PHYSICIAN'S MANUAL
Montana Celiac Society
C
ompiled & Designed by Donald & R. Jean Powell/20012nd Edition, 2003; 3d Edition, 2004
; Web Edition 2005PHYSICIANS'
MANUAL™
Contains Articles presented by Physicians For Physicians & Patients,
describing Celiac Disease and Dermatitis Herpetiformis.
A Manual for Physicians
Presentations By:
Gastroenterologists, Pediatricians, Neurologists, Dermatologists, Dental &
Gastroenterological Researchers, each with long-standing Celiac experience.
Foreword
While Dermatitis Herpetiformis articles are in a category separate from articles
describing Celiac Disease, DH patients are technically and medically Celiac
patients, requiring the same diet and suffering from the same villi involvement.
The diet is imperative for them as well.
Montana Celiac Society is a non-profit corporation that was founded by a small
group of Montanans diagnosed with Celiac Disease in the early 1990's.
Each patient was informed at that time that the ratio of the disorder was
1:10,000. Serological screening in
the United States has, in the 12 years since, proved a demographic among
Northern European Caucasian descendents in the US to be 1 in approximately 120.
This is true in Montana.
The subscription list of the MCS newsletter Gluten-Free Friends has grown
in Montana from the original 7 members in 1990 to over 715 subscribers in 2005,
including subscribers from over 30 states.
As diagnosis improves, numbers grow exponentially.
FOLLOWING IS THE LIST OF MCS OFFICERS AND DIRECTORS 4/2005:
DIRECTORS:
Judy Cass,
Director
Tim Harris,
Director
Pauline Lucas,
Director
Frank Murphy,
Director
Executive Director, Founding President: R. Jean Powell
OFFICERS:
President/Financial Manager: Dorothea Caluori
Vice-President:
Denise McGough
Secretary: Judy
Harris
Patron:
Marlys Werle
Periodical Resources: Houston Celiac Support Group, Janet
Rinehart, Ed.; Tri-County CS Support Group, Jim Lyles, Ed.; Alamo Celiac, Lynn
Rainwater, Ed.; CSA/USA Lifeline, Leon Rottman, Ed.; Montana Celiac Society,
Gluten-Free Friends, R. Jean Powell, Ed.
Revisions, March 2004; September 2004; May 2005.
Celiac Disease & Gluten Sensitivity
Presentation; Questions & Answers:
The Spectrum of Celiac Disease:
Celiac Sprue Research Update:
What is Dermatitis Herpetiformis?:
Dermatitis Herpetiformis:
Dermatitis Herpetiformis:
Diagnosis in the 21st
Century:
by Kenneth Fine, MD
Down's Syndrome: by Lloyd Rosenvold, MD
Schizophrenia:
Infertility:
by Lloyd Rosenvold, MD
Celiac Sprue & Pregnancy:
by Gainer & Phillips, Journal of
Perinatal & Neonatal Nursing
5.
Pediatrics
Pediatric Presentations:
by Alessio Fasano, Pediatrics
Gastroenterologist
If You're Considering Pregnancy:
by Joseph Murray, MD
Cerebellar Atrophy & Patchy
Demyelinization:
by Jerry S. Trier, MD
Epilepsy, Cerebral Calcifications, & CD:
Lancet: by William Dickey
Neurological Manifestations of Adult CD:
Lancet: by Beversdorf, et al.
Cryptic Gluten Sensitivity:
Lancet: Hadjivassillou, et al.
Cerebellum in Cognitive Function:
Discover Magazine,
11/96
Autistic-like Tendencies in a Celiac
child:
Associated with CD:
8. Celiac Disease is the 21st Century
by Dr. Joseph Murray, Mayo Clinic, Rochester, Minnesota
Large Serological Screening Study
Signs & Symptoms of Celiac Disease.
Deficiency Syndromes:
Montana Celiac Society
The correct procedure used to test for
Celiac Disease; MCS, R. Jean Powell
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1. Medical Descriptions
Celiac Disease & Gluten Sensitivity
by Carol E. Semrad, MDAlso referred to as celiac sprue, CD is an inflammatory condition of the small intestine precipitated by the ingestion of wheat in individuals with certain genetic makeups. The onset of illness most commonly occurs around age two, after wheat has been introduced into the diet, and in early adult life [third and fourth decades]. However celiac disease can begin anytime in life. In susceptible individuals, the wheat protein gluten triggers an inflammatory reaction in the small bowel that results in a decrease in the amount of surface area available for nutrient and fluid and electrolyte absorption. The extent of loss of intestinal absorptive surface area generally dictates whether an individual with celiac disease will develop symptoms.
Individuals with celiac disease may experience severe symptoms such as diarrhea, weakness, and weight loss indicating a marked decrease in intestinal absorptive surface area involving much of the small intestine. On the other hand, some individuals present with anemia related fatigue and have no symptoms referable to the gastrointestinal tract. Such individuals likely have disease limited to the proximal small bowel where iron is normally absorbed, the remainder of bowel adequate for nutrient and fluid absorption. Other extraintestinal manifestations of celiac disease include osteopenic bone disease, tetany, and rarely neurologic disorders.
Gluten sensitivity can also manifest itself as a blistering, burning, itchy rash on the extensor surfaces of the body [dermatitis herpetiformis]. Most of these individuals have intestinal biopsies characteristic of celiac regardless of gastrointestinal symptomatology. Recently, with the discovery of antibodies which are specific for celiac disease, screening of families of celiacs and select populations have identified a growing number of asymptomatic individuals who have circulating antibodies and changes on intestinal biopsies characteristic of C.D.
These individuals clearly have a gluten sensitivity but it is unclear if they will develop the clinical features of celiac disease over time.
Removal of wheat [gluten] from the diet of individuals with celiac disease or gluten sensitivity results in regeneration of the intestinal mucosal absorptive surface area and resolution of symptoms in most patients.
There are two important factors that contribute to the development of celiac disease:
1
. The ingestion of wheat:The "Coeliac Affectation" was first reported by Gee in 1888. However it was not until 1950 that wheat was proposed to be the cause of celiac disease. The evidence was based on the observation of a Dutch physician named Dicke who noted during World War II, a time when wheat grains were scarce in Holland, that children with celiac disease who had otherwise failed to thrive, improved on a wheat-poor diet. Since then the large water-insoluble protein, gluten, present in wheat has been identified as the offending substance. Extraction of gluten with alcohol has further narrowed activity to smaller proline-rich proteins called gliadins, which are capable of precipitating disease in previously asymptomatic celiacs. Analogous proteins exist in other grains such as rye, barley, and oats. These grains are also capable of exacerbating celiac disease. The specific peptide sequence of the gliadin responsible for triggering intestinal inflammation has not yet been identified.
2.
The Genetic Background of the Individual:Celiac disease runs in families. First-degree relatives of individuals with celiac disease may or may not manifest symptoms of the disease. Predisposition to gluten sensitivity has been mapped to the major histocompatibility [MHC] D region on chromosome 6. The most important HLA haplotype is Dqw2, which is often in linkage with DR3. Other important HLA haplotypes identified are DR7 and DPB 1, 3, 4.1 and 4.2. The sites on these MHC class 2 expressed proteins responsible for interacting with gliadin and host T cell receptors thereby sensitizing the intestine to gluten have not been identified.
