85

Symposium : Gastroenterology & Hepatology

Crohn’s Disease
Malathi Sathiyasekaran and So. Shivbalan

Kanchi Kamakata CHILDS Trust Hospital and Sundaram Medical Foundation Hospitals, Chennai

ABSTRACT
Crohn’s disease is a chronic inflammatory disease of the gastrointestinal tract and is an important cause of morbidity in children
and adolescents. In India Crohn's disease (CD) was considered a rare disease, however, during the last 10 years CD in adults
is being reported from several centers especially in Southern India. CD is characterized by transmural granulomatous
inflammation involving any part of the gastrointestinal tract in a discontinuous manner. The peak incidence of Crohn’s disease
occurs during the adolescent and young adult years. The clinical presentation and complications are varied and several
extraintestinal manifestations have been recognized. The understanding of the pathophysiology has opened new avenues in
the management. The recognition of this problem in children and adolescents by pediatricians is necessary for proper diagnosis
and management. [Indian J Pediatr 2006; 73 (8) : 723-729] E-mail : ID:[email protected]

Key words : Crohn’s disease; Ulcerative colitis; Inflammatory bowel disease; Children

Crohn’s disease is an idiopathic, relapsing chronic This change in frequency of CD could be due to increased
inflammatory disease of the gastrointestinal tract awareness and availability of better diagnostic facility.
categorized as Inflammatory Bowel Disease (IBD) and is Some authors believe that the recent increase of CD in
an important cause of morbidity in children and India is not apparent but real and consider the improved
adolescents. IBD comprises of two important entities CD sanitation- hygiene hypothesis as an important etiological
and Ulcerative Colitis (UC) based on clinical, laboratory, factor.5
radiologic, endoscopic and histologic features. In 10% of CD can occur in all age groups and follows the same
cases the findings are non-specific and therefore termed bimodal pattern of age distribution as IBD. The
as indeterminate colitis (IC). 1 This subset of IBD has a proportion of patients with CD below the age of 20 years
propensity to progress to CD rather than to UC. varies between 25-40% with around 10% being less than
Approximately 25-30% of CD present before the age of 20 10 years of age.3 The mean age of presentation is about
years and therefore pediatricians need to recognize the 12.1 years. 6 Early onset IBD (EOIBD) i.e. presentation
varied presentations of this disorder2. before the age of 5 years, is a unique subgroup
constituting 4% of pediatric IBD. 2 In this subset it is
difficult to differentiate between UC and CD. In South
EPIDEMIOLOGY
India the youngest age of CD was 4.6 yrs and in their
series 90% were more than 9yrs of age. 7 CD is seen in
The incidence of CD in children is much less than that both sexes. In US there seems to be a preponderance of
seen in adults.3 It is more prevalent in Western countries CD in boys3 whereas in South India it was more prevalent
compared to Asia and Africa. The incidence of pediatric in girls. 7 The effect of breastfeeding and cigarette
CD range from 0.2 to 8.5 per 100,000.3 Recently there have smoking remains controversial. CD occurs with a higher
been reports of CD from Africa, China and Japan. In frequency in patients with Turner’s syndrome,
Singapore the incidence of CD in adults is 3.6 per 100,000.4 Hermansky-Pudlak syndrome, cystic fibrosis and
The incidence of CD is on the rise in children similar to the glycogen storage disease type 1B.8
trend seen in adults whereas UC has shown a more stable Crohn’s disease could represent a persistent infection
pattern. In India, recently there have been several reports with a fastidious organism or an abnormal and prolonged
of CD in adults5 whereas data on pediatric CD is sparse. response to a common pathogen. Various organisms have
been linked with CD but none of them are evident in the
etiopathogenesis. In genetically susceptible individuals
the microvascular injury caused by these infections could
result in a granulomatous vasculitis of the mesenteric
Correspondence and Reprint requests : Dr. Malathi Sathiyasekaran,
No 1- 16 th Cross street, Indranagar, Chennai 600020.
vessels, leading to microvascular thrombosis, multifocal

