Vaccinazioni per l’infanzia ed
gastrointestinali dai Vaccini
Metalli tossici dei vaccini = Autismo vedi:
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vale la pena ricordare che le stesse persone che
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Sentenza 2012 - Trib. Rimini su
Enterocolitis in Children
With Developmental Disorders
University Department of
Medicine, Royal Free and University College Medical
School, London, United Kingdom.
pathology, i.e., ileocolonic lymphoid nodular
hyperplasia (LNH) and mucosal inflammation, has been
described in children with developmental disorders. This
study describes some of the endoscopic and pathological
characteristics in a group of children with
developmental disorders (affected children) that are
associated with behavioral regression and bowel symptoms,
and compares them with pediatric controls.
Ileocolonoscopy and biopsy were performed on 60 affected
children (median age 6 yr, range 3-16; 53 male).
Developmental diagnoses were autism (50 patients),
Asperger's syndrome (five), disintegrative disorder (two),
attention deficit hyperactivity disorder (ADHD) (one),
schizophrenia (one), and dyslexia (one).
ileal LNH was graded (0-3) in both affected children and
37 developmentally normal controls (median age 11 yr,
range 2-13 yr) who were investigated for possible
inflammatory bowel disease (IBD). Tissue sections were
reviewed by three pathologists and scored on a standard
proforma. Data were compared with ileocolonic biopsies
from 22 histologically normal children (controls) and 20
children with ulcerative colitis (UC), scored in an
identical manner. Gut pathogens were sought routinely.
RESULTS: Ileal LNH was present in 54 of 58 (93%)
affected children and in five of 35 (14.3%) controls (p
< 0.001). Colonic LNH was present in 18 of 60 (30%)
affected children and in two of 37 (5.4%) controls (p <
0.01). Histologically, reactive follicular hyperplasia
was present in 46 of 52 (88.5%) ileal biopsies from
affected children and in four of 14 (29%) with UC, but
not in non-IBD controls (p < 0.01). Active ileitis was
present in four of 51 (8%) affected children but not in
controls. Chronic colitis was identified in 53 of 60
(88%) affected children compared with one of 22 (4.5%)
controls and in 20 of 20 (100%) with UC. Scores of
frequency and severity of inflammation were
significantly greater in both affected children and
those with UC, compared with controls (p < 0.001).
CONCLUSIONS: A new variant of inflammatory bowel disease
is present in this group of children with developmental
PMID: 11007230 [PubMed - indexed for MEDLINE]
(trattamenti, Cure, Terapie) +
Amish senza autismo
perche' NON vaccinano +
gastrointestinali da vaccino
Contribution - September 2000 - Volume 95, Number 9
- Pages 2285-2295
in Children With Developmental Disorders
J. Wakefield, F.R.C.S.,a,b
A. Anthony, M.Sc., Ph.D., M.B.B.S.,b
S. H. Murch, Ph.D., F.R.C.P., F.R.C.P.C.H.,b
M. Thomson, MB.ChB., M.R.C.P., F.R.C.P.C.H.,c
S. M. Montgomery, Ph.D.,c
S. Davies, M.R.C.Path.,b
J. J. O'Leary, M.D., D.Phil., M.R.C.Path.,b
M. Berelowitz, F.R.C.Psych.,e
and J. A. Walker-Smith, M.D., F.R.C.P., F.R.A.C.P., F.R.C.P.C.H.d
Intestinal pathology, i.e., ileocolonic lymphoid nodular
hyperplasia (LNH) and mucosal inflammation, has been described in
children with developmental disorders. This study describes some
of the endoscopic and pathological characteristics in a group of
children with developmental disorders (affected children) that are
associated with behavioral regression and bowel symptoms, and
compares them with pediatric controls.
Ileocolonoscopy and biopsy were performed on 60 affected children
(median age 6 yr, range 3-16; 53 male). Developmental diagnoses
were autism (50 patients), Asperger's syndrome (five),
disintegrative disorder (two), attention deficit hyperactivity
disorder (ADHD) (one), schizophrenia (one), and dyslexia (one).
Severity of ileal LNH was graded (0-3) in both affected children
and 37 developmentally normal controls (median age 11 yr, range
2-13 yr) who were investigated for possible inflammatory bowel
disease (IBD). Tissue sections were reviewed by three pathologists
and scored on a standard proforma.
Data were compared with ileocolonic biopsies from 22 histologically normal children (controls)
and 20 children with ulcerative colitis (UC), scored in an
identical manner. Gut pathogens were sought routinely.
Ileal LNH was present in 54 of 58 (93%) affected children and in
five of 35 (14.3%) controls (p < 0.001). Colonic LNH was
present in 18 of 60 (30%) affected children and in two of 37
(5.4%) controls (p < 0.01). Histologically, reactive
follicular hyperplasia was present in 46 of 52 (88.5%) ileal
biopsies from affected children and in four of 14 (29%) with UC,
but not in non-IBD controls (p < 0.01). Active ileitis
was present in four of 51 (8%) affected children but not in
Chronic colitis was identified in 53 of 60 (88%)
affected children compared with one of 22 (4.5%) controls and in
20 of 20 (100%) with UC. Scores of frequency and severity of
inflammation were significantly greater in both affected children
and those with UC, compared with controls (p < 0.001).
A new variant of inflammatory bowel disease is present in this
group of children with developmental disorders.
this article as:
. Wakefield AJ, Anthony A, Murch SH, Thomson M, Montgomery SM,
Davies S, O'Leary JJ, Phil D, Berelowitz M and Walker-Smith JA.
Enterocolitis in Children With Developmental Disorders. Am J
Departments of Medicine, bHistopathology, cPaediatric
Gastroenterology, and dPaediatric Psychiatry, Royal
Free and eUniversity College Medical School, Royal Free
Campus, London, United Kingdom, and University Department of
Pathology, Coombe Women's Hospital and Trinity College, Dublin,
have recently described a characteristic pattern of intestinal
inflammation in a cohort of children with developmental disorders
In these children, the majority of whom had autism, a period of
initial normal development was followed by developmental
regression and loss of acquired skills, sometimes occurring
precipitously over a period of days to weeks. Long-standing
intestinal symptoms, as described previously (1),
were typical of this group of children. These symptoms had often
started at around the same time as the behavioral changes.
lymphoid nodular hyperplasia (LNH) was a consistent feature of
this condition, an observation that has been reported subsequently
in children with attention deficit hyperactivity disorder (ADHD)
and non-IgE-mediated food allergy (2).
There is an anecdotal impression that LNH is a common finding in
children undergoing ileocolonoscopy, although this has not been
subjected to systematic analysis in a controlled study. It cannot
be assumed that LNH is a normal finding in children, as
aymptomatic children are not subjected to ileocolonoscopy, and LNH
may produce symptoms in its own right (3).
Chronic intestinal LNH is a feature of either congenital or
acquired immunodeficient states (4, 5, 6,
and has been described in congenital B cell abnormalities (5,
and common variable immunodeficiency (7,
In its persistent acquired form, ileal LNH has been reported in
association with infection with human immunodeficiency
before the development of AIDS (10).
other consistent feature of the intestinal lesion was a
mild-to-moderate colitis that lacked the specific diagnostic
features of either Crohn's disease or ulcerative colitis (1).
