Leyden University Medical School just finished a large scale investigation. 198 families with a child with DS aged between 1 and 9 years were approached. 115 decided to have their child participate. The first researcher, Elvira George, made home visits and collected blood and urine for testing. A. o. values of anti-endomysium (EmA) were determined. Only if one of the investigated blood or urine values was significantly different from the norm the child was referred to the hospital to take a biopsy. That was the case with 43 of the 115 children. In 9 cases no biopsy was taken, in six because the parents refused it and in 3 because the childs condition didnt allow for it. Of the 34 children that had a biopsy taken eight, or rather 7 % (!) of the original 115, had the intestinal appearance typical for celiac disease (according to international standards).

Retrospectively, five of these eight children had complaints that were compatible with celiac disease, that were considered to be caused by DS as such until then. Three children were free of complaints. Their diagnosis was a complete surprise. In addition, it was proven that the value for EmA was the strongest indicator of a positive biopsy. If EmA was positive there always was celiac disease upon biopsy.

Needless to say that all (so far but one) concerned children were put on a totally gluten free diet. It was reported that their complaints decreased rapidly. Celiac disease is considered to put people involved at risk for particular intestinal cancers, if they do not keep their diet. Therefore, the diet has to be maintained lifelong. This aspect makes testing for celiac disease so important in an at risk population as children with DS are. Even without complaints one in fourteen of our children might have it! It is postulated that the children who had different blood values, but no positive biopsy still can develop celiac disease in the future.

Presently, the complete study is in the process of being published in the international literature. So, Im afraid Im only able to give a you a reference to a pre-publication:

• George, E. et al. The high frequency of celiac disease in DS: screening methods. Gastroenterology 1995; 108 (Supp 4): A 16.iv

Erik de Graaf
director, Stiching Down Syndrome (SDS)
(i.e., the Dutch Down Syndrome Foundation)
Vice-President of the European Downs Syndrome Association (EDSA)
Bovenboerseweg 41
NL-7941 AL Wanneperveen
The Netherlands
Tel.: -31-(0)522-28 13 37
Fax.: -31-(0)522-28 17 99
E-mail: Open Original Shared Link

Leyden University Medical School just finished a large-scale investigation using 198 families who have a child with DS between the ages of 1 and 9 years old. 115 decided to have their child participate. The first researcher, Elvira George, made home visits and collected blood and urine for testing. A. o. values of anti-endomysium (EmA) were determined. Only if one of the investigated blood or urine values was significantly different from the norm was the child referred to the hospital to take a biopsy. That was the case with 43 of the 115 children. In 9 cases no biopsy was taken, in six because the parents refused it and in 3 because the childs condition didnt allow for it. Of the 34 children that had a biopsy taken, eight, or rather 7 % (!) of the original 115, had the intestinal appearance typical for celiac disease (according to international standards).

Retrospectively, five of these eight children had complaints that were compatible with celiac disease, that were considered to be caused by DS as such until then. Three children were free of complaints. Their diagnosis was a complete surprise. In addition, it was proven that the value for EmA was the strongest indicator of a positive biopsy. If EmA was positive there always was celiac disease upon biopsy.

Needless to say that all (so far but one) concerned children were put on a totally gluten free diet. It was reported that their complaints decreased rapidly. Celiac disease is considered to put people involved at risk for particular intestinal cancers, if they do not keep their diet. Therefore, the diet has to be maintained lifelong. This aspect makes testing for celiac disease so important in an at risk population as children with DS are. Even without complaints one in fourteen of our children might have it!

It is postulated that the children that had different blood values but no positive biopsy can still develop celiac disease in the future. Their condition will remain be followed. Presently, the complete study is in the process of being published in international literature. There is the following pre-publication reference:

• George, E. et al. The high frequency of celiac disease in DS: screening methods. Gastroenterology 1995; 108 (Supp 4): A 16

For more information:

• Medical & Surgical Care for Children with Down Syndrome Ed. by DC Van Dyke MD, Woodbine House l995 ISBN ## 0-933149-54-9 p. 185 ...one study found that individuals with DS are 20 times more likely than others to have a particular malabsorption syndrome known as celiac disease. This section is written by Timothy M Buie MD and references DS and Celiac Disease Pediatric Gastroenterology and Nutrition Vol. 10, No.1. l990 41-43 by Dias, J. and Walker-Smith, J.

