Re: gluten/egg/dairy free diet

[Guest guest]

Greetings Spondy Spondies!

Having food allergies is not related to Reiter's or any of the other types

of Spondyloarthropathies as far as medical research's know. There have been

tests done with this theory and all have been negative so far. If we had found a

cure that was so easy to follow as to eliminate food from our diet, that

would be a wonderful treatment form. Not one of us would be here listening

closely to all the information that ever comes out about our

Spondyloarthropathies. There have been many scientific studies done to isolate

the antigens or

triggers which put our immune system into high gear . We do know that most of

these triggers are different forms of bacteria Namely in developed lands the

triggers are usually Chlamydia, Salmonellla, (food poisoning), parasites,

etc. In underdeveloped countries the triggers are usually Yersinia,

Campylobacter jejuni, Shigella, which is found in the soil and in the water they

drink

and wash vegs and fruit with. There has never been shown that food allergies

or molds, or dust mites, or glutton, or dairy products, or poultry/eggs can

cause a flare of spondy. I haven't found one medical abstract on this subject.

Many in the alternative health care pages, may suggest that you can get

Reiter's from these food allergens and they go to great lengths and many tests

to

show there is a correlation between Reiter's/Arthritis and triggers for the

disease.There is spontaneous remission with many diseases. Some may be under

the impression that when they stop a certain food, their Spondy will

disappear. In science this is called Placebo effect.

Many in our group do have problems with food. Either lactose intolerant, or

are allergic to some drug or other foods and pollen, weeds. This has nothing

to do with Spondyloarthropathies. The triggers of foods have been proven to

not be associated with Reiter's. We tend to blame every sickness on our

problem of arthritis. It is natural to do that. The HLA B27 is an antigen that

causes our immune systems to go into hypergear and attack certain areas of our

body. An allergy can do this too...but it is different. It causes rashes,

headache, breathing difficulties. It does not cause arthritis, damage to bones

or

inflammation of joints. Hope this helps.

, unless you had urine track infection many years ago that could have

been Chlamydia...and your arthritis symptoms are usually only on one side of

the body, and you have the other 3 problems associated with ReA...you probably

just have AS. Well, need to get some shut eye. I'm such a rambler, too.

Connie

Connie

[Guest guest]

Hi, my name is Judie and I am new to this group. I was pointed to the South

Beach Diet by the rheumy who diagnosed my USpA. (It was by accident throug a

clinical trial). I have not yet seen a Rheumy for a full workup. In Rochester,

NY where a live, Rheumatologists are as scarce as hens teeth.

You will always have the potential for flare-ups if you have been diagnosed as

having the gene HBLA-27 but staying away from the trigger will keep it under

control. In my son's case, the allergins are wheat gluten and eggs; his

allergin levels to these two are off the charts.

[Guest guest]

Hi Connie:

Let me say that I while I agree with your conclusion that research does not

support an allergic basis for Reiter's, my personal experience does contradict

your conclusion that allergies don't cause stiffness, etc. One evening a couple

of years ago I had a great lobster dinner, accompanied by a bottle of white wine

shared with a friend. I started to feel very hot and slightly ill during the

meal, which I attributed to the wine. When I awoke the next morning I was so

stiff I could hardly get out of bed. It was equivalent to some of my worse

flares, and I swore off alcohol, still assuming that the wine had caused it.

The stiffness and pain decreased over the next few days, and I forgot about it -

except the part about staying away from wine. A couple of months later my

rheumatologist ran allergy tests on me. My one severe allergy was to LOBSTER!

So my body reacted to an allergen with severe stiffness - not breathing problems

or a rash. I've wondered about the relationship

between allergies and my Reiter's ever since, but could not find any research

on it. I don't think we want to discount the possibility. Food allergies has

always been an area where hucksters and conmen take advantage of the public, so

serious researchers seem to shun it. That doesn't mean that no relationship

exists.

in VA

Grannyof9@... wrote:

Greetings Spondy Spondies!

Having food allergies is not related to Reiter's or any of the other types

of Spondyloarthropathies as far as medical research's know.

