Expert Postings
July 1996

Copyright by Michael Jones, Bill Elkus, Jim Lyles, and Lisa Lewis 1996 - All rights reserved worldwide.
Disclaimer

Table of Contents

 
This file contains postings made by the following professionals: 
 
Stefano Guandalini, M.D--a professor of pediatrics at the University of 
   Chicago; formerly with the University of Naples in Italy.  Dr. 
   Guandalini is involved in research on pathophysiology of intestinal 
   transport, and has an interest in coeliac disease in children that is 
   mainly clinical, leading to re-definition of diagnostic criteria in 
   childhood. 
 
Karoly Horvath, M.D.--an associate professor of pediatrics at the 
   University of Maryland at Baltimore.  Dr. Horvath set up the 
   Pediatric Gastrointestinal and Nutrition Laboratory, and is now 
   director of this lab. 
 
Donald D. Kasarda, Ph.D.--a research chemist with the United States 
   Department of Agriculture.  Dr. Kasarda has worked on grain proteins 
   in relation to grain quality for 30 years.  He has colloborated with 
   medical groups working on celiac disease for about 25 years and has 
   often been used as an informal consultant by support groups. 
 
Joseph Murray, M.D.--a gastroenterologist at the University of Iowa, 
   USA, where they have a mutidisciplinary service for the clinical care 
   of people with celiac disease.  They are also involved with clinical 
   research and medical education related to celiac disease. 
 
Kalle Reichelt, M.D.--senior researcher at the Department of Pediatric 
   Research, University of Oslo, Norway.  Dr. Reichelt is looking into 
   the impact of gluten intolerance on certain individuals with 
   developmental delays. 
 
Phil Sheard, Ph.D.--researcher in the Developmental Biology Unit, 
   Department of Physiology, University of Otago Medical School, in 
   Dunedin, New Zealand. 
 
Other expert posting files are available.  The naming convention is: 
 
Disclaimer: Verify this information before applying it to your situation. 
 
========================================================================= 
Date:         Wed, 3 Jul 1996 17:56:48 PDT 
From:         "Donald D. Kasarda" (kasarda@PW.USDA.GOV) 
Subject:      Re: oatrim 
 
With regards to: 
 
) ...I think the findings are that "OATRIM" is used in meats, colas, and 
) other formulated foods.  The Beta Glucans are the specific derivative from 
) "OATRIM" that has been placed in ice tea, fruit juice, sports drinks, and 
) even wine.  The process was developed at USDA's Midwest Area Northern 
) Regional research center and is commercially supplied by ConAgra and Quaker 
) Oats. 
) 
) It is supposed to be a benefit to normal humans.  How it acts on the villa 
) of those with Celiac Disease/Dermatitis Herpetiformis is not something I 
) would deign to presume. AMS 
 
AMS is correct in her posting on oatrim to the best of my knowledge.  I know 
the inventor of Oatrim and will try to find out how it is made and how 
likely it would be to have oat prolamins (or wheat prolamins) as a 
contamination (although oat prolamins may not be harmful to celiac patients). 
 
Don Kasarda 
========================================================================= 
Date:         Sat, 6 Jul 1996 18:28:04 -0400 
From:         Stefano Guandalini (Sguandal@AOL.COM) 
Subject:      Re: return to normal villi 
 
Return of villi to normal after GF diet is a process that may take a 
variable amount of time. However, I believe 2 years has just never been 
reported!  Actually, in the original ESPGAN protocol for diagnosis of CD, 
the lack of return to normal after 1 year of GFD was taken as a convincing 
proof that the cause of flat mucosa can not be CD. 
 
Possibilities are: 
 
1) You are actually still eating gluten in some hidden form (Holy Communion? 
Other?)  Normal blood work-up however (IF including anti-endomysium 
antibodies!) speaks against it. 
 
2) Histology was not performed accurately. Sometimes it may happen that the 
specimen is improperly orientated or tangentially cut, leading to the false 
interpretation of a still flat mucosa. Believe me, it takes a very 
experienced pathologist to realize that the specimen may not be perfectly 
handled for interpretation. 
 
3) You have another disease leading to flat mucosa. This is obviously a real 
possibility, although full clinical and laboratory remission (which I simply 
assume) after GFD are an indirect but sound evidence for CD. Other causes of 
flat mucosa include Crohn's, food allergy (but particularly in the first 2 
years of life!), small bowel bacterial overgrowth, infection by Giardia 
Lamblia. Ask your doctor about these entities. 
 
As for Helicobacter pylori infection, this microrganism is known to be able 
to colonize only gastric mucosa, and is not a known cause for inflammation 
of duodenal-jejunal mucosa leading to shortening of villi. 
 
Hope to have been of some help! 
 
Stefano Guandalini 
========================================================================= 
Date:         Tue, 9 Jul 1996 10:25:56 EDT 
From:         Bill Elkus (Bill_Elkus@JEFCO.COM) 
Subject:      Re: DH diagnosis 
 
)From Karoly Horvath, MD at University of Maryland's celiac clinic: 
 
Date: 07/09/96 09:07:49 AM 
Subject: Re: DH diagnosis 
 
 
If the skin symptoms suggest DH, the diagnosis is based on two tests: 
 
1. Skin biopsy: immunofluorescent staining - linear deposits of IgA. 
 
2. Serology test: positive antiendomysium antibody test. 
 
As a compromise: the positive serology and the typical skin symptoms 
are enough for a clinical diagnosis. However, I think most of the 
dermatologist consider the biopsy as "gold standard" for the diagnosis. 
 
It seems that dermatologist needs some education regarding the DH diagnosis 
("gluten-sensitive dermatopathy"; this is only my terminology) 
 
 
Karoly Horvath 
========================================================================= 
Date:         Wed, 10 Jul 1996 16:50:12 EDT 
From:         Bill Elkus (Bill_Elkus@JEFCO.COM) 
Subject:      Dr. Murray on Biopsies 
 
From: Murray @ intmed-po.int-med.uiowa.edu 
Date: 07/10/96 
 
"Negative biopsies"  may be reported in a celiac patient due one of several 
reasons. 
  -- The patient may already have been on a GFD 
  -- The disease may be somewhat patchy therefore many would advocate doing 
     3-4 samples from the small intestine. 
  -- The pathologist may not recognise subtle changes that can be due to 
     celiac disease. 
  -- There may be some other process such as peptic ulcer disease that may 
     occur simultaneously and mask the celiac disease changes. 
Not medical advice 
Joe Murray 
========================================================================= 
Date:         Wed, 10 Jul 1996 16:45:47 EDT 
From:         Bill Elkus (Bill_Elkus@JEFCO.COM) 
Subject:      Dr Murray on complaints of bones hurting 
 
A forward from Dr Joe Murray about a prior question by Nadia 
)nchychot@gbrownc.on.ca): 
 
N)i'm writing mainly on my mom's behalf. she has been complaining that her 
N)bones hurt for over two years now, and nobody seems to be able to give a 
N)reasonable explanation. 
 
From: Murray @ ntmed-po.int-med.uiowa.edu 
Date: 07/10/96 08:43:36 AM 
 
This may be due to osteoporosis due to loss of bone mineral.  This can result 
in fractures or even sponteneous collapse of vertebra leading to compression 
of nerve roots and severe pain. 
 
Osteomalacia , also can occur though I think it is less common in US patients 
due to high intake of vitamin D and sunlight.  This can result in 
pseudofractures in the hips, pelvis, spine and shouldres with significant 
pain and weakness especially climbing stairs or getting out of a low chair. 
Vitamin D deficiency can also result in a skin pain syndrome. 
 
It is possible that these changes could progress in  diagnosed celiac due to 
poor vit D intake and low calcium intake especially if they are milk in 
tolerant. 
 
