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fredag 5 juni 2015

Peptidaasit keliakiapotilaan suolinukassa taudin akuutissa ja remissiovaiheessa

Clin Chim Acta. 1981 Jan 8;109(1):53-8. Intestinal peptidases and sucrase in coeliac disease.

Abstract

The activities of microvillus
aminopeptidase (microsomal, EC 3.4.11.2),
 dipeptidyl peptidase IV (EC 3.4.14.-),
 glycyl-leucine dipeptidase (EC 3.4.13.11),
proline dipeptidase (EC 3.4.13.9),
 sucrase (EC 3.2.1.48) and
 gamma-glutamyl transpeptidase (EC 2.3.2.2)
were measured in peroral intestinal biopsies taken from patients with coeliac disease in the acute phase and in remission. A comparison with the amounts of corresponding activities from a reference group showed that all the measured activities were significantly decreased in the acute phase of the disease.

 In patients in remission only microvillus
 aminopeptidase and
dipeptidyl dipeptidase IV displayed a substantial depression
 as compared to the reference group.

It is suggested that a primary mucosal digestion defect will result in lack of substrate for other intestinal enzymes. This is a situation comparable to starvation and may explain the variation in the grade of restitution for the different enzymes.
PMID:
7008982
[PubMed - indexed for MEDLINE]

1996 Free paper Abstracts. Oats and other cereals. A126- A138

A126 Fiveryear follow-up study: use of oats and adherence to gluten-free diet. ( Kuopio, Finland)

A127.Oats for patients with dermatitis herpetiformis. (Tamper, Helsinki, Finland)

A128.  Oats in coeliac diet;  A five year follow up study. (Kuopio,. Finland)

A129.  Adult patients with coeliac disease have no antigliadin or antireticulin antibody response to oats.  (Kuopio,, Finland)

A130. The oat - celiac study in Gothenburg (Göteborg, Sweden)

A131.  Effect of heat treatment on solubility of oat proteins (Tallinn, Estland)

A132.  Contamination of rolled oats with wheat, barley and rye. (The Netherlands)

A133.  Oats and gliadin (Berne, Switzerland)

A134. Oats prolamines in vitro activate intestinal cell-mediated immunity in coeliac disease (Rome, Italy)

A135 A small ppeptide from durum wheat prevents cell agglutination induced by cereal prolamin (Rome, Italy)

A136.  MALDI-TOF mass spectrometry as a new tool to detect gliadins in food. (Madrid,. Spain)

A137. Gluten in gluten-free products (Uppsala, Sweden)

A138. Application of PCD methodology to detect wheat DNA in foodstuffs. (Budapest,, Hungary)

1996 Free paper Abstracts. Pathogenesis, immunology and genetics. A139-A181

A139. Purified coeliac disease patient serum IgA inhibits fibroblast and TGF-beta induced epithelial cell (T84) differentiation in vitro. (Tampere, Finland)

A140.  Nitric oxide does not play a role in the initial mucosal response to the instillation of gluten into the rectum (Buenos Aires, Argentina)

A141,  INOS expression in coeliac disease small-bovel biopsy tissue (Maastricht, the Netherlands)

A142. Increased urinary nitric oxide (NO) oxidation  products in children with active coeliac disease (Maastricht, the Netherlands)

A143.  Children with coeliac disease express iNOS in the small intestine epithelium (Norrköping,  Sweden)
http://serials.unibo.it/cgi-ser/start/it/spogli/ds-s.tcl?authors=%22PETERSON+KH%22&language=ITALIANO

A144.  Gluten stimulates NO production in children with coelic disease? (Norrköping, Sweden)

A145. Reduced Na+K+ Pump activity in the erythrocytes of children with treated coeliac disease (Budapest, Hungary)
 http://journals.lww.com/jpgn/fulltext/1996/05000/43_decreased_na__k_atpase_activity_and_increased.56.aspx

A146.Changes in the expression of transcripts of the calcium-binding protein calbindin-D9K in duodenal biopsies in coeliac disease. (London, UK)

A147.  The organe culture of human intestinal biopsies as an in vitro-model for coeliac disease in remission. (Düsseldorf, Germany)

A148.  Integrins and coeliac disease.Pittschieler K, Ladinser B.
 (Italy) http://journals.lww.com/jpgn/fulltext/1996/05000/35_integrins_and_coeliac_disease.48.aspx

A149. Distinct distribution of sulphated glycosaminoglycans within coeliac mucosa, Simon Murch, Alan Phillips  (London, UK)http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4157760/

A150.  Enhanced gliadin peptide binding to intact small intestinal brush border membranes in coeliac disease. (Tübingen, Germany)

A151.  Diversity of epitopes of coeliac disease autoantibodies (Leipzig, Germany)

A152. Studies on IgA-autoantibodies against fibroblast derived antigens in celiac disease (Uppsala, Sweden)

A153. Ig-A antibodies against human proteins in sera from coeliac patients determined by western blotting (uppsala, Sweden)

A154. Cross-reactivity of antigliadin antibodies in coeliac patients with enterocyte antigens (Edmonton, Canada) http://www.ncbi.nlm.nih.gov/pubmed/9400629
 Vasta-aineita kalretikuliinia kohtaan.  ( Tässä sivuhyppu. katsoin akertuuko kalretikuliini APP, Abeeta asioihinja se tarkertuu. Musiiin Mmeoryblogiin  "Calretikuliini".

A155. Deficit  in spontaneous IL-4 secretion by intraepithelial and laminapropria (LPL) lymphcytes from adult coeliac patients.  (France) In conclusion: a defect of IL-4 secretion by intestinal lymphocytes could represent a primary immune dysfunction in adult coeliac disease.

A156. Cytokine production following gliadin stimulation of circulateing peripheral blood mononuclear cells (Maynooth, ireland)

A157. Soluble interleukin-2 (SIL-2R) receptor concentration in serum or children with coeliac disease before and after introduction of a gluten-free diet. (sIL-2R concentration coul be used as an additional method in the coeliac patient therapy response evaluation)

A158.  Leukocyte aggregation and celiac disease. (Milan italy)
http://www.enabling.org/ia/celiac/tamper.htmlhttp://www.enabling.org/ia/celiac/tamper.html

A159.IFN-gamma and IL-4 producin cells in blood of children with coeliac disease.(Uppsala, Sweden)

A160. Effect of alfa-gliadin on intestinal epithelial cell lines; a comparison with G+ and G- antigens( Paris, France)

A161  Gliadin specific, CD4+ T cells are frequntly found in the small intestinal mucosa of both celiac disease and dermatitis herpetiformis patients.  (Oslo, Norway)

A162  Cellular immunity in coeliac disease  (Thessaloniki, Greece)

A163.  Specificity to cereal prolamines an HLA restriction of the T-cell clones isolated from jejunal mucosa of celiac patients.

A164.  T-cell receptor (TCR) repertoire in coeliac disease (CD) conserved junctional sequences in the untreated mucosa (Naples, Italy)

A165. T-lymphocyte sub-populations in healthy human intestinal lamina propria. (Dublin, Ireland)

A166 Quantification of intraepithelial lymphocytes (IEL) subsets by flow cytometry analysis (FCA).

A167. Increased HLA-DR and decreased CD3 on human intestinal intraepithelial lymphocytes: evidence of activation. (Dublin, Ireland)

A168. Quantification of intraepithelial lymphocytes using computerised image analysis.