The main function of the small intestine is to absorb nutrients and fluid and electrolytes, a process depending on adequate surface area. In this regard, the absorptive epithelium [villus] of the small intestine is pleated in the intestinal lumen to increase its surface area. Intestinal inflammation of any etiology, if severe enough, is associated with flattening of the villus epithelium, which results in a decrease in intestinal absorptive surface area. How activated inflammatory cells in the lamina propria beneath the surface epithelium and intersperse between epithelial cells bring about villus flattening remain a mystery. Intestinal biopsies taken from individuals with celiac disease and gluten sensitivity show a spectrum of these mucosal abnormalities. Three distinct patterns have clinical relevance.
Infiltration of the villus epithelium with lymphocytes and a normal villus and crypt architecture.
This pattern is found in 40% of individuals with Dermatitis Herpetiformis and a portion of first-degree relatives of celiacs who have no gastrointestinal symptomatology.
A flat mucosa characterized by villus flattening & crypt elongation with inflammatory cells in the lamina propria.
This pattern is classically found in individuals with celiac disease who have gastrointestinal symptoms, but has also been reported in asymptomatic celiac relatives and individuals with Dermatitis Herpetiformis. It is important to keep in mind that intestinal biopsies are most commonly obtained endoscopically from the duodenum and therefore do not provide information as to the extent of disease along the length of jejunum. Since the duodenum is the first segment of small intestine exposed to gluten, villus flattening might be most severe in this location while much of the jejunal villi remain relatively normal, accounting for an asymptomatic state. In most of these individuals, treatment with a gluten-free diet results in the return of villus and crypt architecture to normal or near normal.
A hypoplastic mucosa characterized by villus flattening and small crypts.This biopsy is found in the small group of patients with presumed severe celiac disease refractory to a gluten-free diet. These individuals have persistent ill-health due to intestinal malabsorption and sometimes require nutritional support parenterally. This intestinal lesion is irreversible.
There is no test yet which is definitively diagnostic of celiac disease. Relief of symptoms or reversion of an abnormal intestinal biopsy to normal on a gluten-free diet is the most convincing evidence that an individual has celiac disease or gluten sensitivity. Intestinal biopsies as discussed above show characteristic findings compatible with celiac disease but are obtained just as often to exclude other intestinal conditions, most importantly infection, which can have a clinical presentation similar to celiac disease.
The first serological marker reported to be of use in the diagnosis of celiac disease was the IgG class antigliadin antibody [AGA]. Though sensitive, this antibody is also found in other diseases and is therefore not specific for celiac disease. IgA class AGA is more specific; however about 2% of patients with celiac disease have selective IgA deficiency. A positive IgG and IgA AGA gives a reported sensitivity of 96% to 100% and specificity of 96% to 97%. If only the IgG AGA is positive an evaluation for selective IgA deficiency should be undertaken. Antireticulin antibodies [ARA] have also been reported in individuals with celiac disease, but are non-specific. IgG ARA is relatively useless, but IgA ARA has a high sensitivity and specificity in adults [97% and 98% respectively]. In children these values are much lower. Recently two antibodies, IgA class antiendomysial antibody [EMA] and human jejunal antibody [JAB], have been identified which are highly sensitive and specific for active celiac disease [100% sensitivity and specifically reported in one study.] The one best characterized is the EMA, an antibody against endomysium reticulin fibers. In adult studies, EMA was only found in patients with active celiac disease and not other diseases.
The test is less powerful in children as EMAs have been detected in other childhood diseases. The more important limitation of EMAs in children is the reported fall in sensitivity observed in children with celiac disease less than 2 years old. Even the EMA and JAB antibody tests in adults are not foolproof as they may not be positive in individuals with celiac disease and IgA deficiency.
A panel of these antibodies seems to be most useful in the diagnosis of celiacs. A combination of IgG AGA, IgA AGA, and EMA have a reported positive predictive value of 99.3% when all were positive and a negative predictive value of 99.6% when all were negative. These antibodies tend to lessen or disappear when individuals are maintained on a gluten-free diet. Antibody testing is important in screening individuals who are at risk for having celiac disease but have no symptomatology, in individuals with atypical symptoms or extraintestinal manifestations of celiac disease, and in individuals with presumed celiac disease who fail to respond to a gluten-free diet. Patients with positive antibody tests must undergo small intestinal biopsy to confirm the diagnosis and assess the degree of mucosal involvement.
Unlike autoimmune diseases in which the precipitating antigen either is not identified or if identified cannot be removed, the antigen precipitating celiac disease, i.e. gluten, can be removed from the diet. This sounds easier than done as wheat is used as a filler and thickener in a number of store bought and restaurant prepared foods. Avoidance of gluten in the diet requires careful scrutiny of food labels for the presence of wheat and other offending grains such as rye, oats, and barley. Products labeled wheat-free are not necessarily gluten-free. Common foods that cannot be eaten include breads, bagels, pastries, pasta and pizza. There are companies throughout the United States that produce gluten-free products made predominately from rice flour. Most patients treated with a gluten-free diet will notice a lessening of symptoms within 2 weeks and no follow-up intestinal biopsy is required. A small group of patients have partial or no response to a gluten-free diet.
One important cause of a poor dietary response is the continued ingestion of gluten in foods thought to be gluten-free or just plain dietary cheating.
Antibody testing while such patients are on a "strict" gluten-free diet may be useful in this situation. A kit that utilizes the Elisa assay has been developed to test food products for the presence of the gluten antigen.
In individuals who have a poor response to a gluten-free diet, a repeat intestinal biopsy is mandatory after 3 months treatment to assure that other intestinal lesions such as infection or intestinal lymphoma were not missed.
In symptomatic patients the obvious answer is to relieve debilitating symptoms. What about individuals who have minimal symptoms or who are asymptomatic? There are two reasons to treat such individuals with a gluten-free diet: 1) a subgroup of these patients will progress to more severe disease and hence develop symptoms and 2) there is an increased incidence of small intestinal lymphomas and adenocarcinomas in individuals with celiac disease. The increased incidence of cancer seems to correlate with the degree of intestinal inflammation [activity] present, as individuals whose disease responded to a gluten-free diet and who remained compliant with the diet had a lower incidence of such cancers. Whether individuals who are found to have elevated antibodies specific for celiac disease but are asymptomatic and have normal intestinal biopsies should be treated with a gluten-free diet is unclear. CAROL SEMRAD, M.D. semrad@columbia.edu/©1995 CU Div. of Gastroenterology
From the video of the Dr. Alessio Fasano Presentation held June 19th, 1999 at Billings Deaconess Hospital, Billings, Montana.
Dr. Alessio Fasano is Professor of Pediatrics and Director of the Department of Pediatric Gastroenterology & Nutrition, University of Maryland School of Medicine. Internationally, he is considered one of the foremost Celiac researchers in the field.
|
THREE POINTS: 1) It’s Permanent: It doesn't go away. 2) Genetic Factors: We are genetically predisposed. 3) Environmental Factors: You must be consuming a diet that includes gluten/gliadins. |
Genetic Predisposition: Familial Occurrence: a. 2 to 4% in general population--10% in first degree relatives. b. 70 % of monozygotal (one egg or identical) twins. c. H(human) L(leukocyte) A(antigen) = HLA fingerprints: 70-80% of Celiacs have positive HLA.
