Clueless mainstream docs - a VENT

[Guest guest]

Okay, our 3 year old daughter with autism has now been hospitalized

for the last three days. She has not eaten one bite of food in 30

days and has refused to drink since Wed. evening. For the past 30

days we've tried everything we know to get her to eat - tons of OT

stuff & ABA - behavioral stuff. The aversion is ovbiously now

INTENSE!

I keep suggesting GI tests to make sure she isn't having pain when

she eats. She had reflux as an infant & has severe constipation

problems. She also has INTENSE oral defensiveness. Is that too much

to ask? It seems to me that she will likely need to get a tube and

we need to make sure she isn't having pain as I mentioned. I'd also

like to try to find a feeding clinic somewhere with experience with

autism/oral defensiveness/feeding issues. Doesn't that just make

sense?

Here is what has happened:

1. Past 3 days - zero nutrition - we are watching her starve - today

she did not even have the energy to hold up her head.

2. Get a load of the consults our pediatrcian ordered - note - no GI

consult:

* Pediatric Neurologist - she wants to do a muscle bioposy & feels

it may be a mitochondrial brain disorder that we can't do anything

for anyway - by the way, this chick had never even heard of ABA!!!!

She said, " What is that anyway, I know there's all sorts of wacky

treatments for autism out there " .

* Speech pathologist - she was actually cool & this consult made

sense to us

* The developmental pediatrician told us to snow her with Risperdal

& maybe she'd eat. We should also put in a NG tube (through her

nose) until she does eat.

* note no GI consult

GIVE ME A FRICKEN BREAK!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

Joy

[Guest guest]

I cannot believe that she has been in the hospital for 3 days (no food

for 30 days) and they have not given her a feeding tube yet! How is that

possible? I would think the first thing they would do is put her on an

IV elemental diet to get some nutrition in.

I wonder if it would be worth a phone call to Dr Krigsman to consult

with him on it?

L

Clueless mainstream docs - a VENT

Okay, our 3 year old daughter with autism has now been hospitalized

for the last three days. She has not eaten one bite of food in 30

days and has refused to drink since Wed. evening. For the past 30

days we've tried everything we know to get her to eat - tons of OT

stuff & ABA - behavioral stuff. The aversion is ovbiously now

INTENSE!

I keep suggesting GI tests to make sure she isn't having pain when

she eats. She had reflux as an infant & has severe constipation

problems. She also has INTENSE oral defensiveness. Is that too much

to ask? It seems to me that she will likely need to get a tube and

we need to make sure she isn't having pain as I mentioned. I'd also

like to try to find a feeding clinic somewhere with experience with

autism/oral defensiveness/feeding issues. Doesn't that just make

sense?

Here is what has happened:

1. Past 3 days - zero nutrition - we are watching her starve - today

she did not even have the energy to hold up her head.

2. Get a load of the consults our pediatrcian ordered - note - no GI

consult:

* Pediatric Neurologist - she wants to do a muscle bioposy & feels

it may be a mitochondrial brain disorder that we can't do anything

for anyway - by the way, this chick had never even heard of ABA!!!!

She said, " What is that anyway, I know there's all sorts of wacky

treatments for autism out there " .

* Speech pathologist - she was actually cool & this consult made

sense to us

* The developmental pediatrician told us to snow her with Risperdal

& maybe she'd eat. We should also put in a NG tube (through her

nose) until she does eat.

* note no GI consult

GIVE ME A FRICKEN BREAK!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

Joy

Many frequently asked questions and answers can be found at

<http://www.autism-rxguidebook.com/forums>

_____

[Guest guest]

The docs not doing gi eval verges on criminal. Perhaps the jack-booted

thugs are goose-stepping away from any possible connection to the Royal

" Free " group's findings -- which have been replicated by Harvard's Buie

and by Arthur Krigsman. Furthermore, the Royal Free group has never

recanted their findings! And their findings confirmed and expanded the

gi-pathology findings of Horvath et al. There are a number of

peer-reviewed citations that document gi pathology in autism. A list of

citations is included hereinbelow, taken from my presentation to

physicians training session after the recent DAN! in Mclean Va.

Perhaps the hospital has some email addresses, eg, for Public Relations

dept, for Hosp Director. Perhaps an email campaign would embarrass

adminstrators sufficiently so that they would quite pretending the

following citations don't exist.