A169. Intraepithelial  lymphocytes (IELs) in the celiac mucosa induce cell death (apoptosis) of enterocytes (Jerusalem, israel)

A170. T cell immune responses to gliadin in coeliac and normal individuals (Ireland)

A171. Immune response in vitro to human fibroblast-derived coeliac disease autoantigen is HLA DR/DQ restricted (Hki, Tre, Finalnd)

A172. Circulating CD45RO+ TcR gammadelta cells in coeliac disease  patients and their healthy family members ( Hki, Tre, Finland)

A173. HLA-DQ2 as a marker of potential coeliac disease among first-degree relatives of coeliac patients 8Spain)

A174.  Relationship between abnormal immunological parameters and the coeliac HLA haplotype in non-coeliac patients. (Edinburgh)

A175. TNF2, a polymorfism of the TNF.-alfa promoter,  is a component of the coeliac disease haplotype.

A176. Restricted T-cell receptor Vbeta gene usage in the skin of patients with dermatitis herpetiformis(DH) . Conclusion: These results support the hypothesis that recognition of an antigen or superantigen is involved in the pathogenesis of DH skin lesions.

A177. Gliadin-induced enteropathy in rats affects activities of intestinal brush-border enzymes (Czech Republic)
Conclusion: Rat model of intestinal enteropathy revealed that alfa-glukosidases increased while lactase, dipeptidylpeptidase (DPP IV)  and  gamma-glutamyltranspeptidase (GGT) decreased after gliadin feeding to newbornd animals.

A178. Experimental model of coeliac disease in non-suckling, artificially fed rats. (Czech republic)

A179. DLA-DQ alleles in Irish setter dogs with naturally occuring gluten-sensitive enteropathy (London, UK)
 
A180. Jejunal leucocyte populations in the early stages of gluten sensitive enteropathy in Irish setter dogs. (London, UK) 

A181. Lamina propria and intraepithelial leucocyte populations in Irish setter dogs with gluten sensitive enteropathy. (London, UK)

torsdag 4 juni 2015

1996 Free Paper Abstracts. A98- A125 Serology.

A98.  Screening relatives of patients with coeliac disedase by means of serum anti-endomysium antibodies .

A99  Human umbilical vein endthelial cells: a new easily available substrate for detecting endomysial antibodies in patients with coeliac disease (Dublin)

A100. Antiednomysium antibody on human umbilical cord vein: a cheap and sensitive diagnostic tool for the screening of celiac disease (Trieste, Italy)

A101.  Evaluation of the endomysiual antibody test in screening for coeliac disease: in a clinical practice setting.  (Dublin)

A102. Human umbilical cord tissue: a suitable substrate for endomysial antibody detection. (UK)

A103. Endomysium autoantibodies on human umbilical cord (HUC) in coeliac disease (Finland)

A104.  Human umbilical cord-derived fibroblasts as antigen in whole cell Elisa for coeliac disease antibodies (Finland)

A105. Connective tissue substrates in serum screening for coeliac disedase (CD).(Tübingen, Germany)

A106. Same substrate for antiendomysium, anti-jejunum and anti-reticulin assay. (Budapest,Hungary)

A107. Endomysium antibodies (EmA) and detection of silent coeliac disease (Barcelona, Spain)

A108.  Human umbilical cord antibodies (HUC-Ab) for CD-screening (Barcelona, spain)

A109 Endomysial antibodies in relation n to celiac disease (CB) activity in lamina propria of jejunal mucosa. (Prague)

A110. Frequency of aspecific staining in the anti-endomysium antibody assay (Budapest, Hungary)

A111.  Improving methods in serum screening for coeliac disease (Tübingen,Germany)

A112. Human liver- suitable antigen for reticulin antibody determination, a prospective study. (Czech Republic)

A113. Three immunological markers may replace intestinal biopsy in the diagnostic approach of coeliac disease (AGA, EMA, ARA)  (Thessaloniki, Greece)

A114. Chronic liver disease may be a cause of false positive anti-endomysium antibody assay. (Scotland, UK)

A115. Screening for coeliac disease with Pharmacia CAP system for detectin anti-gliadin IgG and IgA. (Uppsala, Sweden)

A116.  Dietary intake and false positivity of coeliac disease associated antibodies.(Belfast,  N-Ireland)

A117. UniCAP Gliadin IgA and IgG. New in vitro test system for diagnosis and monitoring of coeliac disease (Uppsala, Sweden)

A118.  The differential diagnosis of coeiac disease and other malabsorption syndromes: IgAEmA and IgGEmA tests (Warsaw, Poland)

A119. Screening tests for coeliac disease using antiendomysium antibody on human umbilical cord section (Budapest, Hungary)

A120. Serological methods for antigliadin antibody (AGA) testing: Secalins as an alternative to gliadins. (Madrid, Spain)

A121. Evaluation of the first quantitative method for the measurement of serum anti-gliadin antibodies (AGA)(Valencia, Spain)

A122. Lack of IgG-type serum anti-endomysium and anti-jejunum antibodies in dermatitis herpetiformis patients. (Budapest, Hungary)

A123. Anti-gliadin antibody producing cells in blood of children with coeliac  disease. (Uppsala, Sweden)

A124. Human  umbilical cord tissue (HUCT) : Substrate for the detection of endomysial antibodies (Dublin, Ireland)

A125.  Screening for coeliac disease among 15- and 16- years old adolescents with gliadin- and endomysial antibodies (Göteborg, Sweden) 

1996 Free Paper Abstracts.Intestinal permeability. A93- A97

A93. Intestinal permeability tests in screening of the general population for coeliac disease (Belfast)

A94.Gut permeability in adults with clinial and silent celiac disease (Sweden)

A95. Lactulose-mannitol test, antigliadin and antireticulin antibodies in the screening for coeliac disease (Finland) 

A96. Intestinal sucrose permeability in celiac disease(CD). Alberta Canada.

A97. A transcellular permeability marker is more efficient than a paracellular one in detecting coeliac disease (Sweden)

1996 Fre Paper Abstracts. Casew reports A87- A92

A87
RHABDOMYOSARCOMA OF THE BILIARY TRACT AND COELIAC DISEASE(CD) (Italy)

A88
CELIAC DISEASE IN ASSOCIATION WITH EOSINOPHILIC GRANULOMA (Uruguay)

A89
ASSOCIATION BETWEEN COELIAC DISEASE AND MULTIPLE SCLEROSIS

A90
TWO CASES OF MELKERSSON-ROSENTHAL SYNDROME ASSOCIATED WITH DERMATITIS HERPETIFORMIS AND GLUTEN SENSITIVE ENTEROPATHY  (Hungary)

A91
TRANSIENT ERYTHROBLASTOPENIA OF CHILDHOOD (TEC) AND COELIAC DISEASE: A CASE REPORT  (ITaly)

A92
PERIPHERAL NEUROPATHY ASSOCIATED WITH COELIAC DISEASE: A CASE REPORT IN A CHILD (Italy) 

1996 Free paper Abstracts. Other associated diseases and complications. A76- A86

A76
OBSTETRIC AND GYNAECOLOGICXAL PROBLEMS AND COELIAC DISEASE (Italy)
Pregnancy may precipitate coeliac disease in some women in whom the disease has not been yet diagnostised

A77
GLUTEN SENSITIVITY: EXPLORING THE NEUROLOGICAL ICEBERG (UK)
Antigliadin antibodies may directly or indirectly be involved. if elimination of these antibodies by a gluten-free diet results in stabilisation or even improvement of the neurological dysfunction,  then the role of the  duodenal biopsy becomes questionable. 