P. McKinney, CPA

434-753-3928

703-919-9856 (cell)

---------------------------------

What are the most popular cars? Find out at Autos

[Guest guest]

Maybe if researchers could find an allergy link they could come up with a drug

that could block the symptoms and make lots of $$$ Just venting, really some

foods do seem to cuase me to flair also.

[Guest guest]

When you are searching for abstracts on diets forAS, please look for ones

authored by a Dr. Erhlangersp?) in London. He has retired, but did much with

diet as related to AS and came up with one which works. I have had so many

other things tthat I haven't gone on it lately, but when I do there is

relief for several months. Then I cycle to the next diet. For me, an ovo

lacto vegetarian diet, cave man's diet or Atkins original diets work best

with my AS. The thing about Dr. Ehrlanger's diet is that he substitutes

beads with sort of breads made from nuts, and most of them don't agree with

me. So I do without that sort of thing.

If any of you are interested in the address for the Londond Diet, write me

off list and I will be happy to give it to you.

GA

[Guest guest]

_Patient Resources - London AS - Low Starch Diet_

(http://www.spondylitis.org/patient_resources/diet_london.aspx)

_Arthritis Diet Claims: Fact or Fiction_

(http://www.webmd.com/content/article/92/101710.htm?z=1681_00000_0000_wk_07)

The low starch diet has been around for a long time. Many studies have been

done and they didn't come out with the same conclusions that Dr. Ebringer

had. Some of his work was done on the " leaky gut " theory and a lot of the

alternative web sites quote this theory. Kick AS, another Ankylosing

Spondylitis

group, has a member/leader who swears by the no starch diet. There is another

group, the Roadback support group, who believe in the long term use of

anti-biotics (long term...meaning for many months) in curing Reiter's. Most of

these

theories have been tested and retested and found to be not consistent with

what we know about genetics, immune systems, and bacteria.

I've tried the no-starch diet for several months, years ago. In the

beginning, I thought that I was getting better, but had the worst ever flare

after a

few weeks on it. Since we have days and weeks where our disease seems

better, it is hard to judge if certain foods cause our arthritis to be worse.

We

can't rely on personal experiences or testimonies because our own bodies and

minds can deceive us. We have to rely on trained research scientists who use

double blind studies over many years time to get correct results. Sometimes,

even these methods turn out to be wrong.

I've tried, without success, to find abstracts where our diet triggers our

arthritis. There are some sites that " say to stay away form " night shades'

etc. and some people have trouble with milk or other foods. It doesn't hurt to

try different diets, but we have to be careful that needed nutrition would be

lacking on some diets. If you try the starch free diet, or the gluten free

diet....a plus for you if you have good results.

Below are listed the known triggers for Reiter's:

Salmonella spp.

Chlamydophila pneumoniae

Yersinia spp.

Mycoplasma hominis

Shigella flexneri

Neisseria gonorrhoeae

Ureaplasma urealyticum

Clostridium difficile

Chlamydia trachomatis

Mycoplasma fermentans

Campylobacter fetus jejuni

Borrelia burgdorferi

Calmette-Guérin bacille*

Clostridium difficile

Escherichia coli

Beta-hemolytic streptococci

Leptospira

Propionibacterium acnes

Bartonella

Tropheryma whippelii

Gardnerella vaginalis

Gambia lamblia

[Guest guest]

When I responded to this topic earlier I had forgotten that research has been

done on non-gluten diets for people with the genetic marker for AS. They found

that gluten and also cassein proteins caused a " leaky gut " which allows

micro-organisms to cross into the blood stream. There was conclusive evidence

that HLA B27 individuals were not able to clear infectious agents via the

digestive system as effectively as others. This research was not claiming that

AS was a reaction to an allergy to gluten proteins, but rather that the gluten

caused a " leaky gut " . I can look up the citations in the medical literature if

anyone is interested.

in VA

Herring <countryms@...> wrote:

When you are searching for abstracts on diets forAS, please look for ones

authored by a Dr. Erhlangersp?) in London.