Why is HLA important? There are receptors on the cells of the intestine, on the enterocytes, which recognize gluten, bring it to the other side of the mucosa (lining), triggering an immune response which activates lymphocytes, producing tissue damage.
Environment: Gliadin: Gliadin is a prolamin, an alcohol-soluble fraction in cereal grains.
Adenovirus 12: There may be a theoretical infectious factor. Up to 85% of Celiacs test positive for Adenovirus 12 but less than 10% of general population test positive. It is still an open issue.
Prevalence: There is data from Europe, but none from the U.S. When we looked at Malmo, Sweden, and Copenhagen, Denmark---20 miles apart--- we saw that in Malmo the incidence was 1:500 but in Copenhagen it was 1:11,000, which has been also claimed in U.S.! (as confirmed by biopsy). If we look for typical presentation we will miss most of it. A decline was claimed in the mid-eighties because babies were being breast-fed & introduction of gluten was late, which made the reason (for the so-called decline) unclear. By delaying the onset of the disease the typical presentation became atypical so that the typical guidelines used brought on a major disaster! Guidelines had to be changed.
Presentation: It is not uniform, and may be typical or atypical. Asymptomatic patients may have latent symptoms which will develop later. The typical (pediatric) patient is 6 to 18 months old, and has symptoms of: diarrhea, steatorrhea (fatty stools), poor weight gain, irritability, anorexia; which equal the Celiac Crisis. We no longer see these (so-called) typical cases (showing a picture of an emaciated baby). . The classical typical form is just the tip of the iceberg--- showing 1:2500. But when looking for all forms including symptomatic atypical Celiac Disease the incidence was 1:300!
Other Organs: The mouth, with Stomatitis (inflammation of the mouth as in ulcers or thrush); the kidneys, with nephropathy (any disease or damage to the kidney); the joints, with arthritis; the skin, with Dermatitis Herpetiformis (DH); all can be related to Celiac Sprue. It is universally accepted that DH = Celiac Disease, even though they may have no intestinal complaints. A biopsy will show typical damage. Dermatologists here (U.S.) said NO, until skin biopsies showed deposits of immuno-complex with gliadin and gliadin antibodies present in typical lesions of the skin. All over the world, this is no longer an issue---except in the U.S. I don’t know why.
Atypical: Short Stature: 20% of idiopathic short stature in Europe is due to Celiac Disease. At the University of Maryland serum bank there were kids who did and didn’t respond to growth hormones. We analyzed these samples for IgG antigliadin antibodies. The kids who responded to growth hormone had normal antibody levels---some of those who didn’t respond to growth hormone had high levels of anti-gliadin antibodies, and all who agreed to the biopsy were found to have Celiac disease. Another example of misdiagnosis.. Now children with short stature are screened for Celiac Disease with routine lab work.
Enamel Dysplasia: This discoloration is due to gliadin and gliadin antibodies on the matrix of the teeth. You can see the damage lines on the matrix of the teeth when gluten was introduced, then withdrawn, and reintroduced.
Seizures:
Described to be frequently associated with Celiac Disease, due to
intercranial calcification, particularly in the posterior of the brain, causing
seizures. We had a four year old
girl with recurrent seizures who did not respond to anti-epileptic drugs and was
brought to our office because of weight loss.
She had had seizures for 2 years.
She tested positive for the anti-gliadin and anti-endomysial antibodies. The
biopsy showed her to be Celiac, and for the first time her seizures were
controlled.
Folic Acid deficiency secondarily causes the calcification.
Rarely
does the calcium deposit almost disappear, but it did in this case.
Other Immune Disorders:
Diabetes Mellitus, where the genes are on the same chromosome as CD;
the rate is much higher than in the general population; thyroid disease;
Sjogren’s syndrome; Rheumatoid Arthritis, collagen vascular disease, and liver
disease (this list is from the GIG article describing Dr. Fasano’s lecture).
Mood Changes: Children come in crazy, screaming, yelling. A molecule seems to be involved in the internal control of subjects, and gliadin changes behavior by interfering with the inter-active receptors of endorphins. Endorphins are able to change the activity and alert(ness) of people. We calculated that there are 23,000 receptors per cell, in which alpha-gliadin could cause abnormal interaction.
Asymptomatic Celiac Disease: The person is healthy, with no symptoms, but has the typical intestinal histology. 10% of Celiac relatives have intestinal damage, and it is crucial that they be treated as Celiac!
What was the difference between Malmo and Copenhagen? It was in the screening in Denmark. Where once they claimed to have the same incidence as the United States, they now have the same as the rest of Europe: 1:300! The difference is that the clinical presentation is absolutely different.
How do you make the diagnosis of Celiac Disease?
In European Pediatrics it once
was with 3 biopsies: 1. Symptoms on a normal diet---Biopsy showing tissue damage.
2.
Gluten-free diet for one year free of symptoms---Biopsy
3.
Challenge---Re-expose subject for 3 months or until relapse, then have 3d Biopsy.
This was painful for patients and physicians. Compliance was very poor, and it was a complicated process. We asked What can we do to improve this painful process? The breakthrough was the use of anti-gliadin anti-bodies found in the lab in the early 1980’s. There has been tremendous improvement of this assay to reach the point now where:
IgG sub class: highly sensitive, not very specific
IgA sub class: not sensitive, but highly specific
Anti-endomysial & anti-reticulin antibodies: Highly sensitive and highly specific
The anti-endomysial antibody test required monkey esophagus. Since I like monkeys and hate to use them for even a very noble issue, I was glad for the alternative, which is much cheaper: Human umbilical cord. We get permission in the delivery room. It is cheap, very specific, and very sensitive.
If Anti-gliadin and Anti-endomysial Antibodies are positive: we are 99.6% sure it is Celiac Disease, the Positive Predictive value. But there still needs to be a biopsy. The test is highly predictive so it is very useful for diagnosis. It is a different tool, considering the pain people were going through. Tests on 3000 children showed that the same results were produced with the alternative approach as with the three biopsies.
Policy: To check antibodies once a year. If you’re getting high signals then, even though you thought you---or your child--were eating appropriate foods you later on discover this is not the case.
Serological Screening: Anti-gliadin and anti-endomysial antibody screening shows a much higher prevalence of the disease than expected before. On the same European map, the triangles are the same size everywhere. 1:300! There is a uniformity of incidence.
Clinical Presentation: Very few (in Denmark) had typical presentation. Most had Osteoporosis, DH, Short Stature, whatever is on that list. Awareness of physicians was pretty low. When we did the screening again of Malmo and Copenhagen, the prevalence of the disease was exactly like the rest of Europe, solving a mystery for us that’s the same mystery we have in U.S. How come---having the same genetic background---we have such a difference in the incidence of the prevalence of the disease compared to European countries?? Is this because we are different---or merely indifferent?
Pilot Study: At the Univ. of Maryland we did a study with 159 kids with atypical symptoms such as 1.Short Stature 2. Poor weight gain 3. abdominal pain. Some tested positive for antibodies and six kids were diagnosed with CD. One Grandmother was Celiac, and her two grandchildren tested sky-high for antibodies, but we couldn’t do the biopsies. Their primary physician said “No Way!” They were healthy. Their insurance company also said no way, because they are healthy. But they will be back as future customers!
