BIOMEDICAL
GASTROINTESTINAL
Lenny González, MD, specializes
in pediatric gastroenterology and
nutrition and is a member of the staff
of SOVENIA (Venezuelan Society of
Autistic Children). Her focus is on
the diagnosis and treatment of GI
pathology in children with autism
and children with developmental
delays. Dr. Gonzalez sees children
from all over South America and has
performed intestinal endospcopies
on more than 956 children with
autism. She has collaborated with
Thoughtful House and Dr. Andrew
Wakefield in Austin, Texas, where
she investigated the histological
findings of gastrointestinal mucosa
of patients and diagnosed infections
and immune system disorders. She is
actively involved in the Defeat Autism
Now! Conference. In addition, she
has presented her findings in most
Latin American countries. She is
dedicated to education, research, and
support for families with children who
have autism and/or gastrointestinal
diseases.
74 THE AUTISM FILE | www.autismfile.com | info@autismfile.com REPRINTED WITH PERMISSION © THE AUTISM FILE
PATHOLOGY IN AUTISM
SPECTRUM DISORDERS:
THE VENEZUELAN
EXPERIENCE
By Lenny G. González, MD
R
ecent studies in the medical
literature have confirmed that
gastrointestinal (GI) symptoms
are common in patients with autism
spectrum disorders (ASD). In two
prospective studies, GI symptoms were
present in 80% and 70% of autistic
children, respectively.1 In contrast with
the ASD group in the latter study,
Valicenti-McDermott et al. reported GI
symptoms in only 28% of neurotypical
controls.1,2,10 Retrospective studies
that rely only upon review of the
children’s existing clinical records are
likely to underestimate the true size
of the problem since these records
rarely document GI symptoms. The
inadequacy of this approach means that
it is impossible to determine whether
symptoms were not present or, more
likely, that the clinician just failed to
document them. On the other hand,
prospective studies that systematically
ask about the presence or absence
of specific symptoms provide a much
more accurate picture of the size of the
problem.
Clinical manifestations of GI disease
in ASD children
Physical symptoms in ASD children
are often misinterpreted as just
autistic behaviors. In our experience,
symptoms of what turns out to be GI
distress often present as inexplicable
irritability, aggressive or auto-aggressive
(self-injurious) behaviors, discomfort,
sleep disorders, and other behavioral
disturbances. The problem of physical
symptoms such as abdominal pain being
interpreted simply as aberrant behaviors
is particularly problematic in children
who are nonverbal and who have serious
difficulties expressing themselves.10
Detailed case histories often provide
evidence of abdominal colic and
sleep disorders during the nursing
stage and frequent infections of the
upper respiratory tract (such as otitis
and tonsillitis) and GI tract caused
by bacterial, viral, parasitic, or yeast
infections. Affected children are often
hypersensitive to sounds, light, flavors,
smells, and clothing labels. In addition,
there is often a history of intolerance
to certain foods containing gluten and
casein as well as indicators of food
allergies.5-7
Children with autism often present
with GI and extra-intestinal symptoms.
The digestive symptoms include
abdominal pain, pyrosis (heartburn),
chronic diarrhea, flatulence, drooling
or excessive salivation, vomiting,
regurgitations, weight loss, rumination,
bruxism (teeth grinding), irritability,
dysentery, constipation, and fecal
impaction. During symptomatic
episodes, periods of irritability,
insomnia, and auto-aggressive behaviors
are observed. In ASD children, it is
common to observe abnormal toileting
patterns. Diarrhea and constipation are
common, and constipation can coexist
ISSUE 32 2009
 One explanation might be that part of the neurological disability in children with autism
results from absorption across an inflamed intestinal lining of molecules that are toxic
to the developing brain.
with episodes of diarrhea. In the case
of diarrhea, the stools are semi-liquid,
very fetid with mucus and undigested
food; sometimes they can have a sandy/
grainy consistency and other times
show blood. Diarrhea is one of the most
common symptoms as reported in the
studies of D’Eufemia, Torrente, Horvath,
Wakefield, Furlano, and Sabrá. This has
been our experience in Venezuela, also.14
The extra-intestinal problems
experienced by our ASD children with
GI symptoms include respiratory,
neurological, and dermatological
disorders. These include frequent
coughing (often dry), upper respiratory
tract infections, skin rashes, eczema,
atopic dermatitis, seborrheic dermatitis,
and itching.