P. McKinney, CPA

434-753-3928

703-919-9856 (cell)

---------------------------------

Bring words and photos together (easily) with

PhotoMail - it's free and works with .

[Guest guest]

Hi ,

Good to hear from you again...I've missed your posts.

I, for one, would be very interested in this article.

Thanks,

in CA

When I responded to this topic earlier I had forgotten that research has been

done on non-gluten diets for people with the genetic marker for AS.

[Guest guest]

Hi Nicky,

Thanks - I'm hoping that with my Dad's improved health I may not have to make

any more trips to England in the near future. Since he's 91 though, I'm not too

hopeful. I haven't been able to find the exact studies that I saw a couple of

years ago. One problem is that a lot of medical research websites are now

charging a lot for articles and subscriiptions. However, I've found a few

articles that tie together gluten intolerance, intestinal permeability and

spondyloarthropies. I'll keep looking and post articles as I find them. I

don't think the link is totally proven but for most of us it's worth trying a

gluten free diet. I know I felt much better on it - but obviously I didn't do a

controlled trial!

Bowel permeability and CD45RO expression on circulating CD20+ B cells in

patients with ankylosing spondylitis and their relatives.

Vaile JH, Meddings JB, Yacyshyn BR, AS, Maksymowych WP.

Department of Medicine, University of Alberta, Edmonton, Canada.

OBJECTIVE: Ankylosing spondylitis (AS) is reportedly associated with subclinical

endoscopic gut inflammation in up to 57% of patients. Studies of bowel

permeability, however, have not consistently revealed abnormalities in these

patients. CD20+CD45RO+ expression is associated with increased antigen exposure,

and previous work has shown increased expression in this B cell isoform in

patients with Crohn's disease and their relatives, correlating with intestinal

permeability abnormalities. We sought to re-examine intestinal permeability in

patients with AS and their relatives, and relate any observed alterations in

permeability with evidence of increased antigen presentation as assessed by the

number of circulating B cells that were CD45RO positive. METHODS: We studied

small intestinal and gastric permeability by measurement of excretion of

lactulose, mannitol, and sucrose in 60 patients with AS and 24 of their

first-degree relatives. We also studied expression of CD20+CD45RO+ by flow

cytometry in these patients. RESULTS: Both patients and first-degree relatives

had significantly increased small intestinal, but not gastric, permeability

compared to controls. Among patients, current users of nonsteroidal

anti-inflammatory drugs (NSAID) had significantly increased small intestinal

permeability compared to nonusers, but relatives not using NSAID also had

increased permeability. CD20+CD45RO+ expression was increased in one-third of

patients but did not correlate with permeability abnormalities. CONCLUSION:

Patients with AS have altered small intestinal, but not gastric, permeability.

NSAID use cannot explain all the abnormality. Bowel permeability abnormalities,

possibly genetically determined, may antedate development of bowel or joint

symptoms. Increased CD20+CD45RO+ expression suggests increased antigen exposure,

which may be related to previous or current intestinal permeability

abnormalities.

Course of gut inflammation in spondylarthropathies and therapeutic consequences.

Mielants H, Veys EM, Cuvelier C, De Vos M.

Department of Rheumatology, University Hospital, Ghent, Belgium.

Gut inflammation plays a crucial role in the pathogenesis of

spondylarthropathies (SpA) since ileocolonoscopic studies have demonstrated the

presence of gut inflammation in different forms of this concept: in ankylosing

spondylitis (AS) (60%), in enterogenic (90%) and urogenital reactive arthritis

(20%), in undifferentiated SpA (65%), in the pauciarticular and axial forms of

psoriatic arthritis (16%), in late onset pauciarticular juvenile chronic

arthritis (80%) and in acute anterior uveitis (66%). The strong relationship

between gut and joint inflammation was demonstrated by performing a second

ileocolonoscopy: remission of the joint inflammation was always connected with a

disappearance of gut inflammation, whereas persistence of locomotor inflammation

was mostly associated with the persistence of gut inflammation. During further

evolution 20% of the non-ankylosing spondylitis SpA patients can develop AS.