Intestinal pathology, vMV, MMR

23: D'Eufemia P et al. Abnormal intestinal permeability in children

with autism. Acta Paediatr. 1996 Sep;85(9):1076-9. PMID: 8888921

" We determined the occurrence of gut mucosal damage using

the intestinal permeability test in 21 autistic children who had no

clinical and laboratory findings consistent with known intestinal

disorders. An altered intestinal permeability was found in 9 of the 21

(43%) autistic patients, but in none of the 40 controls. "

24. Reichelt KL, Knivsberg AM. Can the pathophysiology of autism be

explained by the nature of the discovered urine peptides? Nutr

Neurosci. 2003 Feb;6(1):19-28. PMID: 12608733

25. Mercer ME, Holder MD. Food cravings, endogenous opioid peptides, and

food intake: a review. Appetite. 1997 Dec;29(3):325-52. PMID: 9468764

26. Lucarelli S et al. Food allergy and infantile autism. Panminerva

Med. 1995 Sep;37(3):137-41. PMID: 8869369

" The aim of the present study has been to verify the

efficacy of a cow's milk free diet (or other foods which gave a positive

result after a skin test) in 36 autistic patients. We also looked for

immunological signs of food allergy in autistic patients on a free

choice diet. We noticed a marked improvement in the behavioural symptoms

of patients after a period of 8 weeks on an elimination diet and we

found high levels of IgA antigen specific antibodies for casein,

lactalbumin and beta-lactoglobulin and IgG and IgM for casein. The

levels of these antibodies were significantly higher than those of a

control group which consisted of 20 healthy children. "

27a. Arnold GL et al. Plasma amino acids profiles in children with

autism: potential risk of nutritional deficiencies. J Autism Dev Disord

2003 33(4):449-54. PMID: 12959424

" No amino acid profile specific to autism was identified.

However, children with autism had more essential amino acid deficiencies

consistent with poor protein nutrition than an age/gender matched

control group. There was a trend for children with autism who were on

restricted diets to have an increased prevalence of essential amino acid

deficiencies and lower plasma levels of essential acids including the

neurotransmitter precursors tyrosine and tryptophan than both controls

and children with autism on unrestricted diets. "

28. Chauhan V et al. Alteration in amino-glycerophospholipids levels in

the plasma of children with autism: a potential biochemical diagnostic

marker. Life Sci 2004 Feb 13;74(13):1635-43. PMID: 14738907

" the levels of AGP [amino-glycerophospholipids] were found

to be significantly increased in the plasma of children with autism as

compared to their non-autistic normal siblings. "

29a. Knivsber AM et al. Reports on dietary intervention in autistic

disorders. Nutr Neurosci. 2001;4(1):25-37. PMID: 11842874

" ...Gluten and/or casein free diet has been implemented to

reduce autistic behaviour, in addition to special education, since early

in the eighties. Over the last twelve years various studies on this

dietary intervention have been published in addition to anecdotal,

parental reports. The scientific studies include both groups of

participants as well as single cases, and beneficial results are

reported in all, but one study. While some studies are based on urinary

peptide abnormalities, others are not. The reported results are,

however, more or less identical; reduction of autistic behaviour,

increased social and communicative skills, and reappearance of autistic

traits after the diet has been broken. "

29b. Karyn Seroussi -- Dietary Intervention for Autism

<http://216.117.159.91/powerpoint/dan2003/KarynSeroussi.htm> DAN! 2003

Philadelphia

http://216.117.159.91/powerpoint/dan2003/KarynSeroussi.htm

30: Wakefield AJ, Murch SH, A, Linnell J, Casson DM, Malik M,

Berelowitz M, Dhillon AP, Thomson MA, Harvey P, Valentine A, Davies SE,

- JA. Ileal-lymphoid-nodular hyperplasia, non-specific

colitis, and pervasive developmental disorder in children. Lancet. 1998

28;351(9103):637-41. PMID: 9500320

31: Ashwood P et al. Intestinal lymphocyte populations in children

with regressive autism: evidence for extensive mucosal immunopathology.

J Clin Immunol. 2003 Nov;23(6):504-17. PMID: 15031638

" At all sites, CD3(+) and CD3(+)CD8(+) IEL as well as CD3(+)

LPL were significantly increased in affected children compared with

developmentally normal noninflamed control groups (p<0.01) reaching

levels similar to inflamed controls. In addition, two

populations--CD3(+)CD4(+) IEL and LP CD19(+) B cells--were significantly

increased in affected children compared with both noninflamed and

inflamed control groups including IBD, at all sites examined (p<0.01).

Histologically there was a prominent mucosal eosinophil infiltrate in

affected children that was significantly lower in those on a gluten- and

casein-free diet, although lymphocyte populations were not influenced by

diet.The data provide further evidence of a pan-enteric mucosal

immunopathology in children with regressive autism that is apparently

distinct from other inflammatory bowel diseases. "

32: Wakefield AJ. Enterocolitis, autism and measles virus. Mol

Psychiatry. 2002;7 Suppl 2:S44-6. PMID: 12142948

33a: Wakefield AJ. The gut-brain axis in childhood developmental

disorders. J Pediatr Gastroenterol Nutr. 2002 May-Jun;34 Suppl 1:S14-7.