A78
NERVOUS SYSTEM MANIFESTATION IN PATIENTS WITH COELIAC DISEASE 8Finalnd)
Neurological disorders are common in patients with coeliac disease. Patients with neurological symptoms can have atypical coeliac disedase.

A79
COELIAC DISEASE AND EPILEPSY?  (Lithuania) 

A80
DOWN SYNDROME AND COELIAC DISEASE  THE PREVALENCE OF IgA-AGA  AND  IgA-EmA.   (SWEDEN)

A81
ANTI_GLIADIN AND ANTI_ENDOMYSIUM ANTIBODIES IN CHILDREN WITH DOWNS SYNDROME  (Sweden)

A82
CELIAC DISEASE IN WLLIAMS SYNDROME (Italy)


A83
COELIAC DISEASE IN PATIENTS WITH ORAL MUCOSAL SYMPTOMS (Finland)
(Patients with aphtous ulceration  and longlasting oral mucosal  symptoms   screened) 

A84
ORAL MUCOSAL CHANGES IN PATIENTS WITH COELIAC DISEASE (Finland)
(Aphtous ulcers, atrophy of the epithelium, moderate to severe inflammation;  persistent oral mucosal changes , especially ulcers  screened )
 
A85
ORAL MUCOSA IS FREQUENTLY AFFECTED IN PATIENTS  WITH DERMATITIS HERPETIFORMIS (DH)  (Finland)
Oral mucosal changes are frequent in DH, even in patients with a strict GFD. oral manifestations might even be an early sign of undiagnosed DH or DH complicated with CD.

A86
INTRAEPITHELIAL LYMPHOCYTES (IEL) BEARING GAMMA/DELTA TcR  IN THE ORAL AND JEJUNAL MUCOSA OF PATIENTS WITH DERMATITIS HERPETIFORMIS (DH)(Finland)
( Not related to gluten ingestion, because their numbers were similar in the untreated and GFD-treated DH patients)

1966 Free paper Abstracts. Endocrinological diseases. A67- A75

A67
CELIAC DISEASE IN DIABETIC CHILDREN AND ADOLESCENTS. SCREENING WITH IgA-ANTIGLIADIN ANTIBODIES ( IgA-AGA) 

A68
INSULIN SECRETION DECLINE UNRELATED TO JEJUNAL MORPHOLOGY OR EXOCRINE PANCREATIC FUNCTION IN CELIAC CHILDREN 

A69
COELIAC DISEASE IN IDDM: ANTIBODY DEteRMINATIONS AND HLA GENOTYPING LEAD the way

A70
THE COEXISTENCE OF INSULIN  DEPENDENT  DIABETES MELLITUS AND CELIAC  DISEASE

A71
COELIAC DISEASE AND ENDOCRINOLOGIC DISORDERS 

A72
CELIAC DISEASE (CD) AND INSULIN DEPENDENT DIABETES MELLITUS (IDDM) A MULTICENTRIC STUDY

A73
COELIAC DISEASE (CD) AND INSULIN-DEPENDENT DIABETES MELLITUS (IDDM) IN CHILDREN OF WEST AFRICA 
(Retrospective analysis of 100 CD-IDDM children, Oran,Algeria)  In the anamnese, the mean age of digestive symptoms was 7,8 +- 5,6 years. The course was complicated by 5 retinopathies, 2 nephropathies, 1 pulmonary tuberculosis and 5 deaths. Another disease was noted in 7 cases.  The high prevalence of CD-IDDM in our context would justify the serological screening CD in IDDM in order to reduce the diagnosis delay of CD and the complications related to these 2 diseases. 

A74
COELIAC DISEASE AND AUTOIMMUNE THYROID DISORDERS (HYPERTHYROIDISM) 

A75
PREVALENCE OF AUTOIMMUNE THYROID DISORDERS ION A COHORT OC COELIAC PATIENTS

1996 Free Paper Abstracts. Osteopenia. A61- A66

A61
IS BONE MINERAL DENSITY IN ADULTS WITH UNTREATED COELIAC DISEASE ASSOCIATED WITH CIRCULATING INSULINLIKE GROWTH FACTOR-I

A62
DOES INCREASED IL-6 SERUM LEVELS IN UNTREATED CELIAC PATIENTS PARTICIPATE IN THE PATOPHYSIOLOGY OF OSTEOPENIA?

A63
LONGITUDINAL STUDY ON THE IMPACT OF LONG-TERM TREATMENT ON BODY COMPOSITION AND ANTROPOMETRY OF CELIAC DISEASE PATIENTS

A64
PROPEPTIDE OF TYPE I PROCOLLAGEN IS PREDICTIVE OF POST-TREATMENT BONE MASS GAIN IN ADULT COELIAC DISEASE 

A65
SPINE AND TOTAL BONE MINERAL DENSITY IN YOUNG ADULTS WITH NEGLECTED CELIAC DISEASE 

A66
VITAMIN D RECEPTOR PHENOTYPES AND BONE DENSITY IN CELIAC DISEASE 

1996 Free Paper Abstracts. Malignancy. A57- A60

A57
NEOPLASTIC DISORDERS IN 100 CONSECUTIVE PATIENTS WITH ADULT CELIAC DISEASE (CD) 

A58
FULMINANT LIVER FAILURE IN A PATIENT WITH CELIAC DISEASE DUE TO HEPATO-SPLENIC (PERIPHERAL T-CELL) LYMPHOMA

A59
HOW MUCH IS COELIAC DISEASE (CD) PREVALENCE INCREASED IN PATIENTS WITH MALIGNANCY?

A60
IS THERE AN INCREASED INCIDENCE OF ORAL PREMALIGNANT AND MALIGNANT LESIONS IN PATIENTS WITH COELIAC DISEASE?

1996 Free Paper Abstracts. A47- A56 Gluten Challenge and coeliac disesase latency

A47
CLINICAL AND MUCOSAL RESPONSES IN COELIACS TO CHALLENGE OF VARIOUS DURATION ANDAMOUNTSD OF GLUTEN

A48
HOW LONG DSOES IT TAKE TO EXCLUDE COELIAC DISEASE?

A49
GLUTEN CHALLENGE FOR DIAGNOSIS OF GLUTEN SENSITIVE ANTEROPATHY

A50
A PILOT STUDY OF BIOCHEMICAL GROWTH MARKERS DURING GLUTEN CHALLENGE IN CHILDREN WITH  COELIAC DISEASE

A51
MORPHOMETRIC AND IMMUNOHISTOCHEMICAL ANALYSIS OF SMALL BOWEL MUCOSA IN CHILDREN WITH COELIAC DISEASE AND THEIR FIRST-DEGREE RELATIVES 

A52
SEROLOGICAL MARKERS FOR COELIAC DISEASE: CHANGES WITH TIME AND REALATION TO ENTEROPATHY 

A53
SEROLOGICAL SCREENING FOR COELIAC DISEASE INDICATES THAt  LATENCY IS UNCOMMON

A54
IMMUNOHISTOcHEMICAL CHANGES , SEROLOGICAL MARKERS AND HLA GENES IN PATIENTS WITH COELIAC DISEASE AND IN PATIENTS SUSPECTED FOR COELIAC DISEASE BUT HAVING NORMAL JEJUNAL MUCOSA

A55
IMMUNOHISTOCHEMICAL ANALYSIS OF JEJUNAL BIOPSIES FROM SUBJECTS WITH SERUM ENDOMYSIAL ANTIBODIES AND NORMAL MUCOSA 

A56
IS MUCOSAL ENZYME DEFICIENCY A MARKER OF LATENT COELIAC DISEASE?

