Vaccinazioni per l’infanzia ed Autismo  

Sindrome infiammatoria chiamata "Asia" scatenata dai vaccini !
ASIA_Sindrome infiammatoria-dai-vaccini-Riassunto.pdf
Tratto da:  http://www.assis.it/wp-content/uploads/2014/12/ASIARiassunto.pdf
... ed e' noto che... le infiammazioni sono foriere di qualsiasi tipo di sintomi, che i medici impreparati allopati chiamano erroneamente "malattie"....

vedi: Malattie gastrointestinali dai Vaccini + Metalli tossici dei vaccini = Autismo vedi: PDF -  dott. M. Proietti

I Tribunali anche USA, confermano tranquillamente che il vaccino MMR causa l'autismo. Austin (USA) - 27 Luglio 2013
Dopo decenni di appassionato dibattito, per i genitori che probabilmente hanno perso i ripetuti ricorsi richiesti dalle aziende farmaceutiche e governi, che i vaccini infatti causano l'autismo.
Per i genitori interessati alla ricerca della verità, vale la pena ricordare che le stesse persone che possiedono le aziende farmaceutiche di tutto il mondo possono anche possedere agenzie di stampa americane.
La Ricerca di informazioni prive di propaganda è stata fino ad ora molto difficile.
Ma Whiteout Press non è qui per sostenere o contrastare i vaccini. Siamo qui per portare i lettori la notizia che è il tema e’ in black-out, cover-up e censurato dalle autorita’Sanitarie e Governative.
Tratto da: http://www.whiteoutpress.com/timeless/courts-quietly-confirm-mmr-vaccine-causes-autism/

La prova della FRODE del CDC per le cause dei Vaccini nell'Autismo - CONFESSIONE di un alto dirigente CDC, davanti al Congresso US

In CINA dopo le campagne vaccinali esplode l'Autismo ! - Maggio 2016
http://yournewswire.com/autism-rates-explode-in-asia-after-introducing-western-vaccines/
VERISSIMO, ma non solo l'autismo....ma una innumerevole sequela di altre malattie....
Autismo e non solo dai Vaccini:

Sentenza 2012 - Trib. Rimini su Vaccini=Autismo

Enterocolitis in Children With Developmental Disorders
Wakefield AJ, Anthony A, Murch SH, Thomson M, Montgomery SM, Davies S, O'Leary JJ, Berelowitz M, Walker-Smith JA.
University Department of Medicine, Royal Free and University College Medical School, London, United Kingdom.

OBJECTIVE: 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.
METHODS: 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.
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 disorders.
PMID: 11007230 [PubMed - indexed for MEDLINE]
vedi anche:
Autismo (trattamenti, Cure, Terapie) + Amish senza autismo perche' NON vaccinano + Malattie gastrointestinali da vaccino

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Original Contribution - September 2000 - Volume 95, Number 9 - Pages 2285-2295

Enterocolitis in Children With Developmental Disorders
http://www.ncbi.nlm.nih.gov/pubmed/11007230

A. 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

OBJECTIVE: 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.

METHODS: 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.

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 disorders. Cite 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 Gastroenterol September;95:2285-2295.

^aUniversity 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, Eire

Introduction
We have recently described a characteristic pattern of intestinal inflammation in a cohort of children with developmental disorders (1). 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.

Ileocolonic 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, 7, 8, 9, 10) and has been described in congenital B cell abnormalities (5, 6), and common variable immunodeficiency (7, 8). In its persistent acquired form, ileal LNH has been reported in association with infection with human immunodeficiency virus (HIV) before the development of AIDS (10).

The 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, 12, 13, 14), although the origin and significance of the findings are uncertain. These immune changes, plus the presence of myelin basic protein (MBP) antibodies (15) 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, 16).
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, 18, 19), a situation that may have some overlap with hepatic enephalopathy. An early childhood enterocolitis would be more consistent with the latter mechanism.

This 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.

Materials and Methods
This 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 disorders (20). 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 investigation.

Autism 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).

The 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.
All but three affected children had a developmental disorder that was associated with a clear history of regression, with loss of acquired skills after 1 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.

Investigations
Medical 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).

Ileocolonoscopy and Histology
All 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. 1), 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.

Figure 1 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).

Mucosal 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 (Table 1). 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.

Table 1. Histopathology Proforma Used for Scoring of All Biopsies From Affected Children (Autistic Enterocolitis), Non-IBD Controls, and Those With Ulcerative Colitis

In 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.

Selection Criteria

To 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.

Ethical Approval

All clinical investigations were undertaken with fully informed, written consent from the parents. The initial phase of these studies (1) 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.

Statistical Analysis

The analyses were performed using SPSS 7.5 for Windows and EpiInfo 6.04b. The ² 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.

Results

Ileocolonoscopy

ILEUM. 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 Figure 2. Representative grades of ileal LNH are shown in Figure 1.
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 < 0.001).
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.

Figure 2 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).

COLON. 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 Figure 3. 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 group.
 

Figure 3 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).

Histological Findings

Ileal 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 proforma (Table 1). 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.

Ten 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 group.
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.

ILEAL 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.
The 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 some cases.
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.

COLONIC 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 colitis.
The numbers and percentage of biopsies in each group showing pathological changes are shown in Table 2 and Figure 4, 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 ulcerative colitis.
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 2). 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 in Figure 5. 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 colitis.
The difference between affected children and non-IBD controls is statistically significant (p < 0.001).
The 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).
Although 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).

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Figure 4 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).

Figure 5 (A) 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.

