 5, p-678-680

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ALSTROM SYNDROME

Ref : M S, R.,

Rajan

, M.G., A, P. 

et al.

 

Alstrom

syndrome—a diagnostic dilemma. 

Int J Diabetes Dev

Ctries

 

37, 

88–91 (2017).

Early onset blindness - Congenital progressive cone-rod retinal dystrophy

Sensorineural deafness with h/o

f

requent serous otitis media

Truncal obesity

Hyperinsulinemia, Type 2 diabetes and acanthosis nigricans

Hypertriglyceridemia leading to pancreatitis.

Hypothyroidism and hypogonadism

Gynecomastia and reduced fertility

Childhood obesity

Acanthosis Nigricans

Flat feet

Features

Alstrom

Bardet-Biedl

Visual impairment

+

+

SNHL

+

-

Short Stature

+

+/-

Diabetes mellitus

+

+

Hypogonadism

+

+

Hypertriglyceridemia

+

-

DCM

+

-

Poly/

Syn

-

dactyly

-

+

Mental delay

-

+

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Leptin-melanocortin pathway

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Leptin/LEPR/POMC/MC4R mutations

Gene

Mutation type

Obesity

Associated phenotypes

Leptin

Homozygous mutation

Severe, from the first days of life (major hyperphagia and ravenous hunger)

Gonadotropic and thyrotropic insufficiency Alteration in immune function

LEPR

Homozygous mutation

Severe, from the first days of life (major hyperphagia and ravenous hunger)

Gonadotropic, thyrotropic and somatotropic insufficiency Alteration in immune function

POMC

Homozygous or compound heterozygous

Severe, from the first months of life (major hyperphagia and ravenous hunger)

ACTH insufficiency Mild hypothyroidism and ginger hair if the mutation leads to the absence of POMC production

MC4R

Usually heterozygous

Severe obesity (major hyperphagia and ravenous hunger)

Acanthosis nigricans or signs of hyperandrogenism (in girls), , early puberty, increased linear growth tall stature, a lower tendency for developing hypertension, hypothyroidism

Rare monogenic forms of human obesity

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HEALTH CONSEQUENCES

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CLINICAL EXAMINATION

Pubertal stage (e.g. using Tanner staging) ,

Micropenis

(GH deficiency, hypogonadism), Undescended testis (Prader-Willi Syndrome)

Acne and hirsutism ,

Menstrual irregularity (<9 cycles per year)

- PCOD

Check for hypertension

Dysmorphic facies, developmental delay (Genetic syndromes)

Small hands and feet (Prader Willi or Albright’s Hereditary Osteodystrophy), Polydactyly (Bardet-Biedl syndrome)

Morning headache, transient visual loss, visual field defects (potential benign intracranial hypertension)

Bowing of legs, limp, limited hip range of motion (Orthopedic problems)

Fundus -

Papilloedema

(

Pseudotumour

cerebri)

,

Retinitis pigmentosa (Bardet-Biedl syndrome)

GI symptoms with H

epatomegaly - NAFLD

G

oitre

- Hypothyroidism

Acanthosis nigricans,

skin

tags, keratosis pilaris

- significant insulin resistance

Short stature, a low growth velocity, (may indicate an endocrine cause for weight gain)

, Moon facies, buffalo hump, or bruising or purple striae -

Cushings

Skin and hair– Dry and brittle hair are seen in hypothyroidism, ginger or red hair in POMC mutation; dry and coarse skin in hypothyroidism.

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THE

APPROACH

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Investigations

Cause

Disease

Laboratory

ENDOCRINE

Cushing Syndrome

Dexamethasone Suppression Test

GH Deficiency

Evoked GH response, IGF-1

Hyperinsulinism

Insulin, C-peptide

Hypothyroidism

FT

4

, TSH

Pseudohypoparathyroidism

Ca, PO4, Urine cAMP after synthetic PTH

GENETIC

Prader Willi Syndrome

DNA methylation, partial deletion of

chr

15

Bardet-Biedl Syndrome

BBS1 gene

Carpenter Syndrome

RAB 23 gene mutation

chr

6

Cohen Syndrome

VPS13B gene mutation

chr

8

Down Syndrome

Trisomy 21 karyotyping

Turner Syndrome

XO karyotyping

FTO gene polymorphism

Homozygous FTO allele

MC4R mutation

MC4R mutation

POMC deficiency

POMC loss of function mutation

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Investigations For Comorbidities

FBS, HbA1C, insulin and c-peptide level, OGTT - Type 2 DM

Fasting Total Cholesterol, HDL, LDL, TG –

Dyslipidemia

Fasting glucose, LDL , HDL – Metabolic Syndrome

Pelvic USG, Free testosterone , LH, FSH – PCOS

Abdominal USG, AST, ALT – Gall bladder disease, NAFLD

Knee and Hip Radiographs – Blount Disease, SCFE

CSF opening pressure, CT, MRI – pseudotumor cerebri

Pulmonary function tests – Asthma

Polysomnography – Obstructive sleep apnoea

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SCREENING

Screening with fasting glucose, fasting lipid profile and liver enzymes (ALT, AST) is recommended in children with BMI ≥85th percentile and any two risk factors (acanthosis nigricans, PCOS or family history of diabetes/cardiovascular disease) or those with BMI ≥ 95th percentile.

Screening

should start at puberty or 10 y of age and then 2 yearly

Patients with ALT or AST values more than two times upper limit of normal on two occasions require evaluation by an ultrasound abdomen.