This combination of features, i.e., LNH and nonspecific
colitis, indicates the possibility of chronic mucosal and/or
systemic immune dysregulation. Systemic immunological
abnormalities are not infrequent in children with autistic
spectrum disorders (11,
although the origin and significance of the findings are uncertain.
These immune changes, plus the presence of myelin basic protein (MBP)
and inhibition of macrophage migration to MBP (16),
have led some workers to suggest that the behavioural syndrome may
be associated with cerebral damage due to an autoimmune response
to myelin or other structural components of the CNS (15,
As part of our initial study (1)
we undertook cerebral magnetic resonance imaging, EEG, and
biochemical analysis of cerebrospinal fluid; none of these
investigations indicated cerebral inflammation that would be
consistent with autoimmune demyelination, although a more subtle
lesion remains a possibility.
Alternatively, others have proposed
that some forms of autism may arise from the toxic effects of
intestinal products on the developing brain (17,
a situation that may have some overlap with hepatic enephalopathy.
An early childhood enterocolitis would be more consistent with the
study sought to describe some of the characteristic endoscopic and
histopathological features of this syndrome in a larger cohort of
children with developmental disorders and intestinal symptoms, and
to compare the findings with those in developmentally normal
children undergoing ileocolonoscopy.
study involved the analysis of data from 60 consecutive children
with developmental disorders (affected children) including those
12 children described in a preliminary report (1).
The median age of the children was 6 yr (range 3-16 yr) and 53
were boys, consistent with the male bias of developmental
Developmental diagnoses in the affected children were autism (50
patients), Asperger's syndrome (five), disintegrative disorder (two),
attention deficit hyperactivity disorder (ADHD) (one), and
schizophrenia (one). The latter child was the oldest in the cohort,
at 14 yr of age.
The remaining child in this cohort, a girl 8 yr
of age, had dyslexia and learning difficulties: she underwent
developmental regression from approximately 54 months of age,
which was associated with mouth ulcers, conjunctivitis, and severe
constipation. Her developmental status is currently under
is a behavioral syndrome that consists of qualitative impairments
in social interaction and communication, with restrictive,
repetitive, and stereotypic patterns of behavior. Delays or
abnormal functioning in at least one of these areas occurs before
the age of 3 yr. Asperger's syndrome is a high-functioning
autistic spectrum disorder, and disintegrative disorder is a
regressive condition occurring at age >3 yr in a previously
normal child. Loss of acquired skills may occur precipitously or
over a period of months. The behavioral features are similar to
those of autism but may be accompanied by loss of bowel and
bladder control (20).
majority of affected children were white (57),
but two were of Middle-Eastern origin, and one child had an Indian
father and a white mother.
but three affected children had a developmental disorder that was
associated with a clear history of regression, with loss of
acquired skills after
year of documented normal development (general practitioner/health
visitor records). In three cases, affected children who had been
developmentally normal failed to progress beyond a certain point,
but did not regress.
All but one of the affected children had
current intestinal symptoms consisting of abdominal pain,
constipation, diarrhea (or alternating constipation and diarrhea),
and bloating. The one affected child who did not have current
intestinal symptoms was investigated at his parents' and general
practitioner's request. Affected children were consistently
fastidious in their eating habits, with a diet limited largely to
cereals, potato crisps, and bread.
Despite this, they typically
seemed well nourished, with anthropomorphic indices within normal
limits. Certain foodstuffs such as dairy products were reported by
parents to produce deterioration in behavior, whereas withholding
such foods apparently produced behavioral improvement—in
particular, for aggression, eye contact, and sleep pattern.
According to parental reports, recognizably undigested food was
often seen in stools.
and developmental histories were taken, and a routine physical
examination was conducted. A fasting, morning blood sample was
taken for routine hematology and biochemistry. Sera were screened
for antigliadin and antiendomyseal antibodies. Common enteric
pathogens were sought by routine serology, microscopy, and
culture. A review of the children was undertaken by an experienced
child psychiatrist to confirm the developmental diagnosis using
DSM-IV criteria (20).
children underwent routine ileocolonoscopy and mucosal biopsy.
Ileal LNH was classified subjectively according to prominence and
extent as mild (grade 1), moderate (grade 2), or severe (grade 3),
or as grade 0 if the ileum showed no LNH (Fig.
according to the report provided by one of three physicians.
Similarly, ileal appearances were graded in 37 developmentally
normal children (median age 11 yr, range 2-13 yr). All of these
children had been investigated for symptoms of possible
inflammatory bowel disease, although the final diagnosis was
neither Crohn's disease nor ulcerative colitis. Diagnoses in these
children included idiopathic constipation (five patients), polyps
(two), and LNH (five). In the majority (thirty), including those
with constipation, the colonoscopy was reported as normal, and
follow-up has not revealed any other abnormality.
Lymphoid nodular hyperplasia (LNH) of the terminal ileum in
affected children showing representative grades of LNH: (A)
none (score 0); (B) mild (score 1); (C) moderate
(score 2); and (D) severe (score 3).
biopsies were taken from the ileum, cecum/ascending colon,
transverse colon, descending/sigmoid colon, and rectum.
Hematoxylin and eosin-stained histological sections from all
biopsies were reviewed in the routine pathology laboratory,
followed by independent review and scoring on a standard proforma
In those cases where there was disagreement between these two
reports, sections were examined and reported by a third senior
pathologist, whose arbitration provided the final score. In an
identical manner, histological sections from the ileum and colon
of children without developmental disorder were scored (median age
11.5 years; range 2-13).
These included 22 consecutive ileocolonoscopic biopsy series that had been reported as normal
after routine histopathology assessment. All children in this
non-IBD control group had undergone ileocolonoscopy for
investigation of intestinal symptoms and are included in the 37
endoscopic controls, as described above. To validate further the
evaluation and scoring, 10 coded ileocolonic biopsy series (five
affected children and five non-IBD controls) were reviewed at
another institution by a senior pathologist in an observer-blinded
fashion. Data from these independent assessments were compared.
Histopathology Proforma Used for Scoring of All Biopsies From
Affected Children (Autistic Enterocolitis), Non-IBD Controls, and
Those With Ulcerative Colitis
interstitial neutrophils in lamina propria (LP)
neutrophils in LP
increase in LP mononuclear cells
increase with loss of stratification within LP
of epithelial basal lamina.
changes: prominent germinal centres; tingible body
enlargement with confluence
order to compare the site and degree of pathological changes in
biopsies from affected children with those of a well characterized
IBD, ileocolonic biopsy series from 20 children with established
ulcerative colitis (median age 14 yr, range 8-15 yr) were examined
and scored in an identical manner.
avoid selection bias, children in all groups were chosen
consecutively on the basis that they fulfilled the primary
criteria; that is, developmental disorder with bowel symptoms,
developmentally normal with bowel symptoms, developmentally normal
with normal histology, or ulcerative colitis.
clinical investigations were undertaken with fully informed,
written consent from the parents. The initial phase of these
was approved by the Ethical Practices Committee of the Royal Free
Hampstead NHS Trust. Thereafter, children were investigated
according to clinical need after a formal referral from each
child's General Practitioner or Consultant.
analyses were performed using SPSS 7.5 for Windows and EpiInfo
test was used to investigate differences in endoscopic and
histopathological features between the affected children and the
control groups. Where any cell in the analysis contained five or
fewer subjects, two-tailed Fisher's exact test was used to assess
significance, to adjust for the potential effect of small numbers.
