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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:bwcs@md4.vsnl.net.in

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

Crohn’s disease is an idiopathic, relapsing chronic
inflammatory disease of the gastrointestinal tract
categorized as Inflammatory Bowel Disease (IBD) and is
an important cause of morbidity in children and
adolescents. IBD comprises of two important entities CD
and Ulcerative Colitis (UC) based on clinical, laboratory,
radiologic, endoscopic and histologic features. In 10% of
cases the findings are non-specific and therefore termed
as indeterminate colitis (IC). 1 This subset of IBD has a
propensity to progress to CD rather than to UC.
Approximately 25-30% of CD present before the age of 20
years and therefore pediatricians need to recognize the
varied presentations of this disorder2.
EPIDEMIOLOGY
The incidence of CD in children is much less than that
seen in adults.3 It is more prevalent in Western countries
compared to Asia and Africa. The incidence of pediatric
CD range from 0.2 to 8.5 per 100,000.3 Recently there have
been reports of CD from Africa, China and Japan. In
Singapore the incidence of CD in adults is 3.6 per 100,000.4
The incidence of CD is on the rise in children similar to the
trend seen in adults whereas UC has shown a more stable
pattern. In India, recently there have been several reports
of CD in adults5 whereas data on pediatric CD is sparse.
Correspondence and Reprint requests : Dr. Malathi Sathiyasekaran,
No 1- 16 th Cross street, Indranagar, Chennai 600020.
This change in frequency of CD could be due to increased
awareness and availability of better diagnostic facility.
Some authors believe that the recent increase of CD in
India is not apparent but real and consider the improved
sanitation- hygiene hypothesis as an important etiological
factor.5
CD can occur in all age groups and follows the same
bimodal pattern of age distribution as IBD. The
proportion of patients with CD below the age of 20 years
varies between 25-40% with around 10% being less than
10 years of age.3 The mean age of presentation is about
12.1 years. 6 Early onset IBD (EOIBD) i.e. presentation
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
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
both sexes. In US there seems to be a preponderance of
CD in boys3 whereas in South India it was more prevalent
in girls. 7 The effect of breastfeeding and cigarette
smoking remains controversial. CD occurs with a higher
frequency in patients with Turner’s syndrome,
Hermansky-Pudlak syndrome, cystic fibrosis and
glycogen storage disease type 1B.8
Crohn’s disease could represent a persistent infection
with a fastidious organism or an abnormal and prolonged
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
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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87
Pediatric Crohn's Disease
inflammation. The immunological profile in CD is
predominantly a cell-mediated response. Active mucosal
inflammation of the small and large intestine results in
diarrhea, protein-losing enteropathy, bleeding, abdominal
pain and stricture formation. Proinflammatory cytokines
and eicosanoids increase vascular permeability and cause
electrolyte secretion, and augment smooth muscle
contraction. Many cytokines promote the recruitment and
activity of collagen forming cells leading to fibrous tissue
proliferation and thereby resulting in bowel wall
thickening and stricture formation. The causal role of
TNF-a in the etiopathogenesis of CD has gained
importance.
PATHOLOGY AND DISTRIBUTION
The transmural inflammation and discontinuous
involvement are the characteristic features of CD
differentiating it from UC where the inflammation is
continuous and restricted to the mucosa. The distribution
of the lesions in CD though discontinuous may involve
any part of gastrointestinal tract from the oral cavity to the
colon. In the West isolated colonic involvement is seen in
10-20 %, ileo-colonic disease in 50-70% and diffuse small
bowel disease in 10-15 % 10. Isolated gastroduodenal
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
intestine differentiates CD from UC and is a pointer for
diagnosis. Perirectal disease is seen in 20% of patients and
is associated with recto sigmoid inflammation.
Noncaseating granuloma is the hallmark of CD.2
CLINICAL PRESENTATION
The clinical presentation in CD depends upon the site of
involvement of the gastrointestinal tract. Abdominal pain
and systemic symptoms are generally more severe in CD
than in UC. A dyspeptic-type of epigastric pain is seen in
children with gastro duodenal involvement. Diarrhea
occurs in two-third of affected children. In children with
predominantly ileal involvement, constipation may be a
rare presentation. Gross blood in the stools is unusual
with isolated small bowel disease and more common
when the colon is involved. Fever occurs in
TABLE 1. The clinical Profile of the Patients Seen in South India
Clinical Features Percentage
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
Indian Journal of Pediatrics, Volume 73—August, 2006
approximately 50%. Fatigue, anorexia, weight loss and
diminution in growth velocity are other presenting
symptoms in children. Perirectal involvement fistulae,
fissure and skin tags are important clues to the diagnosis.
