Re: Gluten sensitivity/sprue

[Guest guest]

,

The following abstract shows that it is really inappropriate to use

digestive symptoms as the marker for the need for a gluten free diet in

celiac disease. I've put more sources for you below that, so keep reading...

Nutr J. 2006 Sep 14;5:24

Patterns of clinical presentation of adult coeliac disease in a rural setting.

S, D'Souza C, Haboubi NY.

Dietetics, Royal Gwent Hospital. Newport, Gwent, South Wales, UK.

sian.jones2@...

BACKGROUND: In recent years there has been increasing recognition that the

pattern of presentation of coeliac disease may be changing. The classic

sprue syndrome with diarrhoea and weight loss may be less common than the

more subtle presentations of coeliac disease such as an isolated iron

deficiency anaemia. As a result, the diagnosis of this treatable condition

is often delayed or missed. Recent serologic screening tests allow

non-invasive screening to identify most patients with the disease and can

be applied in patients with even subtle symptoms indicative of coeliac

disease. Both benign and malignant complications of coeliac disease can be

avoided by early diagnosis and a strict compliance with a gluten free diet.

AIM: The aim of this study is to evaluate the trends in clinical

presentation of patients diagnosed with adult coeliac disease. In addition,

we studied the biochemical and serological features and the prevalence of

associated conditions in patients with adult coeliac disease. METHODS: This

is an observational, retrospective, cross-sectional review of the medical

notes of 32 adult patients attending the specialist coeliac clinic in a

district general hospital. RESULTS: Anaemia was the most common mode of

presentation accounting for 66% of patients. Less than half of the patients

had any of the classical symptoms of coeliac disease and 25% had none of

the classical symptoms at presentation. Anti-gliadin antibodies,

anti-endomysial antibody and anti-tissue transglutaminase showed 75%, 68%

and 90% sensitivity respectively. In combination, serology results were

100% sensitive as screening tests for adult coeliac disease. Fifty nine

percent patients had either osteoporosis or osteopenia. There were no

malignant complications observed during the follow up of our patients.

CONCLUSION: Most adults with coeliac disease have a sub clinical form of

the disease and iron deficiency anaemia may be its sole presenting symptom.

Only a minority of adult coeliac disease patients present with classical

mal-absorption symptoms of diarrhoea and weight loss. Patients with

atypical form of disease often present initially to hospital specialists

other than a gastro-enterologist. An awareness of the broad spectrum of

presentations of adult coeliac disease, among doctors both in primary care

and by the various hospital specialists in secondary care, is necessary to

avoid delays in diagnosis. It is important to include serological screening

tests for coeliac disease systematically in the evaluation of adult

patients with unexplained iron deficiency anaemia or unexplained

gastro-intestinal symptoms and in those who are considered to be at

increased risk for coeliac disease.

PMID: 16972991 [PubMed - indexed for MEDLINE]

Also, the following sites discuss comorbid diseases that can develop in

untreated celiac disease, but they mention these issues may not carry the

obvious intestinal symptoms that she considers " overt " .

See

http://celiacdisease.about.com/od/symptomsofceliacdisease/a/complications.htm

and

http://celiacdisease.about.com/od/whatisceliacdisease/f/CanYouOutgrowCD.htm

Can you get her to visit a gastroenterologist who is maybe more current in

the research for celiac disease? I was active for many years in a celiac

support group on the internet where scientists and doctors from Europe

told us constantly that celiac disease is way underdiagnosed in the US

because of a failure of US doctors to understand which conditions celiac

disease causes when there aren't " overt " GI symptoms. Maybe her doctor was

one of those who hasn't kept up with the literature. There are 218

articles on celiac sprue and how it affects the brain, for instance.

Part of the missing education in the US involves how people with celiac

disease carry their own risks from oxalates because of poor fat

digestion. (see abstracts below)

If you consider that bypass surgery also carries its own risks of

developing oxalate issues, this sounds like what she is thinking about

doing might involve a serious double whammy if she doesn't follow the

gluten free diet and allow the diet to heal the unobvious issues in her gut.