1996 Free Paper Abstracts. Clinics. A28- A46

A28
AN INSTRUCTIONAL VIDEO ON THE MANAGEMENT OF CELIAC DISEASE
Molloy M, Davidson AGF, B.C:  Chapter of the Canadian Celiac Association. Vancouver BC , Canada
Feedback regarding the video has been very positive and supports the premise that video is an effective medium for isntruction or trnafer of information.  
 http://www.powershow.com/view/3b1b30-NTk4M/Celiac_Sprue_Review_of_a_Multisystem_Disease_Thomas_Repas_powerpoint_ppt_presentation

A29
CEREAL INTAKE OF ESTONIAN INFANTS
Mitt K, Uibo O. Tartu, Estonia 

A30
GLUTEN FREE DIET (GFD);: EFFECTS ON THE GROWTH PROGNOSIS OF COELIAC CHILDREN DIAGNOSED LATELY AND FOLLOWED AT LONG TERM
 Boudraa G, Benbouabdellah M, Moussaoussaid S, Haddou A, Touhami M.  Oran. Algeria
Th CD screening should be made early and the CD follow-up should be prolonged after the adolescence because the statural gain is always possible. 

A31
PECULIARITIES OF COELIAC DISEASE IN CHILDREN OF THE URAL REGION
Bolotova MF, Koruykina LP, Surinov VA. Perm, Russia
Background: Noninfectious pathology of gastrointestinal tract in children is an actual problem. Coeliac disease diagnosis is difficult.  
The aim of our study was to investigate clinico-laboratory peculiarities of this disease  in children of Perm and region. 
Methods. Clinico-laboratory examination of 17 patients included general and biochemical analysis of blood with determination of protein fractions, lipogramme, electrolytes, enzymes: coprogramme, determination of trypsin and disacharide content in feces, estimation of intestinal flora, sweat test, T-, B-lymphocytes and immunoglobulins, USI of liver and spleen, bone roentgenography.  
 Results:  During the last 3 years coeliac disease was diagnostised in 17 children. The first symptoms appear, when children take gliadincontaining food: loose, butter stool (100%), body mass decrease. Arrest of physical development, xeroderma, muscle hypotension, anorexia, vomiting, abdominal pain were revealed in 70% of children, pseudoascites in 2, osteoporosis in 4 children. Half of children demonstrated hypochromic anemia of the I stage and eosinophilia.. Dysproteinemia was determined in 30%, cholesterol, beta-lipoprotein,  calcium decrease  in 50% . Fatty acids, neutral fat, muscle fibers, iodophilic bacteria, protein detritus were revealed in coprogramme. Disturbance of intestinal microflora correlation was estimated.  Decrease of theophyllinesensitive T-lymphicytes and IgA level was obtained in immunogramme in 1/3 of children. USI demonstrated pancreas changes in 50%. Prescription of agliadin diet and enzymes led to appetite improvement, stool normlization, body mass growth , anemia disappearance.



A32
UNCHANGED CLINICAL PATTERN OF CHILDHOOD COELIAC DISEASE IN SICILY
Cataldo F, Bottaro G, Traverso G, Violante M, Palermo, Catania, Italy

A33
A TYPICAL FORMS OF COELIAC DISEASE (CD),
Olazabal JI, Alvarez R, Ariza F, Ramos A., Loza C,  Asturias, Spain.

A34
PREVIOUS MISDIAGNOSIS AND DIAGNOSTIC DELAY IN COELIAC DISEASE
Brusco G, DiStefano M, Andreani ML, Bisgi F, Jorizzo RA, Arfilli L, Taglieri G, GAsbarrini G, Corazza GR, Italy 

A35
COELIAC DISEASE, A COMPARATIVE STUDY OF TWO PERIODS; 1975 TO 1984 AND 1985 TO  1994. 
Junqueira JC, Calcado AC, Percope S, Tao M.  Rio de Janeiro, Brazil

A36
COELIAC DISEASE IN THE ELDERLY: A MULTICENTRIC STUDY
DeVitis I, S´Addesa , Pasqualetti MR, Brusco G, Corazza GR, Gasbarrini G.  L-Aquila, Italy

A37
PATIENTS WITH SUBTOTAL VILLOUS ATROPHY: DIFFICULTIES OF MAKING ETHIOLOGICAL DIAGNOSIS AND FOLLOW UP
Tao MT, Junqueira JC, Carvalho CRF, MAfra CNC, Gracia J,,Calcado AC, Guerra SNRP. Rio De Janiero, Brazil 

A38
NUTRITIONAL STATUS OF NEWLY DIAGNOSED COELIAC PATIENTS- ASSOCIATION WITH THE GRADE OF VILLOUS ATROPHY
(Partial atrophy, Subtotal atrophy, Total villous atrophy) 
Kemppainen T, Kosma V-M, Janatuinen E, Julkunen R, uusitupa M.

A39
SUPERIOR MESENTERIC ARTERY BLOOD FLOW IN CELIAC CHILDREN 
Ertem, D, Tüney D, Pehlivanoglu E, Istanbul, Turkey

A40
ULTRASONOGRAPHY OF THE ABDOMEN IN CHILDREN WITH COELIAC DISEASE
Kuleta-Bosak E, Kalita B, Sikora A, Slimok M,, Urban K, Bytom, Poland. 
Ultrasonographic examination was carried out by means of Sonoline SL1, S1250 transducer sectoral 5 MHz and linear 5 and 7,5 MHz.   All the organs of the abdomen were examined and special attention was paid to the appearance of the loops of the intestine i.e. width, contents, speed of peristalsis. In all cases, serum was tested for IgA EmA/IgG EmA and in particular cases duodenal biopsy was performed. Altogether 85 ultrasonic examinations of the abdomen were performed on 58  children with coeliac disease. Twenty-seven children were in process of the initial diagnosis (IgA EmA positive  and villous atrophy (VA)  III-IV degree). In 20 children a characteristic picture of the abdomen was observed with overflowing liquid contents in the lumen ( pseudoascites)  and meteorismus. ( Suoliäänet vilkaat ja loiskivat).  On gluten challenge ( 7 children), in all cases we noticed changes in the ultrasonographic picture of the intestines.  Conclusions: (1) Enlarged intestinal loops with  a considerable amount of liquid contents in the lumen and live peristalsis seen in ulttrasound examination may be a symptom of malabsorption syndromes and should accelerate gastroenterological diagnosis.  (2) Appearance of such a picture of intestines in ultrasonic examination in children being treated by gluten free diet may be  a first sign of not properly observing gluten-free diet. (3)  During gluten provocation the changes in the ultrasonographic picture of intestines may preceed the appearane of antiendomysial antibodies (anti-EmA) .