The Spearman rank correlation was used to investigate the
relationship between grade of LNH (0-3) and absolute lymphocyte
count among the affected children.
Complete ileoscopy, in which the terminal ileum was visualized and
biopsied, was successful in 58 of 60 (97%) affected children and
in 35 of 37 (95%) non-IBD controls. The frequency and grade of
ileal LNH in these two patient groups is shown in
Representative grades of ileal LNH are shown in
The data demonstrate not only the consistent presence of LNH in
the ileum of affected children 54 of 58 (93%), but also its
relative infrequency in developmentally normal children undergoing
investigation for similar intestinal symptoms (five of 35; 14.3%);
this difference is statistically significant (p <
In affected children, 76% scored either moderate or
severe; in non-IBD controls, all five children with ileal LNH
scored either moderate (n = 4) or severe (n = 1). Of these five
controls, symptoms that were the indication for ileocolonoscopy
included chronic abdominal pain in four and change in bowel habit
in one; endoscopically, there was no other demonstrable pathology
to account for these symptoms.
Percentage of children showing ileal lymphoid nodular hyperplasia
(LNH), comparing affected children
with developmentally normal children
, investigated for symptoms of inflammatory bowel disease, in whom the
final diagnosis was neither Crohn's disease nor ulcerative colitis.
LNH was significantly more common in affected children than in
controls (p < 0.001).
Complete colonscopy was successful in all 60 (100%) of the
affected children and all 37 (100%) non-IBD controls. Colonscopies
were scored for either the presence or absence of the following:
LNH (not graded), red halo sign surrounding follicles (21),
loss of vascular pattern, mucosal granularity, mucosal erythema,
and presence of ulcer(s).
These features, which are recognized
correlates of associated histopathological abnormality, were noted
previously to be characteristic of this patient group (1).
These features were recorded both for cases and for non-IBD
controls; the data are shown in
Colonic LNH was present in 18 of 60 (30%) affected children
compared with only two of 37 (5.4%) non-IBD controls (p
< 0.01). Similarly, of the other six endoscopic features
described above, all but ulceration are significantly more common
in affected children compared with controls (p < 0.05).
Although the mean age of the developmentally normal comparison
group was significantly greater than that of the affected children,
the presence or absence of LNH was not related to age in either
Colonoscopic features in affected children
and non-inflammatory bowel disease controls
. Colonoscopies were scored for either the presence or absence
of lymphoid nodular hyperplasia, red halo sign, loss of vascular
pattern (LVP), mucosal granularity, mucosal erythema, and
ulceration. All of the features except ulceration were
statistically significantly more common in affected children than
in controls (p < 0.01).
and colonic biopsies from 60 affected children, 22 non-IBD control
children, and 20 children with ulcerative colitis were examined
initially by a clinical histopathologist, and were subsequently
evaluated and scored by another pathologist using a standard
In the 60 affected children, there was discordance between the two
reports in five cases: these were resolved by a third pathologist,
whose independent review agreed with the first pathologist in two
cases and the second pathologist in three cases. There was
disagreement between pathologists concerning the interpretation of
biopsies from only one of the non-IBD controls (which was resolved
as showing mild inflammation in a cecal biopsy) and in none of the
children with ulcerative colitis.
ileocolonic biopsy series were reviewed and scored in an
observer-blinded fashion at an independent institution. No
indication was given of how many samples came from each patient
Cases were clearly distinguished from controls by the
blinded reviewer. Out of a possible total of 15 points,
independent scores were identical for the same criterion in four
of 10 cases (40%), within one point of each other in five of 10
cases (50%), and within two points of each other in one of 10
cases (10%) (Spearman rank correlation 0.79; p < 0.006).
No reviewer scored systematically higher or lower than the other.
HISTOLOGY. A total of 86 ileal biopsies were assessed and scored.
This total comprised 52 biopsies from affected children (seven
biopsies, consisting of fragments of villi only, were considered
inadequate for evaluation), 20 from non-IBD controls, and 14 from
children with ulcerative colitis. Reactive follicular hyperplasia
(RFH) was identified in 47 of 51 (92%) biopsies from affected
children and in four of 14 (29%) with ulcerative colitis. It was
not present in any of the 20 biopsies from non-IBD controls.
differences between biopsies from affected children and from both
non-IBD controls and those with ulcerative colitis are significant
(p < 0.001 and p < 0.01, respectively).
Qualitatively, ileal lymph nodes in those children with LNH showed
marked expansion of lymphoid tissue in histological section, as
described previously (1).
Follicle numbers per biopsy were increased from 2-3 follicles per
biopsy in normal ileal biopsies to 4-5 per biopsy in those with
LNH: follicles were confluent with loss of follicle-to-follicle
demarcation. In comparison with normal follicles, the germinal
centers were grossly enlarged and reactive, as indicated by
numerous tingible body macrophages.
The outer margins of the T
cell zone were not well defined as they were in normal ileal
follicles, with the lymphoid compartment extending into, and
apparently expanding, adjacent villi.
There was also disruption,
but not destruction, of adjacent crypts. Expansion of lymphoid
tissue around crypts gave the impression of a decrease in crypt
numbers, a histological appearance similar to that described by Fiber and Schaefer (3).
In addition, neutrophils and lymphocytes were often seen
infiltrating the epithelium overlying follicles: neutrophils were
also seen infiltrating the crypt epithelium (acute cryptitis) in
Overall, active ileitis (neutrophilic infiltration)
was seen in four of 51 (8%) ileal biopsies from affected children.
Aphthoid ulceration was seen in two of 51 (4%) biopsies.
In the 20
non-IBD control ileal biopsies, none showed active inflammation.
Only two (4%) biopsies from affected children scored positively
for the presence of an increase in intraepithelial lymphocytes,
and two (4%) for the presence of eosinophil infiltration of the
lamina propria. These features were not present in either non-IBD
or ulcerative colitis controls. These differences were not
statistically significant because of small numbers.
HISTOLOGY. A total of 380 colonic biopsies were examined and
scored; these included 229 biopsies from affected children, 80
from non-IBD controls, and 71 from children with ulcerative
The numbers and percentage of biopsies in each group
showing pathological changes are shown in
Table 2 and
respectively. Only one cecal biopsy in the non-IBD controls showed
evidence of inflammation, which was scored as mild. In contrast, a
high percentage of biopsies from throughout the colon showed
pathological changes in both affected children and those with
The differences between both affected children
and those with ulcerative colitis and non-IBD controls, for the
proportion of biopsies exhibiting pathological change are, for
each site, significant (p < 0.001) (Table
Inflammatory changes in biopsy series from individual affected
children, although distributed throughout the colon, were patchy.