There are many other reasons one could have bone pain, from injuries, 
arthritis, lupus and malignancies.  A careful phyical , biochemical and 
radiographic examination may be warranted. 
 
Not medical advice 
========================================================================= 
Date:         Thu, 11 Jul 1996 10:43:25 PDT 
From:         "Donald D. Kasarda" (kasarda@PW.USDA.GOV) 
Subject:      Oatrim 
 
Comments from Don Kasarda, Albany, CA 
 
I have talked with the inventor of Oatrim about what it is and how it is 
prepared.  The main constituent of this fat replacement product is 
carbohydrate, specifically malto-dextrins from oats.  These are prepared by 
fungal amylase digestion of the starch in oats.  Although there is not 
likely to be much contamination from oat proteins in the final product, 
slight contamination cannot be ruled out.  It would require some extensive 
research work to devise a method for measuring oat proteins or peptides at 
very low levels in the final product--and there may be none there. Because 
Oatrim is likely to be incorporated as a minor component of a food product, 
at most in 1:4 ratio with other constituents, this further diminishes the 
amount of oat proteins or peptides that might turn up in the final product. 
However, anyone who is allergic to oats may wish to avoid Oatrim. If there 
is any wheat contamination of the oats used to make the product, then wheat 
proteins or peptides might also make it into the final product, but because 
the amount of such contamination is likely to be very small, the chances for 
wheat proteins or peptides being passed along is also very small, much 
smaller than the possibility for the presence of oat proteins or peptides. 
 
As for celiac patients, some may not wish to take a chance on products 
containing Oatrim.  It seems likely to me that the risk is extremely small 
insofar as I think the data on oats (at least in pure form) being harmless 
to celiac patients look quite good. 
 
This is not to be considered medical advice. My comments are correct to the 
best of my knowledge, but I hope it is clear that absolute statements are 
not possible. 
========================================================================= 
Date:         Fri, 12 Jul 1996 12:24:42 -0400 
From:         Karoly Horvath (khorvath@UMABNET.AB.UMD.EDU) 
Subject:      Re: Return to normal villi (fwd) 
 
        Ronal Hoggan cited a paper published in 1988 showing an incomplete 
histological and functional recovery in adult patients with CD. I have no 
doubt that the conclusion of this paper was correct that time. However, it 
is important to emphasize that the authors did not have the opportunity to 
check the sctrictness of diet by measuring the antibody titers or the in 
vitro cell-mediated immune response to gluten in their patients. It is 
well known that the immunological alterations return to the normal within 
months. If they are still present it suggest gluten ingestion. 
 
        If a found an incomplete recovery of intestinal structure and 
function in children, all these patients had positive in vitro immune 
response to gluten suggesting accidental gluten consumption. 
 
        To clarify this question a new well designed study necessary, 
which proves that the examined patients group do not ingest gluten. 
 
        I agree with Dr. Guandalini and I believe in a complete 
restoration of intestinal structure in patients on a really strict 
gluten-free diet. 
 
Karoly Horvath, M.D., Ph.D. 
Baltimore 
========================================================================= 
Date:         Tue, 16 Jul 1996 10:59:53 +0000 
From:         Phil Sheard (phil.sheard@STONEBOW.OTAGO.AC.NZ)
Subject:      Re: Let's hear it for sprue! 
 
Hi all, with many scientific definitions the real is often less interesting 
than the fanciful. "Sprue" is derived from the Dutch word "sprouw", meaning 
"a kind of tumour". Sorry to disappoint those who thought it may have a 
more interesting derivation. To be an even bigger wet blanket for those of 
you who have DH and thought "herpetiformis" might have something to do with 
lizards, in fact it means "resembling Herpes". 
cheers 
Phil 
 
Philip Sheard 
Developmental Biology Unit, 
Department of Physiology, 
University of Otago Medical School, 
Dunedin, New Zealand. 
Ph (64 3) 479-7344 
Fax (64 3) 479-7323 
========================================================================= 
Date:         Thu, 18 Jul 1996 21:05:19 PDT 
From:         "Donald D. Kasarda" (kasarda@PW.USDA.GOV) 
Subject:      Re: Lemon Grass 
 
Comments from Don Kasarda, Albany, California. 
 
Lemon grass, Cymbopogon citratus, is a member of the grass family. According 
to Hitchcock it is placed in the same tribe as sorghum and therefore I think 
it is not likely to contain any proteins harmful to celiac patients on the 
basis of plant classification. 
 
Lemon grass has not been specifically tested, however, and I make my 
judgement only on the basis of its position in the taxonomy. 
 
 
)Can anyone on the list tell me about GF status of lemon grass?  Is it a member 
)of the grass family? 
) 
)Mildred Oberkotter, New York City 
========================================================================= 
Date:         Wed, 24 Jul 1996 20:25:00 CST 
From:         Murray@INTMED-PO.INT-MED.UIOWA.EDU 
Subject:      RE diabetes and celiac disease, gastroparesis 
 
There is a definite incidence of celiac disease in type one diabetes in 
causcasians at least.  Anywhere from of 3.3% to 10 % of people with type one 
diabetes willl have or develope celic disease.  Any form of diabetes can lead to 
gastroparesis, usually after many years of diabetes.  The symptoms can be 
similar in many ways, bloating after meals, abdominal pain.  Diarrhea is not 
usually caused by the gastroparesis itself.  ( diabetic diarrhea may occur as 
part of the the nerve damage caused by the lonGstanding diabetes).  I have 
several patients who have diabetes, gastroparesis and celiac disease.  Certainly 
identifying the celiac disease oftenn makes a big difference to the symptoms. 
Joe Murray 
Univ of Iowa 
Not medical advice 
========================================================================= 
Date:         Thu, 1 Aug 1996 04:58:32 EDT 
From:         Bill Elkus (Bill_Elkus@JEFCO.COM) 
Subject:      Dr. Horvath on Intussusception & CD 
 
Recently, there was a post asking about a possible relationship between 
Intussusception and Celiac.  I asked Dr. Karoly Horvath, one of the directors 
of the Celiac clinic at University of Maryland, for his thoughts, which follow: 
 
Bill Elkus 
Los Angeles 
 
Dr. Horvath writes: 
 
 Intussusception is a common cause of intestinal obstruction 
between 3 month and six years of age. Generally a segment of intestine 
goes into the other segment, the circulation is compromised, which may 
lead to necrosis.  It occurs frequently after infection involving the 
distal small intestine and causing lymph node enlargement in this area. Up 
to 75 % of causes can be solved by barium enema studies, which is 
diagnostic and therapeutic. The remaining cases need surgery. Even after 
surgery the prognosis is good, there are no complications associated with 
the surgery. There are cases of recurrent intussusception, they may need a 
sugery. 
 In my knowledge there is no association between celiac disease and 
intususception. 
========================================================================= 
Date:         Tue, 13 Aug 1996 09:58:41 PDT 
From:         "Donald D. Kasarda" (kasarda@PW.USDA.GOV) 
Subject:      Re: GF Fast Food 
 
I was very pleased to see this posting (appended) as I suspect that for the 
majority of all celiacs the concern about gluten contamination in products 
that are not likely to have any gluten (or minute amounts, as in drugs taken 
occasionally) is far too great. 
 
Don Kasarda 
 
)...as many on the list know many 
)fast food hamburgers are NOT "diluted with fillers which may be oats or 
)heaven knows what else" -- to say "almost all" is quite misleading.  All 
)french fries are NOT coated with wheat nor cooked in "forbidden oils". 
) Lastly, milk shakes are typically GF....As we have 
)seen from the many posts on this subject, all fast food is not bad, nor is 
)all fast food GF.  Let's not make GF life more difficult than it already is! 
========================================================================= 
Date:         Fri, 16 Aug 1996 14:34:00 CST 
From:         Murray@INTMED-PO.INT-MED.UIOWA.EDU 
Subject:      Maximum tolerable gluten debate 
 
My opinion based on seeing a large number of patients with celiac 
disease both in Ireland and in the USA, is that there is a 
remendous variablity in sensitivity to gluten in patients.  I am 
frequently asked what is the most gluten a patient can tolerate 
and get away with it. How often can they deliberately cheat on 
the diet and get away it? 
How do they know if they have overdone it? 
Therre are no absolutely good answers to these questions. 
 