A41
SOME PARAMETERS OF SERUM LIPID PROFILE IN CHILDREN WITH COELIAC DISEASE
Obuchowicz A, Marek M, Kalita B, Slimok M, Z Szcepanski. Silesian Academy of Medicine,  Bytom,, Poland

 A42
THE USEFULNESS OF BETA-2 MICROGLOBULIN DETERMINATION IN CHILDREN WITH COELIAC DISEASE
Beta-2-m levels were raised , indicating indirectly the state of intestinal mucosa and the changes caused in it by glutren. Beta-2-m determiantion can be useful as a non-invasive means of monitoring treatment with a gluten-free diet. 
 Sikora A, Kalita B, Bukowska C,  Slimok M,  Szczepanski Z. , Sulej J, Chorzelski TP

A43
ABNORMAL RECTOSIGMOID MOTILITY IN UNTREATED CELIAC DISEASE: IMPROVEMENT ON GLUTEN-FREE DIET:
Low levels of TG and VLDL in all children  with CD.
 In children   with CD ,correctly observing a gluten-free diet, both total cholesterol levels and arterosclerosis risk factor are higher as compared to children with CD  and not observing a gluten free diet and children  without CD. 
Iantorno G, Bilder C, Pedreira S, Niveloni S, Smecuol E, Vazquez H, Mazure R, Boerr L, Maurino E, Bai JC.

A44
PERINUCLEAR ANTINEUTROPHIL CYTOPLASMIC ANTIBODIES (p-ANCA) IN CELIAC DISEASE (CS)
Freeman HJ.  University of British Columbia, Vancouver, Canada. 

A45
SCANNING ELECTRON MICROSCOPY IN COELIAC DISEASE
Magliocca FM, Bonamico M, Petrozza V, Mariani P, MontuoAi M, Carpino F. Rome, Italy

A46
HELICOBACTER PYLORI INFECTION IN COELIAC CHILDREN
Slimok M, Sikora A, Kalita B, Zdmudzinzka-Kitczak J, Stoltny L, Szczepanski Z. Bytom,, Poland

1996 Free Paper Abstracts. Epidemiology. A20- A27 Poster Presentations.

A20
 COELIAC DISEASE. HOW BIG IS THE ICEBERG
Dotti M, Montanelli A, Farina GP, Ravelli A, Catassi. University of Brescia, university of Ancona,, Italy
http://www.ncbi.nlm.nih.gov/pubmed/8783752

Acta Paediatr Suppl. 1996 May;412:29-35.The coeliac iceberg in Italy. A multicentre antigliadin antibodies screening for coeliac disease in school-age subjects.

BACKGROUND: Recent studies suggest that coeliac disease (CD) is one of the commonest, life-long disorders in Italy. The aims of this multicentre work were: (a) to establish the prevalence of CD on a nationwide basis; and (b) to characterize the CD clinical spectrum in Italy.

PATIENTS AND METHODS: Fifteen centres screened 17,201 students aged 6-15 years (68.6% of the eligible population) by the combined determination of serum IgG- and IgA-antigliadin antibody (AGA) test; 1289 (7.5%) were IgG and/or IgA-AGA positive and were recalled for the second-level investigation; 111 of them met the criteria for the intestinal biopsy: IgA-AGA positivity and/or AEA positivity or IgG-AGA positivity plus serum IgA deficiency.

RESULTS: Intestinal biopsy was performed on 98 of the 111 subjects. CD was diagnosed in 82 subjects (75 biopsy proven, 7 not biopsied but with associated AGA and AEA positivity). Most of the screening-detected coeliac patients showed low-grade intensity illness often associated with decreased psychophysical well-being. There were two AEA negative cases with associated CD and IgA deficiency. The prevalence of undiagnosed CD was 4.77 x 1000 (95% CI 3.79-5.91), 1 in 210 subjects. The overall prevalence of CD, including known CD cases, was 5.44 x 1000 (95% CI 4.57-6.44), 1 in 184 subjects. The ratio of known to undiagnosed CD cases was 1 in 7.

CONCLUSIONS: These findings confirm that, in Italy, CD is one of the most common chronic disorders showing a wide and heterogeneous clinical spectrum. Most CD cases remain undiagnosed unless actively searched


A21
HIGH PREVALENCE OF COELIAC DISEASE AMONG SWEDISH ADULTS
Hernell O, Ivarsson A, Persson LÅ, Juto P, Suhr O, Umeå University, Sweden
http://www.researchgate.net/profile/Olle_Hernell/publication/13195006_High_prevalence_of_undiagnosed_coeliac_disease_in_adults_a_Swedish_population-based_study/links/5421691e0cf203f155c66c43.pdf


A22
 REGIONAL DANISH COELIAC DISEASE
Weile B, Krasilnikoff PA, Gentofte Hospital, Hvidövre Hospital, Copenhagen
http://www.biomedsearch.com/nih/Low-incidence-rates-by-birth/1498504.html

A23
INCIDENCE OF COELIAC DISEASE IN NORTHERN GERMANY 
Peters U, Kayser H, Jung A, Erbersdobler HF. University of Kiel, Germany
http://www.wjgnet.com/1007-9327/ejournals/WJGv16i16.pdf


A24
 FAMILIAL INCIDENCE OF COELIAC DISEASE IN POLAND
Grzenda-Adamek Z, Stopyrowa J, Pituch-Noworolska A, Miezynski W.  University, Krakow, Poland
http://www.advances.am.wroc.pl/pdf/2007/16/2/297.pdf
 http://www.ncbi.nlm.nih.gov/pubmed/8775318

A25
A POPULATION BASED STUDY OF COELIAC DISEASE IN A EUROPEAN COUNTRY. THE SAN MARINO
Blagi F, Andreani ML, Stefano M, Corrao G,Pretolani S, Giulianelli G, Brusco G, Arfilli L, Malservisi S, Ghironzi G,Taglieri G, GasbarriniG, Corazza GR.
 http://www3.med.unipmn.it/docenti/b/biagi.federico/Biagi%20Federico.pdf

A26
COELIAC DISEASE RISK IN USA: HIGH PREVALENCE OF ANTIGLIADIN AND ANTIENDOMYSIUM ANTIBODIES IN HEALTHY BLOOD DONORS IN THE USA
Not T, Horvath K,  Hill I, Partanen J, Magazzu G, Fasano A.
Prevalence 1:250 .  Coeliac disease is underdiagnosed in USA. 
http://informahealthcare.com/doi/abs/10.1080/00365529850172052?journalCode=gas

A27
HIGH PREVALENCE OF CELIAC DISEASE AMONG HEALTHY CHILDREN AND YOUNG ADULTS IN FINLAND
May be 1:75 in population under 30 years.  Using  antigliadinantibody (AGA)  testing as a primary screening method, only a proportion of patients with silent celiac disease may be found.
Kolho K-L, Åkerblom H, Viikari J, Savilahti E.
 http://www.gastrolab.net/ks1refer.htm#24

1996 Free Paper Abstracts. A12-A19. Pathogenesis, Immunology and Genetics


A12
BINDING OF GLIADIN PEPTIDES TO HLA-DQ2,- DQ8 and -DR3 MOLECULES
Godkin A, Davenport M, Hill A, Jewell DP. Oxford UK
http://www.ncbi.nlm.nih.gov/pubmed/9199974
IDDM, Coeliac disease

A13
CYTOKINE PROFILE IN COELIAC DISEASE
Karban A, Shapiro S, Lerner A, Gershtein R,, Kinarty A, Lahat N.
http://www.ncbi.nlm.nih.gov/pubmed/10219772
Markers of disease activity