The most common clinical signs are
Dennie Morgan infraorbital skin folds
(caused by edema or fluid collecting
in areas of inflammation), dark circles
under the eyes, long eyelashes,
abdominal distension, halitosis, perianal
erythema (diaper rash), anal fissures,
dry skin, angular cheilosis (sore cracks
at the corners of the lips), and greenish
anterior rinorrhea (runny nose).
There are also alterations in the stool
consistency, color, and smell (excessively
offensive) as well as the presence of
mucus or blood, food remains, and
visible fat (often semi-liquid, acidic,
excessively fetid, greasy feces, with
mucus and/or blood).
Etiopathogenesis
Recent studies of ASD children
report chronic inflammation of the
gastrointestinal tract that may be
present anywhere from the esophagus
down to the rectum: this inflammation
may well explain the GI symptoms and
at least some of the behaviors.18-15, 35-40
Several theories have been proposed
for how deterioration in gastrointestinal
function might influence neurological
functioning. The epithelial cell layer
that lines the GI mucosa forms a
ISSUE 32 2009 REPRINTED WITH PERMISSION © THE AUTISM FILE info@autismfile.com | www.autismfile.com | THE AUTISM FILE
barrier that restricts the contents of
the gut from getting into the blood
stream. It it is composed of cells with
absorptive surfaces (the brush border)
that interact with the contents of the
lumen. Between these cells are gates
called tight junctions, the integrity
of which is important in preventing
noxious substances from entering the
bloodstream without passing directly
through the cells.10
One explanation might be that part
of the neurological disability in children
with autism results from absorption
across an inflamed intestinal lining
of molecules that are toxic to the
developing brain.10-14 Inflammation of
the intestinal wall can be induced by
diverse causes such as food allergy,
use of antibiotics and non-steroidal
anti-inflammatory drugs, infection,
or by enzymatic insufficiency,
mycotoxins from yeast/fungi, gluten,
casein, chemical additives, colorings,
preservatives, malabsorption of
proteins, heavy metal intoxications, and
pesticides.3-6
The integrity of the intestinal wall also
plays an important role in the adequate
absorption of nutrients and the exclusion
of potentially harmful toxins, bacteria,
allergens, and peptides coming from
certain foods. In our experience, food
components such as gluten and casein
can provoke the behavioral abnormalities
characteristic of autism 4 , possibly when
they enter the systemic circulation.
Increased intestinal permeability (leaky
gut) may be the link that explains the
association of autism with an abnormal
intestinal immune response, multiple
food allergies, dysbiosis, fungal
overgrowth (Candida albicans), as well
as with micronutrient deficiencies.4,5
Probably due to GI inflammation and
abnormal immune function, children
with autism may have increased levels
of harmful bowel organisms. Frequent
antibiotic use in the first years of life can
also contribute to the chronic imbalance,
referred to as intestinal dysbiosis. Several
investigators have found evidence of
this imbalance in autistic children. A
good example of a pathogenic (disease-
causing) bacterium is Clostridium difficile.
This organism is a common cause of
severe colitis that occurs when broad-
spectrum oral antibiotics have killed
off the beneficial gut bacteria and
have allowed this antibiotic-resistant
opportunistic organism to overgrow and
cause inflammation.10
The gut-brain connection is
recognized as playing a role in the
neurological complications of a number
of gastrointestinal diseases. Symptoms
like constipation, pain, or abdominal
distension are reported by adults with
degenerative disorders of the central
nervous system like Parkinson’s disease, 4
while parents of autistic children report
similar symptoms, although the precise
nature of any link between the gut and
the brain is unknown.