Collin P et al. (1994) Celiac disease - associated disorders and survival. Gut vol 35 (9):1215 1218.

Abstract: The associated diseases in 335 celiac patients diagnosed 1980-1990 were compared with age and sex matched control patients with various gastrointestinal symptoms. Endocrine disorders were found in 11.9% of celiac and 4.3% of control patients (p=0.0003). Celiac patients had insulin dependent diabetes mellitus significantly (p=0.0094) more often (5.4%) than control patients (1.5%). Connective tissue diseases were found in 7.2% of celiac and 2.7% of control patients (p=0.011). Sjogrens syndrome occurred in 3.3% of celiac patients and 0.3% of controls (p = 0.0059). Autoimmune thyroid diseases were found in 5.4% and asthma in 3.6% of celiac patients but also in 2.7% and 3.6%, respectively, among control patients. The incidences of malignant disease and the survival rate in celiac patients were compared with those in the Finnish population. Ten celiac patients developed a cancer during the follow up (mean 5.3 years, range 1-12) but none had a lymphoma. The risk of malignant disease did not differ from that in the Finnish population in general. Eleven celiac patients died during the follow up. The five year survival rate of celiac patients did not differ from those in the general population. At least 83% of the celiac patients adhered strictly to the gluten free diet, which may explain the favorable outcome.

The following piece was written by Ronald Hoggan who is a teacher at Queen Elizabeth High School in Calgary, Alberta, Canada.

The Polish one is: Kozlowska, Z.E. Results of Investigation on Children with Coeliakia Treated many Years with Gluten Free Diet Psychiatria Polska 1991; 25(2): 130-134.

The German one is: Paul, et. al. EEG-befunde Zoeliaki-kranken Kindernin Abhaengigkeit von der Ernaehrung Zeitschrift der Klinische Medizin 1985; 40: 707-709.

The first indicates that 71% of celiac children, when newly diagnosed, demonstrate EEG abnormalities. Now please note this caution: I HAVE NO TRAINING IN THE INTERPRETATION OF EEG READINGS.

Nonetheless, when I compare the authors descriptions of the EEG abnormalities in celiac children, and the abnormalities in children who have been diagnosed with ADD or ADHD, there are some startling similarities.

Paul, et. al. are paraphrased by Reichelt et. al. in THE EFFECT OF GLUTEN-FREE DIET ON GLYCOPROTEIN ATTACHED URINARY PEPTIDE EXCRETION Journal of Orthomolecular Medicine 1990; 5: 223-239.

They say: In celiac children provocation with gluten after diet causes alarmingly high frequency of EEG changes that persist up to a year (Paul et al 1985).

I would urge (those with ADD) to be very careful to avoid contamination in (their) diets, and I would ask you to consider some alternatives to stimulant therapy (Ritalin is a brand name of the most commonly used stimulant.).

The concept of drugging a child to facilitate learning is upsetting to me, especially when there is cause to suspect that, on the Gluten-free diet, she may improve without intervention. I know that she is falling behind now, but if her experience is similar to mine, many of my ADD type symptoms did go away during the first year. I will also forward a part of report that was forwarded to me, that showed that vitamin B-6 supplementation was as beneficial to a group of children with attention deficits, as Ritalin was. Especially in celiac disease, where vitamin deficiencies are so common, that seems a viable alternative.

In the Friday, February 9, 1996 edition of the Independent newspaper (UK), there was a short article reporting research into ME (myalgic encephalomyelitis) by doctors at the Royal Hallamshire Hospital in Sheffield. Their research was published that same weeks Lancet.