Why is it so crucial to be Gluten-Free even if asymptomatic? Here you would teach me. For years you’ve been unhappy and unhealthy. In Pediatrics if the diagnosis is not on time there is no catch-up growth. We as physicians have a tremendous responsibility---kids with Short Stature can recover totally their potential growth. But if we’re late---too late---they will be short forever and ever, and it will be our responsibility! It is the same with skeletal disorders---osteoporosis. Every single person with osteoporosis is a failure of a physician to make a diagnosis. Infertility is also described to be associated with C.D., and the physician has a strong responsibility.
Consequences of Prolonged Exposure: I am sure you are aware of the consequences of long-term exposure and the incidence of intestinal lymphoma, which is much higher among Celiacs chronically exposed to Gluten than among the general population. But with a strict gluten-free diet, after five years the difference is negligible with the general population.
Questions & Answers
Q:
What is the ratio of men to women with Celiac Disease?A:
Of the 1400 we’ve tested so far, 58% are females; of those who’ve tested positive, the ratio is half and half.Q:
The information that you’re sending back in 3 or 4 weeks—is it acceptable with doctors? Will Montana physicians be able to understand what we’re dealing with?A: Your coordinator will be the connection between the physician and us. If the results are an indication that you need to go to the biopsy and the physician is unsure--for instance if there are no symptoms--he/she may fear that the HMO will never approve to do this.
If this is the case--if the HMO
WON’T agree to the test, we will pay for the procedure. This is one way we invest our money. But if you have SYMPTOMS, test POSITIVE, and the HMO refuses still, the lawyer comes into the picture!We would like to review the slides of your biopsy in a blind study. We want to be involved, to help your Internist/Gastroenterologist through this journey if there are such difficulties. If you have a Medical Advisor, then he or she can take the lead and talk with colleagues. We want to facilitate this story as much as we can, either economically or conceptually.
Q:
Is there a list of the labs that you use?A:
I use mine. There are 5 or 6 labs total that can do this test. The antiendomysial test is a subjective one (done by a person, not mechanically). The lab person doing the test who does three a year has a different level of experience than the lab person doing it 50 times a day. We have a tremendous volume. On both a clinical and a research basis, every single time that we have found the antiendomysium to be positive, we’ve found the biopsy to be pathological. That means that we’ve found our quality to be very high.Q: I can think of no one in my family who has a related auto-immune disorder such as lupus or diabetes. Is that something I still need to be concerned about?
A:
Not necessarily. It is not a given. For every Celiac to have an auto-immune disorder would be a disaster.Q:
Have you noticed a correlation between non-compliance with the GF diet and autoimmune disorders being more prevalent?A:
Yes! Stick with your diet!Q:
After you stop eating gluten, how long before symptoms subside?A:
Good question. Our experience is based on how long you’ve been exposed. For kids it may be just a few days; but if you’ve been exposed for years and years, it is sometimes 4 to 6 months.Q:
Is there a connection between Celiac Disease and Multiple Sclerosis?A:
There is no clear association. There are some anecdotal reports, but again we’re talking about two autoimmune diseases. We can’t conclude that there is such a strong association at this stage—the numbers aren’t there.Q:
I’ve been on the celiac diet for 15 years and have never been tested—blood-wise or biopsy-wise. Would you recommend going back to have that done?A:
If you have been so-o-o-o good to be on a gluten-free diet for 15 years, I would not recommend that you make any kind of changes, because you may eventually taste things that you’ve forgotten! Seriously, you’ve shown to yourself a high level of commitment—you’re convinced. On the other hand if you discover you’re not really celiac, you might be very upset!!!Q:
About the gluten challenge: my four-year-old has been on a GF diet for about a year now, and it is extremely obvious that he gets sick if he eats anything with wheat in it. He has not had a biopsy.A:
Again, I think you’re in the kind of situation in which you are extremely convinced and committed to the disease. Believe it or not, you are in a very lucky situation, because if you were to do the challenge, as I would strongly recommend, the time needed to do the entire thing would be brief: he would react immediately, the antibodies would go crazy immediately, and you could do the biopsy immediately.The entire thing could be done in a matter of a couple of weeks. It’s an investment in the future. You have to understand—and this is well demonstrated—your child may react within a few seconds now, but when he is 14 or 15 this is not necessarily going to happen.
I don’t want to scare anybody, but I want to share with you a sad story.
A few months ago a lady came from Philadelphia, 44 years old, with intestinal lymphoma. She, as a child 6 years old, was diagnosed celiac. When she was 10 she was told that she would grow out of it. She exposed herself to gluten and indeed she did not have any relapse of symptoms until she was 42—and her symptom was intestinal lymphoma. She came to me because she has a 6 year old girl who she wanted screened and indeed the daughter happened to be celiac. You can bet the girl will be on a GF diet for the rest of her life!
So—a few weeks of aggravation now, biopsy now, will be a tremendous investment in the future.
Audience member’s comment: If you can put your child through 2 weeks of misery in the summer, then get him diagnosed before school starts, you will avoid the label of ADD. Also, with a biopsy diagnosis, doctors will not be so apt to try to convince him when he is 20 that he’s "not really" a celiac and then encourage him to go off the diet.
Dr. Fasano: That’s true and has been our experience as well…
Q: If I get the biopsy, should I also say that I am looking into the possibility of lymphoma as well?
A:
If you’re celiac and you’ve been diagnosed, and put yourself on the GF diet, it’s the same as the general population. The prevalence of lymphoma will go back to normal, absolutely.Q:
I just got this disease within the last 2 years or so and I am 71… A: You did not get it in the last 2 years.Q:
I’ve always had it then?A:
You’ve always had it. The problem is, while the 4 year old got sick very quickly, the damage expressed itself to someone so young, you took your time! Your immune system was slow-paced; it’s been a continuous experience. But remember, it has an encounter with your genes and your environment. It has been always, always there.Q: How old do you want children to be before you do the biopsy?
A:
I don’t want children to have the biopsy unless there’s some indication that the antibodies are there, there is a family history, and there are symptoms (due to the environmental exposure to gluten). There is no age limit; we do the endoscopy to neo-nates who are having problems…Montana Celiac Society has been told by parents that there are no pediatrics gastroenterologists or instruments to do the biopsy in Montana, so parents must travel to Seattle or Denver.Audience member’s comment:
Dr. Fasano’s answer: This is surprising to me. If I ever consider going into private practice, I will come here! (Applause!). If you have a choice between going to an adult gastroenterologist here and a child’s gastroenterologist, I would prefer that you go to Seattle to a pediatric gastroenterologist.
In fact, Seattle has the highest prevalence at 30% that has been found in any of the states. The gastroenterologist there is very, very good. Also, I will let my students know that there is no pediatrics’ gastroenterologist in Montana.
Q: My son did have a biopsy, which came back negative. He had the stool test and was malabsorbing; he had the blood test and one of the antibodies was positive, one negative…
A: Which one? It makes a world of difference…
Q: The doctor said if it had been the other one, he wouldn’t have done the biopsy, just assumed he was celiac. About a month after the blood test he put him on a gluten-free diet, and did the biopsy 5 days later.
A: Wait a minute! He was placed on a gluten-free diet before the biopsy??? Q: Yes.