Ileo-colonoscopy and autistic
enterocolitis
In 1998, a team of doctors at the Royal
Free Hospital in London reported the
results of ileocolonoscopies on 12
children who presented with autism
and GI symptoms. In a series of papers,
Wakefield and colleagues described a
new variant of intestinal inflammatory
disease, which was named autistic
enterocolitis. The disease is characterized
by mild-to-moderate chronic patchy
inflammation of the mucosa and
lymphoid nodular hyperplasia (LNH)
(swelling of the lymph glands) in the
bowel lining. Visible features suggestive
of inflammatory bowel disease included
the red halo sign – an expression of
pre-ulcerative reddening around the
swollen lymphoid tissues – typically
located at the terminal ileum, potentially
extending to involve the whole colon,
loss of vascular pattern, and mucosal
granularity, erythema (redness), and
ulceration. When compared with
75
 BIOMEDICAL
neurotypical children, including those
with ulcerative colitis (a well described
inflammatory bowel disease), the
findings suggested a novel disease
process.14
In the UK study and in our own
experience, these abnormal findings
are more frequent in autistic children
than in developmentally normal children
with GI symptoms. The only exception
was ulceration, which was uncommon
in both groups. The biopsies from the
children with autism showed reactive
LNH in 88.5% of the children compared
with only 29% of children with ulcerative
colitis, and 0.0% in the control group
without IBD. In many cases, the
researchers also saw infiltration of
inflammatory cells like neutrophils
(pus cells) and lymphocytes (chronic
inflammatory cells) in the epithelium of
the bowel mucosa. Active neutrophilic
inflammation in the ileum was present
in 8% of the children with autism and
in none of the non-inflammatory bowel
disease controls. Chronic lymphocytic
inflammation in the colon was present
in 88% of the autistic cases, 4% of the
controls, and 100% of ulcerative colitis
cases.
In our published study of 45 ASD
children and 57 developmentally normal
controls presenting for GI assessment,
chronic inflammation and LNH in the
colon and ileum was present in 100%
of the autistic cases compared with
66.66% of the controls, reflecting a
high background rate of infectious
enterocolitis in Venezuelan children
(see below.)13 Since then, other studies
carried out in the United States, Brazil,
Italy, and Venezuela have confirmed
the finding of inflammation and LNH in
ASD.10-14, 29
Immune profiling of the intestinal
disease in ASD
Furlano (2001), Torrente (2002),
and Ashwood (2004) have described
immune abnormalities and abnormal
cytokine profiles in the intestine
of ASD children with GI symptoms.
Cytokines are chemical messengers that
communicate between cells to increase
or decrease the activity of the immune
system. In ASD children, upper and
76 THE AUTISM FILE | www.autismfile.com | info@autismfile.com REPRINTED WITH PERMISSION © THE AUTISM FILE
Reflux Esophagitis (Endoscopy)
Figure 1: (a) endoscopic image typical of reflux esophagitis (b) matches the 4 histological
criteria for diagnosis of reflux esophagitis.
lower gastrointestinal inflammation
have been found to different degrees
of severity;6 the relationship, if any,
between the severity of the bowel
inflammation and the autistic features
is not yet known. Using techniques that
identify specific immune cell types,
under the microscope these investigators
have shown characteristic patchy
inflammation in many ASD children
including a pronounced infiltrate of
CD4, CD8, gamma delta T cells and
antibody producing plasma cells. The
inflammatory response is different from
that seen in IBD (inflammatory bowel
disease) patients and in the normal
controls. The inflammation was more
localized to the epithelium and basement
membranes (superficial layers) of the gut
mucosa than that which is commonly
seen in classic IBD.34-38
Intestinal symptoms are not necessary
for the presence of intestinal disease.
An increase in intestinal permeability
in patients with ASD who were not
symptomatic from the GI perspective
and who had no other evidence of GI
illness was described by D’Eufemia in
1996 8 and in 1998-2000. Wakefield
and colleagues suggest the association
of inflammatory intestinal chronic
disease and autism from an analysis
of ileal and colonic biopsies where the
frequent presence of LNH and unspecific
colitis are evidenced.9-15 Currently, the
structure and function of the digestive
Reflux Esophagitis (Biopsy)
mucosa in autistic children is being
studied in the search for an association
between the histological changes and
the etiopathogenesis of autism.