PMID: 12082381

33b. Binstock T. Anterior insular cortex: linking intestinal pathology

and brain function in autism-spectrum subgroups. Med Hypotheses 2001

57(6):714-7. PMID: 11918432

" Numerous parents and some physicians report that an

autistic child's attention and language improve in response to

treatments which eliminate certain dietary antigens and/or which improve

intestinal health. For at least some autism-spectrum children, the link

between intestinal pathology, attention, and language may derive from

shared neuroanatomic pathways within the anterior insular cortex (aIC);

from a neurotrophic virus such as herpes simplex (HSV) migrating within

afferents to the insular cortex; and/or from synaptic exhaustion in the

aIC as induced by chronically inappropriate neuronal activity in the

enteric nervous system and/or its vagal efferents. "

34: Torrente F et al. Small intestinal enteropathy with epithelial IgG

and complement deposition in children with regressive autism. Mol

Psychiatry. 2002;7(4):375-82, 334.

PMID: 11986981

" Most strikingly, IgG deposition was seen on the basolateral

epithelial surface in 23/25 autistic children, co-localising with

complement C1q. This was not seen in the other conditions. These

findings demonstrate a novel form of enteropathy in autistic children,

in which increases in mucosal lymphocyte density and crypt cell

proliferation occur with epithelial IgG deposition. The features are

suggestive of an autoimmune lesion. "

35: Uhlmann V et al. Potential viral pathogenic mechanism for new

variant inflammatory bowel disease. Mol Pathol. 2002 Apr;55(2):84-90.

PMID: 11950955

" AIMS: A new form of inflammatory bowel disease (ileocolonic

lymphonodular hyperplasia) has been described in a cohort of children

with developmental disorder. This study investigates the presence of

persistent measles virus in the intestinal tissue of these patients (new

variant inflammatory bowel disease) and a series of controls by

molecular analysis... RESULTS: Seventy five of 91 patients with a

histologically confirmed diagnosis of ileal lymphonodular hyperplasia

and enterocolitis were positive for measles virus in their intestinal

tissue compared with five of 70 control patients. Measles virus was

identified within the follicular dendritic cells and some lymphocytes in

foci of reactive follicular hyperplasia. The copy number of measles

virus ranged from one to 300,00 copies/ng total RNA. CONCLUSIONS: The

data confirm an association between the presence of measles virus and

gut pathology in children with developmental disorder. "

36: Wakefield AJ et al. Review article: the concept of entero-colonic

encephalopathy, autism and opioid receptor ligands.Aliment Pharmacol

Ther 2002 16(4):663-74. PMID 11929383

37: Furlano RI et al. Colonic CD8 and gamma delta T-cell infiltration

with epithelial damage in children with autism. J Pediatr. 2001

Mar;138(3):366-72. PMID: 11241044

" OBJECTIVES: We have reported colitis with ileal lymphoid

nodular hyperplasia (LNH) in children with regressive autism. The aims

of this study were to characterize this lesion and determine whether LNH

is specific for autism. METHODS: Ileo-colonoscopy was performed in 21

consecutively evaluated children with autistic spectrum disorders and

bowel symptoms. Blinded comparison was made with 8 children with

histologically normal ileum and colon, 10 developmentally normal

children with ileal LNH, 15 with Crohn's disease, and 14 with ulcerative

colitis. Immunohistochemistry was performed for cell lineage and

functional markers, and histochemistry was performed for

glycosaminoglycans and basement membrane thickness. RESULTS: Histology

demonstrated lymphocytic colitis in the autistic children, less severe

than classical inflammatory bowel disease. However, basement membrane

thickness and mucosal gamma delta cell density were significantly

increased above those of all other groups including patients with

inflammatory bowel disease. CD8(+) density and intraepithelial

lymphocyte numbers were higher than those in the Crohn's disease, LNH,

and normal control groups; and CD3 and plasma cell density and crypt

proliferation were higher than those in normal and LNH control groups.

Epithelial, but not lamina propria, glycosaminoglycans were disrupted.

However, the epithelium was HLA-DR(-), suggesting a predominantly T(H)2

response. INTERPRETATION: Immunohistochemistry confirms a distinct

lymphocytic colitis in autistic spectrum disorders in which the

epithelium appears particularly affected. This is consistent with

increasing evidence for gut epithelial dysfunction in autism. "

38: O'Leary JJ et al. Measles virus and autism. Lancet. 2000 Aug

26;356(9231):772. PMID: 11085720

39: Wakefield AJ et al. Enterocolitis in children with developmental

disorders. Am J Gastroenterol. 2000 Sep;95(9):2285-95. PMID: 11007230

" 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.