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Malathi Sathiyasekaran and So. Shivbalan

gastrointestinal infarction, and finally gross pathologic IMMUNOLOGIC FACTORS

sequelae such as ulcerations, fistulas, fibrosis, and
strictures.
CD may represent an aberration in the normal balance
between physiologic inflammation and pro-inflammatory
GENETICS cytokines. This imbalance results in the conversion of
physiological inflammation to a pathologic one and leads
to tissue destruction. The defect may be at several sites
A single well accepted risk factor for the development of
including increased antigen uptake through a leaky gut
CD is having a first-degree relative with the disease. The
epithelium, defective antigen processing, abnormal
age-adjusted risk of developing CD during lifetime for a
vascular endothelial cell function, and abnormalities in
first-degree relative of a proband is about 4%, which is
the production of interleukins and eicosanoids.
more than for UC. Familial IBD is particularly common
with EOIBD and the incidence of IBD among first-degree
relatives may be as high as 56%.2 PATHOPHYSIOLOGY
The CD susceptible gene NOD2/CARD 15 (Cathapse
Activation Recruitment Domain) has been identified on
The prevailing hypothesis regarding the pathogenesis of
chromosome 16. The NOD2/CARD 15 encodes the
CD is an interaction between environmental factors and
protein recognizing lipopolysaccharides of the bacterial
an altered immune response in genetically predisposed
cell wall membrane. Mutations of this gene predisposes to
children, leading to chronic inflammation of the
CD by exhibiting inappropriate response to bacterial
gastrointestinal tract. (Fig 1) In CD there is a disordered
components and thereby altering the signaling pathways
regulation of mucosal and systemic immune response
of the innate immune system leading to the development
resulting in the perpetuation of the inflammatory cascade.
and persistence of intestinal inflammation. This genetic
A dysregulated TH1 response (T helper 1) seems to be
make up is associated more with ileal disease, early onset
crucial in the conversion of physiologic to pathologic
CD or stricturing disease.9