Mysterious symptoms, including muscle weakness, wasting, and poor coordination and balance may be due to an undiagnosed allergy to wheat, barley, oats or rye, according to new research which may have implications for some people with ME...A study of 53 patients with these and other unexplained neurological symptoms, found that nearly three-fifths of them had antibodies to gluten in their blood...none of the patients in the Sheffield group had been diagnosed with celiac disease but when samples of tissue were removed from their gut, more than a third showed evidence of the disease or inflammation of the middle and lower gut.

The following piece was written by Ronald Hoggan who is a teacher at Queen Elizabeth High School in Calgary, Alberta, Canada.

Gall bladder disease or malfunction is often associated with celiac disease. It can cause pain in the upper right quadrant of the abdomen, just at the lowest rib on the right side. In one study of 1300 celiacs in Canada, 9% indicated that gall stones were the earliest presentation, sometimes followed by many years prior to correct diagnosis of their celiac disease. In another report, Dr. Kozlowska indicated that 13 of the 41 newly diagnosed celiacs she investigated were suffering from atresia, a condition which is a partial or complete blockage of the bile duct.

CCK (cholecystokinin) is the hormone responsible for gall bladder contraction. The bulk of this hormone is produced in the duodenum.

Active celiac disease would be likely, then, to cause a reduction or a cessation of duodenal production of CCK. A radiologist in Hungary is currently researching this problem. In private correspondence, one gastroenterologist reports having found (accidentally) a gallstone in a 12 year old girl who had active celiac disease.

The 30% incidence of atresia among celiac children, as reported by Dr. Kozlowska, would suggest an even higher number among adults with active celiac disease. Given the low level of clinical suspicion for celiac disease in North America, it would not be at all surprising if a large portion of patients with gall bladder disease were suffering from occult celiac disease. Future research may reveal that gall stones and atresia are only symptoms of celiac disease.

I did a Medline search on cck and celiac disease. I got 65 hits. Researchers repeatedly identified a connection between celiac disease and gall bladder malfunction with such comments as: Thus the already impaired fat absorption in celiac sprue is magnified by the lack of bile delivery.....; and We conclude that there is a reversible defect of gallbladder emptying and cholecystokinin release in celiac disease. and Cholecystokinin (cck) release and gall bladder emptying in response to a fatty meal are completely abolished in celiac disease. and the abnormally decreased gallbladder contraction in celiac patients is the result of endogenous cck secretion and not a lack of end-organ responsiveness to cck.

There just isnt much ambiguity there. If youve got celiac disease, you have gall bladder malfunction, of the sort that may well develop into atresia and gallstones.

Upon receiving a diagnosis of gall bladder disease, whether gall stones or atresia, one might be wise to request a blood test for celiac disease. The anti-endomysial antibody test is currently the most reliable and available test.

Now, given the low level of clinical suspicion for celiac disease, I anticipate the suggestion that absent gall bladder emptying, atresia, and gall stones might occur in the absence of celiac disease. I did another Medline search, and I cant find a single study that has tested atresia patients or gallstone patients for celiac disease. My answer to the suggestion that gall bladder disease may occur in the absence of celiac disease is that there is no evidence to support such a contention. Considerable evidence exists, however, which points to celiac disease as a likely cause of gall bladder malfunction, atresia, or stones. As for childhood gallstones, there appears to be only one answer.... it is associated with celiac disease.

A view that incorporates the association of gall bladder disease, and celiac disease, but does not preclude the above, has been expressed by Dr. Joseph Murray, of the University of Iowa, who is a gastroenterologist specializing in treating celiac disease. He believes there are several triggers that can activate Celiac disease in genetically susceptible people. One of them is: Surgery, particularly GI (gall bladder, etc.) In any case, the connection between celiac disease and gall bladder disease is well known.