Some of the histological characteristics of this colitis are shown
Overall, chronic inflammation was identified in colonic biopsies
from 53 of 60 (88%) affected children, compared with one of 22
(4.5%) non-IBD controls and 20 of 20 (100%) children with
ulcerative colitis. The differences between both affected children
and children with ulcerative colitis versus the non-IBD
controls are statistically significant (p < 0.001).
There is no statistically significant difference between affected
children and those with ulcerative colitis for the proportion of
biopsies showing chronic inflammation (p > 0.1). An
excess of intraepithelial lymphocytes scored positively in eight
of 60 (13%) of affected children, 0 of 22 (0%) non-IBD controls,
and 0 of 20 (0%) with ulcerative colitis.
There are no
statistically significant differences between the respective
groups (p > 0.1). Eosinophil infiltration of the lamina
propria was observed in 24 of 60 (40%) affected children, 0 of 20
(0%) non-IBD controls, and four of 20 (20%) with ulcerative
The difference between affected children and non-IBD
controls is statistically significant (p < 0.001).
differences between affected children and those with ulcerative
colitis, versus those with ulcerative colitis and non-IBD
controls, are not statistically significant (p > 0.1).
Subepithelial apoptosis/nuclear debris was present in 30 of 60
(50%) affected children, in eight of 22 (36%) non-IBD controls,
and in 16 of 20 (80%) with ulcerative colitis. These differences
are not statistically significant (p > 0.2).
not scored prospectively, it was the clear impression of all
reviewing pathologists that, whereas the presence of subepithelial
apoptosis/nuclear debris was a feature of normal biopsies, its
extent was much greater in inflamed biopsies (that is, those from
either affected children or children with ulcerative colitis).
Distribution of histopathological changes in the ileum and colon
(C/A = cecum/ascending, T = transverse, D/S = descending/sigmoid,
and R = rectum) of affected children
compared with controls whose biopsies were reported as normal (non-IBD
controls), and children with ulcerative colitis. The differences between both affected children and those with
ulcerative colitis, and non-IBD controls, for the proportion of
biopsies showing histological change at each site, are
statistically significant (p < 0.001).
Normal colonic mucosa from a non-inflammatory bowel disease
control child. The surface epithelium is uniform, and the lamina
propria shows loosely organized connective tissue and normal
stratification of cellular density, which characteristically
increases toward the epithelial surface. The demarcation between
lamina propria and epithelial basement membrane is distinct (magnification
×40). (B) Colonic mucosa from an autistic child. There is
mild disruption and lymphocytic infiltration of the surface
epithelium. The crypt epithelium is infiltrated by lymphocytes and
neutrophils. The superficial subepithelial basement membrane is
indistinct compared with (A).
The upper two-thirds of the
lamina propria contains an excess of lymphocytes, plasma cells,
and macrophages, with loss of stratification. The matrix of the
lamina propria appears hyaline in nature (magnification ×40). (C)
Crypt abcess formation in a child with autistic enterocolitis (magnification
×100). (D) Crypt distortion in a child with autistic
enterocolitis; bifid crypts are seen to the left and right of the
micrograph (magnification ×100). Micrographs (B-D) come
from different affected children.
Pathological Changes in Biopsies From Affected Children, Children
With Ulcerative Colitis, and Non-IBD Controls
Enterocolitis (Affected Children)
< 0.001 compared with non-IBD controls. † p
< 0.01 compared with affected children.
the overall severity of pathological change in the respective
groups, by expressing the scores as a percentage of the total
possible score (Table
for biopsies from each site. This format contrasts the
histological normality of the non-IBD control biopsies with the
progressively increasing severity of ulcerative colitis from the
proximal to the distal colon. The data from affected children
reflect a subtle variant consisting of an intermediate condition
of mild to moderate inflammation that, overall, seems not to vary
in severity according to site. The differences between both
affected children and those with ulcerative colitis and non-IBD
controls, for severity of histological change at each site, are
statistically significant (p < 0.001). Ulcerative
colitis biopsies showed statistically significantly more severe
change at each site compared with those from affected children (p
Severity of histopathological changes in the ileum and colon (C/A
= cecum/ascending, T = transverse, D/S = descending/sigmoid, and R
= rectum) of affected children
compared with controls whose biopsies were reported as normal (non-IBD
controls), and children with ulcerative colitis. The differences between both affected children and those with
ulcerative colitis, and non-IBD controls, for severity of
histological change at each site are significant (p <
Ulcerative colitis biopsies showed statistically
significantly more severe change at each site, except the ileum,
compared with those from affected children (p < 0.001).
blood biochemistry, including liver function tests, was
unremarkable. Of the inflammatory markers, the ESR was raised
(>15 mm/h) in seven of 44 (16%, range 18-26 mm/h), and the CRP
was raised (>5 mg/L) in four of 38 (11%, range 6-17 mg/dl)
affected children for whom these data were available. Hemoglobin
was low (<11.5 g/dl) in nine of 55 (16%, range 9.8-11.2 g/dl),
whereas hematocrit was low (<0.37) in 19 of 54 (35%, range
0.3-0.36). On routine differential white cell count, eight of 55
(14.5%) affected children had a neutrophil leucocytosis (>8.5
× 109/L, range 13.8-19.7 × 109/L), whereas
34 of 50 (68%) were lymphopenic compared with the age-standardized
reference range. There was no statistically significant
relationship between absolute lymphocyte count and grade of LNH
when analyzed by the Spearman rank correlation (p >
is notable that all four of the affected children with active
ileitis had a raised ESR (range 19-30 mm/h), and that seven of the
eight affected children with a neutrophil leucocytosis had active
colitis. Only one child had both active ileitis and active colitis:
in this child the ESR, but not the neutrophil count, was elevated.
microscopy and culture, and serum antibody studies identified no
common gut pathogens except in one child, in whom Giardia cysts
were identified by microscopy.
Findings and Developmental Diagnosis
the gastrointestinal findings were similar in affected children,
irrespective of their developmental diagnosis.
The one possible
exception was that a girl with dyslexia associated with
developmental regression at 54 months of age, who had ileocolonic
LNH without ileitis or colitis.
data both confirm and extend our original observations (1),
and indicate a subtle and consistent pattern of intestinal
pathology in this cohort of consecutively referred children. The
combination of ileocolonic LNH and colitis in children with
developmental disorders distinguished them from developmentally
normal children with similar symptoms (including abdominal pain
and constipation) in whom LNH and histopathological change were
These observations, in a broader diagnostic group of
children with developmental/psychiatric disorders, and the recent
report of Sabra et al. (2)
of similar intestinal pathology in children with ADHD, suggests
that the findings may be relevant more widely to childhood
study provides a quantitative assessment of a qualitative
interpretation of histopathological changes in the ileocolonic
mucosa. We have previously reported the quantitative assessment of
cellular infiltration of the mucosa in biopsies from these
children, employing immunohistochemistry and cell counting (22).