ANTIGENIC STIMULATION

Microbial/Dietary Antigen

INTESTINAL MUCOSA
Gut immune system

PHYSIOLOGICAL INFLAMMATION

Genetic Predisposition

Susceptible
Normal Host
Host
Environmental Factors

Limited Inflammation Uncontrolled Inflammation

Healing with no tissue injury Extensive tissue injury

I.B.D.
Fig. 1. Pathophysiology of IBD

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Pediatric Crohn's Disease

inflammation. The immunological profile in CD is approximately 50%. Fatigue, anorexia, weight loss and
predominantly a cell-mediated response. Active mucosal diminution in growth velocity are other presenting
inflammation of the small and large intestine results in symptoms in children. Perirectal involvement fistulae,
diarrhea, protein-losing enteropathy, bleeding, abdominal fissure and skin tags are important clues to the diagnosis.
pain and stricture formation. Proinflammatory cytokines CD is subcategorized as predominantly inflammatory,
and eicosanoids increase vascular permeability and cause fistulizing or stricturing disease based on the clinical
electrolyte secretion, and augment smooth muscle phenotype. The clinical profile of the patients seen in
contraction. Many cytokines promote the recruitment and South India is shown in table 1.
activity of collagen forming cells leading to fibrous tissue
proliferation and thereby resulting in bowel wall
COMPLICATIONS
thickening and stricture formation. The causal role of
TNF-a in the etiopathogenesis of CD has gained
importance. Hemorrhage, obstruction, perforation, abscess and fistula
formation are well known in CD. Perianal disease may
present with abscess formation, perirectal and perianal
PATHOLOGY AND DISTRIBUTION
fistulization and can precede the intestinal manifestation
by years. Perforation with internal fistulae is another
The transmural inflammation and discontinuous serious complication. Carcinoma of the colon is a long­
involvement are the characteristic features of CD term complication of inflammatory bowel disease. The
differentiating it from UC where the inflammation is two well accepted risk factors for cancer are duration and
continuous and restricted to the mucosa. The distribution severity of the disease. Complications such as perianal
of the lesions in CD though discontinuous may involve and rectovaginal fistula, esophageal stricture and small
any part of gastrointestinal tract from the oral cavity to the bowel obstruction necessitating resection were also seen
colon. In the West isolated colonic involvement is seen in in children from South India
10-20 %, ileo-colonic disease in 50-70% and diffuse small
bowel disease in 10-15 % 10. Isolated gastroduodenal
EXTRA INTESTINAL MANIFESTATIONS
disease may be seen in less than 5% whereas endoscopic
and histologic gastroduodenal disease may be as high as
30-40% of children. 2 The involvement of the small Several extra intestinal manifestations which may have
intestine differentiates CD from UC and is a pointer for some prognostic significance are seen in 25-30% 2 of
diagnosis. Perirectal disease is seen in 20% of patients and patients with CD. The important skin manifestations
is associated with recto sigmoid inflammation. include erythema nodosum and pyoderma gangrenosum.
Noncaseating granuloma is the hallmark of CD.2 Apthous ulcerations are the most common oral
manifestation of CD. The oral manifestations may occur
along with intestinal disease or precede it. Oral
CLINICAL PRESENTATION
ulcerations was the primary presentation documented in
two children from South India.7 Ocular manifestations
The clinical presentation in CD depends upon the site of such as episcleritis and anterior uveitis are less common in
involvement of the gastrointestinal tract. Abdominal pain children than in adults and occur when the disease is
and systemic symptoms are generally more severe in CD active. Arthritis is the most common extraintestinal
than in UC. A dyspeptic-type of epigastric pain is seen in manifestation in children and occurs in 7-25 % of pediatric
children with gastro duodenal involvement. Diarrhea IBD and may occur years before the intestinal
occurs in two-third of affected children. In children with symptoms.11 Hepatobiliary complications such as chronic
predominantly ileal involvement, constipation may be a hepatitis, sclerosing cholangitis, cholelithiasis and
rare presentation. Gross blood in the stools is unusual elevated aminotransferase may precede the active
with isolated small bowel disease and more common disease. 12 The renal manifestations of IBD include
when the colon is involved. Fever occurs in nephrolithiasis, hydronephrosis and enterovesical fistula.
TABLE 1. The clinical Profile of the Patients Seen in South India
Other extraintestinal manifestations are thromboembolic
manifestations, vasculitis, pancreatitis, interstitial
Clinical Features Percentage pneumonitis and pericarditis.
Weight loss is seen in more than 50% of children with
Weight loss 100

Abdominal pain 80
CD and is a clue in the evaluation of children with
Diarrhoea, Blood in stools 70
abdominal pain. 8 Failure to thrive is therefore an
Fever 60
important presentation of CD. Malnutrition can be due to
Vomiting 50
suboptimal dietary intake, increased gastrointestinal
Anemia 40
losses, malabsorption, delayed gastric emptying and

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Malathi Sathiyasekaran and So. Shivbalan