Upper gastrointestinal endoscopy
Based upon our experience, we stress the
importance of a full examination of the
GI tract in symptomatic children with any
degree or type of ASD, to include upper
GI endoscopy (esophagus, stomach and,
duodenum). The literature supports
the existence of upper gastrointestinal
disease in these children.3-15 In our
Venezuelan series,13 we found that 88%
of the patients had reflux esophagitis,
55% had nonspecific gastritis due to
Helicobacter pylori, 52% of ASD children
had Giardia intestinalis infection,
and 37% had chronic unspecific
inflammation of the small intestine.
This was in addition to the findings of
colitis with LNH (69%), of which 11%
had eosinophilic colitis, and 100% of the
children presented chronic inflammation
and lymphoid nodular hyperplasia (LNH)
of the terminal ileum.
Esophagus
Over the past decade, the expanding
body of literature on esophageal
physiology and pathology has led to
the perception that the esophagus is
an immunologically active organ. It
can respond to a variety of stimuli by
augmenting certain immunological
ISSUE 32 2009
defenses, including recruitment and
activation of eosinophils – immune
cells involved in allergic responses.
Esophageal pathology is common in
Venezuelan children with ASD (in our
study, degrees of esophagitis were
described according to the guidelines
of the European and American Society
of Pediatric Gastroenterology and
Nutrition. 11,12). One of the most
common visual findings in eosinophilic
esophagitis is linear streaks of nodular
mucosa. Eosinophilic esophagitis is a
common pathology in ASD children and
is defined as an increase in the number
of eosinophils seen microscopically per
high-power field (HPF). For eosinophils,
the normal range in the esophagus is
between 0-2 cells/HPF. In eosinophilic
esophagitis associated with various food
allergic disorders, we often see 20 cells/
HPF or more.14, 24, 40, 41
Reflux esophagitis, in which stomach
acid moves back up into the lower
esophagus, is also common. Visually
this is indicated by esophageal rings,
mucosal erythema, linear ulcers, and
erosive esophagitis when damage from
the acid reflux is extreme. The finding
is confirmed by biopsy. (Figure 1) In
our series, the most frequent diagnosis
was reflux esophagitis that was present
in 89% of the children with autism
compared with 49% in the control group,
with a significant difference between the
groups of p<0.001.14 A neurotypical child
with esophageal pathology as described
above would complain bitterly; for the
nonverbal child, drawing attention to
the source of their distress is particularly
challenging, and doctors should retain a
high index of suspicion.40
Stomach
Our experience with gastric disease in
Venezuela is somewhat different from
the experience of others since we have
a high rate of infection with H. pylori
in children. H. pylori can be a painful
bacterial infection, and children who
Since then, other studies carried out in the United States, Brazil, Italy, and
Venezuela have confirmed the finding of inflammation and LNH in ASD.
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have it in their stomach characteristically
Endoscopic Image of Duodenum
have a very obvious nodular gastritis.
(Figure 4) We observed chronic H.
pylori-associated gastritis in 55.6% of the
children with autism and 33.3% in the
controls, compared with active chronic
gastritis without H. pylori in 33.33% of
the children with autism and 2.56% of
the controls. This compares with a finding
of gastritis in 15 of 36 ASD children by
Horvath et al. in US children.14
(When assessing stomach pathology,
we used the Sydney System for
classification and grading of gastritis14 Figure 2: nodular duodenal bulb
and a raised eosinophil count as one
greater than 20 cells per HPF).
One of the characteristic lesions we see
in the stomach is reactive gastropathy,
which can be associated with the reflux of
bile into the stomach from the duodenum.
Endoscopic findings include congestion,
enanthema (an eruption on the mucus
membrane of the stomach), erythema
(reddening), micro- and macro-nodularity
in the body and antrum, ulcers, and biliary
reflux as a result of hypomotility (reduced
peristalsis) moving food from the antrum
of the stomach into the duodenum. One Figure 3: lymphoid accumulations cumulus
observation in affected children is that in the esophagical mucosa of a 4-year-old
they have very distended bellies. child with diagnosis of severe autism.