That study confirmed the presence of a statistically significant
increase in mucosal macrophage infiltrate and cells expressing
class-II MHC antigen in biopsies from affected children, compared
with normal controls. Further quantitative studies have shown a
statistically significant excess of CD3+, CD8+,
cells, and of Syndecan-1+ plasma cells in the lamina
propria, and evidence of increased epithelial proliferation in
affected children compared with both normal children and those
with chronic constipation (R. Furlano et al., submitted for
The pathology seems to reflect a subtle new variant
of inflammatory bowel disease that lacks the specific diagnostic
features of either Crohn's disease (e.g., granulomata) or
ulcerative colitis (e.g., contiguous distal to proximal
The inflammatory features were accompanied
by endoscopic changes and included a patchy, mild-to-moderate pancolitis, where (with the proviso that only mucosal
biopsies were studied) they were confined to the upper lamina
propria/epithelium. It is of possible clinical relevance that
active disease in the ileum and colon was reflected systemically
in a raised ESR and a neutrophil leucocytosis, respectively.
view of the presenting symptoms in the affected children, the
majority underwent ileocolonscopy rather than investigation of the
upper gastrointestinal tract. However, Horvath et al. have
recently reported compelling evidence of inflammatory changes in
the esophagus, stomach, and duodenum in a majority of autistic
children with symptoms similar to those described here (23).
Where it is indicated, we have included upper endoscopy and biopsy
in our protocol. Our initial findings are consistent with those of
Horvath et al. and will be reported later.
median age of affected children was lower than that in either of
the two control groups. However, within the controls groups there
was no relationship between age and either endoscopic or
histopathological features of disease, indicating that the
comparisons made here are valid. The natural history of this
condition—autistic enterocolitis—is not known; because Crohn's
disease and ulcerative colitis are rare in this age group, it is
too soon to say whether or not the pathology will progress to a
typical IBD phenotype.
is notable that 68% of affected children had a lymphopenia.
Immunological abnormalities are a recurring feature in studies of
children with autism (25,
and detailed immunological studies of affected children will be
reported as a follow-up to this report. Reactive follicular
hyperplasia is an antigen-driven response (9).
In a preliminary study, we have reported evidence of measles virus
nucleocapsid protein in follicular dendritic cells of the reactive
ileal lymphoid tissue and raised serum measles IgG
immunoreactivity in some affected children (26).
An association between measles virus, immunodysregulation, and
autism was also suggested by the recent study by Singh et al.
Measles virus is recognized not only for its ability to establish
persistent infection, but also to induce prolonged T helper cell,
type II immune skewing and immunosuppression (28).
The follicular dendritic cell would be an ideal location from
which to mediate such a response (29).
is tempting to suggest that a gut-brain interaction may be
responsible for some of the behavioral features of this syndrome.
Although the opioid excess hypothesis for autism was first
proposed by Panksepp (17)
in 1979, and reiterated independently by Reichelt et al. (18)
and Shattock et al. (19),
it has only recently found increasing acceptance in the pediatric
psychiatry community. Opioid peptides of dietary origin, i.e.,
gliadomorphine and bovine casomorphine, have been identified in
the urine of some of these children with autistic enterocolitis (unpublished
observations), and the possible significance of these findings is
summary, an endoscopically and histologically consistent pattern
of ileocolonic pathology has been identified in a cohort of
children with developmental disorders. Reactive follicular
hyperplasia, particularly prominent in the ileum, provides a focus
for investigating the nature of antigen(s) that may be driving the
intestinal inflammation in these children.
This syndrome may
reflect a subset of children with developmental disorders with
distinct etiological and clinical features.
express our gratitude to the following for their financial support:
Basil Samuel Charitable Trust, Normanby Charitable Trust, PF
Charitable Trust, and the Scott of Yews Charitable Trust. We are
grateful for the advice and expert assistance of our colleagues in
the Departments of Medicine (Roy Pounder), Histopathology (Amar
Dhillon), and Microbiology.
Wakefield AJ, Murch SH, Anthony A, et al. Ileal-lymphoid nodular
hyperplasia, non-specific colitis, and pervasive developmental
disorder in children. Lancet 1998;351:637-41.
Sabra S, Bellanti JA, Colon AR. Ileal lymphoid nodular hyperplasia,
non-specific colitis, and pervasive developmental disorder in
3. Fiber SS, Schaefer HJ.
hyperplasia of the terminal ileum. Gastroenterology 1983;50:83-98.
Katz AJ, Rosen FS. Gastrointestinal complications of
immunodeficiency syndromes. Ciba Foundation symposium no. 46:[zsbt]
Immunology of the gut. Amsterdam: Elsevier Scientific,
Hermans PE, Huizenga KA, Hoffman et al. Dysgammaglobulinaemia
associated with nodular lymphoid hyperplasia of the small
Am J Med 1965;40:78-89.
6. Ajdukiewicz AB, Youngs GR,
Bouchier IAD. Nodular lymphoid hyperplasia with
hypogammaglobulinaemia. Gut 1972;13:589-95.
7. Bastlein C, Buriefinger R, Holzberg E, et al.
variable immunodeficiency syndrome and nodular lymphoid
hyperplasia in the small intestine. Endoscopy 1989;20:272-5.
van den Brande P, Goboes K, Vantrappen G, et al. Intestinal
nodular lymphoid hyperplasia in patients with common variable
immunodeficiency: Local accumulation of B and CD8+
lymphocytes. J Clin Immunol 1988;8:296-306.
Webster ADB, Kenwright S, Ballard J, et al. Nodular lymphoid
hyperplasia of the bowel in primary hypogammaglobulinaemia: Study
of in vivo and in vitro lymphocyte responses. Gut 1977;18:364-72.
Levendoglu H, Rosen Y. Nodular lymphoid hyperplasia of gut in HIV
J Gastroenterol 1992;87:1200-2.
Stubbs EG, Crawford ML, Burger D et al. Lymphocyte responsiveness
in autistic children. J Autism Child Schizophr 1977;7:49-55.
Warren RP, Yonk LJ, Burger RA, et al. Deficiency of
suppressor-inducer (CD4+CD45RO+) T cells in
autism. Immunol Investi 1990;19:245-51.
Warren RP, Foster A, Margeretten NC. Reduced natural killer cell
activity in autism. J Am Acad Child Adolesc Psychiatry
Ferrari P, Marescot MR, Moulias R, et al. Immune status in
infantile autism. L'Encéphale 1988;14:339-44.
Singh VK, Warren RP, Odell JD, et al. Antibodies to myelin basic
protein in children with autistic behaviour. Brain Behav Imm
Weizman A, Weizman R, Szekely GA, et al. Abnormal immune response
to brain tissue antigen in the syndrome of autism.
Am J Psychiatry 1982;139:1462-5.
Panksepp J. A neurochemical theory of autism. Trends Neurosci
Reichelt KL, Hole K, Hamberger A. Biologically active
peptide-containing fractions in schizophrenia and childhood autism.
Adv Biochem Psychpharmacol 1993;28:627-43.
Shattock P, Kennedy A, Rowell F, et al. Role of neuropeptides in
autism and their relationships with classical neurotransmitters.
Brain Dysfunction 1991;3:328-5.
American Psychiatric Association. Diagnostic and statistical
manual of mental disorders (DSM-IV). 4th Edition. Washington, DC:
American Psychiatric Association, 1994.
Fujimura Y, Kamoni R, Iida M. Pathogenesis of aphthoid ulcers in
Crohn's disease: Correlative findings by magnifying colonoscopy,
electronmicroscopy, and immunohistochemistry. Gut 1996;38:724-32.