A14
ACTIVE COELIAC DISEASE IS CHARACTERISED BY CHANGES IN  SUBPOPULATIONS OF SMALL INTESTINAL LYMPHOCYTES ( gammadelta TCR+)  AND   CD4+CD8+  IN BOTH EPITHELIAL LAYER AND LAMINA PROPRIA.
Carton J, Madrigal L, O´Donoghue DP, O´Farrelly C.
 http://www.researchgate.net/publication/8342866_CD4CD8_human_small_intestinal_T_cells_are_decreased_in_coeliac_
patients_with_CD8_expression_downregulated_on_intra-epithelial_T_cells
_in_the_active_disease

A15
IMMUNODEFICIENT MOUSE MODEL OF GLIADIN INDUCED ENTEROPATHY
Tlaskalova H, Farre MA, Funda DP, Tuskova L,, Horak I, Horakova D, Rehakova Z,Kozakova H,Verdu E,, Stepankova R. Prague, Wurzburg, Germany
 http://uthscsa.edu/micro-immunology/faculty/pclab/print/2008%20Atassi%20Autoimmunity.pdf

A16
COELIAC DISEASE AUTOANTIGENS HOMOLOGOUS WITH GLIADIN
Börner H, Osman AA, Bär J, Mothes T.  University of Leipzig, Germany
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1727378/
Gut. 1999 Feb; 44(2): 168–173.
PMCID: PMC1727378 Identification of common epitopes on gliadin, enterocytes, and calreticulin recognised by antigliadin antibodies of patients with coeliac disease
S Krupickova, L Tuckova, Z Flegelova, M Michalak, J Walters, A Whelan, J Harries, J Vencovsky, and H Tlaskalova-Hogeno...

A17
INTRAEPITHELIAL CLONAL T CELL PROLIFERATION IN THE GUT OF PATIENTS WITH REFRACTORY  SPRUE.
Cellier C., Patey N, Mauvieux L, Cuenod B, Cervoni J-PC, Guy-Grand D, Macintyre E, Barbierr J-Ph, Brousse N, Cerf-Bensussan N.
  https://www.karger.com/Article/Pdf/7779

A18
HUMAN T CELL CLONES FROM THE SMALL INTESTINE AND PERIPHERAL BLOOD EXPRESS VERY SIMILAR ADHESION MOLECULES
Lundin KEA, Gaudernack G,  Oslo University, Norway
http://www.researchgate.net/profile/Knut_Lundin/citations?sorting=citationCount&page=5 

A19
USE OF DIFFERENTIAL DISPLAY REVERSE TRANSCRIPTION  PCR TO IDENTIFY NOVEL DIFFERENTIALLY- EXPRESSED GENES IN COELIAC DISEASE
Aldersley MA, Smith NR, Robinson PA, Markham AF, Howdle PD.
 http://www.ncbi.nlm.nih.gov/pubmed/10672836
IBD
 http://www.ncbi.nlm.nih.gov/pubmed/?term=Smith+NR%2C+Robinson+PA%2C+Markham+AF%2C+Howdle+PD.

1996 Free Paper Abstracts A9- A11. Prolamins

A9
STUDIES OF GLIADIN TOXICITY USING SYNTHETIC PEPTIDES
Cornell H, Mothes T.
University of Leipzig, Germany.
Royal  Melbourne Institute of Technology, Australia
 http://www.ncbi.nlm.nih.gov/pubmed/7727540
" PSQQ motif was not solely responsible for toxicity"
"QQPY motifs,  importance of the flanking amino acids"- 

A10
ABSENCE OF OATS CEREAL TOXICITY IN ADULT COELIAC DISEASE
Srinivasan U, Leonard N, Jones E, Weir DG, O´Farrelly C, Feigherry C.  Dublin, Ireland
 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809658/

A11
ISOLATION OF omega1-SECALIN, A SENSITIVE AND SPECIFIC MAJOR RYE PROLAMIN FOR COELIAC DISEASE DIAGNOSIS
Alfonso P, Camafeita E,, S-Sebastian J, Ribes C, Escobar H, Suarez L,Mendez E,, Madrid, Spain

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2696423/
Multiple myeloma

Toxic repetitive pentapeptide epitopes in gliadin:
http://www.researchgate.net/profile/Thomas_Mothes/publication/11643013_A_monoclonal_antibody_that_recognizes_a_potential_coeliac-toxic_repetitive_pentapeptide_epitope_in_gliadins/links/00b49515dc2a78c3a8000000.pdf

1996 Free Paper Abstracts, Epidemiology and clinics

Epidemiology and clinics,  A1- A8

A1
COELIAC DISEASE HAS A MULTIFACTORIAL ETHIOLOGY 
Ivarsson A, Persson LA, Hernell O. Umeå University, Sweden.
Coeliac disease has a multifactorial etiology. 
 http://www.karger.com/Article/Pdf/86234

A2
COELIAC DISEASE IN NORWEGIAN BLOOD DONORS 
Hovdenak N, Bovlid E, Fkluge G, Aksnes L, Erichsen M, Eide J, Deaconess Hospital and Haukeland Hospital, Bergen, Norway.
http://www.ncbi.nlm.nih.gov/pubmed/10102231

A3
MARKERS OF COELIAC DISEASE LATENCY IN PATIENTS WITH POSITIVE RETICULIN AND GLIADIN ANTIBODIES
 Kaukinen K, Collin P, Holm K, Karvonen A-L, Pikkarainen P, Mäki M, University Hospital and University of Tampere, Finland
http://www.ncbi.nlm.nih.gov/pubmed/9759950

A4
 QUANTITATIVE EVALUATION OF ADHERENCE TO A STRICT GLUTEN-FREE DIET (GFD) IN ADULT COELIAC DISEDASE (ACD): RELIABILITY OF IgA-ANTI-ENDOMYSIAL ANTIBODIES (EMA) AND INTRAEPITHELIAL LYMPHOCYTE (IEL) COUNTS.
QUANTITATIVE EVALUATION OF ADHERENCE TO A STRICT GLUTEN-FREE DIET (GFD)
Vahedi K, Laberenne JE, Bouhnik Y, Mascart-Lemone F, Desreumaux P, Morin MC, Velly C, Rambaud JC, Colombel JF, Matuchansky C, Hopital Saint-LAzare, Paris, CHRU, Lille, Hopital Erasme, Bruxelles. Ranska, Belgia   http://serials.unibo.it/cgi-ser/start/en/spogli/df-s.tcl?prog_art=1708128&language=ENGLISH&view=articoli 

A5
PSYCHIATRIC ILLNESS IN ADULT COELIAC DISEASE 
Hallert C,, Bengtsson B-O, Ekerling L, Reckner Olsson Å, Ström M, Valdimarssoon T, University of Linköping, Sweden
 http://www.ncbi.nlm.nih.gov/pubmed/7134833

A6
AUTOIMMUNE DISORDERS IN COELIAC DISEASE   (IDDM, Dermatitis herpetiformis,, Atrophic gastritis)
Ventura A, Magazzu G, Balli F, Bertolani P, Caruselli C, Cataldo F, Chiaravalloti G, Greco L,, lambertini A, Martelossi S, Mostaccfio L,, Torre Gg, Ughi C, Zaniboni G,  University of Bolagna, Italy.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1773487/

A7
POST-BULBAR DUODENAL STENOSIS IN CELIAC DISEASE
Murray JA, Schweiger GD, University of Iowa, USA
http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010000700007
 http://eurekamag.com/research/032/879/032879883.php#close

ISBN 952- 9705- 07-7.
  Free Paper Abstracts . All on Coeliac Disease.  Editors P Coollin, M Mäki.
Short oral presentations (Näistä minulla on luentomuistiinpanot olemassa)

Epidemiology and clinics,  A1- A8
Prolamins,  A9- A11
Pathogenesis, immunology and genetics,,  A12- A19
Poster presentations (Tampere-hallissa)
Epidemiology,  A20- A27
Clinics, A28- A46
Gluten challenge and coeliac disease latency, A477- A56
Malignancy, A57- A60
Osteopenia, A61- A66
Endocrinological diseases, A67- A75
Other associated diseases and complications, A76- A86
Case reports, A87- A92
Intestinal permeability, A93- A97
Serology A98- A125
Oats and other cereals, A126-A138
Pathogenesis, immunology and genetics, A139- A181.