A: No-no—No, No! I would do two things: you would be more than welcome to send me the results and copies of the slides so I can take a look at them. Sometimes there are subtle changes as the tissue repairs itself, which an experienced pathologist can pick up. I would be more than pleased to take a look at that.
Second, if the biopsy is normal, unfortunately you do not have any other alternative but to go back on the regular diet, do the challenge, the whole nine yards, until the antibodies turn positive again.
Since he’s on a gluten-free diet now, I would test him first to make sure all the antibodies are normal, expose him to gluten, wait either for the symptoms to appear or for six months if he has no symptoms, then redo the blood test. If you see the antibodies elevate then we do another biopsy. Sadly, you’re in LaLa Land right now… Q: I know…
Q: My sister, mother, grandmother and brother have CD. I took the blood test today; but let’s say I don’t have it and I have kids. Can I just carry it over?
A: Absolutely! Suppose you need a combination of 10 genes to have celiac. You may have 8 of the 10 genes, so you will not be celiac—ever. Still, you have 8 genes—the likelihood that you can marry someone who has the other two genes that will mesh and carry it to your child is possible.
Q. For the past week or so, I’ve been gluten-free. Does that skew this test?
A: Yes. There’s a possibility that it does. My suggestion is to go back on the regular diet, get sick and repeat the test. Alessio Fasano
You may contact Dr. Alessio Fasano at: The University of Maryland School of Medicine, 22 South Greene Street N5W70, Box 140, Baltimore, Maryland 21201-1595; Phone #: [410] 328-0812; FAX: [410] 328-1072.
e-mail: afasano@umaryland.edu.
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The Spectrum of Celiac Disease
DR. JOSEPH MURRAY, Mayo Clinic, Rochester, Minnesota
From The Sprue-nik Press, Issue Jan/Feb. 1998; Jim Lyles, Editor
There are many different terms that have been used to describe the disease that we generally call celiac disease (CD); only the first of these is preferred:
Gluten Sensitive Enteropathy
--this is the most precise definition, as it describes intestinal damage related to the intake of gluten.Celiac Sprue
--sprue implies diarrhea, which many newly-diagnosed celiacs do not have.Idiopathic Steatorrhea
--this means "unexplained foul-smelling, fatty stools". Many celiacs do not have this symptom either, and in any case the cause is known (damaged villi), so it can hardly be unexplained.Non-Tropical Sprue
—[as distinguished from Tropical Sprue, which responds to antibiotics. RJP, Ed.] Again the implication is that diarrhea is a major symptom, which is not always the case.A GOOD WORKING DEFINITION OF CD IS:
Joseph Murray, MD"A PERMANENT INTOLERANCE TO GLUTEN THAT RESULTS IN DAMAGE TO THE SMALL INTESTINE, WHICH IS REVERSIBLE WITH THE AVOIDANCE OF DIETARY GLUTEN. "
UNUSUAL SYMPTOMS
Some of the more unusual non-gastrointestinal symptoms of CD include:
Rickets, dental enamel defects, epilepsy with intra-cranial calcification, delayed menarche in teenage girls, arthritis (synovitis), neurologic disorders, mental "fuzziness", and lupus and other connective tissue diseases.
There are also some unusual gastrointestinal symptoms, which include:
Heartburn, gastrointestinal lymphomas and carcinomas (two forms of cancer), abnormal transaminases (liver abnormalities), and unexplained weight loss.
DERMATITIS HERPETIFORMIS
Dr. Murray believes that ALL Dermatitis Herpetiformis [DH] patients also have Celiac Disease and the gluten sensitivity which occurs in the gastrointestinal tract, producing antibodies. In DH, those antibodies are "dumped" under the lining of the skin, where they sit like small land mines for days, months, or years. One day something triggers them (sunlight, iodine in a cleanser, etc.) into bursting forth as the immune system of the skin begins attacking the deposits, forming the blisters. However, the antibodies originate from the intestine when it is exposed to gluten.
VILLI DAMAGE
Both iron and folic acid are absorbed in the first third of the small intestine, which is often where much of the villi damage occurs in celiacs. Other nutrients can be absorbed further down in the small intestine. This explains why newly-diagnosed celiacs often have unexplained anemia and/or low folic acid levels with no other apparent symptoms.
CHANGES IN CRITERIAIn recent years the "typical" presentation of CD has been changing. CD tends to appear at an older age now. The symptoms are more often atypical instead of the "classic" symptoms of diarrhea, bloating, wasting, and fatty, smelly stools. It is diagnosed more often in adults now than in children. The pediatric age of diagnosis is now 4-7 years, whereas it was much younger in the past. There tends to be less marked growth retardation and fewer deficiencies in newly-diagnosed celiacs, [because of recognition of the early symptoms.
Ed.].THE MANY REASONS
Breast feeding is encouraged today, whereas in the past it was actually discouraged; this means the introduction of gluten to the diet will occur later. Also, the IgA/IgG antibody blood tests often help to "find" celiacs sooner, before damage has become too severe. There is a trend towards more aggressive screening for CD in many countries.
CELIAC DISEASE DIAGNOSIS
The rate in Europe varies from 1:200 (one out of every 200 people) to 1:2,000.
It appears to be rare in Negroid and Asian populations.
The rate of diagnosis in most areas is proportional to the degree of suspicion!
6% of adult Type I diabetics in Iowa have CD.
1:10,000 children in Buffalo, New York have been diagnosed with CD.
1:4,700 Olmsted, Minnesota residents have been diagnosed with CD (from a Mayo Clinic study).
The rate in healthy blood donors in most tested countries varies from 1:100 to 1:300.
Among diagnosed celiacs, the ratio of females to males is 2:1. However, in screening tests the ratio is 1:1. Does this occur because males delay in seeking medical help?
INCREASES IN DIAGNOSES:At the University of Iowa, the rate of diagnosis has gone up dramatically, perhaps because there is a higher degree of suspicion regarding CD. Prior to 1988, about 2 cases of CD were diagnosed per year at the University of Iowa. In 1991, there were 18.
Currently 55-60 Iowa cases of CD are diagnosed per year!
From 1980-1988 in Iowa,70% of the diagnosed celiacs presented with "classic" celiac symptoms. Since 1992, only about 30% have the classic symptoms at the time of diagnosis.
[This suggests that the remaining 70% display the so-called "atypical" symptoms. Because of improved diagnoses, a redefining of terms is essential. rjp, Ed].OTHER MALADIES
Many celiacs have been diagnosed or misdiagnosed with other maladies prior to their diagnosis of CD, including:
Irritable bowel syndrome (IBS), sometimes a catchall for unexplained GI symptoms
Primary lactose intolerance
Inflammatory bowel disease (IBD)
Psychiatric illness
Pernicious anemia
Menstrual blood loss
Peptic ulcer disease
Diabetic diarrhea
Chronic fatigue syndrome
Giardia
Pancreatitis/SOD dysfunction
Fibromyalgia
Fiber deficiency
Multiple Sclerosis
LOOKING AGGRESSIVELY
Dr. Murray believes in aggressively looking for CD:
If you are already doing an endoscopy, then always do a duodenal biopsy. You are "down there" anyway, and it only takes a few more minutes.
Screen all high-risk groups for CD. Along with the "usual" groups, you should look at those with IgA deficiency (which is more common in celiacs) and Caucasians with lactose intolerance.