Table 2. Pathological Changes in Biopsies From Affected Children, Children With Ulcerative Colitis, and Non-IBD Controls

Figure 6 compares the overall severity of pathological change in the respective groups, by expressing the scores as a percentage of the total possible score (Table 1) 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 < 0.001).
 

Figure 6 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 < 0.001).
Ulcerative colitis biopsies showed statistically significantly more severe change at each site, except the ileum, compared with those from affected children (p < 0.001).

Routine Laboratory Tests

Routine 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 > 0.5).

It 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.

Stool microscopy and culture, and serum antibody studies identified no common gut pathogens except in one child, in whom Giardia cysts were identified by microscopy.

Clinical Findings and Developmental Diagnosis

Overall, 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.

Discussion

These 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 uncommon.
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 developmental disorders.

This 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⁺, and T 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 publication).
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 colonic inflammation).
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.

In 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.

The 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.

It is notable that 68% of affected children had a lymphopenia. Immunological abnormalities are a recurring feature in studies of children with autism (25, 26), 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. (27). 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).

It 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 under investigation.

In 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.

Acknowledgments

We 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.
 

References

1. 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.

2. Sabra S, Bellanti JA, Colon AR. Ileal lymphoid nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children. Lancet 1998;352:234-5.

3. Fiber SS, Schaefer HJ. Lymphoid hyperplasia of the terminal ileum. Gastroenterology 1983;50:83-98.

4. Katz AJ, Rosen FS. Gastrointestinal complications of immunodeficiency syndromes. Ciba Foundation symposium no. 46:[zsbt] Immunology of the gut. Amsterdam: Elsevier Scientific, 1977:243-61.

5. Hermans PE, Huizenga KA, Hoffman et al. Dysgammaglobulinaemia associated with nodular lymphoid hyperplasia of the small intestine. 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. Common variable immunodeficiency syndrome and nodular lymphoid hyperplasia in the small intestine. Endoscopy 1989;20:272-5.

8. 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.

9. 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.

10. Levendoglu H, Rosen Y. Nodular lymphoid hyperplasia of gut in HIV infection. Am J Gastroenterol 1992;87:1200-2.

11. Stubbs EG, Crawford ML, Burger D et al. Lymphocyte responsiveness in autistic children. J Autism Child Schizophr 1977;7:49-55.

12. Warren RP, Yonk LJ, Burger RA, et al. Deficiency of suppressor-inducer (CD4⁺CD45RO⁺) T cells in autism. Immunol Investi 1990;19:245-51.

13. Warren RP, Foster A, Margeretten NC. Reduced natural killer cell activity in autism. J Am Acad Child Adolesc Psychiatry 1987;26:333-5.

14. Ferrari P, Marescot MR, Moulias R, et al. Immune status in infantile autism. L'Encéphale 1988;14:339-44.

15. Singh VK, Warren RP, Odell JD, et al. Antibodies to myelin basic protein in children with autistic behaviour. Brain Behav Imm 1993;7:97-103.

16. 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.

17. Panksepp J. A neurochemical theory of autism. Trends Neurosci 1979;2:174-7.

18. Reichelt KL, Hole K, Hamberger A. Biologically active peptide-containing fractions in schizophrenia and childhood autism. Adv Biochem Psychpharmacol 1993;28:627-43.

19. 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.

20. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (DSM-IV). 4th Edition. Washington, DC: American Psychiatric Association, 1994.

21. 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.

22. 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.

23. 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. Autism and the immune system. J Child Psychol Psychiatry 1997;38:337-48.

25. 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.

26. 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.

27. 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. Measles virus. In: Fields BN, Knipe PM, Howley PM, et al., eds. Fields virology. 3rd ed. Philadelphia: Lippincott-Raven, 1996; 1280.

29. Bhardwaj N. Interactions of viruses with dendritic cells: A double-edged sword. J Exp Med 1997;186:759-99.
 

Reprint 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.

Received Jul. 28, 1999; accepted Feb. 25, 2000.
 

Copyright ©2000 the American College of Gastroenterology - Published by Elsevier Science Inc.  (Articolo eliminato dal sito, chissa' perche'...?)
vedi: Autismo ed enterocolite, in Italiano  +  Bibliografia su Autismo dai vaccini

REFERENCES:

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Autism: a Novel Form of Mercury Poisoning

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The Neurobiology of Lipids In Autistic Spectrum Disorder

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Intervista al Dr. Philippe Raymond  - 25 Mag. 2012
Membro del gruppo di ricerca "Chronimed" (vedi sotto l’articolo), diretto dal premio Nobe: Luc Montagnier

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 con autismo.

Quali sono secondo voi le cause dell'autismo?
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 doppio cieco?
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 studio?
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 sistema immunitario?
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 antibiotici.

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.
Riferimenti: 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 Jan. 2012
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’ samples.
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, bw2101@columbia.edu. 1. Editor Christine Biron, Brown University
Tratto da: chronimed.over-blog.com

Commento NdR : questi ricercatori, sono ancora all’oscuro che le malattie non sono prodotte dai germi, bensi dal Terreno che nel caso di alterazione bioelettronico-chimica, (pH, rH, ro') produce e favorisce la prolificazione di batteri e funghi e/o virus, in 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 l'apparire dei parassiti.
Ma ricordo che, molta importanza hanno anche i cibi assunti non adatti al gruppo sanguigno del soggetto.

vedi:  AUTISMO + Autism REFERENCES + Autismo dai VACCINI + Autismo - La prova dei Danni dei Vaccini + Bibliografia su Autismo dai vaccini + Bibliografia Danni dei vaccini  +  Bibliografia danni 2  +  1.000 studi sui Danni dei Vaccini  

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