The work of Fasano on zonulin's role in celiac disease bring up the issues

related to how eating gluten in someone with celiac disease opens up gut

permeability....something that doesn't cause GI symptoms, but does cause a

score of associations with developing autoimmune disease, as Fasano himself

is prone to remind everyone! In fact, I believe he talked about that issue

particularly at the international celiac conference I attended in New York

two years ago. But the excess permeability is also what leads to dietary

oxalate becoming a problem.

Can someone develop neurotoxicity from oxalate when you have no kidney

symptoms? Absolutely.

In a recent study of the toxicity of oxalate to the nervous system, a high

percentage of patients given platinum oxalate though an IV as a cancer

treatment developed neurotoxicity from the oxalate without any sign of

kidney problems developing. This study obviously invalidates the notion

that kidney disease will be the first presentation of oxalate trouble, just

like it isn't anymore valid to say that GI problems are the first and only

valid signs of celiac disease. It is amazing how long it takes for people

to " unlearn " things they've always heard or assumed after the studies are

done to show those ideas to be invalid!

I hope these resources are helpful to you.

Am J Dig Dis. 1977 Oct;22(10):921-8.

Related Articles, Links

Hyperoxaluria and intestinal disease. The role of steatorrhea and dietary

calcium in regulating intestinal oxalate absorption.

Stauffer JQ.

Hyperoxaluria was documented in patients with pancreatic insufficiency,

adult celiac disease, regional enteritis after ileectomy and partial

colectomy, and jejunoileal bypass. The degree of hyperoxaluria correlated

directly with the severity of the steatorrhea and inversely with the

dietary calcium content. High-calcium diets suppressed oxalate excretion to

normal when fecal fat excretion was approximately 30 g/day or less. In

patients with more severe steatorrhea, decreasing dietary fat and oxalate

content further reduced urinary oxalate excretion. These data suggest that,

while steatorrhea is the most important determinant for enhanced absorption

of dietary oxalate, variations in dietary calcium content modulate the

amount of oxalate absorbed.

Publication Types:

Comparative Study

Research Support, U.S. Gov't, P.H.S.

PMID: 920694 [PubMed - indexed for MEDLINE]

1: J Urol. 2008 Sep;180(3):974-9. Epub 2008 Jul 17.

Urinary stone disease in adults with celiac disease: prevalence, incidence and

urinary determinants.

Ciacci C, Spagnuolo G, Tortora R, Bucci C, Franzese D, Zingone F, Cirillo M.

Department of Clinical and Experimental Medicine, Federico II University,

Naples,

Italy.

PURPOSE: Intestinal diseases may cause urinary stone disease via

hyperoxaluria or

diarrhea induced hyperconcentrated acidic urine. Data are missing on urinary

stone disease in celiac disease, a common malabsorptive disorder. In this study

we analyzed urinary stone disease and urine composition in adults with celiac

disease. MATERIALS AND METHODS: Study patients were 18 years or older,

untreated,

and newly diagnosed with celiac disease by serum markers and jejunal biopsy.

Clinical presentation of celiac disease was assessed focusing on 5 disorders of

diarrhea, and deficiency of calorie (low body mass index or weight loss), lipid

(low prothrombin time or low serum lipids), iron (low hemoglobin or low serum

ferritin) and calcium (low serum calcium or low bone densitometry). Urinary

stone

disease history was assessed by questionnaire (imaging, stone excretion, stone

disruption/removal). Urinary variables were measured in a 24-hour

collection in a

subgroup of patients. RESULTS: Under untreated conditions (baseline) urinary

stone disease was independent of celiac disease presentation and more prevalent

in patients with celiac disease than in a population sample used as a control

(608 and 3,540, 7.9% and 5.0%, sex and age adjusted odds ratio 4.0, 95% CI

2.7-5.9). Excluding from analysis individuals with baseline urinary stone

disease, the incidence of urinary stone disease history was not significantly

different between the treated celiac disease (gluten-free diet) and control

population (458 and 3,003, 2.4% vs 3.9%). The urine of untreated patients with

celiac disease differed from that of healthy volunteers with 120% higher

oxalate

and 43% lower calcium (in 45 and 45, p <0.001). A gluten-free diet corrected

urinary abnormalities (p <0.01). CONCLUSIONS: Urinary stone disease risk is

high

in untreated patients with celiac disease independent of overt malabsorption.