Look for CD in children with non-specific abdominal pain.
PSYCHOLOGICAL PROBLEMS
Many factors can lead to psychological problems in untreated or undiagnosed celiac patients:
1. Fatigue 2. Feeling Ill 3. Dietary illness 4. Social isolation 5. Vitamin deficiencies
6. Direct toxic effect of gluten on a leaky gut.
RECOMMENDED FOLLOW-UP
·
Ensure a well-balanced gluten-free diet.·
Take vitamins for 100% of the Recommended Daily Allowance [RDA].·
Take Calcium and Magnesium supplements.·
Cholesterol may rise, since malabsorption may have caused it to be unnaturally low.·
Check for lactose intolerance after the villi have healed.·
Check for complications and associated diseases such as bone density problems.
A RECOMMENDED TEXT
Dr. Murray recommends the book Celiac Disease, by Michael Marsh, (Blackwell Scientific Publications, Nov. 1992) to physicians associated with Celiac patients. It thoroughly explains the disease. It's priced at about $175.00, well worth the cost if it helps a physician become more interested and to learn about this misunderstood disease.
Contact Dr. Murray at:
Dr. Joseph Murray, Mayo Clinic, 200 1st Street SW, Rochester, Minnesota 55905, [507] 284-2631 % Carol
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CELIAC SPRUE RESEARCH UPDATE
by KENNETH FINE, MD
Dr. Fine has been serving the celiac/gluten sensitive community as a clinical researcher, support group advisor and clinician for over 12 years.
I would like to announce the formation of two new public service websites serving the needs of the celiac and gluten sensitive community. The first is a website called FINERHEALTH AND NUTRITION at the address www.finerhealth.com containing a wealth of information on celiac sprue and the closely related syndrome, microscopic colitis. I have made myself available for consultation by phone for anyone feeling they need guidance relating to celiac sprue, microscopic colitis, or for more general preventive health-related issues. Gluten-free dietary consultation with experienced registered dietitians also is offered. Online "chats" take place Sundays through Wednesdays beginning at 8:00 PM US Central time for topics related to celiac sprue. The chat room is available to anyone anytime. There are slide shows of medical information and intestinal biopsy and endoscopy photographs relating to celiac sprue and microscopic colitis, as well as a very large message board.
To help potential celiacs or their family members in need of testing for immunologic reactions to gluten and other dietary sensitivities, I have devised a mechanism for such individuals to be tested by mail without a blood test or intestinal biopsy. The new stool test I have developed is carried out in a specialty laboratory called ENTEROLAB and can determine if an individual is gluten-sensitive and/or is experiencing malabsorption of nutrients and vitamins. Through extensive research, the test has proven to be more sensitive than blood antibody screening for antigliadin and antitissue transglutaminase antibodies, the diagnostic antibodies for this syndrome. The testing can be carried for a cost below that of most commercial laboratories' gluten sensitivity testing panels. At a relatively low cost this test can also be carried out by mail without drawing blood. In this way, all samples can be collected by the individual at home and returned to EnteroLab by overnight mail. Tests can be ordered at www.enterolab.com
As an extension of the services offered at FinerHealthTM & Nutrition Nutrition & EnteroLabTM, I have founded the INTESTINAL HEALTH INSTITUTE to serve the public directly through medical research, education and awareness. Additional information on the Intestinal Health Institute is located at www.intestinalhealth.org. Proceeds from the consulting and lab testing service are donated to this institute.
Thank you for your interest in FinerHealth and Nutrition, EnteroLab, and the Intestinal Health Institute. My interest is in helping those who suffer needlessly from gluten and other food sensitivities. Please let me know how I may serve you. You may phone: [972] 686-6869. Kenneth Fine, MD.
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2. Dermatitis Herpetiformis
What is
Dermatitis Herpetiformis?CSA/USA Brochure
Dermatitis Herpetiformis is a form of gluten-sensitive enteropathy in which the skin is the major organ involved, with skin manifestations usually the most prominent. Red raised patches of skin develop with tiny blisters. These are accompanied with burning and itching. There may be raised swollen areas that appear similar to patches of hives.
The most common areas of occurrence are the elbows and knees, along with the buttocks, the shoulder blades, and face involved, with the eruptions frequently appearing symmetrically. Eruptions can also occur in the mouth, but are not as common. The severity of the symptoms varies and can wax and wane when untreated. It can appear at any time after wheat, rye, or barley, are added to the diet, but occurs more often after the teen years.
It has been generally recognized that all patients with DH show similar intestinal damage, although often less severe, as those seen in Celiac Disease. There are some medications available for treating the rash, but the medication [Dapsone] does not heal the damage to the intestinal mucosa. If grains are consumed, damage to the mucosa continues with repeated damage causing the greatest health risk.
CSA/USA: Celiac Sprue Association/US of A, Inc.Box 31700, Omaha, Nebraska 68131-0700 [402] 558-0600
Dermatitis Herpetiformis
P. Brian Rogers,
M.D., PS. Dermatology & Allergy1727 West College Avenue Bozeman, Montana 59715 [406] 587-4432
DERMATITIS HERPETIFORMIS was first described by Louis Duhring in 1884. This is a rare blistering disease of the skin with an unknown prevalence. It is very rare in blacks and almost unheard of in Japanese people. The peak incidence of DH is in the 2nd, 3rd, and 4th decades of life.
The primary skin lesion in dermatitis herpetiformis is an extremely itchy vesicle or blister. Occasionally hive-like plaques or erythematous papules are also seen. The lesions have symmetrical grouping and often are found over the elbows, knees, shoulders, buttocks, and sacrum. A biopsy of the lesions shows a blister beneath the epidermis with collections of neutrophils [white blood cells] in the upper layers of the dermis. Immunofluorescence shows a granular deposition of IgA ,one of the five types of immunoglobulins normally found in all humans.
Dermatitis herpetiformis is thought to result from a hyperresponsive immune system. This disease most commonly occurs in a certain genetic type termed HLA B-8. Other diseases of the immune system sharing this genetic characteristic include celiac sprue, chronic hepatitis, Grave’s disease [hyperthyroidism], diabetes, and systemic lupus erythematous.
Eighty percent of patients with DH have an abnormal flattening of the villi in the small intestine. It is felt that the wheat-related cereal protein, gluten, is responsible for this change in the intestinal villi. An identical gastrointestinal disorder is found in Celiac Disease.
The mainstay of treating dermatitis herpetiformis is a gluten-free diet. It is felt that avoiding gluten also reduces the chance of lymphoma of the small bowel or adenocarcinoma of the small bowel in patients with both DH and celiac sprue. In addition, patients with DH should avoid iodides since the skin lesions may worsen.
In many patients diet alone can control the disease but if medications are needed Dapson or sulfapyridine are indicated. Dapsone is the more effective of the two and probably works by inhibiting the chemotaxis of neutrophils into the skin. It has numerous side effects such as hemolytic anemia [in people of Mediterranean descent], peripheral neuropathy, liver damage, kidney damage, agranulocytosis, or even psychosis. In the majority of the cases, strict adherence to a gluten-free diet will greatly reduce or eliminate the need for Dapsone or other drugs. Spontaneous remission in this disease is rare, but it has been reported. Brian Rogers, MD.