increased requirements associated with marked consider CD or tuberculosis in the Indian setting. A
inflammatory activity. The severe mucosal inflammation perianal and rectal examination is necessary to detect skin
leads to the loss of cellular constituents and hematochezia tags, fissures and fistulae. Laboratory tests such as
and results in protein-losing enteropathy, iron-deficiency complete blood count, C reactive protein, motion for
anemia, vitamin deficiencies, increased fecal loss of occult blood and total protein albumin/globulin ratio
calcium, zinc and magnesium. should be included.
Growth failure and decrease in growth velocity may An ultrasound (US) examination of the abdomen may
precede gastrointestinal symptoms and an absolute detect thickened bowel loops, pseudo kidney sign and
height deficiency may be present in 30% at the time of enlarged lymph nodes in CD. The US findings of free
diagnosis.2 Permanent growth failure can also occur. The fluid, lymph nodes, thickened mesentery or omentum are
probable reasons for growth failure are chronic under more diagnostic of abdominal tuberculosis than CD. The
nutrition, administration of corticosteroids, low levels of child should then be referred to the pediatric
insulin-like growth factor (IGF 1), and alteration of gastroenterologist for a more complete work up. The
cytokine profiles. diagnosis of CD in children is made by a combination of
The delay in sexual maturation seen in some children clinical observations and confirmed by laboratory,
with CD may have a significant effect on self-esteem and radiologic, endoscopic, and histologic findings. CD can be
socialization. There is irreversible loss of growth potential classified as mild, moderate and severe based on the
in those who develop secondary sexual characters before clinical presentation.. The popular scoring system for
attaining remission whereas if they attain remission pediatric CD is the Pediatric Crohn’s Disease Activity
before puberty there is good catch up growth and height Index (PCDAI) 13 which helps in assessing the severity of
velocity. the disease.
Bone disease is a common problem in children with The differential diagnosis depends on the age and
CD. The causative factors include malnutrition, various clinical presentation and includes ulcerative colitis, HIV
effects of cytokines and glucocorticoid therapy. Despite enteropathy, yersenia enterocolitis, allergic enterocolitis,
the potential for children with CD to develop tuberculosis, lymphoma, intestinal polyps and diarrhoea
osteoporosis, the bone mineral density in adulthood is predominant IBS. In India it is a dictum though difficult
normal if they are managed appropriately. to differentiate CD from TB.

DIAGNOSIS ENDOSCOPIC EVALUATION

The initial evaluation of a child with suspected CD In CD the characteristic lesions on ileo-colonoscopy are
includes a detailed elicitation of clinical, family and the skip lesions, cobble stoning of mucosa, apthous ulcers
treatment history by the pediatrician. Any child or or deep irregular ulcers of varying sizes with normal
adolescent with recurrent abdominal pain associated with intervening mucosa (Fig 2). Rectal sparing and terminal
or without fever, diarrhoea and growth failure is a ileal involvement are features of CD rather than UC.
possible candidate for CD and requires complete Histopathologically the presence of noncaseating
examination. A careful assessment of the growth and granuloma is diagnostic of CD but often difficult to
development of the child is essential. The abdominal differentiate from TB. The inflammatory cells have a
examination may not be contributory however if a mass is transmural distribution and the fissuring ulcers extend to
palpable especially in the right iliac fossa one may the muscularis propria. Normal appearing colonic

Fig 2. Colonoscopic appearance of CD showing irregular ulcers with normal intervening

mucosa.

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Pediatric Crohn's Disease

mucosa should always be biopsied since microscopic small bowel CD 16 . Gandolium enhanced Magnetic
inflammation is a feature of CD Gastric antral biopsy and Resonance Imaging (MRI) Scan has been beneficial in
identification of focal active gastritis or microgranuloma some cases of IBD to differentiate between CD and UC.
also increases the diagnostic yield.14
CD VS UC
RADIOLOGIC EVALUATION
The distinction between CD from UC though essential
may be difficult in some circumstances. Some of the
Barium Meal Series is useful to identify small bowel differentiating clinical and endoscopic features are shown
involvement and lesions such as strictures, fistulae, and in table 2.
ulcerations may be identified. This contrast study has
largely been replaced by contrast enhanced computerized CD VS TB
tomography.
Contrast Enhanced Computerized Tomography It is crucial to differentiate CD from TB for administrating
(CECT) is more sensitive than barium studies to identify appropriate therapy. Tuberculosis has always been
bowel wall thickening and assess the length and site of considered a possible differential diagnosis in the
strictures in small bowel CD. Ultrasound abdomen is evaluation of granulomatous colitis resulting in patients
done as a primary modality of investigation and may be with CD being treated as tuberculosis. There are some
used as screening test. differentiating features between CD and intestinal TB.
The ulcer in CD are longitudinal whereas it is more
transverse in TB. Perianal involvement is a feature of CD
SEROLOGICAL MARKERS
and not TB. The granulomas are smaller, ill formed,
numerous and non-caseating in CD whereas they are
Perinuclear anti-neutrophil cytoplasmic antibody larger, well formed confluent and caseating in TB 17.
(pANCA) and anti sacchromyces cerevisiae antibody Isolated lymphnode involvement can occur without
(ASCA) are potentially important addition to the bowel involvement in CD but not in TB.
diagnostic panel of IBD. Combination of these markers
has shown a specificity of 95% and sensitivity of 55% in
THERAPY
children with CD.15 They are not considered as a screening
test for CD. The detection of ASCA antibodies in
individuals with CD may depend on the duration of The general goals of treatment are to achieve best clinical
exposure to sacchromyces cerevesiae. and laboratory control of inflammatory disease with least
possible side effects from medication, promote growth
through adequate nutrition and permit the child to
NEWER INVESTIGATION MODALITIES
function as normal as possible. 3 5-Aminosalicylates like
sulfasalazine or 5-ASA remain the cornerstone of
Isolated small bowel CD may be diagnosed using a treatment for CD. The 5 ASA drugs (mesalamine,
double balloon enteroscope that helps to directly visualize balsalazide) exert local anti-inflammatory effects through
and biopsy the lesions. The wireless capsule endoscopy a number of mechanisms, which includes inhibition of 5 –
has been used as a diagnostic tool in adults with isolated lipoxygenase with a result in decreased production of