This is a short and generalised summary of my answers 
If eating it makes you sick avoid it.( dont assume its gluten 
that makes you sick ; it could be lactose intolerance) 
If you know it has gluten ( like wheat bread, bagels etc) avoid 
it. 
Follow up with your doctor with some objective test such as a 
biopsy and or blood tests ( antibodies to gliadin or similar 
tests).  If these show there is still a problem, you must ask 
yourself if you gluten free enough? 
There are people who are exquisitily sensitive to minute 
quantities of gluten but they make up the minority of people with 
CD. 
What is minute?  for some it is vinegar, others malt flavoring, 
others think of minute as a small slice of bread( wheat that is) 
What I mean by minute is  less than the codex alimentarius agreed 
amount. 
People are unique, in their make up, hence their reactions to 
things are different both in type and severity. 
Those with a professional interest in any topic have to make some 
general assumptions based on aggregate data,  Individuals must 
make their own minds up as to what is best for them, obviously 
and hopefully gaining some benefit from the experiences of others 
that gone before and from observers like Don Kasorda and myself. 
 
Discussing celiac disease can evoke some emotive issues, and 
responses, that in the e-mail world are not qualified by tonal 
inflections in the voice or gestures or mannerisms of the face to 
face conversations.  Netiquette is a whole new skill that is 
strange to most of us, and we are all learning. 
 
Get well 
Stay well 
and be happy 
 
This opinion is not medical advice 
Nor is it the opinion of the US Government, the State of Iowa, 
the University of Iowa, 
 
Joe Murray MD 
University of Iowa 
========================================================================= 
Date:         Mon, 19 Aug 1996 09:17:49 EDT 
From:         Bill Elkus (Bill_Elkus@JEFCO.COM) 
Subject:      Reichelt on Fanconi and Downs syndrome 
 
Forwarded with permission: 
 
To: Bill_Elkus@jefco.com 
From: K.L.Reichelt@rh.uio.no (Kalle Reichelt) 
Date: 08/19/96 04:39:59 PM EDT 
Subject: Downs syndrome 
 
Hi. 
I know nothing about the mechanisms causing the Fanconi syndrome.It is 
correct that there is s slight increasein the frequency of coeliac disease 
in Downs. More important though is the fact that without Downs syndrome 
more than 1/3 of the children have extremely high IgA antibodies against 
gliadin, gluten,lactoglobulin and casein as well as ovalbumin without 
endomycium antibodies being increased.(1,2) There is an inverse 
relationship size of the children and level of IgA to gliadin and gluten. 
C P Reading in Australia thinks that there is a causal relationship Downs 
because of the increase in antibodies found also by him (3). 
Ref: 
1:Kanavin \ et al (1988) Immunological studies of patients with Down's 
syndrome. Acta med Scand. 224: 474-477. 
2: Reichelt KL et al (1994) Increased levels of antibodies to food proteins 
in Down Syndrome. Acta Paed japon 36: 489-492. 
3:Reading CM (1984) Down's syndrome:Is Gluten/Alpha-gliadin 
sensitivity/coeliac disease the cause? Int J Biosocial Res 6: 62-65. 
 
All the best                                    Cheers 
 
                                                        TINY 
 
K. Reichelt 
Pediatric Research Institute 
N-0027 Oslo, Norway 
Tel: +47 22 86 90 45 
Fax: +47 22 86 91 17 
E-mail: K.L.Reichelt@rh.uio.no 
========================================================================= 
Date:         Tue, 20 Aug 1996 16:00:04 +0000 
From:         Phil Sheard (phil.sheard@STONEBOW.OTAGO.AC.NZ)
Subject:      Fanconi 
 
G'day from the southern hemisphere. I read with interest a recent posting 
by Tom Hennessy which described a possible link between Fanconi syndrome 
and other disorders of interest to this group. His description did not 
resemble my memory of the disease, so I looked it up in the American 
Medical Association Encyclopedia of Medicine (1989). This book describes 
the disease as a rare kidney disorder occurring mainly in childhood, in 
which various important nutrients and chemicals such as amino acids, 
phosphates, calcium and potassium are lost in the urine. This leads to 
failure to thrive. It describes a number of possible causes, including 
inheritance, drug side effects, and ingestion of heavy metals. I looked up 
the url which Tom listed in his posting,and this seems to back up the 
encyclopedia's description. I found no obvious direct links with other 
diseases, and no mention of the endocrine abnormalities, although another 
(unrelated) disease (Fanconi's anaemia) is a fatal anaemia which may have 
associated endocrine changes. Since the latter is fatal and usually results 
in early death, it would be reasonable for most of you to assume you don't 
have it. 
I offer this information to contribute to the discussion, and it is no way 
intended as a criticism of Tom Hennessy or his findings, I am not a medical 
practitioner and my findings are also open to dispute. 
Tom mentioned one other thing which I would like to expand upon, as a point 
of general interest. He said "..the *muscle proteins* one of which is 
myosin which controls the face and throat..". Most of you will be aware 
that meat is muscle. Those of you who eat meat do so because it is a good 
source of dietary protein. The major proteins in muscle are the contractile 
proteins actin and myosin, these are the molecules which use energy to 
produce work, and which allow you to move your limbs (among other things). 
So, myosin is in all muscle (in various forms, but myosin nonetheless), and 
is not specifically related to face or throat musculature. 
best wishes 
Phil 
 
Philip Sheard 
Developmental Biology Unit, 
Department of Physiology, 
University of Otago Medical School, 
Dunedin, New Zealand. 
Ph (64 3) 479-7344 
Fax (64 3) 479-7323 
========================================================================= 
Date:         Sat, 24 Aug 1996 17:37:04 PDT 
From:         "Donald D. Kasarda" (kasarda@PW.USDA.GOV) 
Subject:      Re: the real culprit 
 
)I was under the impression that because gluten is insoluble in water, it is 
)pretty difficult to digest for a significant number of persons. And our 
)digestive systems have not evolved as quickly as cereal domestication. 
)We started out as hunter/gatherers. Dr. Lutz' article provided by Don Wiss 
)suggests this explanation. 
 
I have not read the article referred to (Dr. Lutz), but as a scientist 
specializing in gluten proteins, I am fairly aware of nutritional research 
related to the gluten proteins.  I am not aware myself of any scientific 
evidence that gluten proteins are difficult to digest--there is some 
evidence in the direction that they are easy to digest.  Also, most gliadin 
proteins (at present considered the most active fraction of gluten) are only 
slightly soluble in water, but are fairly soluble in acidic solutions. 
There is a high concentration of hydrochloric acid in the stomach where 
initial breakdown of proteins by the protease enzyme pepsin (which has low 
specificity, breaking down many different amino acid linkages) begins. The 
ability to be digested by various proteases probably outweighs solubility 
considerations for gluten proteins.  Proteins that start out insoluble 
rapidly become soluble as enzymes fragment them into smaller pieces.  The 
gluten proteins appear to be adequately attacked by the array of proteases 
available in our gastrointestinal tracts. I think it is not likely that the 
basis of celiac disease lies in the digestibility of the gluten proteins, 
although I know of one scientist who disagrees with me on this. I think, 
however, that most scientists would agree with me. 
 