Dr. Brian Rogers, M.D., P.S., 1727 West College, Bozeman, Montana, 59715 [406] 587-4432
Dermatitis Herpetiformis
by
Dr. Joseph Murray, Mayo Clinic, Rochester, MinnesotaDH is an extremely itchy skin rash. Even poison ivy may not come close according to those who have had both. It affects the elbows, knees, buttocks, back of the head, and scalp. (Dr. Murray described one lady who developed lesions in her outer ear canal). Coming in waves, crops of little bumps appear and soon turn into the extremely itchy blisters.
DH is often considered a skin disease, but that is not strictly true. DH is a manifestation of intestinal intolerance to gluten. Research has been done in which gluten was injected under the skin of DH patients, and it did not produce blisters, because DH is not a skin allergy to gluten. However, if a Dermatitis Herpetiformis patient takes gluten by mouth, lesions can then appear as DH blisters on the skin. Dr. Marsh in Manchester (England) introduced gluten into the rectums of patients and in several instances the patients claimed that attacks of DH followed.
What happens when a DH patient ingests gluten? In the intestine the body’s immune system mounts a response to the gluten. Part of that response is the production of antibodies, which are little chemical messengers the body produces in defense. In DH patients those antibodies often get dumped under the lining of the skin, where they sit like small land mines for days, months, or years. Then one day something triggers them (sunlight, iodine in a cleanser, etc.) and there follows a bursting forth as the skin’s immune system begins attacking the deposits, thereby forming the blisters. But the deposits occur originally when the intestine is exposed to gluten.
DH is the skin manifestation of intestinal gluten sensitivity that is indistinguishable from CD. Most, if not all, DH patients will have some degree of damage in their small intestines, even if they may have no gastrointestinal symptoms
.Q. Is the danger of intestinal cancer as high with DH if the patient is not completely compliant to the GF diet?
"It is probably not quite as high in DH as in CD, but it happens; and there still is occurring an excess of lymphoma patients, especially in middle-aged men."A.
Q. Can you have dermatitis herpetiformis (DH) without having CD?
A. If you have DH, then you have an intestinal sensitivity to gluten that will cause some damage to your intestine and may become more significant as you get older. The treatment for both CD and DH is a GF diet. If you have DH you may...find some relief from dapsone, a medicine that suppresses the symptoms until the diet takes effect.
Dr. Murray is convinced that ALL Dermatitis Herpetiformis [DH] patients also have Celiac Disease, whether they realize it or not. This (type of) Celiac Disease is often latent or silent. Earlier reports of patients with DH who did not have enteropathy may not have counted milder forms of the celiac disease damage.
Since CD is an autoimmune disease, it follows that there are other autoimmune diseases that are associated with it. Rheumatoid Arthritis, Lupus, Type 1 Diabetes, and some eye problems occur more frequently in CS patients. This is not because of gluten or CS itself; it is because CS patients are part of a group that is genetically predisposed toward auto- immune complications.
About 5% of CD patients have DH. At the University of Iowa, there have been 350 patients diagnosed with DH, which Dr. Murray believes have celiac disease. If DH patients are only 5% of the Celiac population, then there would be approximately 7,000 Celiacs in the Iowa area. The number of diagnosed Celiacs is much less than 7,000. Even if this extrapolation is exaggerated, it is still clear that there are many undiagnosed Celiacs in the general population.
Most DH patients are prescribed Dapsone, which treats the symptoms. In many cases, patients are told of the GF diet, but it is not stressed and so most do not follow it.
Dr. Murray finds this most distressing, because even if DH patients do not have GI-related symptoms, there is continuous damage being done to their small intestines.
Dermatologists in general don’t give enough consideration to a gastrointestinal involvement as the source of DH. This places DH patients at an even greater risk of developing lymphoma in the small intestine.
Lymphoma in the small intestine is extremely rare in the general population, while untreated Celiacs have a 70 or 80 times greater chance of developing it. A lifetime of being exposed to gluten gives a Celiac patient about a 7% chance of developing lymphoma. There is also an increased risk of other GI-related and lymphatic cancers. The risk of developing lymphoma immediately begins to decrease when the patient adopts the GF diet. The risk continues to decrease until, after 3-5 years, it approaches that of the general population.
Dr. Murray makes a small intestine X-ray a routine part of the treatment of a newly-diagnosed adult Celiac patient, especially those over 40 years of age. He is looking for lymphoma in the small intestine. It is difficult to detect, but if found can usually be successfully treated.
Dr. Joseph Murray, Mayo Clinic, 200 1st Street SW, Rochester, Minnesota 55905,
[507] 284-2763*****************************************************************************
3. Associated Disorders
Diagnosis of Gluten Sensitivity: Time for a Change?
by KENNETH FINE, MD.
Gastroenterology, Director of FinerHealth & Nutrition, and EnteroLab at WWW.intestinalhealth.orgWhat is the Difference Between Gluten Sensitivity and Celiac Sprue?
Gluten sensitivity implies that a person’s immune system is intolerant of gluten in the diet and is forming antibodies or displaying…evidence of an inflammatory reaction. When reactions cause small intestinal damage visible on a biopsy, the syndrome has been called celiac sprue, celiac disease, or gluten sensitive enteropathy. The clinical definition of celiac sprue usually requires a clinical and/or pathologic improvement following a gluten-free diet.
In the past, celiac sprue could only be diagnosed after certain symptoms developed. A biopsy of the small intestine would be performed and if abnormal and typical of celiac sprue, and if a gluten free diet brought resolution of diarrhea, with weight gain or growth, only then would a diagnosis of celiac sprue be made. However, recent advances in diagnostic screening tests and application of these tests to people at heightened risk or to general populations, have allowed earlier detection of celiac sprue, sometimes even before damage to villi has occurred. This latter scenario would…be called gluten sensitivity.
What Role Does Genetic Testing Play In the Diagnosis of Gluten Sensitivity?
Currently, tests are available to detect the genes that control the immune system's reaction to gluten. These genes are called human leukocyte antigens or HLA. It is a particular type called HLA-DQ that is most useful in the assessment of the probability that a person may be gluten sensitive. The reason gene testing assesses probability rather than disease itself is because some people have the genes for gluten sensitivity but have no detectable evidence of the immune reaction to gluten or have no symptoms. In such people, gluten sensitivity is still possible but the probability is lower than in a person who may be having symptoms attributable to gluten or who has had antibodies detected.
Can I have gluten Sensitivity with Negative Screening Blood Tests?
With heightened awareness of the possibility of gluten sensitivity in family members of diagnosed celiacs, or in people with syndromes associated with celiac sprue, it has become clear that not all people suspected of being immunologically intolerant to gluten have positive blood tests. This is problematic…and is because the reaction to gluten begins inside the intestinal tract, not in the blood per se. I had an idea about a year ago that these antibodies should be more frequently detected in the stool of gluten sensitive individuals than in the blood. This turned out to be the case.
Who Should be Tested for Gluten Sensitivity?
Because my research has shown that as many as 40% of all Americans may be gluten sensitive, and from recent prevalence studies up to 1 in 150 have the severe form of this sensitivity causing celiac sprue, a case can be made that everyone in America should be tested for gluten sensitivity (similar to the concept that everyone should have their cholesterol checked to ensure they are not at high risk for having a heart attack). However, there are people with various risk factors or diseases who are at greater risk and should undoubtedly be tested.