About 6% of the total group SpA patients, in whom inflammatory bowel disease

(IBD) was excluded, developed Crohn's disease 5 to 9 years later. All these

patients initially presented with gut inflammation, which indicates that this

finding has prognostic value. The high prevalence of evolution to IBD in SpA

patients confirms the thesis that both disease entities bear common pathogenic

mechanisms, and confirms the place of IBD in the concept of SPA. Sulphasalazine

(SASP), a successful drug in the treatment of IBD, has demonstrated its

effectiveness in the treatment of SpA. The beneficial effect of the drug in this

disease entity could be due to its anti-inflammatory effect on the gut wall, by

normalizing its permeability and by preventing the entrance of antigens through

the defective gut wall. However, SASP could not prevent the evolution to IBD.

Bowel inflammation and the spondyloarthropathies.

De Keyser F, Elewaut D, De Vos M, De Vlam K, Cuvelier C, Mielants H, Veys EM.

Department of Rheumatology, University Hospital, Ghent, Belgium.

The concept of spondyloarthropathies gathers together a group of chronic

diseases in which not only the locomotor system is involved but also other

organs, especially the gastrointestinal tract. In humans, ileocolonoscopic

studies demonstrated the presence of inflammatory gut lesions in all the

diseases in the spondyloarthropathy group; their presence varied in the

different diseases between 20% and 70%. The inflammation could be related to

specific disease features in the spondyloarthropathies. Further research

supports the hypothesis of subclinical inflammatory bowel disease in some

patients with spondyloarthropathy, in which the locomotor inflammation was the

only clinical manifestation. The link between gut inflammation and arthropathy

has also been demonstrated in animal models, notably the human leukocyte antigen

B27 transgenic rats. The temporal relationship between activity and severity of

colonic involvement and flares of peripheral arthritis directs treatment of

choice. For

all forms of enterogenic arthropathies, nonsteroidal anti-inflammatory drugs

remain the acute treatment form. Caution is in order, however, because of their

possible harmful effects on intestinal integrity, permeability, and even on gut

inflammation.

Intestinal permeability in patients with ankylosing spondylitis and their

healthy relatives.

ez- O, Cantero-Hinojosa J, e-Sastre P, Gomez-Magan JC,

Salvatierra-Rios D.

Department of Rheumatology, University of Granada Hospital, Spain.

Patients with AS were previously found to have increased intestinal permeability

using the 51Cr-EDTA resorption test. In order to discover whether this

alteration has taken place prior to, or as a consequence of the disease, we

studied the intestinal permeability to 51Cr-EDTA in 20 patients with AS, 65 of

their healthy relatives, and 25 normal volunteers. We also considered the HLA

B27 antigen, the serum immunoglobulin A levels, the disease activity, the

existence of peripheral arthritis, the ESR, the CRP values and the intake of

drugs at the time of study. Gut permeability was found to have increased in the

patients and their healthy relatives compared to the control group. No

difference in gut permeability was found between patients and relatives

regardless of whether they had the HLA B27 antigen or not. The increased

intestinal permeability in the patients had no relation to the disease activity,

to the presence of peripheral arthritis or to the intake of NSAIDs. Gut

permeability

was shown to bear no relation to IgA levels, ESR or CRP. Our findings suggest

that the increase in gut permeability in AS patients and their relatives is a

primary defect and may be an aetiologic factor in this disease.

Intestinal mucosal permeability in inflammatory rheumatic diseases. II. Role of

disease.

Mielants H, De Vos M, Goemaere S, Schelstraete K, Cuvelier C, Goethals K,

Maertens M, Ackerman C, Veys EM.

Department of Rheumatology, Gastroenterology, Pathology and Nuclear Medicine,

University Hospital, Ghent, Belgium.

Gut permeability as measured by the 51Cr-EDTA resorption test was determined in

56 patients with rheumatoid arthritis (RA), 73 patients with

spondyloarthropathies (SpA), 18 patients with inflammatory bowel disease (IBD)

and 97 controls (42 patients with no inflammatory rheumatic diseases and 55

healthy controls). Gut permeability was found to be increased in the 3 patient

groups, partially due to the intake of antiinflammatory drugs. When only

patients not taking these drugs were considered, an increased gut permeability

was found in patients with SpA and IBD. In patients with RA gut permeability

could not be evaluated as they were all taking antiinflammatory medication.

