Thursday, 9 May 2013

Testing Blood and Biopsy. Yes, I'm against it.

Here is a paper I picked up years ago and had posted in the files of my long defunct yahoo support group.

I didn't want to lose it again and so just copied it here in case it would be useful to others considering testing.

Testing is tricky for many reasons:

1. Not accurate. Many, many false negatives.

2. If you have cut gluten out of your diet, adding it back in for the sake of testing could land you with extra chronic issues:

thyroid disorder
irreparable intestinal damage

3. Less than Marsh III and you don't get Celiac diagnosis.

4. Government does not give tax breaks on meat, fruit and veggies.

5. Gluten free junk food, just because you get a tax break, does not warrant ingestion. 
     It is not a REQUIRED food source.

I have more but am so limited in time these days. 
Please do sit down with a tea and read this VERY interesting article.

                    The Widening Spectrum of Celiac Disease
                              by Joseph Murray, MD, PhD
                   summarised by Jim Lyles (Sprue-nik Press, Nov. 1996)

        Dr Joseph Murray, one of the leading US physicians in the diagnosis
        of celiac disease (CD) and dermatitis herpetiformis (DH),
        originally came from Ireland and got his
        medical degree and a doctorate from the National University of Ireland
        in Galway.  His residency was at the University of Dublin and he
        completed his fellowship in gastroenterology at the University of Iowa
        College of Medicine, where he has been since 1988.  What follows are
        some highlights of a talk by Dr Murray in November, 1996.

        Dr Murray started off by endearing himself to the audience:  He
        spoke of TCCSSG in glowing terms and compared our group favorably with
        other active support organizations, both local and national.  Because
        our newsletter appears on the Internet, he wanted us to know that we
        are helping not only our local members but also people thousands of
        miles away.

        The Standard Definition of CD

        Dr Murray gave us the "standard" definition of CD:  "CD is a
        permanent intolerance to gluten that results in damage to the
        intestine and is reversible with avoidance of dietary gluten."  There
        are some important parts in this definition:

          *  "permanent":  The effects of CD may change from time to time.
             You may be sicker at one phase of your life than at another.  For
             example, you may be sicker at age two, may seem to get better
             during the teenage years, may be sick again in your 20's (but
             with different symptoms), and then present with bone problems
             when you are in your 50's.  So there may be different phases, but
             it is a PERMANENT intolerance.  You do NOT outgrow it; you do not
             go through phases where you don't have it anymore.  (That used to
             be what was thought and TAUGHT in medical schools.)

          *  "damage to the intestine":  There is definitely intestinal
             damage; without it you cannot define CD.  For some people the
             damage is severe, for others it is not so severe.  It is the
             cases which are not so severe that can be difficult to diagnose.
             If the damage is mild then the person interpreting the biopsy
             might not even think of CD as being a possible cause of the

          *  "reversible":  The damage should be reversible.  Dr. Murray says
             there are about 5% of people with what he believes is CD in whom
             at one point in their lives the damage becomes irreversible.  In
             these cases there is intestinal damage that does not completely
             recover.  It may partially heal, but not completely.  One can
             infer that they have the same condition as celiacs that do
             recover, based on their history.  There may be something
             different about that group of patients in their immune systems
             that makes them different, but that is an area that is still
             being actively researched.

        Effects of CD
        "Classic" CD is what most medical students are taught about.  It is
        characterized by diarrhea, steatorrhea (smelly, floating, pasty, fatty
        stools), weight loss, abdominal bloating or distention, and flatulence
        (farting [yes, he really did say that--ed.]).

        Dr. Murray showed a lovely slide depicting steatorrhea, but warned
        that you can't identify it just from its appearance; it is the smell
        that distinguishes it.  There is nothing that smells quite like
        steatorrhea.  (Dr. Murray admitted that he sometimes has trouble
        keeping nurses in his clinic because he does frequently collect stool
        samples, which they find rather "challenging".)  Steatorrhea (fat in
        the stool) was thought to be synonymous with CD.  In fact, CD has also
        been called idiopathic steatorrhea, which refers specifically to this
        particular symptom.  So it was thought that if you didn't have this
        symptom, you didn't have CD.  Nothing could be further from the truth;
        Dr. Murray says fewer than a third of his celiac patients have ever
        produced this sort of stool.

        What are the consequences of the damage to the small intestine?

          * Anemia, particularly iron-deficiency anemia or folate-deficiency anemia.  
          Why these two types (there are other types of anemia)?
             Because iron and folic acid are absorbed in the first part of the
             small intestine, which is also the part that is most affected by

          * Hypocalcimia (low calcium level).  This happens for two reasons:
             1) You are deficient in Vitamin D, a fat-soluble vitamin.  Fat
             mostly passes through the intestine into the stool, and carries
             the fat-soluble vitamins with it.  2) If there is severe damage
             throughout the small intestine, then calcium is not going to be
             absorbed well.