ASSOCIATED DISORDERS, Kenneth Fine, MD
: People with the Following Conditions are at Increased Risk for Gluten Sensitivity/Celiac Sprue:|
Relatives of gluten-sensitive individuals Microscopic colitis Chronic diarrhea of unknown origin Hepatitis C Autoimmune liver disease Other causes of chronic liver disease Dermatitis herpetiformis Diabetes mellitus, type 1 Rheumatoid arthritis Sjogren's syndrome Lupus Autoimmune thyroid disease Any autoimmune syndrome Asthma |
Osteoporosis Iron deficiency Short stature in children Down's syndrome Mothers of kids with neural tube defects Female infertility Peripheral neuropathy Seizure disorders Irritable bowel syndrome Inflammatory bowel disease Gastroesophageal reflux disease Autism AIDS |
Kenneth Fine, MD, 10851 Ferguson Rd., Suite B, Dallas, TX 75228, [972] 686-6869
Down’s Syndrome
by
Dr. Lloyd Rosenvold, 1992Down’s Syndrome (DS) is a genetic birth abnormality that occurs in about 1:700 live births. The genetic defect is situated on chromosome #21 and at birth these children usually have 47 chromosomes instead of the normal 46.
The infants suffer from weakness, misshaped small heads and mental deficiencies. Most do well to have an IQ of about 50. Many die at a young age but some live on into middle life of 30s and 40s. General development is much slower than that of normal children. The facial appearance is Mongoloid and for that reason the condition is often referred to as mongolism. Other congenital defects and skeletal deformities are not regarded with surprise in these cases. There has been no treatment of value for these patients except to provide good custodial and nutritive care in order to make the best of a disappointing situation.
An Australian physician, Chris Reading, together with associates, has over a period of years carefully evaluated the family histories of more than 2000 patients. Among many of his discoveries relating to genetic data, he relates that out of the 18 children who had Down’s Syndrome, 17 positively had gluten intolerance. In the remaining case he suspected gluten intolerance in that child also.
Dr. Reading found that by placing the DS children on a gluten-free diet fortified with various vitamins and minerals he could report as follows: the DS children "have made rapid and measurable improvement in height, head circumference, weight, mental and motor development and general health."
Having observed that these children seemed to be deficient in various minerals and vitamins, and knowing that persons with gluten intolerance all have a malabsorption problem with nutrients, Dr. Reading fortified their diets with formulations featuring vitamins: B1, niacin, B12 and various minerals, particularly zinc. Certainly if I had a Down’s Syndrome child in my family I would not hesitate to investigate whether or not the child also had celiac disease. There could be much to gain, and nothing to lose, investigating the possibility of there being a concomitant presence of celiac disease.
DS children should all be tested for gluten intolerance and if any are found they should be placed on a gluten-free program. In fact, it would be well for the mother to also be tested. We don’t know yet if any gluten-derived toxins might be transmitted in breast milk to an infant. Lloyd Rosenvold, MD
To order Can a Gluten-Free Diet Help? How? write to Dr. Lloyd Rosenvold, % Mrs. Leola Rosenvold, Box 330 Hope, Idaho 83836
Schizophrenia
by Lloyd Rosenvold, MD, box 330 Hope, Idaho 83836
CAN A GLUTEN-FREE DIET HELP? HOW?
Republished 2001For many years the cause of schizophrenia was shrouded in mystery. But a few decades ago it became evident that altered brain chemistry was involved and then followed suitable drugs that could modify the chemistry. A number of investigators have now demonstrated that diet and nutrition can be definite factors in causing the disease. In the Fall 1966 issue of Clinical Ecology, Beatrice Trum Hunter has made an extensive review of the literature on the topic. Here are some of her findings:
Is gluten Intolerance related to schizophrenia? Dohan (Dr. F. Curtis Dohan of the Medical College of Pennsylvania) thinks that it is. He has been studying the biochemical associations with schizophrenia. As early as 1966, he reported four observations:
1. Children with celiac disease, more often than by mere chance, become schizophrenic adults.
2. Psychoses occur in adult celiacs more often than by mere chance.
3. Gluten can induce common behavioral disturbances in both children and adults who are celiacs, and these disturbances subside after introduction of a gluten-free diet.
4. Often, during times of psychic stress or acute infection, the severity of celiac disease symptoms increases. In some instances, this is accompanied by an increased severity of schizophrenic symptoms.
Dohan suggested that in gluten-intolerant individuals, gluten may enter the brain and affect the nerve receptor sites. Peptides from gliadin may be the neuroactive substances that go from gut to brain. Dohan's subsequent studies strengthened his original observations.
About ten years after Dohan's initial report, MM Singh and SR Kay of the Bronx Psychiatric Center studied schizophrenics who had been improved under neuroleptic drug therapy and who were on cereal grain-free diets.
When adding gluten foods they noted that the patients regressed in their improvement and after removing the gluten challenge they would improve again. Suitable control cases were maintained. They concluded that there were schizophrenia-promoting properties in the wheat gluten. (Their findings were reported in Science magazine 191:401-402, 1976.)
Other studies have demonstrated that where gluten-containing grains are freely used, such areas have a higher incidence of celiac disease than areas that are similar except for a lower use of the cereals.
Other associated disorders Gluten-Free Friends, MCS Student Brochure, R. Jean Powell, Editor
The following disorders have a related incidence with Celiac Disease that is significantly higher than the general population incidence:
ADULTS: Arthritis, Chronic Anemia, Type II Diabetes Mellitus, Fibromyalgia, IBS, Infertility, Intestinal Lymphoma, Lactose Intolerance, Lupus, Osteomalacia & Osteoporosis, Multiple Sclerosis-type Neuropathy, Sjögren's Syndrome, Thyroid Disorders.
CHILDREN: ADD, Chronic Anemia, Type I Diabetes Mellitus, Down's Syndrome, Osteomalacia [Rickets], Seizures, Schizophrenia, Short Stature.
At Denver Children's Hospital, Denver, Colorado, pediatric patients with Diabetes Mellitus are routinely tested for Celiac Disease.
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4. Reproductive Disorders
Infertility by Dr. Lloyd Rosenvold
Millions of couples sorrow over their infertility—inability to bear children. Millions of dollars are spent each year of sophisticated tests and procedure to overcome or circumvent this disability. Individual couples may spend thousands of dollars in the process—at times fruitlessly. The problem may lie sometimes in the female, and sometimes in the male, partner.
A recent report from Ireland (Ulster Medical Journal 57 (1): 88-89, 1998) details a case of infertility of at least three years' duration. Merely two months after undertaking a gluten-free (GF) diet, the individual was able to conceive.
The investigators mention that there have been other cases of infertility (both male and female) with fertility restored by changing to a GF diet.
We know of no extensive data on how dependable this method for overcoming infertility might be statistically. And in no way would we wish to lead to the impression that this method is a cure-all. But a trial of a GF diet by both parties for several months might merit consideration, if it is seriously believed that there is other evidence that CD exists. Certainly the dietary trial costs essentially nothing but some diligent kitchen effort.
by Lloyd Rosenvold, MD: Can A Gluten-Free Diet Help? How? (2001 Revision) Box 330 Hope, Idaho, 83836Celiac Sprue & Pregnancy
by Gainer & Phillips <