CD is subcategorized as predominantly inflammatory,
fistulizing or stricturing disease based on the clinical
phenotype. The clinical profile of the patients seen in
South India is shown in table 1.
COMPLICATIONS
Hemorrhage, obstruction, perforation, abscess and fistula
formation are well known in CD. Perianal disease may
present with abscess formation, perirectal and perianal
fistulization and can precede the intestinal manifestation
by years. Perforation with internal fistulae is another
serious complication. Carcinoma of the colon is a long­
term complication of inflammatory bowel disease. The
two well accepted risk factors for cancer are duration and
severity of the disease. Complications such as perianal
and rectovaginal fistula, esophageal stricture and small
bowel obstruction necessitating resection were also seen
in children from South India
EXTRA INTESTINAL MANIFESTATIONS
Several extra intestinal manifestations which may have
some prognostic significance are seen in 25-30% 2 of
patients with CD. The important skin manifestations
include erythema nodosum and pyoderma gangrenosum.
Apthous ulcerations are the most common oral
manifestation of CD. The oral manifestations may occur
along with intestinal disease or precede it. Oral
ulcerations was the primary presentation documented in
two children from South India.7 Ocular manifestations
such as episcleritis and anterior uveitis are less common in
children than in adults and occur when the disease is
active. Arthritis is the most common extraintestinal
manifestation in children and occurs in 7-25 % of pediatric
IBD and may occur years before the intestinal
symptoms.11 Hepatobiliary complications such as chronic
hepatitis, sclerosing cholangitis, cholelithiasis and
elevated aminotransferase may precede the active
disease. 12 The renal manifestations of IBD include
nephrolithiasis, hydronephrosis and enterovesical fistula.
Other extraintestinal manifestations are thromboembolic
manifestations, vasculitis, pancreatitis, interstitial
pneumonitis and pericarditis.
Weight loss is seen in more than 50% of children with
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Malathi Sathiyasekaran and So. Shivbalan
increased requirements associated with marked
inflammatory activity. The severe mucosal inflammation
leads to the loss of cellular constituents and hematochezia
and results in protein-losing enteropathy, iron-deficiency
anemia, vitamin deficiencies, increased fecal loss of
calcium, zinc and magnesium.
Growth failure and decrease in growth velocity may
precede gastrointestinal symptoms and an absolute
height deficiency may be present in 30% at the time of
diagnosis.2 Permanent growth failure can also occur. The
probable reasons for growth failure are chronic under
nutrition, administration of corticosteroids, low levels of
insulin-like growth factor (IGF 1), and alteration of
cytokine profiles.
The delay in sexual maturation seen in some children
with CD may have a significant effect on self-esteem and
socialization. There is irreversible loss of growth potential
in those who develop secondary sexual characters before
attaining remission whereas if they attain remission
before puberty there is good catch up growth and height
velocity.
Bone disease is a common problem in children with
CD. The causative factors include malnutrition, various
effects of cytokines and glucocorticoid therapy. Despite
the potential for children with CD to develop
osteoporosis, the bone mineral density in adulthood is
normal if they are managed appropriately.
DIAGNOSIS
The initial evaluation of a child with suspected CD
includes a detailed elicitation of clinical, family and
treatment history by the pediatrician. Any child or
adolescent with recurrent abdominal pain associated with
or without fever, diarrhoea and growth failure is a
possible candidate for CD and requires complete
examination. A careful assessment of the growth and
development of the child is essential. The abdominal
examination may not be contributory however if a mass is
palpable especially in the right iliac fossa one may
Fig 2. Colonoscopic appearance of CD showing irregular ulcers with normal intervening
mucosa.
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88
consider CD or tuberculosis in the Indian setting. A
perianal and rectal examination is necessary to detect skin
tags, fissures and fistulae. Laboratory tests such as
complete blood count, C reactive protein, motion for
occult blood and total protein albumin/globulin ratio
should be included.