          *  Other fat-soluble vitamin deficiencies:  Vitamin E, which can be
             related to nerve damage; Vitamin A, which can cause night
             blindness; and Vitamin K, which is for blood clotting (lack of
             Vitamin K can lead to nosebleeds, easy bruising, or easy

        Dr Murray then showed a few pictures of a young woman who is one of
        his more unusual celiac patients:  She was extremely obese.  She was
        an inpatient at the hospital on the psychiatry floor (which is
        interesting in itself).  She had complained of nighttime abdominal
        pain.  The most common cause of this symptom is a regular duodenal
        ulcer, but medication to treat an ulcer wasn't working so the
        gastrointestinal (GI) department was consulted.  They performed an
        endoscopy, expecting to find an ulcer.  They also did a biopsy because
        that is Dr. Murray's habit whenever he does an endoscopy.  They were
        surprised to find active CD.  Her symptoms were chronic constipation
        (she had diarrhea as a child), malodorous flatus (smelly gas), had
        gained 200 lbs.  in the preceding four years, and practiced
        lactose-avoidance.  Being overweight and constipated, she was just
        about the exact opposite of what most people would conceive of as the
        typical celiac.  She had completely normal serum chemistries.  Routine
        blood tests were normal; there was no clue to the physician suggesting
        CD.  Yet the biopsy showed completely flattened villi and an antiendomysial
        antibody test came back positive.  She had a good clinical response to a 
        gluten-free (GF) diet which included some weight loss.

        The degree or type of symptoms that a person with CD presents with
        does NOT depend on the severity of the disease where you take the
        biopsy.  In CD the damage starts in the intestine just after the
        stomach and works its way down.  The small intestine is about 26 feet
        long and has a tremendous ability to compensate.  So if the damage is
        mostly near the stomach (which is where biopsies are done) then you
        may never have diarrhea; the rest of the small intestine can
        compensate and absorb all the liquid and food that passes by the first
        few damaged feet.

        When somebody presents with severe diarrhea and wasting, that means
        most of the small intestine is damaged and it is not able to
        compensate for the damage closer to the stomach.  So it is the amount
        of the small intestine that is damaged which determines the symptoms.
        If you have all of the small intestine damaged you'll have diarrhea and 
        weight loss.  If only a small portion of the small intestine is
        damaged, you may have pain, bloating, and discomfort after eating but
        not diarrhea.
        Dr Murray discussed some of the different types of presentations
        that they see at the University of Iowa:

          *  Iron-deficiency anemia.  At the University of Iowa this is the
             most common symptom other than diarrhea.

          *  Lactose intolerance.  This is a very common cause of diarrhea in
             certain populations, including people of African and Asian
             descent.  In these populations lactose intolerance is genetically
             predetermined.  Something happens in the lining of their
             intestine at a certain age that makes them unable to break down
             lactose.  (Lactose is milk sugar.  It has nothing to do with the
             fat content of the milk.)  In Caucasians this genetically
             predetermined lactose intolerance is not very common, occurring
             in less than 5% of the population.  So when a Caucasian complains
             of lactose intolerance Dr. Murray looks for damage to the small
             intestine as a possible cause.

          *  Constipation.  About 20% of Dr. Murray's celiac patients present
             with constipation instead of diarrhea.

          *  "Nutritionally-compensated".  In other words, they are not skinny
             and have never been skinny.

          *  Osteopenia.  This refers to weak, thin bones.

          *  Chronic fatigue.  This is a very common symptom in untreated celiacs.

          * Arthralgias.  These are joint aches or pains.

          *  Brittle diabetes.  [This is a form of Type I diabetes that is
             difficult to control--Dr. Alexander.]

          *  Short stature.  Many people with CD are short.  Untreated CD can
             cause malabsorption of nutrients.  Lack of nutrition in turn can
             cause short stature in children, in which they fail to follow a
             normal growth curve.  Of course there are also many tall celiacs.
             But if you are a celiac and you have a child that isn't growing,
             even if there are no GI symptoms you should consider CD as one of
             the possible causes.

          *  Neurological disorders.  There are some associated neurological
             disorders.  Thankfully these are fairly rare.

          *  Dental enamel defects.  This is a problem when CD is otherwise
             silent in children during the time when their permanent teeth are
             developing.  What happens is the enamel (the hard coating on your
             teeth) does not develop properly.  With no enamel, your teeth
             wear down and you get cavities very quickly.  Dr. Murray has
             seen terrible dental loss in 20-year-old celiacs, where they've
             lost an entire mouthful of teeth.  This is not as much of a
             problem in the United States as it is in other countries, where
             dental care is not as frequent and aggressive.  If dental enamel
             defects are detected, you can't really regrow it because it has
             never developed.  But now there are new dental bonding techniques
             where they can put special films over the tooth to protect the
             defective area.

        As we see, CD can present in its "classic" form with multiple symptoms
        such as steatorrhea, weight loss, typical blood test abnormalities,
        and a flat biopsy.  But perhaps more often it presents in an
        "atypical" form with only one symptom such as anemia or bone problems.
        In atypical cases the biopsies are not always flat; there may be
        varying degrees of damage.