Hyperoxaluria is likely the underlying disorder. A gluten-free diet reduces

urinary stone disease risk and oxaluria.

PMID: 18639267 [PubMed - indexed for MEDLINE]

2: Gut. 1977 Jul;18(7):561-6.

Hyperoxaluria correlates with fat malabsorption in patients with sprue.

Mc GB, Earnest DL, Admirand WH.

The effect of fat malabsorption on the absorption and renal excretion of

dietary

oxalate was studied in four patients with sprue and in two patients with

dermatitis herpetiformis and sprue-like jejunal histology. Hyperoxaluria was

present in all patients with sprue when fat malabsorption was severe. Urinary

oxalate excretion decreased in two of the three patients with coeliac sprue

when

their fat malabsorption had improved after three months of dietary gluten

restriction. Neither patient with dermatitis herpetiformis and sprue had

steatorrhoea. In these patients, urinary oxalate excretion was always within

normal limits. A significant positive linear relationship (y=28.25 +4-84x;

r=0-82; P less than 0-01) was demonstrated between faecal fat and urinary

oxalate

excretion. The results of this study support the concept that severe

malabsorption of dietary fat plays a primary causative role in enteric

hyperoxaluria.

Publication Types:

Research Support, U.S. Gov't, P.H.S.

PMID: 873337 [PubMed - indexed for MEDLINE]

Clin Cancer Res. 2007 Nov 1;13(21):6359-68.[] Links

Predictive factors of oxaliplatin neurotoxicity: the involvement of the

oxalate outcome pathway.

Gamelin L, Capitain O, Morel A, Dumont A, Traore S, Anne le B, Gilles S,

Boisdron-Celle M, Gamelin E.

Laboratory of Oncopharmacology-Pharmacogenetics, Institut National de Sante

et de Recherche Medicale U564, Angers, France.

PURPOSE: Oxaliplatin displays a frequent dose-limiting neurotoxicity due to

its interference with neuron voltage-gated sodium channels through one of

its metabolites, oxalate, a calcium chelator. Different clinical approaches

failed in neurotoxicity prevention, except calcium-magnesium infusions. We

characterized oxalate outcome following oxaliplatin administration and its

interference with cations and amino acids. We then looked for genetic

predictive factors of oxaliplatin-induced neurotoxicity. EXPERIMENTAL

DESIGN: We first tested patients for cations and oxalate levels and did

amino acid chromatograms in urine following oxaliplatin infusion. In the

second stage, before treatment with FOLFOX regimen, we prospectively looked

for variants in genes coding for the enzymes involved (a) in the oxalate

metabolism, especially glyoxylate aminotransferase (AGXT), and ( in the

detoxification glutathione cycle, glutathione S-transferase pi, and for

genes coding for membrane efflux proteins (ABCC2). RESULTS: In the first 10

patients, urinary excretions of oxalate and cations increased significantly

within hours following oxaliplatin infusion, accompanied by increased

excretions of four amino acids (glycine, alanine, serine, and taurine)

linked to oxalate metabolism. In a further 135 patients, a minor haplotype

of AGXT was found significantly predictive of both acute and chronic

neurotoxicity. Neither glutathione S-transferase pi nor ABCC2 single

nucleotide polymorphisms we looked for were linked to neurotoxicity.

CONCLUSION: These data confirm the involvement of oxalate in oxaliplatin

neurotoxicity and support the future use of AGXT genotyping as a

pretherapeutic screening test to predict individual susceptibility to

neurotoxicity.

PMID: 17975148 [PubMed - indexed for MEDLINE]

1: Scand J Gastroenterol. 2006 Apr;41(4):408-19.

Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac

intestinal mucosa and intestinal cell lines.

Drago S, El Asmar R, Di Pierro M, Grazia Clemente M, Tripathi A, Sapone A,

Thakar

M, Iacono G, Carroccio A, D'Agate C, Not T, Zampini L, Catassi C, Fasano A.