Ileocolonoscopy with biopsies of the gut was performed in 62 of the 73 patients

with SpA and disclosed subclinical gut inflammation in 21. No difference in gut

permeability was found between patients with or without gut inflammation.

However, when the type of gut inflammation was considered, a significant

increase of

gut permeability was found in patients with chronic gut inflammation compared

with patients presenting acute lesions. Our findings again suggest that the

chronic gut inflammation seen in SpA is fundamentally different from acute gut

inflammation and possibly related to the gut inflammation of IBD.

Importance of intestinal mucosal immunity and luminal bacterial cell wall

polymers in the aetiology of inflammatory joint diseases.

Sartor RB.

The distal intestine contains bacterial cell wall polymers capable of inducing

acute and chronic polyarthritis if systemically distributed. Parenteral

injection of peptidoglycan-polysaccharide (PG-PS) polymers from certain

bacterial species produces spontaneously relapsing erosive synovitis in

susceptible rat strains, and normally subarthropathic amounts of PG-PS and

lipopolysaccharide (endotoxin) can reactivate arthritis initially induced by

PG-PS. These experimental results illustrate the inflammatory potential of

luminal bacterial products and the importance of genetically determined host

susceptibility factors in the pathogenesis of arthritis. Normally, luminal

complexing by secretory IgA and an intact epithelial barrier limits uptake of

luminal antigen; however, intestinal inflammation enhances mucosal uptake and

systemic distribution of potentially injurious macromolecules, including PG-PS

and lipopolysaccharide. Occult intestinal inflammation, which may be related to

non-steroidal anti-inflammatory drugs or may be disease-associated, occurs in

approximately two thirds of patients with rheumatoid arthritis, idiopathic

reactive arthritis and ankylosing spondylitis. Enhanced mucosal permeability to

macromolecules occurs in rheumatoid arthritis, enteric infections and idiopathic

inflammatory bowel disease. Intestinal inflammation is associated with increased

mucosal IgG production and circulating immune complexes. Hyperactive IgA

synthesis occurs in many types of inflammatory joint disease. Polyclonal IgA is

increased in rheumatoid arthritis, Sjogren's syndrome, ankylosing spondylitis,

Reiter's syndrome, and reactive arthritis following Yersinia infection.

Anti-Klebsiella IgA cross-reacts with HLA-B27 antigen, and antibodies to enteric

bacteria are able to lyse lymphocytes from HLA-B27 patients with ankylosing

spondylitis. Anti-Yersinia IgA is produced at the mucosa in increased quantities

in patients who develop arthritis following Yersinia

enteritis, possibly as a consequence of defective cellular immunity. Serum

concentrations of IgA correlate with activity of rheumatoid arthritis and

ankylosing spondylitis, and serum IgA immune complexes are associated with

rheumatoid vasculitis, suggesting that IgA contributes to the pathogenesis of

arthritis. We speculate that intestinal injury may also induce or perpetuate

arthritis by systemic distribution of inflammatory mediators produced by

intestinal immune effector cells.

Abnormal bowel permeability in ankylosing spondylitis and rheumatoid arthritis.

MD, Gibson RA, PM.

Intestinal permeability was measured using a low molecular weight polyethylene

glycol as a permeability marker in patients with osteoarthritis, ankylosing

spondylitis (AS) and rheumatoid arthritis (RA). Patients with AS showed a

significant increase in bowel permeability when compared to controls. Intestinal

permeability was also increased in patients with active RA but was less than the

control group in RA patients who did not have active joint disease.

I

ntestinal permeability in long-term follow-up of patients with celiac disease

on a gluten-free diet.

Duerksen DR, Wilhelm-Boyles C, Parry DM.

University of Manitoba, Winnipeg, Manitoba, Canada. duerksn@...

Intestinal permeability is frequently abnormal in patients with celiac disease.