        Lactose Intolerance
        Dr Murray revisited the topic of lactose intolerance.  About 50% of
        celiac patients are lactose intolerant at the time of diagnosis.  Here
        is why:

        Lactose is a double sugar.  The small intestine has an enzyme called
        lactase which breaks that double sugar down into single sugars which
        your body can then absorb.  Lactase is produced right at the tips of
        the villi.  If the villi are damaged then you can't produce that
        enzyme to split that double sugar.  So the lactose stays intact in the
        intestine, passes through it, and then acts as a laxative.  You will
        get diarrhea, bloating, or gas, depending on the severity of the

        After you go on a GF diet and get healing in your intestine, usually
        those villi will regenerate and begin producing lactase again,
        allowing your body to break down the lactose and absorb it.  Dr.
        Murray looks for improvement in lactose tolerance as a measure of
        healing.  If you do not recover the ability to digest lactose, then
        either the intestine has not yet healed or you are one of the few celiacs 
        that are also genetically-predetermined to never be able to
        break down lactose, as was discussed earlier.  So continued lactose
        intolerance is not necessarily a sign of villi damage (though highly
        suggestive); but improvement in lactose tolerance is a sign of

        Dr Murray tells patients who have a lot of problems with milk to
        wait about six months after starting a GF diet before trying it again.
        After about six months they should start testing themselves with a
        little skim milk first thing in the morning, to see if they get any
        symptoms.  If they get symptoms (bloating, gas, or diarrhea) then they
        probably are still lactose intolerant.  If that continues then they
        need to revisit their doctor to find out if there is still evidence of
        damage in the intestine.

        The important point is that in most (over 90 percent) newly-diagnosed 
        celiacs with lactose intolerance, it should get better.

        Dermatitis Herpetiformis
        Next Dr Murray discussed dermatitis herpetiformis (DH).  DH is an
        extremely itchy skin rash.  There is nothing that is as itchy as DH;
        even poison ivy may not come close according to those who have had
        both.  It effects the elbows, knees, buttocks, back of the head, and
        scalp.  Dr. Murray even had one lady who got it in her outer ear
        canal.  It comes on in waves.  Crops of little bumps appear and soon
        turn into blisters that are extremely itchy.

        DH is often thought of as 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 has been injected under the
        skin of DH patients, and it does not produce a blister.  So DH is NOT
        a skin allergy to gluten.

        However, if a DH patient takes gluten by the mouth, then it can come
        out as DH on the skin.  In fact, Dr. Marsh in Manchester (England)
        has put gluten in the rectum and in a couple of cases he had DH
        patients claim that they got an attack of DH afterwards.

        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 like little
        chemical messengers the body produces to attack things and help defend
        itself.  In DH patients those antibodies often get dumped under the
        lining of the skin, where they just sit like little land mines for
        days, months, or years.  Then one day something triggers them
        (sunlight, iodine in a cleanser, etc.)  and you get this little
        bursting forth as the skin's immune system begins attacking these
        deposits thus forming the blisters.  But the deposits occur originally
        due to the intestine being exposed to gluten.

        So DH is the skin manifestation of intestinal gluten sensitivity which
        is indistinguishable from CD.  Most, if not all, DH patients will have
        some degree of damage in their small intestines.  They may have no GI
        symptoms but they have some degree of damage.

        Villi Damage
        The villi are the most important part of the absorptive system in the
        small intestine.  Normal villi are long and slender, giving a healthy
        small intestine the appearance of a deep pile carpet.  All these villi
        give the small intestine an enormous absorptive surface; if laid out
        flat it would cover an area the size of a tennis court.

        Now consider the "worst case" scenario for CD, where the villi are
        completely flattened.  This decreases the absorptive surface down from
        a tennis court to about the size of a small table.  So you have a
        dramatic reduction in the amount of area for digesting and absorbing
        nutrition from your food.  But there are other factors to consider as
        well.  The villi aren't just flattened, they are also inflamed; just
        like your skin is inflamed after being burned.  It can produce pain.
        (But the pain is not as obvious and localized as it is for inflamed
        skin; you just know that there is pain in there somewhere.)

        Often the villi are not completely flat.  Dr. Murray showed a slide
        in which the villi were a little "stubby".  In these cases the villi
        are still different enough to be classified as not fully formed.  But
        then he showed a slide in which the villi appeared to be normal size.
        Many pathologists would look at such a case and be tempted to rule out
        CD as a possibility.  However, if you carefully examine the surface of
        the villi you'll see that there is a marked increase in lymphocytes,
        the small immune cells that reside in the intestine.  It is the
        lymphocytes which are mostly responsible for the damage in the small
        intestine.  These are the cells that are responding to gluten.

        Dr Murray talked about five degrees of severity of villi damage:

          1. Healthy, undamaged villi.

          2. Infiltrated villi.  The villi are still standing up long and
             straight, but the is an increase in the surface lymphocytes.

          3. Partially-shortened villi.  The villi are somewhat short and
             stubby, and the crypts (the basement parts of the villi) are
             expanding and becoming inflamed.