An ultrasound (US) examination of the abdomen may
detect thickened bowel loops, pseudo kidney sign and
enlarged lymph nodes in CD. The US findings of free
fluid, lymph nodes, thickened mesentery or omentum are
more diagnostic of abdominal tuberculosis than CD. The
child should then be referred to the pediatric
gastroenterologist for a more complete work up. The
diagnosis of CD in children is made by a combination of
clinical observations and confirmed by laboratory,
radiologic, endoscopic, and histologic findings. CD can be
classified as mild, moderate and severe based on the
clinical presentation.. The popular scoring system for
pediatric CD is the Pediatric Crohn’s Disease Activity
Index (PCDAI) 13 which helps in assessing the severity of
the disease.
The differential diagnosis depends on the age and
clinical presentation and includes ulcerative colitis, HIV
enteropathy, yersenia enterocolitis, allergic enterocolitis,
tuberculosis, lymphoma, intestinal polyps and diarrhoea
predominant IBS. In India it is a dictum though difficult
to differentiate CD from TB.
ENDOSCOPIC EVALUATION
In CD the characteristic lesions on ileo-colonoscopy are
the skip lesions, cobble stoning of mucosa, apthous ulcers
or deep irregular ulcers of varying sizes with normal
intervening mucosa (Fig 2). Rectal sparing and terminal
ileal involvement are features of CD rather than UC.
Histopathologically the presence of noncaseating
granuloma is diagnostic of CD but often difficult to
differentiate from TB. The inflammatory cells have a
transmural distribution and the fissuring ulcers extend to
the muscularis propria. Normal appearing colonic
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Pediatric Crohn's Disease

mucosa should always be biopsied since microscopic
inflammation is a feature of CD Gastric antral biopsy and
identification of focal active gastritis or microgranuloma
also increases the diagnostic yield.14
RADIOLOGIC EVALUATION
Barium Meal Series is useful to identify small bowel
involvement and lesions such as strictures, fistulae, and
ulcerations may be identified. This contrast study has
largely been replaced by contrast enhanced computerized
tomography.
Contrast Enhanced Computerized Tomography
(CECT) is more sensitive than barium studies to identify
bowel wall thickening and assess the length and site of
strictures in small bowel CD. Ultrasound abdomen is
done as a primary modality of investigation and may be
used as screening test.
SEROLOGICAL MARKERS
Perinuclear anti-neutrophil cytoplasmic antibody
(pANCA) and anti sacchromyces cerevisiae antibody
(ASCA) are potentially important addition to the
diagnostic panel of IBD. Combination of these markers
has shown a specificity of 95% and sensitivity of 55% in
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
exposure to sacchromyces cerevesiae.
NEWER INVESTIGATION MODALITIES
Isolated small bowel CD may be diagnosed using a
double balloon enteroscope that helps to directly visualize
and biopsy the lesions. The wireless capsule endoscopy
has been used as a diagnostic tool in adults with isolated
small bowel CD 16 . Gandolium enhanced Magnetic
Resonance Imaging (MRI) Scan has been beneficial in
some cases of IBD to differentiate between CD and UC.
CD VS UC
The distinction between CD from UC though essential
may be difficult in some circumstances. Some of the
differentiating clinical and endoscopic features are shown
in table 2.
CD VS TB
It is crucial to differentiate CD from TB for administrating
appropriate therapy. Tuberculosis has always been
considered a possible differential diagnosis in the
evaluation of granulomatous colitis resulting in patients
with CD being treated as tuberculosis. There are some
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
and not TB. The granulomas are smaller, ill formed,
numerous and non-caseating in CD whereas they are
larger, well formed confluent and caseating in TB 17.
Isolated lymphnode involvement can occur without
bowel involvement in CD but not in TB.
THERAPY
The general goals of treatment are to achieve best clinical
and laboratory control of inflammatory disease with least
possible side effects from medication, promote growth
through adequate nutrition and permit the child to
function as normal as possible. 3 5-Aminosalicylates like
sulfasalazine or 5-ASA remain the cornerstone of
treatment for CD. The 5 ASA drugs (mesalamine,
balsalazide) exert local anti-inflammatory effects through
a number of mechanisms, which includes inhibition of 5 –
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
metabolites, prevention of the upregulation of leucocyte
adhesion molecules and inhibition of interleukin 1
synthesis. 5 ASA is rapidly absorbed from the upper
intestinal tract and various drug delivery systems have
been employed so that it reaches the distal small bowel or
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
enema for use in left sided lesions. Mesalamine is used in
the dose of 40-60mg/kg/day as the first line drug in mild
CD and also as maintenance drug.
STEROIDS
Corticosteroids are used in acute stages of moderate to
severe CD or when aminosalicylates are ineffective
Prednisolone is started at a dose of 1-2 mg/kg day in
moderate CD. Once clinical remission is reached attempts
are made to wean the medication to alternate day 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
side effects of steroids.