Asetan nämä abstraktit ryhmänimiensa alle.  jatkossa


Vuoden 1996 keliakiasymposiumin vapaista abstrakteista

Nämä olivat minulle henkilökohtaisesti merkitseviä abstakteja,, varinkin kun olin juuri alkanut toipuva verisolujen vähenemästä , jokma oli 1981 8 leukosyytit 2,1, trombosyytit alle normaalin,  punasolut  anemian puolela, GT kohollal,  seerumi hemolyyttinen ja kellertävä.  Aloitin  gluteenittoman dieetin , raudan ja B12 vitamiinin.
 Symposiumi 1996 oli  fokusoinut   valkosoluihin ja niiden laatuun.  Jos valkosoluja on 2,1 niin laatuakin on vähemmän,  tietysti, mutta mihin ne minulla katosivat.  Joka tapauksissa  GFD toi niitä takaisin ja nyt ne ovat   4. ( Vuonna 2015).
Tuo abstraktikirja oli minun mielestäni  erittäin  valaiseva, joten.  koetan asettaa niitä muistiin. Niitä voi löytyä nyt netistä. Niitten lukumäärä on 181 , joten  niitten muistiinpanemiseen menee   monta minuuttia per otsikko. Mutta se kannattaa. 
ISBN 952- 9705- 07-7.  Free Paper Abstracts . All on Coeliac Disease.  Editors P Coollin, M Mäki.

Kansainvälisistä keliakiaa käsittelevistä symposiumeista ja konferensseista

 http://www.transglutaminase-what.org/Meetings/

11th International Symposium on Coeliac Disease

28-30 April 2004, Waterfront Hall, Belfast, Northern Ireland Call for abstracts. For further information and registration, see: Web: www.happen.co.uk/iscd2004
NIH Consensus Development Conference on Celiac Disease June 28-30, 2004, William H. Natcher Conference Center, National Institutes of Health, Bethesda, Maryland
by:National Institutes of Health Consensus Development Conference on Celiac Disease
eBook
OCLC: 776004357

 1996, 1998 TAMPEREFinland
  • 7. kansainvälinen symposiumi ja sen jälkeen päätetty kokoontuminen 1998.
http://www.gastroenterologiayhdistys.fi/@Bin/179453/nettimaki_cveurojan13.pdf

1990  HOLLANTI
  Coeliac disease : proceedings of the second International Coeliac Symposium by:International Coeliac Symposium
Book ISBN: 902070463X, 9789020704631
OCLC: 1365969

1992  IRLANTI 
Gastrointestinal immunology and gluten-sensitive disease : proceedings of the Sixth International Symposium on Coeliac Disease held at Trinity College, Dublin, in July 1992 by:International Symposium on Coeliac Disease Dublin :Oak Tree Press, 1994.
Book ISBN: 9781872853437, 1872853439
OCLC: 31518974
 

Kansainvälinen keliakiasymposiumi 2015 . Gluteeniyliherkkyys fokuksessa yleisesti

http://www.icds2015prague.com/guidelines-for-authors/

16th International Coeliac Disease Symposium
2015  21.06-24.06.2015
Pre Conference Workshop on Non Coeliac Gluten Sensitivity; 
The evolving planet of Gluten Related Disorder 

Clinical Forum

Tuesday, June 23
08.30 - 08.50 What celiac patients expect from experts and community
Deutsch H (Austria)


08.50 - 10.10 Fundamental issues
Chairs: Koning F, Guandalini S
20 min Celiac disease  in childhood and adults: 2014
Koning F (The Netherlands)
20 min New view on celiac iceberg – the „Prague“ definition 2015
Ludvigsson JF (Sweden)
20 min Pathogenesis of celiac disease: orchestration of genetic and enviromental factors
Catassi C (Italy)
20 min Progress in diagnosis: Pitfalls in the ESPGAN-work-up
Husby S (Denmark)



10.30 - 12.00 Behind the intestine
Chairs: Ulčová-Gallová Z, Kaukinen K
20 min Skin manifestation of celiac disease: not only dermatitis herpetiformis
Kaukinen K (Finland)
20 min Celiac disease and autoimunity associated conditions in reproductive tract and other organs
Ulčová-Gallová Z (Czech Republic)
20 min Bone Alterations in Celiac Disease
Di Stefano M (Italy)
20 min Psychiatry and neurology
Hadjivassiliou M (UK)
10 min Do extra intestinal manifestations of celiac disease improve on GFD?
Sansotta N (USA)

13.30 - 15.10 Behind the intestine
Chairs: Lundin K, Bureš J
20 min Celiac disease nd malignancies
Sanders DS (UK)
20 min Could we prevent celiac disease and associated autoimunity?
Troncone R (Italy)
20 min Eosinophil disease of GIT
Bouma G (The Netherlands)
20 min Other non-coeliac enteropathies
Bureš J (Czech Republi)
20 min Non celiac gluten sensitivity
Lundin K (Norway)


20 min Early diagnosis and prevention of CD - Is its relevance appraised in practice?
Frič P (Czech Republic)
20 min FODMAP:  Non-nutritional effects of food
Gibson PR (Australia)
20 min Towards optimal gluten-free diet
Welstead L (USA)
20 min Progress in non-dietary therapies
Sollid LM (Norway)
20 min How to measure the response to gluten in clinical trials
Schuppan D (Germany)




Abstrakti 135, vuodelta 1996.IN: All on Coeliac Disease. The 7.th International Symposium On Coeliac Disease