          4. Flattened villi.  This is the typical or classic form of CD, in
             which the villi are destroyed.

          5. Burned-out villi.  This can occur in older celiacs, where the
             villi don't necessarily have the ability to recover on a GF diet.

        Causes of CD
        There are three factors involved in CD:

          *  the immune system
          *  environment
          *  genetics

        The immune system comes into play through the lymphocytes we
        previously discussed.  There are lymphocytes in the intestines of
        celiac patients that respond specifically to something in gluten.
        These are called T-cells, and are actually responsible for the damage
        in the villi.  There are also cytokines, which are chemical messengers
        floating around that our bodies produce to fight infection.  The
        lymphocytes also produce cytokines which cause even more damage.

        The environment comes into play in the form of gluten.  For example,
        in the early '70s there was a trend towards a macrobiotic diet,
        meaning a lot of grains.  As a result, a lot of people presented with
        celiac disease.  This was a result of challenging themselves with a
        lot of gluten, causing the damage in the intestine to become more
        extensive.  So a gluten challenge can cause symptoms, though Dr.
        Murray does not think it triggers the disease itself.  Instead, some
        other event may "trigger" the beginning of CD.  Possible triggers of
        CD include:

          *  A significant change in nutritional status (such as deciding to
             lose weight).

          *  An infection.  Any kind of infection can inflame the lymphocytes
             in the intestine so that they start responding, possibly to

          *  The aftermath of pregnancy.  During pregnancy the body's immune
             system must be prevented from responding to the fetus, which is a
             foreign organism that is immunologically separate from the
             mother.  So the immune system is suppressed to accommodate that
             foreign being.  Immediately after delivery the immune system
             reconstitutes and raises its defenses.  What happens is that any
             kind of autoimmune disease can get worse after delivery, and one
             of these is CD.  Many of Dr. Murray's patients' symptoms started
             after childbirth; though not necessarily after the first child.
             Sometimes symptoms would start after the second, third, or even
             fourth child.

             DH is different and often gets worse during pregnancy, not
             afterwards.  It is not clear why, though it is thought to have
             something to do with changes in the skin.

          *  Surgery.  It is thought that this also has something to do with
             stimulating the immune system.

        There is a tissue type called HLA.  This is similar in nature to blood
        types, where A, B, and O are the three standard blood types.  Tissue
        typing takes that a whole generation further, taking it down to very
        specific subtypes of the genetic material in our white blood cells
        (and most other cells in the body).  It identifies us as "self",
        because we have a specific genetic type in our cells.  Our body uses
        this to avoid attacking anything that it can identify as "self";
        anything else it readily attacks.  This is what makes organ
        transplants difficult.  The body automatically recognizes the
        transplanted organ as a foreign body and tries to attack it as an
        invader.  It is the immune system that mounts this attack, and one of
        the things it uses to distinguish foreign bodies from "self" is the
        HLA typing in the body's cells.

        Why is this relevant for celiacs?  There is a very particular tissue
        type that is seen in most celiacs called DQ2.  (Dr. Murray noted that
        the HLA names keep changing every year or two, so that a different
        term might be in use now; but DQ2 was what it was previously called.)
        Studies in the USA on this subject are sparse, but in studies in
        Czechoslovakia, the United Kingdom, and Italy 87% or more of the celiacs 
        had this tissue type.

        The risk of CD increases within the families of known celiacs.
        According to Dr. Murray, here are the approximate risk factors for
        various relatives of a diagnosed celiac:

          -- identical twin:  70% (but not 100%, thus proving CD is not
                entirely genetic)
          -- HLA-matched sibling:  30-40%
          -- non-HLA-matched sibling:  10% (some say even 20%)
          -- child:  less than 10%
          -- parent:  5-7%
          -- others (nieces, nephews, grandparents, grandchildren):  even less

        Why is there a difference in risk factors for an identical twin and an
        HLA-matched sibling?  Clearly there must be another gene involved
        besides the known DQ2 tissue type.  Up until three months ago we
        didn't have any clue as to what that other gene might be.  But at the
        symposium in Finland<1> a collaborative study done jointly in Galway,
        Ireland and Alabama, USA provided some new information.  A series of
        families from the Galway group were studied.  A new method of looking
        for gene site associations was used.  They took some of the
        chromosomes from blood samples of these patients and looked for
        genetic similarities.  [Human beings have 23 pairs of chromosomes.
        Each chromosome is composed of a multitude of genes.--editor] They
        found one spot on chromosome #6 which it seemed to be very highly
        associated with CD; in other words, those that have CD seem to have
        this "spot" on chromosome #6; those that did not have CD did not tend
        to have this "spot".  It is not known what the genes in that "spot"
        do, because i t is one of those uncharted areas of human genetics.  It
        is hoped that over the next two years we will learn which specific
        gene is involved and how it confers a risk for CD.  So there are
        probably at least two separate genes that come together to result in a
        genetic predisposition towards CD.