The long-term effect of a gluten-free diet on intestinal permeability and the

correlation of intestinal permeability with a gluten-free diet are not known.

The objectives of this study were to determine the responses of intestinal

permeability and antibody testing to gluten free diet and the degree of

correlation of these measurements with gluten ingestion. In this prospective

study, patients with celiac disease were divided into three groups based on

length of time on a gluten-free diet: Group A, < 1 month; Group B, 1 month-1

year; Group C, > 1 year. Patients in Groups B and C were tested at baseline and

at 4-12 weeks later for the following: lactulose/mannitol intestinal

permeability, endomysial antibody, and 3-day food record. Permeability tests

were also performed in Group A and control subjects. Intestinal permeability was

elevated in newly diagnosed celiac disease and in individuals on a gluten-free

diet for less than 1 year. Intestinal permeability was normal in 80% at visit 1

and 87% at visit 2 in individuals with celiac disease on a gluten-free diet for

more than a year. Trace gluten ingestion was associated with increased

intestinal permeability on visit 2 (P = 0.0480). The sensitivity of detecting

gluten ingestion as measured by a 3-day food record was higher for permeability

testing (29 and 36%) compared with endomysial antibody testing (18 and 18%) for

visits 1 and 2, respectively. Intestinal permeability normalizes in the majority

of individuals with celiac disease on a gluten-free diet. Gluten ingestion as

measured by a 3-day food record correlates with intestinal permeability

measurements. The role of permeability testing in the follow-up of patients with

celiac disease warrants further investigation.

Celiac Sprue

Also known as gluten enteropathy, celiac sprue is characterized by diffuse

damage to the proximal small intestinal mucosa that results in villous atrophy

and altered gut permeability. It is strongly associated with the HLA class II

antigens: DR3 and DQw2. Arthritis is a well-known complication in children and

adults. It was present in 52 of 200 adult celiac disease patients attending a

routine gastroenterology follow-up clinic (16). The distribution of arthritis

was peripheral in 19 patients, axial in 15, and an overlap in 18 subjects. The

prevalence of joint disease was less common among patients on gluten free diet.

Recently, Usai et al found axial joint inflammation in 63% of patients with

celiac disease (17); 22 patients with celiac sprue underwent bone scintigraphy

using 99mTc methylene diphosphonate. Changes compatible with sacroiliitis were

found in 14 cases, 11 of whom had low back pain. Five patients with low back

pain had negative scintigraphy. Sacroiliac radiographs were obtained in only

four patients, and all had bilateral sacroilitis. One patient had rheumatoid

arthritis but all studied individuals were HLA-B27 negative.

Arthritis and other rheumatic complaints have been the presenting symptom in

patients with gluten enteropathy with improvement in the clinical abnormalities

on a gluten-free diet (18,19,20). An increased level of antigliadin antibodies

was seen in 9 of 74 patients with spondyloarthropathies, 1 of whom had elevated

antiendomysium antibodies and biopsy proven celiac disease (21). Thus,

antiendomysial antibody testing is recommended as a screening tool in patients

with suspected gluten enteropathy. Another study found that 3.3% of sprue

patients had Sjogren’s syndrome (22).

Serial bone mineral density measurements of 55 patients with celiac disease

detected osteoporosis (defined as a Z score equal or below 2) in 50% of the men

and 47% of the women (23). Celiac disease was an independent risk factor for the

development of osteoporosis.

.

Rheum 413-Volume 51, Number 2

http://www.arthritis.org/research/bulletin/vol51no2/51_2_celiac.asp

A vegan diet free of gluten improves the signs and symptoms of rheumatoid

arthritis: the effects on arthritis correlate with a reduction in antibodies to

food antigens.

Hafstrom I, Ringertz B, Spangberg A, von Zweigbergk L, Brannemark S, Nylander I,

Ronnelid J, Laasonen L, Klareskog L.

Department of Rheumatology, Karolinska Institutet at Huddinge University

Hospital, Stockholm, Sweden.