Sarcoidosis is the disease; and sarcoid of the lungs is a location affected by the disease. According to a report by the U.S. Department of Health and Human Services Public Health Service National Institutes of Health: Sarcoidosis is a disease due to inflammation. It can appear in almost any body organ, but most often starts in the lungs or lymph nodes. As sarcoidosis progresses small lumps, or granulomas appear in the affected tissues. Symptoms are usually general. Weight loss, fatigue, night sweats, fever, or just an overall feeling of ill health. In some cases it shows up with the appearance of skin rashes. red bumps on the face, arms, shins, ect., and sometimes inflammation of the eyes.

Further: Sarcoidosis was once considered a rare disease. It is now known to be a common chronic illness that appears all over the world. It is the most common of the fibrotic lung disorders, and occurs often enough in the United States for Congress to have declared a national Sarcoidosis Awareness Day in 1990. Sarcoidosis is currently (1993) thought to be associated with an abnormal immune response. Whether a foreign substance; a chemical, drug, virus, or some other substance is the trigger and how the immune disturbance is caused are not known. No one can predict how sarcoidosis will progress. In general, sarcoidosis appears briefly and heals naturally. However, 20 to 30% of sarcoidosis patients are left with some permanent lung damage. In 10 to 15% of the patients, sarcoidosis can become severe and chronic. When either the granulomas or fibrosis seriously affect the function of a vital organ; the lungs, heart, nervous system, liver, or kidneys, for example, sarcoidosis can be fatal.

From Ron Hoggan:

Sarcoidosis has repeatedly been associated with celiac disease. Some researchers seem to view it as a condition which results from untreated celiac disease, while others see it as coincident with celiac disease. Here are a couple of references you might want to look at:

• Douglas, et. al. Sarcoidosis and Celiac Disease: An Association? Lancet, 1984; July 7:13-15
• Karlish Celiac Disease and Diffuse Lung Disease Lancet, 1971; May 22: 1077

A Medline search might reveal more information to you, and I would suggest that you satisfy yourself of the connection. In #1, it says, in part: These cases suggest there may be an association between celiac disease and sarcoidosis, but formal studies of small bowel function in sarcoidosis are needed to confirm this. It is important to recognize that these two conditions can occur together and that unexplained weight loss in a patient with sarcoidosis may be caused by celiac disease. You might consider suggesting that your friend get a full panel of blood tests for celiac disease, as it is usually a very treatable condition. And I have been pleasantly surprised by the resolution of other, apparently unrelated health problems, that have cleared up on the diet since I was diagnosed. I hope she is similarly surprised.