Man no doubt started out as a hunter and gatherer, but that doesn't 
necessarily mean that he lived off easily digested materials only.  I would 
guess that a wide range of plant foods were gathered and consumed, varying 
according to type in the degree of ease with which they could be digested. 
It is certainly possible, even likely, that wild wheats were gathered for a 
long time before they began to be cultivated (about 10,000 years ago, 
although I doubt that any special evolution of the digestive tract was 
necessary to adapt to the eating of grains, at least once they were cooked. 
If I recall correctly the pertinent publications on the subject, it is 
thought by anthropologists that adherent glumes (characteristic of wild 
wheats and spelt) had to be removed from the grains by charring, then the 
wheat grain was stone ground in a mortar for preparation of something like a 
gruel or porridge by cooking in water. 
 
Don Kasarda, Albany, California 
========================================================================= 
Date:         Mon, 26 Aug 1996 09:02:44 -0400 
From:         khorvath@MEM.po.com 
Subject:      Endomysial IgA 
 
Peter L. Warren's question: 
 
"Does anyone know the range for positive and negative test results for 
endomysial IgA ?" 
 
        We are using different dilutions of patient serum and incubate them 
with tissue slides. Generally, a fluorescence  at the dilution of  1:4 
or 1:5  is considered as borderline positive. Any fluorescence in the 
tissue above this  dilution indicates a real positive result. Most of 
our patients with CD or DH  have a value higher than 1:32. 
 
Karoly Horvath, M.D., Ph.D. 
Associate Professor of Pediatrics 
Director, pediatric GI and Nutrition Laboratory 
University of Maryland at Baltimore 
Tel: 410-328-0812 
Fax: 410-328-1072 
========================================================================= 
Date:         Wed, 28 Aug 1996 09:30:28 PDT 
From:         "Donald D. Kasarda" (kasarda@PW.USDA.GOV) 
Subject:      Re: the real culprit 
 
(If active celiacs 
)DON'T have achlorhydria, how is it that the peptides reach the gut intact 
)enough to be antigenic?). 
 
This comes about because in all people digestion of proteins in the stomach 
is incomplete so that peptides and some intact proteins pass into the small 
intestine where digestion continues by pancreatic enzymes and enzymes 
associated with the brush border of the intestinal epithelium. 
 
Don Kasarda, Albany, CA 
========================================================================= 
Date:         Thu, 5 Sep 1996 23:08:58 -0400 
From:         Bill Elkus (Bill_Elkus@JEFCO.COM) 
Subject:      The Coeliac Symposium - Day 1 
 
The following is a report from the international Coeliac Symposium 
currently being held at Tampere, Finland.  This event occurs once 
every 4 years, and is the most important gathering of researchers 
in our field.  We are very fortunate to have two volunteers as our 
reporters: Dr. Joseph Murray from the Celiac clinic at the University 
of Iowa, who is attending the conference and calling in his reports, 
and Ann Whelan, who is transcribing, summarizing and editing them. 
 
Many of you know Ann Whelan as the editor of the GLUTEN-FREE LIVING 
newsletter.  This is an excellent printed newsletter which covers 
important topics at a level of detail which is difficult to do on 
a listserv just as ours.  It is also an excellent product to give 
to medical professionals to assist them in keeping up with this field. 
It is well researched, and includes quotes and/or articles by many 
well-respected clinicans and researchers in the Celiac field.   One 
year of 6 issues is $29, two years is $49. International orders are 
$5 extra. A sample issue is $5.95. Four issues have been published 
so far, the fifth is about to appear).  Order from Gluten-Free 
Living, P.O. Box 105, Hastings-on-Hudson, NY 10706. Ann plans on 
covering a few selected topics from the Tampere symposium 
in greater detail (and with additional sources) in future issues. 
 
Bill Elkus 
for the Listowners 
 
---------Ann Whelan / Joe Murray report #1 follows------------- 
 
THE DAILY REPORT 
 
Hi, everybody. Although I am not currently on the Internet, I am 
pleased to be involved in this effort to get the word out as 
quickly as possible. After listening to Joe Murray talk about the 
conference, I can tell you that I'd love to be there -- as I'm 
sure most of us would prefer. Joe says he didn't take a head 
count in the hall, but it's packed and just about everyone who is 
anyone in the celiac community -- with very few exceptions -- is 
in attendance. 
 
Today's rundown is pretty descriptive. Time permitting tomorrow I 
will try to get a bit more depth. But I think in the following 
information, you'll find plenty of interesting developments. 
     So, here we go... 
 
The first speaker, Dr. Jarmo Visakorpi, from Finland, gave an 
overview of CD and how it started out being thought of as a rare 
gi disease of children and not a common disease that occurs at 
all ages and may not be limited to the gi tract. Joe remembered 
one quote that he felt would be well worth repeating -- and 
you'll see why. 
 
Dr. Visakorpi said: 
 
"Many people call parts of the celiac iceberg by different names, 
but that's not important. It's  more important to know the size 
of the iceberg and how it floats...In Sweden, the whole iceberg 
is floating. In other European countries,  the tips of the 
iceberg are showing. But in the United States, the whole iceberg 
is submerged." 
 
Wow! I'd call that a great image... 
 
Dr. Luigi Greco, from Italy, spoke next. He talked about origins 
of cultivation and how wheat was the first cultivated plant, at 
least in the middle east. The cultivation of wheat allowed people 
to change from being nomads to being settled. The next big 
occurrence relative to cultivation was that people discovered 
they could ferment wheat and make beer! 
     Dr. Greco went on to comment that in the western part of 
Europe, exposure to gluten has only occurred  very recently in 
genetic terms, with little time having elapsed for the population 
to adapt genetically! 
     Dr. Greco also commented on the perceived differences in 
incidence rates that we see quoted and suggested that these 
differences may be actually due to the different ages of onset in 
different populations and there really is little difference 
statistically between different measures --1 250 and 1 in 500, 
for example. 
 
Dr. Henry Asher from Sweden spoke next. He discussed the Swedish 
experience, which has shown an increased incidence among children 
that is different from other countries. 
     Dr. Asher made several observations about the gluten content 
of commercial foods, which has gone up dramatically since cow's 
milk protein has been eliminated from formulas and replaced with 
gluten-containing material. He says the amount of gluten given to 
young children is correlated with the onset of symptomatic 
disease. He looked at gluten consumption in children: It's 
highest in Italy, next highest in Sweden, next is Finland and the 
next is Denmark and these levels of gluten consumption parallel 
the rise in symptomatic cd in children. 
     Dr. Asher went on to observe that the diagnosis of cd is 
related to a shorter duration of breastfeeding, the earlier 
introduction of solid foods and a higher amount of gluten in the 
diet. He showed news clippings from Sweden, including one that 
said the Justice Minister in Sweden has a daughter who has cd and 
the minister has called for an outright ban on gluten-containing 
baby food! 
     Not surprisingly, Joe says there was a lot of comment on 
this question. Some suggested the need to look for other factors 
for the change in childhood incidence. Also, if the amount of 
gluten given to children is reduced, they may develop not 
symptomatic CD but silent or delayed CD. Joe says it's too soon 
to decide what can be done with childhood dietary content, but 
that it seems reasonable to prolong breastfeeding and to reduce 
the amount of gluten in the child's diet. 
 
Dr. Carlo Catassi, from Italy, spoke about screening. He used a 
quote (not his own) that said screening should only be undertaken 
if there's a risk of complications and we can alter the natural 
history of the disease in a significant proportion of those 
screened. Dr.  Catassi claims in Italy, CD is one of the 
commonest lifelong disorders. He suggested that for every one 
diagnosed CD individual in Italy, there may be 7 others who have 
asymptomatic disease. In Italy, they screened 17,501 students and 
came up with a high incidence. 
 