Anthony A, Sim R, Murch SM, et al. Lymphonodular hyperplasia of
the ileum with increased MHC class II antigen expression and
macrophage infiltration of the colon in children with regressive
developmental disorder. Gut 1998;42(suppl 1):A24.
Horvath K, Papadimitrou JC, Rabsztyn A, et al. Gastrointestinal
abnormalities in children with autistic disorder.
J Paediatrics 1999;135:559-63.
24. van Gent T, Heijnen CJ, Treffers PDA.
and the immune system. J Child Psychol Psychiatry 1997;38:337-48.
Gupta S, Aggarwal S, Rashanravan B, et al. Th1 and Th2-like
cytokines in CD4+ and CD8+ T cells in autism.
J Neuroimmunol 1998;85:106-9.
Wakefield AJ, Anthony A, Schepelmann S, et al. Persistent measles
virus infection and immunodeficiency in children with autism,
ileo-colonic lymphoid nodular hyperplasia and non-specific colitis.
Gut 1998;42(suppl 1):A86.
Singh VK, Lin SX, Yang VC. Serological association of measles
virus and human herpes virus-6 with brain autoantibodies in autism.
Clin Immunol Immunopathol 1998;89:105-8.
28. Griffen DE, Bellini WJ.
virus. In: Fields BN, Knipe PM, Howley PM, et al., eds. Fields
virology. 3rd ed. Philadelphia: Lippincott-Raven, 1996; 1280.
Bhardwaj N. Interactions of viruses with dendritic cells: A
double-edged sword. J Exp Med 1997;186:759-99.
requests and correspondence: Dr.
Andrew J. Wakefield, F.R.C.S., Inflammatory Bowel Disease Study
Group, Department of Medicine, Royal Free and University College
Medical School (Royal Free Campus), Hampstead, London NW3 2QG, UK.
Jul. 28, 1999; accepted Feb. 25, 2000.
©2000 the American College of Gastroenterology -
(Articolo eliminato dal sito, chissa' perche'...?)
Bibliografia su Autismo dai vaccini
Autismo ed enterocolite, in Italiano
Black C, Kaye J, Jick H (Aug
24 2002). "Relation
of childhood gastrointestinal disorders
to autism: nested case-control study
using data from the UK General Practice
BMJ 325 (7361): 419-21.
Chakrabarti S (Oct 2001). "No
evidence for a new variant of
Pediatrics 108 (4): E58.
Davídsdóttir K, Agnarsson U, Sigthórsson
G, Kjeld M, Bjarnason I (Dec 2002). "Inflammation
and Inflammatory Bowel Disease: Effect
of Pentavac and measles-mumps-rubella
(MMR) vaccination on the intestine.".
Gut 51 (6): 816-7.
Murch S, Anthony A et al. (1998).
hyperplasia, non-specific colitis, and
pervasive developmental disorder in
children". Lancet 351
PMID 9500320. Retrieved on
Wakefield A, Anthony A,
Murch S, Thomson M, Montgomery S, Davies
S, O'Leary J, Berelowitz M, Walker-Smith
J (Sep 2000). "Enterocolitis in children
with developmental disorders.".
Am J Gastroenterol 95
Autism-BioMed.org - 'MMR vaccine and
autism, revisited' (commentary)', Ronald
J. Kallen, MD,
Autism Biomedical Information Network
(May 31, 2000)
MelaniePhillips.com - 'MMR: the
Daily Mail, (October 31, 2005)
"The MMR skeptic who just doesn't
understand science", Ben Goldacre,
The Guardian (November 2, 2005)
MelaniePhillips.com - 'Evidence-based'
ignorance over MMR,
Daily Mail, (November 08, 2005)
BrianDeer.com - 'The MMR-autism
scare - Summary of a
Brian Deer (2005)
CDC.gov - 'FAQs about measles
vaccine and inflammatory bowel disease',
Centers for Disease Control
Cochrane.org - 'The Cochrane Library
publishes the most thorough survey of
MMR vaccination data which strongly
supports its use',
Cochrane Library (October 19, 2005)
MedAdNews.com - 'Impact of
Gastrointestinal Dysfunction in Autistic
PRNewswire (January 11, 2006)
NeuroDiversity.com - 'Autism &
RxPGNews.com - 'MMR vaccine - An End
to the Controversy' (October 19, 2005)
Tripod.com - 'Autism, Viral
Infection and the Gut-Brain Axis',
Andrew J. Wakefield, Scott M.
Journal of Pediatric Gastroenterology
and Nutrition. vol 34 p S14-S17
Autism and Mercury Detoxification
Autism: a Novel Form of Mercury Poisoning
Studies on the Effects of Secretin in
Children With Autism
Single Injection Of Secretin Does Not
Objections to the Study That
Showed Secretin Does Not Work for Autism
Short-Term Benefit In Treating Autism
The Neurobiology of Lipids In Autistic
Link Between Autism and
Autism May Be Caused By an
Immune System Response To a Virus
Vaccine - Autism Link Feared
Vaccine Induced Autism
Milk Link To Autism
Intervista al Dr.
Philippe Raymond - 25 Mag. 2012
Membro del gruppo di ricerca "Chronimed"
(vedi sotto l’articolo), diretto dal premio Nobe:
Il premio Nobel, Luc
Montaigner, il primo a individuare il virus dell’Aids
nel 1983, lavora da qualche anno su altre malattie
neurodegenerative cercando di indviduarne l'origine. Per
l'autismo indaga la pista infettiva. Malattie come
Parkinson, Alzheimer e autismo potrebbero avere
un’origine infettivaed essere combattuta con terapia
antibiotica. L'autismo in particolare, secondo un suo
studio condotto su 200 bambini, potrebbe essere trattato
con buoni risultati con terapia antibiotica.
Il Dr. Philip Raymond fa parte del gruppo di lavoro "Chronimed",
che riunisce 15 medici intorno al professor Luc
Montagnier, premio Nobel per la Medicina. Questo gruppo
lavora sulle probabili cause infettive di alcune
patologie croniche per cui non si suppone l'origine
infettiva, tra cui l'autismo. Il loro lavoro è iniziato
dopo la constatazione di indizi infettivi, sia somatici
(sintomi clinici) che nel siero (anticorpi) in persone
Quali sono secondo voi le
Secondo P. Raymond, l'autismo è multifattoriale. Ammette
che vi sono ovviamente cause genetiche dell'autismo, ma
di non aver indagato in questa direzione,non essendo un
esperto. Ci si riferisce ad un articolo della
ricercatrice americana Helen V. Ratajczak, che tratta
tutte le cause dell'autismo attualmente accettate
(pubblicato nel 2011 nel « Journal of Immunotoxicology
»). Secondo P. Raymond, le malattie tossiche sono una
possibile causa della sindrome autistica.