• Reunala T, et al. [see Related Articles] Diseases associated with dermatitis herpetiformis. Br J Dermatol. 1997 Mar; 136(3): 315-318. PMID: 9115907; UI: 97247319.
• Papadopoulos KI, et al. [see Related Articles] The occurrence of polyglandular autoimmune syndrome type III associated with celiac disease in patients with sarcoidosis. J Intern Med. 1994 Dec; 236(6): 661-663. PMID: 7989901; UI: 95081757.
• Bianconcini G, et al. [see Related Articles] [Celiac disease (familial) associated with sarcoidosis. Clinical case and review of the literature]. Minerva Med. 1994 Oct; 85(10): 541-553. Review. Italian. PMID: 7800197; UI: 95098301.
• Boruchowicz A, et al. [see Related Articles] [sarcoidosis and the digestive tract]. Gastroenterol Clin Biol. 1994; 18(12): 1119-1128. Review. French. No abstract available. PMID: 7750685; UI: 95269922.
• Riccabona M, et al. [see Related Articles] Sonographic findings in celiac disease. J Pediatr Gastroenterol Nutr. 1993 Aug; 17(2): 198-200. PMID: 8229548; UI: 94046289.
• Papadopoulos KI, et al. [see Related Articles] Polyglandular autoimmune syndrome type III associated with celiac disease and sarcoidosis. Postgrad Med J. 1993 Jan; 69(807): 72-75. PMID: 8446560; UI: 93189522.
• Mainguet P, et al. [see Related Articles] [Celiac disease in adults: clinical aspects--role of endoscopy]. Acta Gastroenterol Belg. 1992 Mar; 55(2): 181-189. Review. French. PMID: 1632135; UI: 92336640.
• Sorokin R, et al. [see Related Articles] Diarrhea presenting as a rare manifestation of sarcoid. Am J Gastroenterol. 1990 Sep; 85(9): 1197-1198. No abstract available. PMID: 2389733; UI: 90358167.
• Rogers P, et al. [see Related Articles] Antibodies to Proteus in rheumatoid arthritis. Br J Rheumatol. 1988; 27 Suppl 2: 90-94. PMID: 3042079; UI: 88294497.
• James DG, et al. [see Related Articles] Overlap syndromes with sarcoidosis. Postgrad Med J. 1985 Sep; 61(719): 769-771. Review. No abstract available. PMID: 3903708; UI: 86042375.
• James DG, et al. [see Related Articles] Overlap syndromes with sarcoidosis. Sarcoidosis. 1985 Sep; 2(2): 116-121. PMID: 3843140; UI: 87177134.
• Lowe G, et al. [see Related Articles] Sarcoidosis and celiac disease. Lancet. 1984 Sep 15; 2(8403): 637. No abstract available. PMID: 6147667; UI: 84294457.
• [No authors listed] [see Related Articles] Sarcoidosis and celiac disease. Lancet. 1984 Aug 18; 2(8399): 408. No abstract available. PMID: 6147488; UI: 84294274.
• Douglas JG, et al. [see Related Articles] Sarcoidosis and celiac disease: an association? Lancet. 1984 Jul 7; 2(8393): 13-15. PMID: 6145934; UI: 84244768.
• Vilaseca J, et al. [see Related Articles] [Granulomatous hepatitis. Etiologic study of 107 cases]. Med Clin (Barc). 1979 Apr 10; 72(7): 272-275. Spanish. PMID: 459594; UI: 79220138.
• Hurley TH, et al. [see Related Articles] Reaction to Kveim test material in sarcoidosis and other diseases. Lancet. 1975 Mar 1; 1(7905): 494-496. PMID: 46962; UI: 75117906.
• Ewe K. [see Related Articles] [Calcium absorption in health and disease. II. Syndromes of imparied calcium absorption]. Klin Wochenschr. 1974 Jan 15; 52(2): 64-73. Review. German. No abstract available. PMID: 4361437; UI: 74122902.
• Mornet P, et al. [see Related Articles] [A case of peripheral neuropathy during terminal ileitis. Crohns disease]? Sem Hop. 1973 Jun 26; 49(30): 2209-2218. French. No abstract available. PMID: 4147181; UI: 73252730.
• Karlish AJ, et al. [see Related Articles] The Kveim test in Crohns disease, ulcerative colitis, and celiac disease. Lancet. 1972 Feb 19; 1(7747): 438-439. No abstract available. PMID: 4110670; UI: 72118038.
• MacGregor GA. [see Related Articles] Inhibition of leucocyte migration in celiac disease. Lancet. 1971 Dec 25; 2(7739): 1431. No abstract available. PMID: 4107620; UI: 72042982.
• Pagaltsos AS, et al. [see Related Articles] In vitro inhibition of leucocyte migration by sarcoid spleen suspension in celiac disease and dermatitis herpetiformis. Lancet. 1971 Nov 27; 2(7735): 1179-1181. No abstract available. PMID: 4107984; UI: 72052439.
• Karlish AJ. [see Related Articles] Celiac disease and diffuse lung disease. Lancet. 1971 May 22; 1(7708): 1077. No abstract available. PMID: 4103011; UI: 71206245.
• Dawson AM. [see Related Articles] Nutritional disturbances in Crohns disease. Proc R Soc Med. 1971 Feb; 64(2): 166-170. No abstract available. PMID: 5548941; UI: 71139887.
• Hill LE. [see Related Articles] Hypogammaglobulinaemia in the United Kingdom. 3. Clinical features of hypogammaglobulinaemia. Med Res Counc Spec Rep Ser (Lond). 1971; 310: 9-34. No abstract available. PMID: 5573491; UI: 71183306.
• Levinson JD, et al. [see Related Articles] Infiltrative diseases of the small bowel and malabsorption. Am J Dig Dis. 1970 Aug; 15(8): 741-766. Review. No abstract available. PMID: 4195473; UI: 70283039.
• Sjaastad O. [see Related Articles] Urinary excretion of free and conjugated histamine in various gastrointestinal disorders. Acta Med Scand. 1969 Jun; 185(6): 495-499. No abstract available. PMID: 4185319; UI: 69281390.
• Pirola RC, et al. [see Related Articles] Whipples disease. Med J Aust. 1967 Nov 25; 2(22): 985-988. No abstract available. PMID: 4170086; UI: 68128282.
• Smith BD. [see Related Articles] Sarcoidosis with recurrent thrombophlebitis and idiopathic steatorrhoea. Proc R Soc Med. 1966 Jun; 59(6): 569-570. No abstract available. PMID: 5937945; UI: 66143622.