Dr. Martin Stern spoke about the standardization of screening 
tests. Joe said his talk was very technical about standardization 
(not screening) in Europe. One important point that he made of 
interest to laypeople is that these tests can either be set as 
screening tests or as diagnostic tests but not both at the same 
time. What makes a good screening test does not make a good 
diagnostic test. Dr. Stern said the normal cutoff point needs to 
be adjusted for whichever aim you have. 
 
Dr. Pekka Collin, from Finland, spoke about diagnostic strategy 
and how to find CD. He did it on the basis of several things: 
actively screening high risk groups, including first-degree 
relatives, and those with insulin dependent diabetes mellitus, 
rheumatologic problems, especially sjogrens syndrome, problems of 
infertility, thyroid disease, and neurologic disease. 
 
The second thing he does is have a service where he gives open 
access endoscopy to primary care doctors who refer patients for 
endoscopy. Third, is to biopsy the duodenum of all patients who 
are endoscoped. Dr. Collin went on to remark that the incidence 
of DH, which is an obvious condition, has been stable and 
unchanging over the years but the diagnosis of CD is increasing 
dramatically. 
 
Next were several short oral presentations not listed in the 
program. First, Dr. Ivarsson and colleagues from Sweden talked 
about different factors leading to cd in children. They mentioned 
the quantity of gluten, a shorter duration of breastfeeding and, 
interestingly Joe says, the socioeconomic status of those 
diagnosed. The lower the socioeconomic status, the greater the 
risk. Additionally, he found that those born in the summertime! 
have a greater risk and, of course, those genetically 
predisposed. 
     Second, Dr. Hovdenak and his colleagues from Norway talked 
about blood donor screening. Joe said he thinks it's very 
interesting that he found a high incidence, 1 in 200, but did not 
find any difference in sex. Joe says that's different from 
symptomatic CD, which is predominately female. 
     Third, Dr. Kaukinen from Finland looked at CD in patients 
who had positive antibody tests and normal architecture in the 
intestine. They show that many of these patients have some subtle 
changes in the intestine, but he's not sure yet what it means. 
(NOTE: The previous seems contradictory to me. I'll try to 
clarify tomorrow. 
     Fourth, Dr. Bahedi from France talked about his findings that 
showed that only 43 percent of adult patients adhere to the GF 
diet. This was detected by biopsy and endomysial antibodies. He 
emphasized that when the antibodies are positive, patients are 
told they are not compliant, but if the antibodies are negative, 
it's  not necessarily saying everything is okay. (NOTE: I'll see 
what else I can find out here tomorrow.) 
 
The next scheduled speaker, Dr. Anne Ferguson from the U.K., said 
that some people just eat a naturally low-gluten diet and that 
aspect needs to be considered when assessing for CD. She also 
talked about the latent forms of CD. 
 
Dr. Auricchio from Italy talked about patients who have symptoms 
due to gluten, but with normal biopsies. These people seem to 
have many differences from celiac patients. Dr. Auricchio 
suggested there may be different genes that determine sensitivity 
to gluten on one hand and the development of small bowel problems 
on the other. 
 
Dr. Lionel Fry from the U.K. talked about DH. He stated that all 
patients with DH have some degree of enteropathy, even though 
less than 1 in 10 patients with DH have GI symptoms. Dr. Fry also 
said 40 percent of DH relatives have gluten-sensitive 
enteropathy. He went on to say that the GF diet can take 6 months 
to two years to get healing of DH, and a relapse of the DH rash 
may take 2 to 12 weeks to occur after someone eats gluten. 
     Total disappearance of IGA skin deposits may take up to 7 
years  after a GF diet is started. 
Dr. Reunala from Finland talked about associated diseases. He 
quoted others who said 5 to 14 percent of DH patients have 
thyroid disease and went on to say that DH patients have an 
increased incidence of lymphoma but a gf diet seems to protect 
against lymphoma. 
 
Dr. Holmes from the U.K. talked about malignancy in CD. He quoted 
that the is risk is between 0 and 7 percent, while in general 
it's 3 to 11 percent and this is reduced by being on a GF diet. 
 
Dr. Carazza from Italy talked about other conditions like 
refractory disease, hyposplenism, and something else, but there 
are no notes. 
 
Then there was a forum. Dr. Hallert talked about psychiatric 
illness in adult CD patients. He studied 180 CD patients and 
found that 22 percent had been to the psychiatric department 
prior to diagnosis of cd and the average time from going to the 
psychiatric department to the eventual diagnosis of CD was 14 
years! (NOTE: I think I've got that right but think I should 
verify the figure tomorrow.) Dr. Hallert also said celiacs were 
four times as likely to be seen in the psychiatric department as 
the general population! He also went on to say that depression 
may occur after the CD diagnosis. 
 
Dr. Ventura from Italy talked about autoimmune disorders. He 
suggested it's more common in patients diagnosed later in life 
than those diagnosed in early childhood. 
 
Next, Dr. Murray himself presented information about seven 
patients who have duodenal strictures as a previously undescribed 
presentation/complication of CD. I'll see if I can get more 
information tomorrow, or perhaps it can wait until he returns. 
 
Dr. Bai, (sorry, don't know from where) described effects of the 
GF diet on bone density. Patients showed marked improvement in 
bone density with the GF diet, although it did not return to 
normal. The improvement was better in the spine than in the hip 
and better in the hip than elsewhere. Dr. Bai went on to say that 
premenopausal women did better than postmenopausal women. 
 
And that's it for today. I'll try to ask Dr. Murray more 
questions tomorrow, when he says the presentation might be much 
more technical. We were on the phone for a very long time just 
relaying the previous notes, which certainly provide a great deal 
of gluten-free food for thought! 
 
Talk to you tomorrow! 
======================================================================== 
Date:         Fri, 6 Sep 1996 23:53:00 EST 
From:         James Lyles (0002002214@mcimail.com) 
Subject:      The Coeliac Symposium - Day 2 
 
)From an oral report by Dr. Murray; transcribed for the list by Ann 
Whelan, editor of the bi-monthly newsletter "Gluten-Free Living". 
To subscribe, write to P.O. Box 105, Hastings-on-Hudson, NY 10706. 
 
 
THE DAILY REPORT 
 
 
The big story today from Finland is oats. There were two talks 
and several posters presented about the topic. 
 
In the first talk, Dr. Risto Julkunen spoke about the Finnish 
five-year follow-up study in which oats were given to a 
population of well-controlled celiacs. They ingested an average 
of 34 grams, which is slightly over one ounce, daily for up to 
five years. The oats used in the study were specially grown and 
tested to be free of wheat, barley and rye. The researchers claim 
there was no difference in those allowed the oats and those who 
were not. 
     There was a second study presented from Dublin, and reported 
by Dr. Conleth Feighery. This 12-week study looked at a small 
group of patients with healed CD to start with, who were given 50 
grams of oats a day. Again, the oats were carefully screened and 
tested to make sure there was no contamination. 
     After 12 weeks, no effect was seen on biopsy or through 
antibody tests. The researchers also took 2 of the 12 
participants and did what they called a "micro challenge" of 500 
milligrams of gluten a day. Both patients got reactions, so the 
researchers felt that at least two of the participants were 
sensitive celiacs -- and they still did not respond to the oats. 
     A poster from Italy showed biopsies taken from celiacs that 
had been studied in the culture plate in the presence of oats, 
which did show some effect on the biopsies. In other words, 
tissue from biopsies from patients with treated CD were put in a 
plate and grown in the presence of oat protein, and the oat 
protein had an effect on the biopsies. 
     This sounded odd, so I made sure I'd really understood what 
Joe reported and paraphrased: In other words, they're seeing no 
reaction from oats within the body in some studies but this one 
showed a reaction outside the body? 
     "Yes," Joe said, "this of course is puzzling." 
     Continuing on the oats issue, a series of short studies from 
several places also showed what the Finns had shown in the body, 
i.e., no problem in the short term. 
 