        Prevalence of CD
        How common is CD?  A few years ago it was thought that the prevalence
        of CD in Europe varied from 1:300 (one out of 300 people) to 1:2000.
        Now the figures vary from 1:90 to 1:600, depending on which study you
        look at.  These figures are mostly based on studies involving
        anonymous blood donors, or screening healthy populations such as
        school children.  These figures are not based on going to hospitals
        and counting the number of diagnosed celiacs.

        CD is rare in the Negroid and Asian races, though not unheard of.
        This may be because the major starch in China and Africa was not wheat
        until fairly recently.  So until these populations are exposed to
        large amounts of wheat, we may not know what the true prevalence of CD
        is in those countries.

        The rate of diagnosis of CD seems to be directly related to the level
        of suspicion of the doctor, hospital, or health care system.  It has
        been well-studied in places like Scotland where the rate of diagnosis
        in one area is found to be high and then in another area it is much
        lower.  Then someone with an interest in CD transfers to the second
        area and the rate of diagnosis of CD suddenly increases.

        There are some population differences that have been noted.  For
        instance, in Sweden CD is very common and mostly diagnosed in
        childhood.  But in neighboring Finland CD tends to be diagnosed more
        often in adults than in children.  In the USA the vast majority are
        diagnosed during adulthood.  At the University of Iowa the rate is 30
        or 40 adults diagnosed with CD for each child.  How does one explain
        these differences.  Is it because the adult doctors aren't looking for
        CD in Sweden and the pediatricians aren't looking for it in the USA?
        Dr. Murray doesn't think so; he believes there truly is a difference
        in the age at which CD is presenting in these countries.  At the
        Finland symposium there was some discussion on this topic.  In Sweden
        commercial baby food products have a lot of wheat in them.  (In the
        past they had lots of milk protein in them, and they changed it 20-30
        years ago due to the incidence of milk allergies.)

        Incidentally, nearly the exact opposite happened in England & Ireland
        in the 1970's.  It had been general practice to begin feeding some
        type of cereal such as oatmeal to a baby as early as two weeks of age.
        Breastfeeding was done only in 10% of the children beyond the age of
        six weeks.  As a result there were several very young celiacs diagnosed.  
        However, due to the incidence of CD public health nurses
        began advising new mothers to avoid giving gluten to their babies
        before the age of one year, and to avoid solids altogether for the
        first four months or so.  As a result the entire feeding patterns of
        infants changed within a year or two and diagnosis of CD in very young
        children dropped considerably.

        So in Sweden the children are challenged with gluten early in life, so
        CD begins presenting early in life; whereas in Ireland gluten is now
        avoided early in life, so CD doesn't show up until a later age.

        One question that arises:  In families with a history of CD, does
        exposure to gluten at an early age increase the chances of getting CD?
        Nobody knows for sure.  Dr. Murray generally advises families with a
        history of CD to not feed gluten to a child before the age of one.
        Then, once they are a year old, put them on a normal gluten-containing
        diet and see what happens.  In these cases Dr. Murray recommends that
        the child then get the celiac antibody blood tests at age two, or a
        full GI evaluation if they develop symptoms or fail to grow.

        Is CD really as rare as you might think in the USA?  Probably not.
        Consider the following:

          *  6% of adult Type I diabetics in Iowa have CD.

          *  A study has shown that 1 in 10,000 people in Utah have DH.  That
             may not sound too common, but in European countries the incidence
             of DH is about the same.  And in European countries you usually
             get 20 celiac patients for every one DH patient.  [That would
             make the incidence of CD about 1:500--editor] So if the Utah
             study is correct then the rate of CD in Utah should be about the
             same as in Europe.  Yet the diagnosis rate is much less.  Why?
             Because either there is a low suspicion of CD among the GI
             specialists, or they just aren't seeing all the people who have
             CD and don't know it.

        Dr. Jarmo Visakorpi is a Finnish researcher who has been studying CD
        for about 35 years.  He gave the introductory talk at the Finland
        symposium and talked about the celiac "iceberg".  The analogy is that
        the diagnosed cases of CD are like the portion of a floating iceberg
        which is above water, and the undiagnosed cases of CD are like the
        portion that is below the water.  Dr. Visakorpi said that the goal is
        to get the entire iceberg above water.  This is mostly a reality in
        Sweden.  In Finland and the rest of Europe some of those peaks are
        sticking out of the water.  Across the ocean [meaning in North
        America] most of the iceberg is underwater.

        At the University of Iowa there are 14-17 full-time
        gastroenterologists on their staff.  Prior to 1990 they diagnosed 2-3
        cases of CD a year.  Then the numbers started to jump up:  8 cases of
        CD diagnosed in 1990; 18 in 1992; 55 or so in 1995, and they are
        running at about the same rate again in 1996.  Prior to 1990, most of
        their newly diagnosed celiac patients presented with either the
        "classic" celiac symptoms, DH, or lymphoma.  In 1992, only a third of
        the newly-diagnosed celiacs fit the representation of classic CD.
        Most of them had a single symptom, not multiple symptoms.  Half of
        them had no diarrhea, and never really had diarrhea at all.  Two
        thirds of those tested did not have steatorrhea (fatty, smelly

        Testing for CD
        Many different tests have been used or proposed for CD screening:

          *  Routine blood count, serum chemistry, etc.  These are general
             health-screening tests.  They are only useful if they come back
             abnormal, and for many celiacs these tests come back normal.