I have only found three reports in the literature suggesting a coincidence of the two above-mentioned conditions (1, 2, 3). And yet, I was recently contacted by Karen Brinser, whose mother had been diagnosed with celiac disease and had a section of her bowel was surgically removed due to a small bowel adenocarcinoma. Karen indicated she had ITP, and asked if there could be any connection with celiac disease.

I responded with the three citations to journal articles, along with some comments from Cooke & Holmes indicating that the platelet count could rise in celiac disease (4) (page 122). I seem to have missed the comment, later on the same page, that the platelet count can also be considerably diminished in the presence of granulopenia. They go on to say that granulopenia is not uncommon in celiac disease, and approximately 10% of celiac patients have total white cell counts less than 3500 per cmm and approximately the same percentage have either a neutropenia of less than 3000 or a lymphopenia of less than 1500 per cmm.

Karen took the initiative and posted to the celiac listserv asking for responses from those who have experience with both celiac disease and ITP. One parent wrote about a daughter who had previously experienced ITP, but had regained her health since the diagnosis and treatment of her celiac disease.

A middle-aged man who had suffered from ITP during the 1960s and 1970s and was treated with corticosteroids, was diagnosed with celiac disease in 1980. His ITP also seems to have resolved.

A woman was diagnosed with both celiac disease and ITP at the same time, three years ago. Her gastroenterologist thought the two were related as both are auto immune diseases.

Another woman had two severe bouts with reduced platelet levels occurring at ages 38 and again at age 45. At age 59 she was diagnosed with celiac disease and now blames the celiac disease for a variety of health problems, including her bouts with abnormal platelet levels.

Another womans ITP eventually led her astute (my opinion) doctor, after excluding leukemia, in the direction that led to the diagnosis of her celiac disease.

A father discussed his own and his daughters symptoms of purpura, as well as some associations between celiac disease and damage to capillaries. He structured some very thoughtful, compelling arguments suggesting that abnormal WBCs and platelet counts may well be associated with celiac disease. He also indicated that his symptoms had abated on the gluten-free diet.

Another parent had one daughter diagnosed with celiac disease. When their other daughter started to develop symptoms of celiac disease they put her on a gluten-free diet. At age five, they re-introduced wheat to her diet to see if she could tolerate it. She was subsequently hospitalized due to ITP. At the time, the parents thought the ITP might have been due to a drug reaction. The daughter was returned to the gluten-free diet due to other celiac-like symptoms, and has not had any significant health problems since. All these anecdotal reports, but in combination with Cook & Holmes comments, and the three journal articles, the possibility of a connection seems reasonable. It is at least a connection worthy of investigation, as ITP can be deadly, as can some of the other sequelae of celiac disease. Given the delays between presentation of ITP, and diagnosis of celiac disease, the former could prove to be a valuable indicator of the possibility of the latter.