OBJECTIVE: Whether food intake can modify the course of rheumatoid arthritis

(RA) is an issue of continued scientific and public interest. However, data from

controlled clinical trials are sparse. We thus decided to study the clinical

effects of a vegan diet free of gluten in RA and to quantify the levels of

antibodies to key food antigens not present in the vegan diet. METHODS:

Sixty-six patients with active RA were randomized to either a vegan diet free of

gluten (38 patients) or a well-balanced non-vegan diet (28 patients) for 1 yr.

All patients were instructed and followed-up in the same manner. They were

analysed at baseline and after 3, 6 and 12 months, according to the response

criteria of the American College of Rheumatology (ACR). Furthermore, levels of

antibodies against gliadin and beta-lactoglobulin were assessed and radiographs

of the hands and feet were performed. RESULTS: Twenty-two patients in the vegan

group and 25 patients in the non-vegan diet group completed 9

months or more on the diet regimens. Of these diet completers, 40.5% (nine

patients) in the vegan group fulfilled the ACR20 improvement criteria compared

with 4% (one patient) in the non-vegan group. Corresponding figures for the

intention to treat populations were 34.3 and 3.8%, respectively. The

immunoglobulin G (IgG) antibody levels against gliadin and beta-lactoglobulin

decreased in the responder subgroup in the vegan diet-treated patients, but not

in the other analysed groups. No retardation of radiological destruction was

apparent in any of the groups. CONCLUSION: The data provide evidence that

dietary modification may be of clinical benefit for certain RA patients, and

that this benefit may be related to a reduction in immunoreactivity to food

antigens eliminated by the change in diet.

Joint manifestations in gastrointestinal diseases. 2. Whipple's disease,

enteric infections, intestinal bypass operations, gluten-sensitive enteropathy,

pseudomembranous colitis and collagenous colitis.

Gran JT, Husby G.

Department of Rheumatology, Central Hospital of Aust-Agder, Arendal, Norway.

This review addresses the clinical picture of rheumatic diseases seen in

Whipple's disease, gluten-sensitive enteropathy, pseudomembranous colitis,

collagenous colitis and that developing after enteric infections and intestinal

bypass operations for morbid obesity. These disorders exemplify the interplay

between antigen entrance through the gastrointestinal canal, specific bacterial

properties and genetic host factors such as HLA B27. In most cases such as

interplay results in formation of circulating immune complexes causing the

development of peripheral joint disease.

Unusual polyarthritis as a unique clinical manifestation of coeliac disease.

Bagnato GF, Quattrocchi E, Gulli S, Giacobbe O, Chirico G, Romano C, Purello

D'Ambrosio F.

Dip. Medicina Interna, Policlinico Universitario, Messina, Italy.

bagnato@...

This report describes a patient who presented with an unusual polyarthritis

accompanied by myalgia, fever and anxiety. After extensive clinical and

serological evaluation, duodenal biopsy and serological tests provided evidence

for the diagnosis of coeliac disease (CD). The patient was promptly put on a

gluten-free diet, which led to an improvement in the clinical abnormalities.

Arthritis as presenting symptom in silent adult coeliac disease. Two cases and

review of the literature.

Slot O, Locht H.

Department of Rheumatology, Copenhagen County Hospital Gentofte, Hellerup,

Denmark.

We report 2 cases of adult silent coeliac disease (CD) presenting with arthritis

of a knee and a sacro-iliac joint, respectively. In both patients the arthritis

was relieved on a gluten free diet. The literature on arthritis in adult CD is

reviewed.

nicki jackson <njacksonbrown@...> wrote:

Hi ,

Good to hear from you again...I've missed your posts.

I, for one, would be very interested in this article.

Thanks,

in CA

---------------------------------

Autos. Looking for a sweet ride? Get pricing, reviews, & more on new and

used cars.

[Guest guest]

That's the truth, Once you find an article you like, you'd better archive it

cause you may never find it again. The number of articles I have lost that

way!!!