          *  Absorption tests.  There is a xylose test in which the patient
             drinks a "foreign" sugar solution and then the level of this
             sugar in the blood or urine is monitored.  If it is properly
             absorbed then the level should rise at a certain known rate.  You
             need to have a normal intestine in order for it to be absorbed
             properly, so it is not a bad test.  It is not painful and picks
             up many celiacs but not all.

          *  Antibody blood tests.  These are fairly specific to CD.  One
             disadvantage is that these tests don't pick up other causes of
             malabsorption, which may be why they have not been as popular in
             the USA as they have been in other countries.

          *  The small intestine biopsy remains the "gold standard" for
             diagnosing CD.  At the Finland symposium there was a whole
             session devoted to debating how many biopsies are needed to
             diagnose CD.  There are still experts who believe that three
             biopsies are needed, while many others think that one is enough.
             However, none of the 392 celiac experts at the symposium thought
             CD could be diagnosed without a biopsy.  (Dr. Murray thinks that
             in the next 4-5 years blood tests may become reliable enough to
             diagnose CD in some circumstances without a biopsy.)

          *  Small bowel x-rays.  This is where you swallow a white chalky
             liquid.  This test is pretty much useless for diagnosing CD.
             (30-40 years ago the barium solution used behaved differently so
             that it wasn't a bad test for CD, but with modern barium it is
             not useful.)

          *  An empirical trial of the GF diet.  Why not just go on the GF diet 
          and see if you get better?  Well, suppose you try a GF diet
             for six months and you feel better.  But you decide the diet is a
             real hassle, so you want to be sure you really have CD.  You then
             visit Dr. Murray to get a definite diagnosis.  What you are
             faced with is a gluten challenge, which is not fun for anybody.
             Otherwise, there is no way to know if you are a celiac or not.
             If you have a biopsy after six months on a GF diet, the
             pathologist is probably not going to be able to tell you anything
             definitive.  So the moral of the story is:  Get a biopsy and a
             confirmed diagnosis before going on a GF diet.  There are very
             few exceptions to this rule.  On rare occasions where the patient
             is not physically well enough to undergo a biopsy, or the health
             care company completely refused to pay for it and the patient
             can't afford to pay for it themselves, Dr. Murray has diagnosed
             CD on the basis of a positive antibody test followed by a good 
             clinical response to the GF diet.  But this is absolutely the
             last alternative to pursue.

        In the past, three biopsies were required to diagnose CD.  The
        European Society for Pediatric Gastroenterology and Nutrition (ESPGAN)
        developed criteria in 1969-1970 for defining CD.  They said you needed
        three biopsies:  The initial biopsy to show the damaged villi, a
        second biopsy after being on a GF diet showing that the villi have
        healed, and a third biopsy showing damaged villi after a gluten

        In 1990 ESPGAN revised their criteria.  They now say that in most
        cases only one biopsy is needed.  If there is a clinical response to a 
        GF diet (meaning the symptoms go away), so that there is some
        definable improvement, then no additional biopsies and no gluten
        challenge are necessary to make the diagnosis.  Now there occasionally
        may still be a second biopsy to show healing, but it is not
        specifically to confirm diagnosis.  The second biopsy is usually for a
        different reason, such as looking for a complication or making sure
        that healing has occurred (and sometimes it doesn't occur despite the
        best efforts of doctor and patient).  The gluten challenge is now
        reserved for less than 10% of the cases that Dr. Murray sees; usually
        those that have minimal damage and in whom it is not easy to determine
        if the GF diet has really helped.

        Older patients may respond to the GF diet but not completely heal.
        Why not?  Well, they may be healing fully further down the small
        intestine but not in the area near the stomach, which has been exposed
        to the most gluten for the longest time.  However, it is only in the
        area near the stomach that you can effectively take small intestine
        biopsies.  So a biopsy might not show the true extent to which healing
        has occurred.

        What about all the atypical cases; people who present, but don't yet
        have symptoms?  Where do they fit in the ESPGAN criteria?  And do
        milder degrees of damage cause problems?  The other thing is the
        response to a gluten challenge.  Some people don't get sick at all;
        they don't get any symptoms.  They may have damage in their gut but no
        symptoms, sometimes even after six months.  There was one patient that
        went 14 years on a gluten challenge before they developed intestinal
        damage.  This tells us that if a celiac eats gluten there won't
        necessarily be any reaction, so you can't use how you react to judge
        whether or not an item is GF.  On the other hand, Dr Murray said
        that some people will get intestinal changes within two hours of
        ingesting gluten; this has been shown by taking a biopsy of a
        fast-reacting celiac before and two hours after some gluten was

        If a celiac is having a gluten challenge Dr Murray looks for
        symptoms to begin occurring again, or if not then he follows the
        antibody tests until they become positive.  After the return of
        symptoms, or a positive antibody test, or after about six months, then
        Dr. Murray generally performs a biopsy.