IMMUNOMODULATORS
The recognition of the central role played by the immune
system in the pathogenesis of IBD has increased the use of
immunomodulators.
6 Mercaptopurine (1-1.5mg/kg/day) and azathioprine
(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
tapering of the corticosteroids. These drugs usually
require three to six months to exhibit efficacy, and are not
effective as primary therapy. Methotrexate has been used
in children with CD with beneficial results.
ANTIBIOTICS
Though no infective agent has been implicated in the
etiology, Ciprofloxacin and metronidazole have shown
some efficacy in active CD especially those associated
with perirectal disease, perianal fistulae and even small
bowel CD.
BIOLOGICAL THERAPY
Several novel therapies have been investigated in the
treatment of IBD. They may be biologic agents such as
infliximab, natalizumab, Interleukin 10 or non-biologic
agents such as thalidomide, granulocyte colony
stimulating factor. 18 Anti-Tumour Necrosis Factor,
728
90
infliximab has been evaluated in pediatric CD and has
proved effective as a short-term therapy in moderate to
severe CD and in children with active draining external
fistulae.19
NUTRITIONAL THERAPY
Children with CD should be supported with proper
nutrition to ensure better results from therapy. Caloric
supplementation is essential in children with growth­
delay or under-nutrition. It is evident that enteral
nutrition with an oligopeptide formula or amino acid
based formula has fewer relapses. Patients who attain
remission with exclusive enteral nutrition have prolonged
remission and improved linear growth. 20 Calcium
supplementation is an important adjuvant to prevent
bone disease.
PSYCHOLOGICAL THERAPY
CD is a chronic condition that may have a profound
influence on the lives of affected children and their family
members. Adolescents have a difficult time in handling
the disease. Every effort should be made to facilitate
normal age appropriate activities and early intervention
by psychologists or psychiatrists should be sought if
problems develop.
SURGICAL THERAPY
The indications for surgery in CD include intractability,
uncontrolled hemorrhage, perforation, obstruction,
fistulae, growth retardation, and carcinoma.
MULTIDISCIPLINARY APPROACH
The care of the child with CD involves a multidisciplinary
approach involving the pediatrician, pediatric
gastroenterologist, nutritionist, psychologist, pediatric
surgeon, social worker and nurse. The team should also
include parents, siblings and teachers who should be well
informed about the child’s problem. This concept in care
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
the adolescent from the child centered health care systems
to the adult oriented health care system should be done
with utmost care.
CONCLUSION
Crohn’s disease is an emerging chronic gastrointestinal
Indian Journal of Pediatrics, Volume 73—August, 2006
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Pediatric Crohn's Disease
disease of childhood and adolescence which affects a
very vulnerable period in the life of the individual
characterized by remissions and relapses and continues
through adulthood. Indian children are not spared from
this problem and it is essential that pediatricians are
aware of this disease to enable proper diagnosis and
prompt referral.
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1. Kirschner BS. Inflammatory Bowel Disease in Children. Pediatr
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2. Baldassano RN, Piccoli DA. Inflammatory bowel disease in
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4. Law NM, Lim CC, Chong R, Ng HS. Crohn’s disease in the
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5. Desai HG, Guptae PA. Increasing incidence of Crohn’s disease
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6. Cosgrove M, Al-Atia RF, Jenkins HR. The epidemiology of
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10. Hyams JS. Crohn’s disease. In Wyllie R, Hyams JS, Eds.
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13. Hyams JS, Ferry GD, Mandel FS, Gryboski JD, Kibort PM,
Kirschner BS, Griffiths AM, Katz AJ, Grand RJ, Boyle JT et al.
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14. Abdullah BA, Gupta SK, Croffie JM, Pfefferkorn MD,
Molleston JP, Corkins MR, Fitzgerald JF. The role of
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15. Ruemmele FM, Targan SR, Levy G, Dubinsky M, Braun J,
Seidman EG. Diagnostic accuracy of Serological assays in
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16. Reddy DN, Kaffes AJ, Sriram PVJ, Venkat Rao G. Capsule
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17. Pulimood AB, Ramakrishna BS, Kurian G, Peter S, Patra S,
Mathan VI. Endoscopic mucosal biopsies are useful in
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from tuberculosis. Gut 1999; 45 : 537-541.
18. Mamula P, Mascarenhas MR, Baldassano RN. Biological and
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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.

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