Also sympathies for you and your dad's situation. Taking care of older

parents and worrying about them when you are not is a major contributor to

my recent health problems and I haven't done near the job I would have if

health had been better. It's a tough road to go down, especially since yours

is in another country. Bet wishes on that one. Please take my advice if you

can and take care of you first. It's a rough order but I know I should have

done just that to keep from being where I am now.

Learn from one who feels like a VERY old woman.

I also agree with the idea of trying the gluten free diet. If it works any

at all, then you have learned something and if you don't then you don't have

to guess about it any more. Hope you have great results.

GA

----- Original Message -----

From: " McKinney "

Hi Nicky,

Thanks - I'm hoping that with my Dad's improved health I may not have to

make any more trips to England in the near future. Since he's 91 though,

I'm not too hopeful. I haven't been able to find the exact studies that I

saw a couple of years ago. One problem is that a lot of medical research

websites are now charging a lot for articles and subscriiptions. However,

I've found a few articles that tie together gluten intolerance, intestinal

permeability and spondyloarthropies. I'll keep looking and post articles as

I find them. I don't think the link is totally proven but for most of us

it's worth trying a gluten free diet. I know I felt much better on it - but

obviously I didn't do a controlled trial!

[Guest guest]

Hallo again!

At first I´d like to thank you three groupmembers who bothered to

reply to my call out for information on links between Reiter´s and

intestinal trouble. After reading your replies and after being

provided with these most interesting medical articles from I

gather it makes sense to go along with my theory as to the cause of

intestinal trouble connected with diagnosed Reiter´s and HLAB-27

presence. You see, I have to put together arguments to convince the

physician I´m going to see, the link between my gut problems and

Reiter´s can´t be ruled out. A poor performance from my side would

probably make the physician to persist in arguing, the causes of

subsequent gut surgeries in a two year period are totally

coincidental and irrational. Not to mention any link to

Spondyloarthropaties. " Never heard of such a thing! " Thus leaving me

waiting for the next intestinal symptom to come along. Can anyone

give me good advice how to behave when seeing the doc? An appointment

is scheduled on Monday, Feb. 6 th.

Anders

[Guest guest]

Thanks for your sympathy and encouragement . I hope your situation is

improving.

in Va

Herring <countryms@...> wrote:

Also sympathies for you and your dad's situation. Taking care of older

P. McKinney, CPA

434-753-3928

703-919-9856 (cell)

---------------------------------

What are the most popular cars? Find out at Autos

[Guest guest]

I have been diagnosed with 2 diseases in the last 6 mos. But I have

had IBS for 4 years, right after my gall bladder was taken out. The

DR who diagnosed me with Reiters, added Fibromyalgia to my list

because I have the hot spots where they test for pain, and a history

of IBS and Migraines.

Now, I am at the point I cannot tell what is the Reactive arthritis

pain and what is Fibro, not to mention what is a side effect of the

Methotrexate I take. I think there are people out there with true

allergies, and others who just have disorders that are not allergy

based. Like my son and his adhd. He did not show any change when his

diet was limited. And as an adult he still has all the problems, he

can just deal with them better. So, I think it is possible for you to

check out diets and I hope you find it helpful. I am forced to take

medication for my IBS and eat a diet with very low fat and no milk

products.

I am glad you found some information. I cannot get on very much to

read, the Reactive arthritis is effecting my eyes and I cannot see

well for a while. My right eye looks like it has a vaseline smear

across it, and the reading glasses do not work. My new glasses will

not be in until next week sometime. The drops help the pitting and

how the light is causing that terrible shadow, but not enough yet for

me to be comfortable. I barely get through work now, so hard to read.

And I am sooooo tired.

Hope you understand that many of us want to read and respond, but

cannot do so every day. I am just too tired these days.

Best of luck to you.

[Guest guest]

Dunno who I am responding to but does it really matter where the pain is

coming from? Just wanna get rid of it myself. I did occasionally wonder if

my flare before Christmas was from AS or FMS but a burst of cortisone cured

that so if I could get over the fatigue from a flu like bug from over a

month now, I'd be so happy I could just_______________(fill in the blank)

GA

> Now, I am at the point I cannot tell what is the Reactive arthritis

> pain and what is Fibro,