Mucosal Biology Research Center, Center for Celiac Research and Division of

Pediatric Gastroenterology and Nutrition, University of land, School of

Medicine, Baltimore, MD 21201, USA.

OBJECTIVE: Little is known about the interaction of gliadin with intestinal

epithelial cells and the mechanism(s) through which gliadin crosses the

intestinal epithelial barrier. We investigated whether gliadin has any

immediate

effect on zonulin release and signaling. MATERIAL AND METHODS: Both ex vivo

human

small intestines and intestinal cell monolayers were exposed to gliadin, and

zonulin release and changes in paracellular permeability were monitored in the

presence and absence of zonulin antagonism. Zonulin binding, cytoskeletal

rearrangement, and zonula occludens-1 (ZO-1) redistribution were evaluated by

immunofluorescence microscopy. Tight junction occludin and ZO-1 gene expression

was evaluated by real-time polymerase chain reaction (PCR). RESULTS: When

exposed

to gliadin, zonulin receptor-positive IEC6 and Caco2 cells released zonulin in

the cell medium with subsequent zonulin binding to the cell surface,

rearrangement of the cell cytoskeleton, loss of occludin-ZO1 protein-protein

interaction, and increased monolayer permeability. Pretreatment with the

zonulin

antagonist FZI/0 blocked these changes without affecting zonulin release. When

exposed to luminal gliadin, intestinal biopsies from celiac patients in

remission

expressed a sustained luminal zonulin release and increase in intestinal

permeability that was blocked by FZI/0 pretreatment. Conversely, biopsies from

non-celiac patients demonstrated a limited, transient zonulin release which was

paralleled by an increase in intestinal permeability that never reached the

level

of permeability seen in celiac disease (CD) tissues. Chronic gliadin exposure

caused down-regulation of both ZO-1 and occludin gene expression. CONCLUSIONS:

Based on our results, we concluded that gliadin activates zonulin signaling

irrespective of the genetic expression of autoimmunity, leading to increased

intestinal permeability to macromolecules.

PMID: 16635908 [PubMed - indexed for MEDLINE]

>We are evaluating our first patient with gluten sensitivity. Diagnosed

>by biopsy and positive antibodies. She wants a bypass and has not been

>following a gluten free diet because she has no " overt symptoms. "

>

>I will be evaluating pt soon and would be interested in your advice

>(questions to ask, pitfalls to avoid) and your suggestions for protein

>supplements, vitamin/mineral supplements and anything else someone with

>more experience than I can offer.

>

>Many thanks,

>

>

>Salem, Or

>

>

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[Guest guest]

As a self-diagnosed Celiac, I would advise her to follow a gluten-free

diet first, as I lost a ton of weight just doing that. If she doesn't

take medical advice now, why would she after getting a bypass? My

nutritional deficiencies were almost identical to those one gets after

RNY. I wouldn't wish that on anyone. Helen

>

> We are evaluating our first patient with gluten sensitivity. Diagnosed

> by biopsy and positive antibodies. She wants a bypass and has not been

> following a gluten free diet because she has no " overt symptoms. "

>

> I will be evaluating pt soon and would be interested in your advice

> (questions to ask, pitfalls to avoid) and your suggestions for protein

> supplements, vitamin/mineral supplements and anything else someone with

> more experience than I can offer.

>

> Many thanks,

>

>

> Salem, Or

>

[Guest guest]

Hi ,

I know Medifast has several meal replacement products that have been tested to be less than 5ppm in gluten. These can be used pre-surgery and some post. You may want to check out their product for gluten intolerance patients.

Tammy Hutchisen RD, LDN CPT

Mid-land Bariatrics

From: cacm1921 <catherine.quinn@...>Subject: Gluten sensitivity/sprue Date: Wednesday, December 10, 2008, 7:20 PM

We are evaluating our first patient with gluten sensitivity. Diagnosed by biopsy and positive antibodies. She wants a bypass and has not been following a gluten free diet because she has no "overt symptoms."I will be evaluating pt soon and would be interested in your advice (questions to ask, pitfalls to avoid) and your suggestions for protein supplements, vitamin/mineral supplements and anything else someone with more experience than I can offer. Many thanks,Salem, Or