Queste tossine hanno origini diverse: possono essere
prodotte da batteri intracellulari che invadono la
parete vascolare e secernono delle tossine vaso
costrittive e neurotossiche, oppure possono anche essere
causate da fattori ambientali (pesticidi, metalli
pesanti, ecc.). La loro origine può invece anche essere
alimentare: intolleranze alimentari diverse favorite da
infezioni croniche (la disbiosi intestinale porta ad una
permeabilità intestinale) e soprattutto le intolleranze
a glutine e caseina, dove i risultati dell'abolizione
sono talvolta spettacolari, soprattuttonei bambini con
autismo con disturbi digestivi associati.
Questi fattori infettivi tossici e ambientali,
potrebbero spiegare da un lato l'esplosione incredibile
della diffusione dell'autismo negli ultimi anni, e in
secondo luogo, il fatto che la stragrande maggioranza
dell' autismo oggi è di tipo regressivo e non più di
nascita, come una volta.
Potete parlarci più precisamente dei vostri trattamenti
in corso e dei risultati?
P. Raymond ci riporta a un articolo dello psichiatra
americano Robert C. Bransfield, che enumera tutti i
batteri o virus coinvolti nei disturbi dello spettro
autistico tra cui, tra gli altri, Borrelia, Clamidia,
Herpes, Micoplasma, ecc. Nella nostra analisi spesso
troviamo i dati sierologici positivi. Questi bambini con
autismo presentano spesso molti segni fisici che
riflettono uno stato infettivo cronico: rialzi
ricorrenti di febbre, sudorazione notturna, estremità
fredde, tosse cronica, rinite cronica, congiuntivite
cronica, pallore, occhi cerchiati, eczema, diarrea
cronica ... Secondo la sua esperienza personale, ognuno
di questi sintomi è presente dal 22% al 56% dei casi.
P. Raymond constata che il trattamento di queste
infezioni con civli di antibiotici sempre più
intervallati, possono ridurre in modo spesso importante
i sintomi dell’autismo. Tuttavia, riconosce un tasso di
fallimento del circa il 20%. Più in dettaglio, i
risultati di un lavoro personale di recente presentato a
Bordeaux su 51 autistici sono i seguenti: per il 51% dei
bambini trattati il miglioramento è rapido e costante
fin dal primo mese di trattamento. Per il 30% è più
lento e può essere ciclico. Per il 19%, infine, il
trattamento fallisce o viene interrotto. Questi
risultati vengono confermati da altri medici che hanno
attuato questo tipo di trattamento (in totale oltre 120
bambini trattati attualmente). Durante i primi mesi del
trattamento, se le interruzioni sono troppo lunghe, si
osserva una recidiva dei sintomi fisici, ma anche di
quelli comportamentali, che erano scomparsi. Tutti
questi sintomi scompaiono di nuovo dopo due giorni dalla
ripresa del trattamento!
Perché non pubblicate i vostri risultati? Quali sono gli
ostacoli attualmente, e quanto costerebbe uno studio in
Questo studio è ancora recente, e il gruppo lavora alla
pubblicazione dei risultati. Purtroppo i neuropsichiatri
seguono metodi vetusti senza considerare e seguire tali
trattamenti anche in presenza degli evidenti sintomi.
Altri studi si faranno più facilmente se ci sarà
collaborazione con i servizi ospedalieri specializzati.
Il gruppo "Chronimed" vorrebbe che aziende farmaceutiche
si interessassero a questo progetto. Ad oggi, i
protocolli di studio sono in fase di sviluppo e si
possono essere significativi risultati in 3 mesi o 6
mesi al massimo. Uno studio più avanzato costerebbe tra
i 200 e i 300.000 euro, e sarebbe quindi anche
potenzialmente finanziabile da un'istituzione.
Ci sono già delle pubblicazioni sul vostro argomento di
P. Raymond spiega che l'associazione tra disturbi dello
sviluppo neurologico e infezioni è stata studiata da
lungo tempo. Cita pubblicazioni internazionali a questo
proposito: uno studio americano del 1988 (Tanoué) ha
mostrato che un bambino aveva una maggiore probabilità
di sviluppare autismo regressivo dopo il ricovero
ospedaliero per polmonite. Successivamente, nel 1995, lo
studio Ciaranello (confermato dallo studio di Wilkerson
2002, e Atlodottir nel 2010) ha dimostrato che le donne
in gravidanza hanno un rischio maggiore di dare alla
luce un bambino autistico se la madre fosse stata
ricoverata nel secondo trimestre della sua gravidanza
per una polmonite.
Ora, i batteri studiati dal gruppo del professor
Montagnier sono appunto responsabili della polmonite.
Fin dal 1989, il dottor Bottero aveva già pubblicato la
notevole riduzione dei sintomi di un bambino autistico
che soffriva di infezione da Rickettsia, fin dalle prime
cure antibatteriche. I canadesi e gli americani hanno
ampiamente dimostrato disfunzioni immunitarie per
l'autismo (V. Singh e El Dahr). Il professor Garth
Nicolson ha spesso pubblicato studi sul rapporto tra
autismo e infezioni croniche, tra cui studi che mostrano
nel 40% dei casi la presenza di infezioni da Micoplasma
nei bambini autistici in California. Robert C.
Bransfield ha anche pubblicato articoli che stabiliscono
il legame tra la Borreliosi di Lyme e l'autismo.
Qual è la sua opinione sulla teoria della vaccinazione
come causa probabile dello scatenamento dei sintomi
autistici in numerosi bambini?
P. Raymond ci ricorda che un certo numero di genitori di
bambini autistici (da 10 a 15% circa) descrivono che la
regressionedel loro bambino avviene improvvisamente
entro ore o giorni dopo la vaccinazione. Helen V.
Ratajczak fa ipotesi diverse in proposito. Siamo in
grado di aggiungere un ipotesi ulteriore: la modulazione
immunitaria indotta dalla vaccinazione consentirebbe ad
una infezione latente in precedenza, di svilupparsi
(nozione di terreno favorevole) P. Raymond cita una
frase che avrebbe detto Louis Pasteur alla fine della
sua vita: "Antoine Bechamp aveva ragione, il microbo non
è niente, il terreno è tutto ".
Il trattamento da mettere in atto è quindi secondo voi
un trattamento antibiotico.
Come rispondete a quelli che spiegano i vostri buoni
risultati con la pratica concomitante della ABA?
Immunostimolanti o antibiotici saranno più efficaci se
sono accompagnati dall’ABA. P. Raymond dà l'immagine di
una macchina parcheggiata, che per riavviarsi, ha
bisogno di una spinta (ABA), ma anche di rimuovere il
freno a mano (trattamento antibiotico). Le tossine
correlate a malattie croniche vanno considerate come
"semplici" inibitori. Una volta rimosse, il lavoro del
ABA è molto più facile e più efficace. P. Raymond dà
vari argomentazioni per dimostrare l'efficacia dei
trattamenti antibiotici al di fuori della pratica dell'ABA:
in primo luogo, ci ricorda che durante i primi mesi di
trattamento, i risultati sono immediati e, appena si
arrestano il trattamenti antibiotici e pur continuando
l'ABA, i sintomi fisici e comportamentali, che erano
migliorati, ritornano. Questi sintomi fisici scompaiono
rapidamente dopo la ripresa del trattamento antibiotico.