40: Wakefield AJ, Montgomery SM. Autism, viral infection and

measles-mumps-rubella vaccination. Isr Med Assoc J. 1999 Nov;1(3):183-7.

PMID: 10731332

41: Wakefield AJ. MMR vaccination and autism. Lancet. 1999 Sep

11;354(9182):949-50. PMID: 10489978

42: Horvath K et al Gastrointestinal abnormalities in children with

autistic disorder. J Pediatr. 1999 Nov;135(5):559-63. PMID: 10547242

" OBJECTIVES: Our aim was to evaluate the structure and

function of the upper gastrointestinal tract in a group of patients with

autism who had gastrointestinal symptoms. STUDY DESIGN: Thirty-six

children (age: 5.7 +/- 2 years, mean +/- SD) with autistic disorder

underwent upper gastrointestinal endoscopy with biopsies, intestinal and

pancreatic enzyme analyses, and bacterial and fungal cultures. The most

frequent gastrointestinal complaints were chronic diarrhea, gaseousness,

and abdominal discomfort and distension. RESULTS: Histologic examination

in these 36 children revealed grade I or II reflux esophagitis in 25

(69.4%), chronic gastritis in 15, and chronic duodenitis in 24. The

number of Paneth's cells in the duodenal crypts was significantly

elevated in autistic children compared with non-autistic control

subjects. Low intestinal carbohydrate digestive enzyme activity was

reported in 21 children (58.3%), although there was no abnormality found

in pancreatic function... CONCLUSIONS: Unrecognized gastrointestinal

disorders, especially reflux esophagitis and disaccharide malabsorption,

may contribute to the behavioral problems of the non-verbal autistic

patients... "

43: Horvath K, Perman JA. Autism and gastrointestinal symptoms. Curr

Gastroenterol Rep. 2002 Jun;4(3):251-8. PMID: 12010627

44: Horvath K, Perman JA. Autistic disorder and gastrointestinal

disease. Curr Opin Pediatr. 2002 Oct;14(5):583-7. PMID: 12352252

" High prevalence of histologic abnormalities in the

esophagus, stomach, small intestine and colon, and dysfunction of liver

conjugation capacity and intestinal permeability were reported. Three

surveys conducted in the United States described high prevalence of

gastrointestinal symptoms in children with autistic disorder. Treatment

of the digestive problems may have positive effects on their behavior. "

45a: Quigley EM, Hurley D. Autism and the gastrointestinal tract. Am J

Gastroenterol. 2000 Sep;95(9):2154-6. PMID: 11007210

45b: Tim Buie, M.D., Harvard/Mass-General, Presentation at 2003 DAN!,

Philadelphia.

http://216.117.159.91/powerpoint/dan2003/Buie.htm

eof

[Guest guest]

In a message dated 5/7/2004 10:31:32 PM Eastern Daylight Time,

thljrm01@... writes:

> * Pediatric Neurologist - she wants to do a muscle bioposy & feels

> it may be a mitochondrial brain disorder that we can't do anything

> for anyway - by the way, this chick had never even heard of ABA!!!!

> She said, " What is that anyway, I know there's all sorts of wacky

> treatments for autism out there " .

>

> RUN away from this woman- I don't think I'd accept her opinion on the

weather!

Keep asking your doctors: " What would you be doing if she DIDN'T have

autism? " So many doctors are so clueless about autism that is scares them and

they

can't see past it to the child they are supposed to treat.

I would INSIST on a GI consult, if for no other reason than to get a feeding

tube in place.

You can't just sit by and watch your daughter starve to death!

I'm praying for you and your little girl!

~Sue

[Guest guest]

I don't even know what to say, this is so shocking. Here goes.

My mother was dying of emphysema, and was in the hospital for pneumonia. My

brother went out to the nurse's station and asked for some to be

administered to her right away, as she had awakened in a great deal of pain.

They said she wasn't due for another 20 minutes. He came back very

distressed. I was pissed off. I went out to that nurse's station and asked

who was in charge of my mother's care. I said, " My mother is going to get

morphine right now, and it's going to happen because if it doesn't, I'm

going to be disturbing a lot of other patients with my angry yelling. I

suggest you do it immediately. "

This got very fast results. It may seem like an unnecessarily long way of

going about telling you to make some noise, but as it really happened, I

think it's more compelling.

Your daughter's life is at stake. These are people who do this for a living.

They are practically immune to pain and death. They need you to shake them

out of their complacency. You will be labeled difficult. Forget it. And when

I say " make some noise, " I mean it quite literally. They will do pretty much

anything to keep a hospital quiet.

Hospitals are vastly understaffed and nurses are horribly overworked. This

is not your problem. The ONLY way to get decent care in a hospital is to

have someone advocating for you 24/7. We are praying for you, your daughter,

and your family.

Liz