        There are two basic serological (blood) antibody tests: antigliadin 
        (antibodies directed against a component of gluten) and connective
        tissue (antibodies directed against our own tissues).  The antiendomysial 
        test is an example of the second type of antibody test.
        It is very operator-dependent (unfortunately).

        A study reported in Gut in 1992 suggests that the celiac antibody
        blood tests are 100% sensitive and 99% specific to CD.  Some HMOs have
        pointed to these studies as proof that a biopsy is unnecessary.  But
        there are some problems with that study.  It was based on a serum bank
        saved from previously-diagnosed celiacs.  These were celiacs who were
        originally found because of screening with these blood tests.  So
        negative results would automatically not be found in the serum bank.

        In September the University of Iowa tested seven reference labs in the
        US.  They took 20 serum samples from untreated celiacs, split them
        seven ways, and sent them to seven different labs across the country
        for analysis.  All of the untreated celiacs were diagnosed by biopsy
        and had not previously had the antibody tests.  They also sent 20
        serum samples from people who were biopsy-proven to NOT have CD.  Dr.
        Murray just got the data back in the last week.  Each lab tested the
        samples blindly, using their own methods.  The results:

          *  The endomysial antibodies at all the labs were 100% specific.  In
             other words, none of the 20 non-celiacs tested positive.

          *  The sensitivity of the endomysial antibodies, meaning how often
             is the test positive for celiacs, varied a lot:  from 55% to 90%.
             So with this test alone, you would not find all the celiacs.  In
             other words, every lab had some false negatives on this test.

          *  The sensitivity of the IgA and IgG antigliadin tests was quite
             variable.  If you combined this test with the endomysial antibody
             test, the sensitivity is about 95-100%.  In other words, if both
             of these tests came back negative from the same lab, the chances
             of having CD are less than one in twenty.  So these tests are not
             bad.  They aren't quite as good as some European studies have
             suggested, but they are not bad.  (This is reassuring.)

        However, there is one caveat with these test results:  the 20 celiac
        samples were "classic" celiac cases.  These were not patients with
        mild damage.  So patients with mild damage might not have abnormal
        antibody levels.  [Yet these are the very patients that are hard to
        diagnose, and for which better tests are needed!--editor]

        Some of the potentials for these antibody tests include:

          *  Screening whole populations, or higher-risk populations such as

          *  Monitoring the response to a GF diet.  These tests should become
             negative after a celiac has been on a GF diet for awhile.

        There are problems with the blood tests.  For example, there is no
        standardization between the various labs.  None of the labs do these
        tests the same way, and none of them report the results the same way.
        A "high" positive from one lab is not necessarily going to be a "high"
        positive from another.  That means you may not be able to compare
        results from one year to the next if the samples are sent to different
        labs.  (This often happens as HMO's change contracts.)

        Who should be screened?  Dr. Murray usually screens people with Type
        I diabetes, unexplained iron-deficiency anemia (Dr. Murray does not
        accept heavy menstrual flow in women as an explanation), unexplained
        bone disease, functional diarrhea, irritable bowel syndrome, history
        of "transient" gluten-sensitivity ("Well, I had it as a child and
        outgrew it..."--you DON'T outgrow CD), or lactose intolerance (if

        How should close relatives of a known celiac be screened?  Obviously,
        a biopsy would be ideal as it would determine for sure whether or not
        villi damage is present.  But a more reasonable first step is to use
        the celiac antibody blood tests to screen close relatives.  Tissue
        typing could also be done to determine whether or not a relative is at
        risk for developing CD, but there is not enough information on the
        American population.  The type of tissue you see in celiacs also
        occurs in about 20% of Caucasians.

        You also have to follow up intermittently, since a relative might not
        develop CD until after the first screening.  For example, suppose you
        are a celiac and you have a child.  Dr. Murray recommends keeping the
        child GF the first year, then putting them on a gluten-containing
        diet.  At the age of two, or at the appearance of any symptoms, they
        would then be screened for CD using the antibody tests.  Then check
        them again at age 9 or 10, before they go into that pubertal growth

        Treating CD
        Dr Murray says that when he tells someone they have CD, and that the
        treatment is to avoid wheat, barley, rye, and oats, he expects a
        "grief" reaction.  This reaction has some fairly standard stages:
        Shock, denial (this lasts a long time for some people), anger, and
        then (eventually) acceptance.  The most dangerous of these stages are
        denial and anger.  In the denial stage you just deny that this is
        really happening to you, or you deny that you are really that
        sensitive ("Well, I can get away with a little bit of gluten.").  This
        reaction is especially common in men.  In the anger stage you may be
        angry at the delay in getting diagnosed, or angry at why you got this
        disease ("God, why did you give this to me?"), anger at the food
        manufacturers for incomplete ingredient information, or anger at the
        difficulties of following the diet.  It is good to channel the anger
        to something useful, but eventually you have to get to the acceptance