Seitsemännen kansainvälisen keliakiasymposiumin ( 5- 7. syyskuuta  1996 Tampere (FINLAND)  abstrakti numero 135 löytyy nyt PubMed hakulaitteella ja on seuraava:
Muistiinpanovihossani on  tästä abstraktin aiheesta myös luento-osuus näiltä tutkijoilta.  He olivat  saaneet hajoitettua entsymaatisesti pepsiinillä ja trypsiinillä Durumvehnän  proteiinien gliadiinsita fraktioita, joissa koeputkitutkimusten ( in vitro) mukaan  ei ollut toksista vaikutusta  suolen  soluun. He alkoviat  tarkemmin tutkia  peptidin  sisäraeknenta ja päätyivät   kymmenen aminohapon jaksoon. He merkkasivat tämän B-fraktioksi, jonka molekyylipaino oli 1157, 5 ja kutsuivat tätä peptidiä  tällä nimelläkin 1157,5.  He syntetisoivat sitä  pätkää jonka aminohapot olivat (H2)N-QQPQDAVQPF-COOH. He huomsivat että  fraktio B esti frraktio C:n toksisuuden  koeputkessa, kun tutkittiin suolisolun suhteen.  He sanoivat luennossaan että mahdollsesti on löydettävissä jokin peptidirakenne, joka  avustaisi gluteiinitoksisuuta vastaan in vivo ( elävässä kehossa, eräänlainsen tulevaisuuden "suojapeptidi". Sen verran kiinnosotava  asia, että katson miten  tämän  outolaisen gliadiinipeptidin  tietellinen jatko  sitten oli. Vai katosiko  tämä tieteenhaara   netistä. Itse alan olla sitä mieltä, että vilja pitää  hajoittaa  peptidijaksoista, jotka ovat  toksisia, jo ennen kuin ihmiset syö ne. Silloin et tarvitsisi  esim odotaa että lapset syövtä  ensin 2- 4 vuotta väärää ruokaa,   ja sitten yhtäkkiä   teho-osaston tasolta asit   koetetaan diagnosoida onko suolen pinta vielä ehjä. Tulisi yhteiskunnalle  havlemmaksi  hydrolysoida   prolamiinit valmiiksi ja samalla riittäisi kyllä koko maailmalle  ruokaakin paremmin kun  prolamiinit  on tehty  saatavaan muotoon.  maailman tergeystilanne kohentuisi olennaisesti ja syöpä vähenis, saati siten allergiat ja suolsitotaudit.  kaikki vilja pitäisi tosiaan käyttää uusissa  viljan käsittelytehtaissa . Eihän sitä enää syödä perunasta sen salaatillista antia.  Monessa   juureksessakin on kovasti toksiineja ja ne ovat kuitenkin stapelvara-

Vuodelta 2000 löytyy vielä yksi tarkennustutkimus asiasta.  ja siinä mainitaan peptidirakenteen aminohapot.
Vuoden 1996  abstraktia edelsi  peptidin  agglutinaation estokyvyn  tutkimukset kooeputkessa   vehnän, ohran, rukiin ja kauran prolamiinien  agglutinaatiovoimia vastaan. 
MAC =  Minimal Concentration of Cell Agglutination ( mg/L)
MIC = Minimal Concentration required  to complete Inhibition of Cell agglutination induced  by a peptide  concentration 6 x higher than the  minimal concentratioon needed to agglutinate practically all the cells.

Abstraktin  työ johti  tarkentaviin jatkotutkimuksiin, joista on artikkeli vuodelta 2000. 
http://www.ncbi.nlm.nih.gov/pubmed/10771132
 Näyttää siltä että löytöpeptidillä  on  edelleen mainetta  aglutinaation estäjänä koeputkessa. 

LÄHDE:
All on Coeliac Disease. Editors Pekka Collin, markku Mäki.  Free paper Abstracts. Seventh International Symposium on Coeliac Disease. September 5-7, 1996. Tampere Hall, Tampere Finland ISBN 952-9705-07-7

tisdag 2 juni 2015

Onko kyse vain entsymaattisesta vajeesta?

Ravinnon gluteeni on evoloitunut , mutta  entsyymikapasiteetti ihmisessä ei.

Tässä näyttää joku tehneen  lääkkeellisen entsyymin gluteenin pilkkomiseksi. Katsokaapa :
http://www.nutridesk.com.au/enzymes-digestion-intestine-digestive-absorption.phtml

 Periaate on  kuten esim.  näin:  Jos insuliinia puuttuu, ei hätää , syö vain niin paljon kuin haluat niin sitten asetetaan insuliini vastaamaan tilannetta. - (  Niinkuin ruotsiksi sanotaan paarataan insuliini ja  hiilihydraatit)

  Samaa on ajateltu gluteenin suhteen. Mutta tuo entsyymihirviö  jo kuvassa näyttää aika moiselta uudelta allergeeniltä.

Mielestäni- jos teoria ihmiskuntaentsyymin heikentymisestä olisi oikea, tulisi testata mikä on ihmiskunnan  gluteenin  sulatuskyky normaalisti,  ja muokataan   prolamiinipitoiset viljat  entsymaattisen kapasiteetin mukaisiksi.

Saattaa olla että  suurimmalla osalla  gluteenia syövistä  gluteeni ei ehdi pilkkoutua koskaan  täydellisesti   osiinsa aminohapoiksi,  vaan  ehkä joko poistuu kehosta  peptidifragmentteina tai tulehdussolut  pilkkovat ja fagit syövät  ne antigeeneina ilman  suurempia vaivoja.

  Suurin osa ihmisistä on tottunut vaivoihinsa, pitämättä mitenkään tilannetta  normaalista poikkeavana. Kaikkien  immuunipuolustus ei omaa  tunnistusmolekyylejä gluteenille.

 Olisi loogista että keliaakikoista useimmat  olisivat A+ veriryhmäisiä,  joilla on  hämmästyttävä  repertuaari  reagointivalmiita tunnistajia. Liekö katsottu  veriryhmiä tässä asiassa.
HLA alue ei ole kuitenkaan katsottu omaksi veriryhmäkseen. 

OHRA, Suomen eräs kotimainen vilja , Hordeum vulgare , Barley, Brygg, Bjugg, Die Gerste

 Keliaakikko ei voi käyttää ohraviljaa.  Toiset  heistä reagoinevat  ohralle miltei voimakkaammin kuin vehnälle.

Ohrasta löytyy hyvä maisterityö Helsingin Yliopistosta
Marko Meskanen.

 https://helda.helsinki.fi/bitstream/handle/10138/38623/Maisterin%20tutkielma%20Meskanen.pdf?sequence=1

ISSN 0355-1180 HELSINGIN YLIOPISTO Elintarvike- ja ympäristötieteiden laitos
EKT-sarja 1572  OHRAN BEETAGLUKAANIN KONSENTROINTI MYLLYTYKSELLÄ 

Tästä löytyy sivulta 19 selvitys ohran proteiineista  gluteliineista ja prolamiineista  eli hordeiineista. 
 
"Albumiinit ovat jyvän itämisen alkuvaiheessa toimivia entsyymejä, jotka sijaitsevat ohran
aleuronikerroksessa. Globuliineihin kuuluu sekä entsyymejä että pienimolekyylisiä varastoproteiineja sub-aleuronissa ja tärkkelysendospermissä. Prolamiinit eli ohralla hordeiinit käsittävät suurimman osan ohran proteiineista (35–55 %) ja esiintyvät pääasiassa endospermin varastoproteiineina (Shewry 1993). Hordeiinit voidaan jakaa neljään ryhmään: Runsaasti rikkiä sisältävät: pienimolekyyliset B-hordeiinit sekä monomeeriset Ȗ-hordeiinit, ja vähän rikkiä sisältävät: C-hordeiinit ja suurimolekyyliset polymeeriset D-hordeiinit. Gluteliinit ovat puolestaan soluseinärakenteiden niukkaliukoisia rakenneosia (Palmer 1989)"

Ohra-allergioista:
 http://www.prism.gatech.edu/~syarlagadda6/PDFs/barley.pdf
Ohra (Hordeum vulgare)  on englanniksi barley, hebreaksi Shibboleth Shual, (ketuntähkä).
Ohra käytetään lähinnä karjan rehuksi, mutta myös maltaina.
Saksaksi Die Gerste.  
Ruotsiksi:
Korn eller brygg (Hordeum vulgare) är ett sädesslag i familjen gräs. Ordet korn refererade ursprungligen till "det vanliga sädeskornet", men har i dag helt tagit över namnet på det sädesslag som tidigare kallades, på fornsvenska bjugg.[1]