(Ref :

Barlow SE, Expert Committee. Expert committee recommendations regarding the prevention, assessment, and treatment of child and adolescent overweight and obesity: summary report. Pediatrics.

2007;120:S164–92.)

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MANAGEMENT for Obesity/Overweight

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Dietary Modification

A planned diet with balanced macronutrients, in proportions consistent with Recommended Daily Allowances

Structured daily meals and planned snacks (preferably home-made)

Diet restriction should not hamper pubertal growth spurt

Minimize sugar-sweetened beverages (ideally eliminated)

Avoid energy dense and low nutrient dense fast foods

Preferred home-made meals rather than restaurant

A healthy breakfast every day

Fruits and vegetables every day

Diet rich in

fibre

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Dietary strategies

VERY LOW CALORIC DIET-

protein-sparing modified fast

(600–800 kcal/day, protein 1.5–2 g/kg ideal weight, carbohydrates 20–25 g/day, multivitamins + minerals, water

> 2000 ml/day), in selected patients

with severe obesity, under close medical surveillance and in specialized pediatric centers.

The aim is to

induce rapid weight loss (duration of this restrictive diet no longer than 10 weeks) followed by a less restrictive

diet regimen balanced in macronutrients.

TRAFFIC LIGHT AND MODIFIED TRAFFIC LIGHT DIET

- Reduced caloric intake (1000–1500 kcal/day) is achieved through categories of foods grouped by nutrient density

NON-RESTRICTIVE APPROACH

-

It does not consider a given caloric intake or nutrient composition, rather it focuses on the consumption of low-fat and high-nutrient density foods

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Behavioral Modification

Family members eat at the table along with the child as a family

Involve the whole family in lifestyle changes

Reduce frequency of snacking in between meals

Vigorous physical activity - begin with 15 minutes per day and work up to at least 60 minutes

Reduction of television and other screen time to 1 hour per day (not more than 2 hours per day for children above 2 yrs of age and no screen time for less than 2 years)

Improvement in routine activity patterns, such as walking to school or performing yard work

Cognitive behavioral techniques - goal setting, self-monitoring (through food and physical activity diaries), contingency training, stimulus control, positive reinforcement, cognitive restructuring, problem solving

Improvement of the home environment

Motivation of the child

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Pharmacotherapy – FDA Approved

Ref :

Farello

G, Patrizi F,

Tambucci

R,

Verrotti

A (2018) Drug Therapy of Childhood Obesity. J

Nutr

Food Sci 8: 702

Drugs

Mechanism of action

Average weight loss

Age of use

Side effects

ORLISTAT

Inhibition of gastric and pancreatic lipases

2,4% (after 4 year of treatment)

>12 years old

Fecal urgency, fecal incontinence, flatulence with discharge, oily stools.

. Interferes with the absorption of fat-soluble vitamins. Hepatic and renal damage in adults

METFORMIN

Decrreased

appetite, intestinal glucose uptake and hepatic gluconeogenesis, increasing insulin sensitivity

3% (after 6-12 months of therapy)

>18 years old

Vomiting, nausea,

diarrhea

PHENTERMIN/

TOPIRAMATE

Phentermine - noradrenergic agonist, topiramate- GABA agonist; anorectic effect and increases energy expenditure

5% (after 1 year of treatment)

>18 years old

Dry mouth, Constipation, insomnia, cognitive dysfunction, headache, nausea, vomiting, anxiety.

LORCASERIN

5-HT2C receptor agonist inhibits food

behaviour

5% (after 1 year of treatment)

>18 years old

Headache, nausea, nasopharyngitis, Symptomatic hypoglycaemia in patients with T2DM. Euphoria, hallucinations, abnormal dreams and impaired perception

NALTREXON/

BUPROPION

Naltrexone - opioid antagonist.

Bupropion inhibits norepinephrine and dopamine transporters

6,4% (after 56 weeks of treatment)

>18 years old

Constipation, nausea, vomiting, headache, dry mouth, dizziness, diarrhea and insomnia. an increased risk of suicidal thoughts and neuropsychiatric symptoms

LIRAGLUTIDE

(

semaglutide

)

GLP-1 receptor agonist.

Induces satiety by delaying gastric emptying and glucagon secretion, increased insulin

6%

>18 years old

Nausea, vomiting, diarrhea, and low blood glucoses and rarely kidney failure, suicidal impulse, pancreatitis, and gallbladder disease

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Pharmacotherapy (other drugs)

OCTREOTIDE

- inhibits secretion of gastric acid, pancreatic enzymes, and bile, prolongs intestinal transit time, and decreases gallbladder contractility

SETMELANOTIDE

– melanocortin-4 receptor agonist given by daily subcutaneous injection. It has received Breakthrough Drug Designation from the FDA for the treatment of obesity related to pro-opiomelanocortin (POMC) deficiency and leptin-receptor-deficient obesity.

Setmelanotide

is also being evaluated for the treatment of PWS, Bardet–Biedl syndrome,

Alstr

ӧ

m syndrome, POMC heterozygous deficiency obesity and POMC epigenetic disorders.

Hormone replacement therapy

– Leptin/POMC deficiency (leptin analogs)

GROWTH HORMONE

– Prader Willi Syndrome

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Bariatic Surgery

Gastric bypass or gastric banding.

Perioperative risks, post procedure nutritional risks, and the necessity of lifelong commitment to altered eating

BMI of 40 kg/m2 with a comorbidity or 50 kg/m2; physical maturity (Tanner IV or V pubertal development and final or near-final adult height); emotional and cognitive maturity; and weight loss efforts for 6 months in a behavior-based treatment program

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