TABLE 2. Differentiating Features Between Ulcerative Colitis and Crohn’s Disease

Features Ulcerative colitis Crohn’s Disease

Bloody diarrhoea Common Unusual

Abdominal Pain Unusual Common
Abdominal Mass Not present May be present
Growth Failure Unusual Present
Failure to thrive Unusual Present
Oral ulcers Not present May be present
Perianal disease Not present Present
Rectal mucosal involvement Present Usually spared
Distribution of lesions Continuous Skip lesions
Ileum involvement Not involved May be involved
Depth of inflammation Involves only mucosa Submucosa, transmural
Ulcers Microulcers common Apthous ulcers, linear ulcers
Complications Toxic Megacolon Strictures, Fistula
Histopathology Cryptitis, crypt abscess Granuloma

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Malathi Sathiyasekaran and So. Shivbalan

leukotriene B4, scavenging of reactive oxygen infliximab has been evaluated in pediatric CD and has
metabolites, prevention of the upregulation of leucocyte proved effective as a short-term therapy in moderate to
adhesion molecules and inhibition of interleukin 1 severe CD and in children with active draining external
synthesis. 5 ASA is rapidly absorbed from the upper fistulae.19
intestinal tract and various drug delivery systems have
been employed so that it reaches the distal small bowel or
NUTRITIONAL THERAPY
colon. Mesalamine is coated with Eudragit, a pH sensitive
acrylic resin or ethyl cellulose to release the drug at the
appropriate site. Uncoated mesalamine is also available as Children with CD should be supported with proper
enema for use in left sided lesions. Mesalamine is used in nutrition to ensure better results from therapy. Caloric
the dose of 40-60mg/kg/day as the first line drug in mild supplementation is essential in children with growth­
CD and also as maintenance drug. delay or under-nutrition. It is evident that enteral
nutrition with an oligopeptide formula or amino acid
STEROIDS based formula has fewer relapses. Patients who attain
remission with exclusive enteral nutrition have prolonged
Corticosteroids are used in acute stages of moderate to remission and improved linear growth. 20 Calcium
severe CD or when aminosalicylates are ineffective supplementation is an important adjuvant to prevent
Prednisolone is started at a dose of 1-2 mg/kg day in bone disease.
moderate CD. Once clinical remission is reached attempts
are made to wean the medication to alternate day therapy PSYCHOLOGICAL THERAPY
and then tapered before stopping within 6-8 weeks.
Newer corticosteroids such as oral budesonide at a dose
of 6-9mg/day may be prescribed to avoid the systemic CD is a chronic condition that may have a profound
side effects of steroids. influence on the lives of affected children and their family
members. Adolescents have a difficult time in handling
IMMUNOMODULATORS the disease. Every effort should be made to facilitate
normal age appropriate activities and early intervention
The recognition of the central role played by the immune by psychologists or psychiatrists should be sought if
system in the pathogenesis of IBD has increased the use of problems develop.
immunomodulators.
6 Mercaptopurine (1-1.5mg/kg/day) and azathioprine SURGICAL THERAPY
(2-2.5mg/kg/day) are effective in patients with active
disease when added on to corticosteroid therapy. They
facilitate the development of remission and promote The indications for surgery in CD include intractability,
tapering of the corticosteroids. These drugs usually uncontrolled hemorrhage, perforation, obstruction,
require three to six months to exhibit efficacy, and are not fistulae, growth retardation, and carcinoma.
effective as primary therapy. Methotrexate has been used
in children with CD with beneficial results.
MULTIDISCIPLINARY APPROACH

