MBBS MDPEDIATRICS DEFINITIONS Diagnostic criteria to classify overweight and obesity AGE 02 YEARS 25 YEARS gt5 YEARS INDEX WEIGHT FOR LENGTH WEIGHT FOR HEIGHT BMI REFERENCE WHO WHO ID: 908580
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Slide1
OBESITY AND OVERWEIGHT
DR. MD ABU SAYEED MULLICK
MBBS. MD(PEDIATRICS)
Slide2DEFINITIONS
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
Slide3ETIOLOGY
Slide4History
Slide5ENDOCRINE CAUSES
Slide6GENETIC CAUSES
Slide7PRADER 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
Slide8BARDET-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.
Slide9CARPENTER 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
Slide10COHEN 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
Slide11ALSTROM 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
-
+
Slide12Leptin-melanocortin pathway
Slide13Leptin/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
Slide14HEALTH CONSEQUENCES
Slide15CLINICAL 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.
Slide16THE
APPROACH
Slide17Investigations
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
Slide18Investigations 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
Slide19SCREENING
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.)
Slide20MANAGEMENT for Obesity/Overweight
Slide21Dietary 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
Slide22Dietary 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
Slide23Behavioral 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
Slide24Pharmacotherapy – 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
Slide25Pharmacotherapy (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
Slide26Bariatic 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
Slide27