This is Joe's summary on Oats: 
 
Over the short term, in well-controlled, healed celiacs who are 
compliant in every other way, it may be safe for them to take 
oats that have been tested to be free of contamination of other 
grains. 
     He also mentioned that there were a few studies showing that 
contamination of commercial oats may be common in several 
European countries. 
 
(NOTE: I went to Digestive Disease Week in May, where I met 
several Irish doctors who have studied oats. I would describe 
their strong beliefs about oats as very "adamant." They are 
adamant in believing that uncontaminated oats are safe for people 
with Celiac Disease. 
     If all of this oats talk pans out as being acceptably 
correct to gluten-sensitive individuals in this country, that 
would seem to be pretty good news. Then, the next big challenge 
would be to figure out how gluten-sensitive people are going to 
get access to contamination-free oats. I, for one, will be all 
ears.) 
 
Moving on to other things: 
 
Dr. Paul Ciclitira spoke about in vivo gluten challenge and 
showed that one gram of gluten produces damage after only two 
hours. 100 milligrams, that's 1/10th gram, produced some damage 
or slow damage and 10 milligrams produced no damage. 
     The limitations of studies such as this are that they are 
highly invasive and there may be some risk. Joe said, "You must 
leave a biopsy capsule down for 24 hours, so it's not a small 
deal." 
 
Dr. Luigi Maiuri from Italy described an in vitro testing of 
intestine biopsies that showed a response could be produced. Joe 
said this wasn't new but what was interesting was that the 
little pieces of tissue could produce endomysial antibodies when 
exposed to gluten. 
 
Dr. Riccardo Trancone from Italy talked about rectal mucosal 
response to gluten challenge. He said he could get a measurable 
response in treated celiac disease patients to gluten, which Joe 
said was new. Dr. Trancone also talked about the idea that there 
may be two separate genetic factors involved in CD. One causes 
the individual to be sensitized to gluten and the second one is 
involved at the stage of severe gut damage. His work was based on 
examination of CD family members who don't have CD. 
 
Dr. Michael Marsh described the effects of specific peptide 
sequences from gluten. He had done studies in only two patients. 
Dr. Marsh said it was very expensive to do tests of this kind 
because it's very expensive to make the peptide artificially. He 
estimated a figure of about $5,000 (dollars) to do one test in 
one patient. 
 
Don Kasarda's talk was very hypothetical, Joe said. Don suggested 
that Celiac Disease may be the result of a collision of two 
separately evolving processes, the first being the storage 
proteins in the grasses and the second being control proteins in 
animals. Both of these have similarities in their proline and 
glutamine content and could lead to molecular mimicry. An 
explanation of what he meant is apparently quite complex, and 
after trying to explain, we gave up. It all has something to do 
with getting your lines crossed -- and this is hypothetical. 
     Don also talked about the possible peptide fragments 
responsible for Celiac Disease. 
 
In his second presentation, Dr. Paul Ciclitira talked about the 
potential for identifying small amounts of gluten in foods. Based 
on what he said in his earlier talk about in vivo challenge, he 
took 10 milligrams per 100 grams of protein content in food as 
being the cutoff or threshold. He said that most commercial oats 
products are contaminated with gluten. Cooking does not alter the 
toxicity. Dr. Ciclitira also commented about toaster 
contamination and said he sees about one patient a year who gets 
contamination from using the same toaster as the rest of the 
family. 
     Dr. Ciclitira also commented on the Skerrit test, which 
tests for gluten in food (it's the Australian test). He has 
"strong reservation" about the test and thinks it's because the 
test identifies omega gliadins, which are a minor component of 
gluten so the test can give variable results. Apparently this 
test is available in Canada. 
     Dr. Ciclitira also mentioned other types of tests that 
really may not be specific and may pick up other non-toxic grains 
but may not pick up rye or barley. 
     This brought on a lot of discussion, Joe said. The proposed 
CODEX Alimentarius threshold for something to be called gluten 
free is 200 parts per million. That's equivalent to 20 milligrams 
of gluten in 100 grams of protein. (I'm afraid I can't provide 
any more information about this.) 
     There was a lot of heated discussion, and a women who may be 
the President of the European Celiac Societies objected to the 
allowance of wheat starch. Dr. Ciclitira and others said wheat 
starch is allowed only because the patients demanded it! Someone 
else also estimated that the market for GF foods in Europe was 
500 million dollars! Joe said that really surprised him. 
     Someone else, perhaps Dr. Ciclitira, said the Vatican now 
allows wheat starch communion hosts. Sorry, no more information 
available at this time. 
 
Dr. Thomas MacDonald from the U.K., gave a very technical talk on 
a model system for gut damage. Dr. Erkki Savilahti from Finland 
spoke about the role of lymphocytes in latent forms of CD. Dr. 
Markku Maki talked about the possible role of the antibodies in 
causing changes in the intestine. Dr. Per Brandtzaeg from Norway, 
whose talk was on "Development of intestinal immunity and its 
relation to coeliac Disease,"  made some interesting comments 
about the mismatch of our genetic makeup and the environmental 
pressure in the modern world. Again, sorry, no more information 
at this time. 
     Dr. Brandtzaeg did mention several reasons why breast milk 
is particularly good for infants and the development of the 
immune system in that it provides antibodies the baby cannot make 
that helps protect the intestinal and respiratory tracts. He also 
talked about other things that are important to the gut like 
bacteria, age, and possible allergies. 
 
Dr. Kagnoff's presentation on "MHC and Coeliac Disease was very 
technical. He reviewed part of the genetic background on tissue 
types and CD. Dr. Kagnoff said virtually all celiacs have a 
specific tissue type but many people with the type do not have 
CD. 
 
Dr. Ludvig Sollid from Norway gave a very technical talk about 
lymphocytes and, finally, Dr. Joseph Michalski from the United 
States described how he has identified a new gene site, a small 
area on chromosome 6 that may be where the other gene for CD is 
located. Joe said it was interesting and mentioned a "race to 
find that gene."  Dr. Michalski does his work at the University 
of South Alabama and uses patient material from County Galway, 
Ireland. 
 
(NOTE: I've spoken to Dr. Michalski a few times recently about 
genetics and HLA typing for a small article that will be in the 
September/October issue of Gluten-Free Living. He is very 
interesting and said he might consider writing an article for the 
newsletter about genes and the search for same. I'll keep you 
posted, because I'm really anxious to see an article that even 
the brain challenged among us on things scientific can understand 
about the genetic mysteries of Celiac Disease.) 
 
That's it for today. The last report will be tomorrow. I suspect 
we will all be talking about the Finland conference for quite a 
long time. I'm sure I'm just like you in being real anxious to 
know more about some of this tantalizing information. 
========================================================================= 
Date:         Sat, 7 Sep 1996 18:58:33 -0400 
From:         Jim Lyles (lyles@TIR.COM) 
Subject:      The Coeliac Symposium - Day 3 
 
)From an oral report by Dr. Murray; transcribed for the list by Ann 
Whelan, editor of the bi-monthly newsletter "Gluten-Free Living". 
To subscribe, write to P.O. Box 105, Hastings-on-Hudson, NY 10706. 
 
 
DAILY REPORT 
 
The thir 
d, and final, session at the conference in Finland was 
shorter and less packed than the previous two, but it was also 
much more technical in some instances. The first morning session 
was devoted to diagnostic criteria and was divided into two 
parts: child and adult diagnosis. 
 