ANTIBIOTICS
The care of the child with CD involves a multidisciplinary
approach involving the pediatrician, pediatric
Though no infective agent has been implicated in the gastroenterologist, nutritionist, psychologist, pediatric
etiology, Ciprofloxacin and metronidazole have shown surgeon, social worker and nurse. The team should also
some efficacy in active CD especially those associated include parents, siblings and teachers who should be well
with perirectal disease, perianal fistulae and even small informed about the child’s problem. This concept in care
bowel CD. ensures an ideal, comprehensive management of the CD
patient and helps in achieving appropriate levels of
physical, mental and social well being. The transition of
BIOLOGICAL THERAPY the adolescent from the child centered health care systems
to the adult oriented health care system should be done
Several novel therapies have been investigated in the with utmost care.
treatment of IBD. They may be biologic agents such as
infliximab, natalizumab, Interleukin 10 or non-biologic CONCLUSION
agents such as thalidomide, granulocyte colony
stimulating factor. 18 Anti-Tumour Necrosis Factor, Crohn’s disease is an emerging chronic gastrointestinal

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Pediatric Crohn's Disease

disease of childhood and adolescence which affects a Diagnosis, Management. WBSaunders. Philadelphia 1999: 401­
very vulnerable period in the life of the individual 418.
11. Burbrige EJ, Huang S, Bayless TM. Clinical manifestations of
characterized by remissions and relapses and continues
Crohn’s disease in children and adolescents. Pediatrics 1975;
through adulthood. Indian children are not spared from 55 : 866-871.
this problem and it is essential that pediatricians are 12. Hyams JF. Extraintestinal manifestation of Inflammatory
aware of this disease to enable proper diagnosis and bowel disease in children. J Pediatr Gastroenterol Nutr 1994;
prompt referral. 19 : 7-21.
13. Hyams JS, Ferry GD, Mandel FS, Gryboski JD, Kibort PM,
Kirschner BS, Griffiths AM, Katz AJ, Grand RJ, Boyle JT et al.
REFERENCES Development and validation of a pediatric Crohn’s disease
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2. Baldassano RN, Piccoli DA. Inflammatory bowel disease in oesophagoduodenoscopy in the initial evaluation of childhood
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1999; 28: 445-455. Gastroenterol 2002; 35 : 636-640.
3. Mamula P, Markowitz JE, Baldassano RN. Inflammatory 15. Ruemmele FM, Targan SR, Levy G, Dubinsky M, Braun J,
bowel disease in early childhood and adolescence: special Seidman EG. Diagnostic accuracy of Serological assays in
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4. Law NM, Lim CC, Chong R, Ng HS. Crohn’s disease in the 115 : 822-829.
Singapore Chinese population. J Clin Gastroenterol 1998; 26 : 27­ 16. Reddy DN, Kaffes AJ, Sriram PVJ, Venkat Rao G. Capsule
29. endoscopic features of crohns disease. Digestive Endoscopy 2004;
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in India; Is it related to improved sanitation? Indian J 17. Pulimood AB, Ramakrishna BS, Kurian G, Peter S, Patra S,
Gastroenterol 2005; 24 : 23-24. Mathan VI. Endoscopic mucosal biopsies are useful in
6. Cosgrove M, Al-Atia RF, Jenkins HR. The epidemiology of distinguishing granulomatous colitis due to crohns disease
pediatric inflammatory bowel disease. Arch Dis Child 1996; 74: from tuberculosis. Gut 1999; 45 : 537-541.
460-461. 18. Mamula P, Mascarenhas MR, Baldassano RN. Biological and
7. Sathiyasekaran M, Raju BB, Shivbalan S, Rajarajan K. Pediatric novel therapies for inflammatory bowel disease in children.
Crohn’s disease in South India. Indian Pediatr 2005; 42 : 459-463. Pediatr Clin North Am 2002; 49 : 1-25.
8. Cuffari C, Darbari A. Inflammatory Bowel disease in the 19. Baldassano R, Braegger CP, Escher JC, DeWoody K, Hendricks
pediatric and adolescent patients. Gastroenterol Clin N Am DF, Keenan GF, Winter HS. Infliximab (REMICADE) therapy
2002; 31 : 275-291. in the treatment of pediatric Crohn’s disease. Am J Gastroenterol
9. Bonen DK, Cho JK. The genetics of Inflammatory Bowel 2003; 98 : 833-838.
Disease. Gastroenterol 2003; 124 : 521-530. 20 Griffiths AN, Ohlsson A, Sherman PN, Sutherland LR. Meta
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Pediatric Gastrointestinal Disease: Pathophysiology, Crohn’s disease. Gastroenterology 1995; 108 : 1056-1067.