Sources:

• Kahn O, Fiel MI, Janowitz HD Celiac Sprue, Idiopathic Thrombocytopenic Purpura, and Hepatic Granulomatous Disease. An Autoimmune Linkage? Clin. Gastroenterol. 1996 Oct;23(3):214-216.
• Sheehan NJ, Stanton-King K Polyautoimmunity in a Young Woman. Br. J. Rheumatol 1993 Mar;32(3):254-256.
• Stenhammar L, Ljunggren CG, Thrombocytopenic Purpura and Celiac Disease, Acta Paediatr Scand, 1988 Sep; 77(5):764-766.
• Cooke W & Holmes G (1984) Celiac Disease Churchill Livingstone, NY.
• Nelson E, Ertan A, Brooks F, Cerda J, (1976). Thrombocytosis in Patients with Celiac Sprue. Gastroenterology 70, 1042-1044.
• Croese J, Harris O, Bain B,(1976). Celiac Disease. Haematological Features and Delay in Diagnosis. Medical Journal of Australia 6, 335-338.
• Bullen A, Hall R, Brown R, Losowsky M, (1977). Mechanisms of Thrombocytosis in Celiac Disease. Gut. 18, 962.

New England Journal of Medicine, May 2, 1996 -- Volume 334, Number 18
Kenneth D. Fine

The New England Journal of Medicine published a study in the May 2, 1996 (Volume 334, Number 18) issue regarding the prevalence of occult gastrointestinal bleeding in patients with celiac sprue. Its goals were to explain the iron deficiency found in many celiacs. The fecal samples of 8 Patients with partial villous atrophy and 28 with total villous atrophy were studied. Their results found 25% of patients with partial villous atrophy and 54% of Patients with total villous atrophy tested positive for blood. They concluded that gastrointestinal bleeding can be found in about 50% of patients with celiac sprue, and should therefore be added to the list of factors that can contribute to iron deficiency in celiacs.

The following are comments on this article by Karoly Horvath, M.D., Ph.D., of Baltimore, Maryland, USA. If you have any questions you can e-mail him at: Open Original Shared Link

Date: 05/02/96 - 08:20:20 AM. Subject: Re: Fecal Occult Blood, Plus Elevated Liver Enzymes FECAL OCCULT BLOOD:

The cited NEJM paper found occult intestinal bleeding in patients who had some degree (partial and total) of intestinal villous atrophy. However, this paper have certain methodological problems. The first, and most important -as you can read in the editorial comment- that they did not place the patient on a specific diet before collecting the stool. It is a rule that the patients should be on a diet which eliminate all the peroxidase containing food. So this may increase the number of false positive cases.

The second problem that the hemoccult test is only a screening method, which does not give information about the degree of blood loss. The test can be positive in the presence of small amount of blood in the stool. While this paper has limitations, I should accept that patients with mucosal atrophy and inflammation have small amount of blood loss. So I do not have any doubt regarding the final conclusion of paper, that patients with active celiac disease have blood loss in the stool. This is not surprising and not a novel finding.

To avoid any panic in the celiac community I do not recommend to post this finding without appropriate comment to the Celiac List. We should emphasize one sentence from this paper: ALL THE PATIENTS WITH PREVIOUSLY DIAGNOSED AND TREATED CELIAC SPRUE HAD NEGATIVE TESTS FOR FECAL OCCULT BLOOD.

LIVER ENZYMES:

It is well known that patient with intestinal inflammation may have elevated liver enzymes. The well known examples are patients with inflammatory bowel disease. Because patients with active celiac disease have significant accumulation of inflammatory cells in the mucosa it is not surprising that a percentage of patients with active celiac disease have elevated liver enzymes. However, this is a temporary elevation, which disappears on gluten-free diet.

The explanation is not clear for this finding. The simplified explanation is that there is an increased permeability in the inflamed intestinal segments and different toxins, which normally are detoxified by the enterocyte Cytochrom P450 enzyme system, enter the portal circulation and there is an increased toxin load into the liver.