Dr. Walker-Smith from the U.K. discussed historical issues of how 
diagnostic criteria were first generated. It started with the 
three biopsies: an initial biopsy, a second showing healing and a 
third done after a gluten challenge. This was in 1969. 
     More recent criteria put together in 1989 suggested that in 
many children, one biopsy could be enough if there were some 
evidence of clinical improvement, demonstrated by antibody 
improvement or in some clinical situation like symptoms or 
anemia. 
     There were some exceptions to this: 
 
o   in patients where the initial biopsy was not entirely flat. 
o   where the first biopsy was done under the age of two. 
o   in communities where there were other diseases that could cause 
a flat biopsy (such as parasite infection). 
o   if there was any doubt about the original diagnosis. 
o   in teenage patients who were going to go off the diet anyway. 
(Apparently the feeling was that teens wouldn't follow the diet, 
and if they were going to be non-compliant, they should be 
encouraged to do it in a controlled fashion with a biopsy done 
before they would go off on their own.) 
 
Another point was made (not by Dr. Walker-Smith) about a finding 
in eight non-compliant teens in whom there was a flat biopsy but 
the endomysial antibodies were negative! (Sorry, no more 
information on that.) 
     Then there was a discussion about serologic tests, and the 
feeling was that the tests are not yet good enough and can't 
completely replace the need for a biopsy. 
     In adult biopsies, another doctor felt that in many cases, 
two biopsies are necessary, one before the gluten-free diet and 
one after starting the diet. It was also noted that how reliable 
this would be would depend on whether there were other diseases 
occurring in the community that could mimic the first biopsy. 
     The next discussion concerned a Finnish study that suggested 
it didn't matter where in the duodenum the biopsies were taken as 
long as they were taken. 
     Dr. Ferguson (I think there may be two Dr. Fergusons and 
don't know which one) commented that doctors should be aware of 
the personal and financial cost of the biopsy and the hope that 
there could be some way to replace this procedure. 
     Then a general discussion pretty much held that a certain 
number of biopsies are essential and there is not yet a zero 
biopsy option. They could not overemphasize the importance of 
doing a biopsy before beginning the gluten-free diet, and that 
there are still some patients in whom more than one biopsy is 
necessary. 
 
     Joe said the rest of the morning presentations were pretty 
scientific. 
 
In the afternoon, Dr. Lloyd Mayer from New York talked about how 
the cells lining the intestine can or cannot take up different 
proteins. Joe described Dr. Mayer as "not a celiac person." 
(NOTE: Since Dr. Mayer is here in New York, where I am, I'm going 
to see what I can find out about how his research work relates to 
Celiac Disease.) 
 
Dr. Cerf-Bensussan from France talked about T cells and said 
there were some very unusual T cells present in the intestines of 
celiacs. She also commented about a group of French children who 
seemed to be doing okay clinically on a gluten-containing diet 
although they did have a prior diagnosis of CD, but the children 
did have an increased number of these unusual T cells, which are 
called gamma delta cells, in their intestines. 
 
Next, Dr. Hayday from Connecticut talked about gamma delta cells 
seen in the lining of the intestines of celiacs that seem to be 
important for regulating immune responses. 
 
Next, Dr. Cerf-Bensussan presented and talked about some unusual 
populations of lymphocytes in patients with refractory sprue. 
These cells may represent a premalignant condition. She showed 
that five patients with refractory sprue had these identical 
types of cells. 
 
Dr. Auricchio from Italy was the last individual presenter. He 
outlined the six topics that are the most important for future 
research: 
 
1. Understanding the entire clinical spectrum of gluten 
sensitivity. 
 
2. Identifying the damaging peptides. 
 
3. What is the mechanism of the damage that occurs (I hope I have 
this one right; my notes were a bit obtuse). 
 
4. The other (non HLA) genes that contribute to CD. 
 
5. Developing an animal model. 
 
6. Developing strategies of immune therapy. 
 
Following his talk, there was a broad-ranging discussion on 
different possibilities for research. 
 
Then, a panel discussion suggested that there are several stages 
in what ends up with CD, the first being the initiation of gluten 
sensitivity, about which very little is known. Second, was non- 
immune reactions to gluten, meaning that the T cells are 
important in the damage, but they are probably not the only 
process in the initiation phase. 
 
At this point, a comment was made that Joe says was worth 
repeating. Here it is, to the best of our abilities, although 
it's obviously not a direct quote: 
 
"Some of the response seen in the challenge studies happen too 
fast to be purely due to immune cells or T cells. It was 
suggested that there are further stages and what we see in CD is 
a stage that is further beyond initiation." 
 
Another comment was made that it's important to replicate studies 
that have been done in only one center and in only two or three 
patients. 
 
Joe then summarized what he thought were the most exciting 
aspects of the conference: 
 
1. The searches for the other non HLA genes. 
 
2. The description of very early or possibly non-immune response 
to gluten. 
 
3. The suggestion of non-gastrointestinal involvement (apparently 
some posters described early changes in the gut within one to two 
hours of a challenge (I'm not sure I have that absolutely 
correct). 
 
4. That it seems as if major progress has been made in 
understanding the mechanism that causes the damage in the 
intestine. 
 
I asked about incidence, our perennial U.S. question, and Joe 
said there were several posters showing that in almost every 
place that was studied, the prevalence varies from between 1 in 
100 to 1 in 500. In this regard, Dr. Fasano's Baltimore blood 
donor study was one of those presented. 
 
Here's the situation regarding publication of the material from 
Finland: 
 
There will be a book that will include all the presentations of 
all the invited speakers, which means they will not be on the 
internet. (Some of the studies already have been published 
elsewhere, so they are available in print.) Apparently there was 
some discussion of this, but Joe emphasized that studies will not 
be accepted by the scientific community unless they are subjected 
to the usual peer review process. 
 
And that's it ... the Finnish conference has ended. I'm sure 
there will be plenty to talk about over the next four years and 
plenty of leads to be investigated. I, personally, look forward 
to finding out more about many of the items discussed over the 
last three days. 
 
     It was a pleasure to be able to reach so many people with 
this information and, especially, to work with Joe Murray. I 
should add that he was positively heroic in his efforts to 
transmit this information in such a timely fashion, and I think, 
as always with Joe, we all owe him an enormous debt of gratitude. 
                                                    -- Ann Whelan 
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ 
 
)From the listowners: 
 
The listowners would like to express our appreciation to Dr. Murray 
for his efforts to keep the list informed.  These reports were 
thorough, enlightening, and represented significant effort on his 
part in taking notes and transcribing them over the phone to Ann 
Whelan.  We also want to thank Ann Whelan for her excellent job of 
capturing the information Joe relayed to her and turning it into 
three well-worded reports.  Finally, we also appreciate the efforts 
of Sue Goldstein, who took Ann's reports and placed them on-line 
for our benefit.  This truly was a team effort, from which we all 
benefitted. 
 
For the Listowners, 
 
Jim Lyles ........ (200-2214@mcimail.com) ........ Holly, Michigan, US) 
========================================================================= 
Date:         Wed, 18 Sep 1996 22:43:30 -0400 
From:         Karoly Horvath (khorvath@UMABNET.AB.UMD.EDU) 
Subject:      Gliadin in pharmaceutical products 
 
I would like to make a correction.  The cited paper was published in 
July 1994 from the Duke University. 
(Miletic et al.  Identification of gliadin presence in pharmaceutical 
products. Journal of Pediatric Gastroenterology and Nutrition 1994; 
19:27-33) 
 
They analyzed 59 prescription and non-prescription medications and 
summarized their results in a table. Their list included cold 
medications, pain-killer medications and medications used for 
gastrointestinal problems etc 
 
It is important to know  that Lactase enzyme supplement (Dairy Ease) had 
gluten in both their tablet and drop form.  Furthermore, Gas-X 
(simethicone), Pepcid (Famotidine), Tagamet (Cimetidine) also contained 
gliadin. 
 