        Professional dietary advice is invaluable--if you can get it. Dietitians
        who are interested, knowledgeable, keep up-to-date, and
        learn as much from their celiac patients as the patients learn from
        them are invaluable, and there are a few.  (Dr. Murray specifically
        referred to our own dietitian advisor, Dorothy Vaughan, as one of the

        The University of Iowa surveyed members of the Iowa Dietetic
        Association, asking how many celiac patients they have, what kind of
        information do they provide, do they routinely give information about
        support groups, etc.  They found that most of them don't treat celiac
        patients, most don't even know what to do because it is so difficult.
        Most dietitians get their material from the American Dietetic
        Association, and up until several years ago it was woefully
        out-of-date. Dietitians can keep up on fat, cholesterol, and diabetic
        information; but it is the celiac information that keeps on changing.
        As a professional, it is very challenging for a dietitian to keep up,
        especially if you are only counseling one or two celiacs a year.

        Local and national support groups are important for your immediate
        benefit.  You don't have to reinvent the wheel all the time.  Also,
        there is strength in numbers to advocate to bigger corporations and
        food providers, and perhaps get them to bend a little bit.

        Nutritional supplementation to correct deficiencies is important.  For
        example, if someone is very anemic they need something to correct it.

        Dr Murray advocates "champagne, not pessimism"<2>.  Initially the GF 
        diet may be overwhelming and dominate a celiac's life.  But after a
        few years to adjust celiacs should expect to have the attitude that
        they are on a healthy diet that is interesting and just happens to be
        free of gluten.

        There are many other aspects of treatment.  A bone density test may be
        important.  You may want to screen family members for CD.  Intense
        nutritional fluid intervention is sometimes necessary in the really
        sick patient.  Consider coexisting malignancy or other disease,
        especially in the older patients.

        Finally, there is the need of follow-up for compliance.  Those that do
        well on the diet may need less follow-up.  The doctor doesn't know at
        the time of diagnosis just how compliant the patient will be to the GF 
        diet (though he may have his suspicions).  By setting up a follow-up
        appointment six months down the road, you give the patient a goal to
        shoot for.

        Most patients come back for a checkup doing very well.  But Dr.
        Murray has had some come back looking terrible.  In some cases he has
        had to admit them because they were suicidally depressed, somewhere
        between the denial and anger stages.  They obviously needed help.
        (Trying to persuade the insurance company to admit them to the
        hospital for dietary management is nearly impossible.)

        Dr. Murray advocates prudence, but not paranoia about what you eat.
        Some people do get to the point of paranoia, avoiding things that are
        reliably GF.  You need to have a "safe haven", where you can simply
        eat without worrying about whether or not the food is GF.  This could
        be your home, a celiac friend's house, whatever; someplace where you
        can completely relax and not worry about the diet.  Some of the GF 
        cruises that have been organized provided such a haven for the
        duration of the trip.  [So did the CSA Conference--editor]

        In Iowa they have about 150 people in their support group.  They have
        split up into smaller subgroups that meet every two months or so in
        somebody's home.  There is no real organization to it, but they know
        they can go to that person's home, bring their food, and then relax
        and not worry about the food being GF or explaining the diet to
        someone.  This provides them with a "relief valve".  You need to be
        able to do something like that from time to time.

        Dr. Murray then spoke on monitoring the GF diet.  Symptoms should go
        away when you are following the GF diet.  Deficiency states (such as
        iron-deficient anemia) should become corrected.  Dr. Murray asks his
        patients, "How many times in the last three months have you put
        anything in your mouth that you suspected beforehand contained
        gluten?"  He says he can look at them as they answer this and know
        whether they have or not.  The last person he asked answered, "well,
        maybe twice a week".  This was a shock, and Dr. Murray told the
        patient that he really was not on a GF diet.  Then he asks why.  The
        answers include:  "I was very hungry"; "I couldn't get anything else
        to eat"; "I was traveling".  The advice he tries to give is to think
        of these situations before they happen and plan for them. Antigliadin 
        antibody tests can be helpful in monitoring compliance.
        How many times do you do them?  Dr. Murray says nobody really has an
        answer; but he likes to see them become normal (negative).  A
        follow-up biopsy is done occasionally, on a case by case basis.

        <1> Dr. Murray is referring to the "7th International Symposium on
            Coeliac Disease" held September 5-7 in Tampere Finland.  See _The
            Sprue-nik Press_, Sept. '96, for a summary of this symposium.

        <2> This quote came originally from Elaine Harstook, the late founder
            of the Gluten Intolerance Group of North America.

        No liability is assumed. Individuals should consult their physicians
        and dietitians before following any medical or dietary recommendations
        published here.

        Original material used in The Sprue-nik Press is placed in the
        public domain for the benefit of all celiacs.  

        The Sprue-nik Press is published by the Tri-County Celiac Sprue
        Support Group (TCCSSG), a local chapter of CSA/USA located in
        southeast Michigan.  Members receive this newsletter, a shopping
        guide, and a new member packet full of articles and useful
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