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Notes and News

CME on “Fetal and Developmental Origins of Childhood and Adult Disease:

Implications for Clinical Practice” November 9th 2006

PHD House, Opposite Siri fort Auditorium, 4/2, Siri Institutional Area, August Kranti Marg,
New Delhi-110 016

This CME on “Fetal and Developmental Origin of Childhood and Adult Disease: Implications for Clinical
Practice” is being organized with participation by global leaders in this field to increase the awareness and
forewarn about the impending explosion of diseases such as Diabetes, Hypertension, Coronary Artery Disease,
Metabolic Syndrome, etc., which are now increasingly being diagnosed in young adults and even in adolescence.
More importantly, this dynamic conference, which is being addressed by eminent clinicians from different
specialities, scientists and researchers, also proposes to discuss early indicators for diagnosis, prevention, burden
of cost and possible strategies with simple, practical and affordable interventions.

Organized by : S.L. Jain Hospital; All India Institute of Medical Sciences; Sitaram Bhartia Institute of Science and
Research, New Delhi; and SNEHA-India.

In association with : International DOHaD Society; MRC Epidemiology Resource Centre, Southampton, UK; The
Centre for Development Origins of Health and Disease, University of Southampton, UK; Liggins Institute, New
Zealand; and Public Health Foundation of India.

Programme co-ordinators : Prof. Santosh K. Bhargava, Prof. K.S. Reddy, Prof. H.P.S. Sachdev

Faculty : India : Anand Pandit, Chitaranjan Yajnik, G.V. Krishnaveni, Nikhil Tandon, D. Prabhakaran,
P. Raghupathy

International : Caroline Fall (UK), Clive Osmond (UK), Mark Hanson (UK), Peter Gluckman (New Zealand),
Katherine O'Connor (New Zealand), Harold Alderman (USA)

Subjects for Discussion Include : Relevance of Barker's Hypothesis to India, Maternal Nutrition and Fetal
Outcome, Diabetes and Insulin Resistance, Gestational Diabetes and Long-term Fetal Effects, Epigenetic and Trans
and Intergenerational Effects, Childhood Growth Monitoring and it's Application in Prediction of Adult Disease,
Medical and Economic Burden of Diabetes, Cardiac Diseases and Low Birth Weight in India.

Registration fee : Before 31. 10. 2006

Individual Rs. 500/-
Group registration 3 Rs. 1050/ for additional beyond 3 Rs 350/each
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Spot Rs. 750/-
Additional CME CD Rs 100/-

Payment by demand draft/cheque in favor of “CME Pediatrics Fetal Origin 2006”

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For registration and further enquiries please write to :

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Mobile : 9810474560; e-mail : [email protected]

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Mobile : 9811093347; e-mail : [email protected]

730 Indian Journal of Pediatrics, Volume 73—August, 2006