Karoly Horvath, M.D., Ph.D. 
Associate Professor of Pediatrics 
University of Maryland at Baltimore 
Tel: 410-328-0812 
Fax: 410-328-1072 
========================================================================= 
Date:         Thu, 19 Sep 1996 08:59:05 PDT 
From:         "Donald D. Kasarda" (kasarda@PW.USDA.GOV) 
Subject:      Glutamine 
 
Glutamine is an amino acid.  It is the major amino acid in wheat gluten 
proteins, making up 30-55% of the amino acids in these proteins.  In itself 
and not as part of a protein or peptide, it is apparently harmless to celiac 
patients on the basis of one early paper.  If the product in question 
includes only the purified amino acid and no proteins or peptides derived 
from wheat, it would not be harmful to celiac patients.  The acid hydrolysis 
product of glutamine is glutamic acid, essentially the same as MSG.  I do not 
know how large amounts of glutamine taken as the pure amino acid would affect 
humans, but I am fairly sure it would not trigger celiac disease in the 
strict sense. 
 
Don Kasarda, Albany, CA 
 
)...Can someone please explain the significance of glutamine. 
========================================================================= 
Date:         Tue, 24 Sep 1996 09:34:37 +0000 
From:         Phil Sheard (phil.sheard@stonebow.otago.ac.nz) 
Subject:      marmite 
 
Hi all, New Zealand dietitians maintain a register of commercial foods and 
their ingredients (using information supplied by the manufacturers), and 
this is called the NZ therapeutic database. From that database they supply 
the NZ coeliac society with a list of all commercial gluten free food 
products currently available in NZ, and the society sends the list to its 
members. The May 1996 list does not include Marmite, so NZ coeliacs would 
generally assume it not to be GF (although I have not called Sanitarium, 
the manufacturer, to check). However, a similar product, Vegemite 
(manufactured by Kraft) is included in the list, and is regularly consumed 
by my coeliac daughter with no ill-effects. Another beef/yeast extract 
(Bovril) is also included in the GF list. 
 
Some of you may also be interested in the following, which is included in 
the introduction to the GF foods booklet: "For the purposes of the GF list 
the criteria used for GF is that defined in the current New Zealand Food 
Regulations: When food products contain ingredients derived from wheat, 
triticale, rye, barley, and oats the nitrogen content of those ingredients 
shall not exceed 0.05 percent calculated as nitrogen on a dry weight basis; 
Starches prepared from gluten containing cereals are not considered to 
contain gluten if there is less than 0.3 percent protein in the dry 
matter." 
cheers 
Phil 
 
Philip Sheard 
Developmental Biology Unit, 
Department of Physiology, 
University of Otago Medical School, 
Dunedin, New Zealand. 
Ph (64 3) 479-7344 
Fax (64 3) 479-7323 
========================================================================= 
Date:         Tue, 24 Sep 1996 10:17:49 PDT 
From:         "Donald D. Kasarda" (kasarda@PW.USDA.GOV) 
Subject:      Re: Spelt Flour 
 
Spelt is wheat and nothing all thqt unusual about it beyond the adherent 
glumes, which represents a gene or two difference from normal bread wheat. 
There are slight variations in analysis of any given sample in comparison 
with an arbitrary sample or samples of bread wheat, but these differences 
don't impress me.  It may have a slightly different flavor from normal bread 
wheat, as does durum wheat.  I don't know about this as I have never eaten 
spelt although I have worked with it in the laboratory. On the basis of my 
experience in blind testing of someone with allergy who felt they could eat 
spelt, I would say that spelt is not suitable for use by people allergic to 
wheat and certainly is not suitable for anyone with celiac disease. 
 
Don Kasarda, Albany, CA 
 
)There was an article by Paul Heiney in the Times (UK Newspaper) on 
)Saturday 21st September on this very old variety of wheat which goes 
)back in the UK to Roman times.  The flour is very high in protein 
)vitamins and minerals and the finished bread does contain gluten which 
)the growers say can be eaten by people normally intollerant to gluten. 
)Does anybody have experience of this flour?  Are there any medical or 
)scientific opions on this variety of wheat? Is this similar to the Oats 
)debate? 
)-- 
)Deryk Ford 
========================================================================= 
Date:         Wed, 25 Sep 1996 09:33:00 CST 
From:         Murray@intmed-po.int-med.uiowa.edu 
Subject:      Inflammed duodenum in celiac disease 
 
The duodenum is the first part of the small intestine after you leave the 
stomach.  It is exposed to acid and stomach digestive enzymes.  It has a 
built-in defense against these corrosive materials.  In many diseases the 
duodenum becomes inflammed.  In duodenal ulcer disease, a bacterium, 
Helicobacter pylori damages alters the amount of acid the stomach produces 
and reduces the defense against the acid resulting in damage of the duodenum 
and ulcers.  This is way and far the most common inflammation of the 
duodenum. 
 
However there are other things that inflame the duodenum and one of those is 
celiac disease.  Celiac disease affects the first part of the small intestine 
( duodenum more than any other part) the damage may get less furhter douwn 
the intestine.  The extent of small intestine involved by the celiac damage 
may determine which symptoms the patient gets.  If a lot of the small 
intestine is involved then diarrhea and malabsorption is more likely. 
However if only a short portion of the intestine is involved then there may 
be no diarrhea.  The major consequence may be the result of the inflammation 
of the duodenum with pain bloating nausea and vomiting, that may be the same 
symptoms as those of the much more common peptic ulcer disease.  Indeed some 
patients may even have ulcers that look like the peptic ulcers further 
confusing the picture and misleading the physician.  Many patients biopsies 
taken by the endoscopists may have been called "non specific duodenitis " in 
the past where the pathologist may have assumed that the inflammation was 
caused by aicd damage and peptic ulcer disease. 
 
There some things that can be done to clarify this. 
 
1. Have a high index of suspicion for CD, especially if the patient does not 
have helicobacter, or is not on large doses of anti-arthritis drugs. 
 
2. Take biopsies in the duodenum past the area that have ulcers or obvious 
inflammation (the findings of celiac disease inflammation is more widespread 
than the damage with peptic ulcer disease which is usually located tio the 
spots whre the ulcers is. 
 
3. The pathologist needs to look for intraepithelial lymphocytosis and the 
chronic inflammatory cells in the lamina propria( deeper layer)  And draw the 
attention of the clinician to the alternate possibility. 
 
4. Antibody tests may be helpful in differentiating the 2 conditions. 
 
The above represents a new approach to this problem and would not have been 
common or usual practise even 3-4 years ago. 
 
This is not medical advice and should not be used as such.  It is intended to 
be general information and is part of the educational mission of the Univ of 
Iowa. 
 
Joe Murray MD 
Univ of Iowa 
========================================================================= 
Date:         Fri, 27 Sep 1996 21:33:17 -0400 
From:         "Donald D. Kasarda" (kasarda@PW.USDA.GOV) 
Subject:      Re: dieticians and sugar 
 
)sugar cane is a grass and thus related to the wheat plant.  Therefore 
)people who cannot tolerate wheat should not eat sugar. 
 
In regard to the query about sugar cane containing gluten.  Sugar cane is a 
member of the grass family as are wheat, rye, and barley, the species that 
contain proteins harmful to celiac patients.  However, not all grasses are 
harmful to celiac patients--for example, rice and corn.  The scientific name 
of sugar cane is Saccharum officinarum and it belongs to the tribe 
Andropogoneae, which also includes sorghum.  On the basis of closer 
relationship to corn or maize than to wheat, I would say that sugar cane is 
not likely to be harmful to celiac patients.  Furthermore, as far as we know 
gluten proteins, or their equivalents in rye and barley, are found only in 
the endosperm of the grain of the plant and not in vegetative tissues, such 
as leaves.  To the best of my knowledge, sugar is obtained from the stalks 
of the plant and, hence, even if the seeds of the plant contained harmful 
proteins (not likely), highly refined sugar would be safe to eat. 
 
Don Kasarda 
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