Small Bowel
The small bowel is the duodenum, the Stomach
jejunum, and the ileum. It is the longest
part of the bowel, and it is important
because it is where the body absorbs
calories and nutrients. Currently, the small
bowel can be visualized using capsule
endoscopy, but, other than the very first
and last parts of the small intestine it is
not routinely accessible to biopsy. We
sometimes find celiac disease in children
with autism, but it is surprisingly rare,
considering that this group is exceedingly
sensitive to gluten. Because celiac disease
Figure 4: corresponds to image of gastric
can only be diagnosed with certainty while
antrum where nodularity (stony antrum) can
the child is ingesting gluten, it is critical
be seen, characteristic of the infection by
to obtain baseline celiac antibodies before
Helicobacter pylori.
beginning a gluten-free diet in order to
confidently exclude celiac disease.
77
 BIOMEDICAL

Treatment gluten and casein, among others (because

The diagnosis and treatment of these may result in an immune/allergic
gastrointestinal disease in children with response that may exacerbate any intestinal
autism involves an exhaustive assessment inflammation) and strengthen their immune
that includes a detailed case history and system throughout with the treatment of
physical examination, investigation of any IgA secretory deficiency.
the macroscopic characteristics of the All of the intestinal lesions, damage, or
stool, laboratory testing, a complete stool abnormalities are potentially treatable.Many
analysis, a search for intestinal infections to children respond very well to combinations
include parasites, Campylobacter jejuni and of the following: of a restricted diet,
Clostridium difficile, and a fungal culture. anti-inflammatory medication, probiotics,
Treatment is designed to reduce damage antibiotics, antifungals, and digestive
and inflammation of the gastrointestinal enzymes, among other things. There is
mucosa, diminish intestinal permeability, correlation between the treatment of GI
improve nutrient intake and micronutrient disease and improved cognitive functions,
Figure 5: histologic specimen with
absorption, and treat any associated decreased self-aggressiveness, and
eosinophilic gastritis
infection(s). In addition, the children improvements in attention, visual contact,
should avoid proteins in the diet such as and sleep disorders.
Colitis with LNH
In summary, particular attention should be paid to:
1. Nutritional intervention (e.g., gluten-free/casein-free diet and appropriate
supplementation)
2. Treatment of gastroesophageal reflux disease (GERD)
3. Treatment of eosinophilic esophagitis
4. Management of gastritis with or without Helycobacter pylori infection
5. Treatment of constipation29
6. Management of pancreatic insufficiency30
Figure 6: image where total loss of normal
7. Antifungal treatment
characteristics of the colon can be observed. 8. Probiotics, prebiotics (foods that support beneficial bacteria), fermented
foods31, 32
9. Treatment of other infections including Clostridium difficile, intestinal
Histological image of Ileum parasites such as protozoarians and helminths, and other bacteria including
ECEP, Klebsiella pneumoniae, Citrobacter feundii, Enterobacter cloacae,
Pseudomona aeruginosa, Proteus mirabilis, Aspergillus, Trichosporum and
Geotrichum sp, among others.

Figure 7: eosinophilic colitis at 10X in a
child with severe autism.
Conclusions
Our experience of Venezuelan children with ASD is that most have GI symptoms that may
not be immediately evident or may not be obviously related to intestinal distress. The
absence of obvious GI symptoms does not mean an absence of the disease. There may be
chronic inflammation anywhere from the esophagus down to the rectum that may be seen
even in asymptomatic patients; the GI evaluation is an essential part of the investigation
protocol in ASD. In our experience, treating GI disease is consistently associated with
improved cognitive functions, decreased self-aggressiveness, better attention, improved
eye contact, and decreased sleep disorders.

In our experience, treating GI disease is consistently associated with improved

cognitive functions, decreased self-aggressiveness, better attention, improved
eye contact, and decreased sleep disorders.
78 THE AUTISM FILE | www.autismfile.com | info@autismfile.com REPRINTED WITH PERMISSION © THE AUTISM FILE ISSUE 32 2009
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