D’altra parte egli cita l’esperienza dell’IME di
Suresues che aveva preso in carico 12 bambini con ABA
intensivo. Di questi 12, 8 sono stati seguiti da
Raymond. Dopo 1 anno soltanto di trattamento, 4 degli 8
bambini seguiti da Raymond, hanno potuto essere
scolarizzati contro nessuno degli altri 4.
Che cosa rispondete a quelli
che affermano che gli antibiotici rendono fragile il
E’ probabilmente il caso di infezioni virali acute,
quando alcuni antibiotici sono somministrati male.
Raymond sottolinea che il Dr. Montagnier è uno
specialista sul tema e che la tesi del gruppo di studio
è la seguente: piuttosto che indebolire il sistema
immunitario, gli si dà sollievo ed esso può più
efficacemente lottare altrove. Infine ci ricorda che gli
antibiotici non sono somministrati in maniera continua
nel loro protocollo, ma con cure sempre più
intervallate, fino all’eliminazione finale. Se gli
antibiotici prescritti indebolissero il sistema
immunitario, la tendenza sarebbe inversa cioè si
andrebbe verso la necessità di usare sempre più
Quali sono le migliori opzioni di screening secondo voi?
Raymond stima che la diagnosi è clinica e dunque tocca
in prima linea a pediatri e medici generici. Si può
secondo lui, rendersi conto che un bambino presenta
tratti autistici a partire da 6 -9 mesi (anche se la
diagnosi precisa si farà più tardi). Sfortunatamente, i
medici sono molto male formati e informati e pensano che
non ci sia alcun trattamento possibile. C’è anche spesso
un rifiuto da parte dei genitori, che è associato al
ritardo della diagnosi, o al ritardo della comunivazione
della diagnosi, che è sempre difficile.
Cosa ne pensate dei test genetici?
Una malattia genetica è l’interazione di un gene con
l'ambiente; si può benissimo avere un gene portatore di
una malattia genetica e non svilupparla. Se si
generalizzassero i test genetici troveremmo malattie a
tutti. P. Raymond ritiene che i test genetici sono una
forma di consulenza, e possono effettivamente fornire un
rischio percentuale più o meno esatto. Riconosce che
possono costituire una forma di
prevenzione, tanto più che ci sono delle cause genetiche
evidenti nell’autismo, come mostrano le statistiche
secondo le quali il 70% dei fratelli gemelli di un
bambino autistico, sono egualmente autistici, contro il
5% dei fratelli ordinari di un bambino autistico.
Riconosce egualmente che il sistema immunitario ha un
ruolo importante nello sviluppo dei sintomi autistici ed
è geneticamente determinato.
Cosa ne pensa dei test sul sangue?
Raymond ci spiega, che allo stesso modo, si può avere
una sierologia positiva e non sviluppare mai la
malattia. Se si generalizzassero i test su sangue, si
troverebbero ancora più ammalati che nella realtà.
Intervista in lingua originale
Tratto da: emergenzaautismo.org
Vedi a cosa serve
la tecnica chiamata ABA, per l'autismo:
Les enfants autistes présentent des bacteries
intestinales differentes - Bacterium Suterella - 15
Autistic Kids Possess A
Bacteria in Their Gut Different From Non-Autistic
Counterparts Autistic kids harbor a form of bacteria in
their guts that is not found in those without autism, a
new study suggests. The study to be published in mBio
journal was carried out by Columbia University research
team that included Brent Williams and colleagues. The
research team pointed out that the microorganism
communities found in autistic kids’ guts are completely
different from those found in non-autistic kids. But
whether these differences have anything to do with
vulnerability to autism is still unclear. The bacteria
that fall under Sutterella group represented a huge
population of microorganisms found in 12 of 23 samples
of tissues taken from autistic kids’ guts, but these
microorganisms were not found in non-autistic kids’
The reason behind this is unknown. Jorge Benach from
Stony Brook University who reviewed the study explains,
“Suterella has been tied to gastrointestinal problems
but it is still unclear whether it’s a pathogen or not.”
According to Benach, the study was exclusively strong
because tissue samples were taken from patients’ guts.
“Stool samples were primly used in most work that linked
the gut microbiome to autism,” says Benach, but the
stool samples do not precisely represent actual microbes
around the intestinal wall.
The Benach believes that despite being statistically
powerful the study is just an observation that has to be
thoroughly followed to determine the role of Sutterella
in causing problems in the gut.
POSTED By ADMIN on MONDAY, JANUARY 9, 2012 AT 5:22 AM
FILED UNDER MENTAL HEALTH · TAGGED
Specific gut bacterium found in autistic children, shows
study Scientists have found that gastrointestinal
problems commonly occur in children suffering from
autism. As an important investigation on this front,
professionals from the Columbia University have put
forth that high proportions of abacteriumcalled
Sutterella in the gut could be the reason behind
gastrointestinal troubles observed in autistic children.
As part of the trial, 23 autistic children and 9 normal
kids were inspected. After examining the subjects’
intestinal biopsies, the team also accessed
Sutterella-specific molecular assays for precise
identification of the bacterium. “These findings shine a
light on a bacterium about which we know very little, in
a disorder for which we have few answers. There is much
work to be done toward understanding the role Sutterella
plays in autism, the microbiota, infections, and
inflammation,” commented Brent Williams, PhD, the lead
author on the study.
The outcomes showed that more than half of the children
suffering from autism and gastrointestinal problems
seemingly carried Sutterella in their intestinal
biopsies. On the other hand, normal children with
gastrointestinal problems did not seem to possess
Sutterella in theirintestines.
Notably, greater proportions of Sutterella were present
in the intestinal tissue of autistic children. However,
the team is not yet clear whether the bacterium could be
considered a humanpathogen. Also, the primary reason for
this association between gastrointestinal conditions and
autism is not known by scientists presently.
The study is published in
the journal, mBio. Application of Novel PCR-Based
Methods for Detection, Quantitation, and Phylogenetic
Characterization of Sutterella Species in Intestinal
Biopsy Samples from Children with Autism and
Gastrointestinal Disturbances 1. Brent L. Williams, 2.
Mady Hornig, 3. Tanmay Parekh, and 4. W. Ian Lipkin
+Author Affiliations 1. Center for Infection and
Immunity, Mailman School of Public Health, Columbia
University, New York, New York, USA 1.
Address correspondence to Brent L. Williams, email@example.com.
1. Editor Christine Biron, Brown University
Commento NdR : questi ricercatori, sono ancora
all’oscuro che le malattie
non sono prodotte dai germi, bensi dal
che nel caso di alterazione
bioelettronico-chimica, (pH, rH, ro') produce e
favorisce la prolificazione di batteri e funghi e/o
esso; quindi e’ sul
terreno che occorre agire in primis,
togliendo la possibilita’ di mutazioni batteriche
endogene e/o di terreno adatto alla proliferazione di
batteri, funghi e simili che mutando divengono co-patogeni
per le tossine che essi producono, oltre a favorire
Ma ricordo che,
molta importanza hanno anche i cibi assunti non
adatti al gruppo sanguigno del soggetto.
Autismo dai VACCINI
Autismo - La prova dei
Danni dei Vaccini
Bibliografia su Autismo dai vaccini +
Danni dei vaccini +
1.000 studi sui Danni dei Vaccini
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