Clwy'r ceudod

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Clwy'r ceudod
Coeliac path.jpg
Data cyffredinol
Enghraifft o'r canlynol Clefyd Edit this on Wikidata
Math Autoimmune disease of gastrointestinal tract edit this on wikidata
Dynodwyr
Thesawrws NCI C26714 edit this on wikidata
Freebase /M/0h1pq edit this on wikidata
OMIM 212750, 607202, 609753, 609754, 609755, 611598, 612005, 612006, 612007, 612008, 612009, 612011 edit this on wikidata
MeSH D002446 edit this on wikidata
UMLS CUI C0007570 edit this on wikidata
Arall
Commons page Ffeiliau perthnasol ar Gomin Wicimedia

Mae Clwy'r ceudod neu glefyd coeliac, sydd weithiau'n cael ei sillafu fel clefyd celiac, yn salwch hunanimíwn o darddiad genetig sy'n effeithio yn bennaf ar y coluddyn bach.[1] Mae'r symptomau yn cynnwys problemau gastrogoluddol megis dolur rhydd parhaus, chwyddo abdomenol, diffyg traul, colli awydd am fwyd, ac ymhlith plant fethiant i dyfu yn normal. Mae hyn yn aml yn dechrau pan fo'r dioddefwr rhwng chwe mis a dwy oed. Mae symptomau nad ydynt yn nodweddiadol yn fwy cyffredin, yn arbennig ymhlith pobl sydd dros ddwy oed.[2][3][4] Gall fod symptomau gastrogoluddol ysgafn neu absennol, nifer eang o symptomau yn effeithio ar unrhyw ran o'r cordd, neu ddim symptomau amlwg o gwbl. Cafodd clwy'r ceudod ei ddisgrifio gyntaf mewn plant;[5][6] fodd bynnag, gall ddatblygu unrhyw bryd ym mywyd y dioddefwr.[7] Mae'n cael ei gysylltu a chlefydau hunanimíwn eraill, megis diabetes mellitus teip 1, a thyroiditis, ymhlith eraill.

Mae clwy'r ceudod yn cael ei achosi gan adwaith i glwten, sef protinau amrywiol sydd i'w cael mewn gwenith a grawn eraill, megis barlys a rhyg.[8][9][10] Mae swmpiau cymhedrol o geirch, sydd heb eu difwyno gan grawn sy'n cynnwys glwten, fel arfer yn gallu ei oddef.[11] Gall y problemau gael eu hachosi gan fathau penodol o geirch.[12] Wrth ddod i gysylltiad a glwten, gall ymateb imiwn annormal arwain at cynhyrchu gwahanol hunanwrthgyrff sy'n gallu effeithio ar nifer o organau.[13][14] Mae hyn yn achos adwaith ennynol yn y coluddyn bach all fyrhau'r leinin fili (crebachiad filaidd) yn y coluddyn bach.[15] Mae hyn yn effeithio ar amsugno maetholion, gan arwain yn aml at anemia.

Mae diagnosis fel arfer yn cael ei wneud trwy gyfuniad o brofion gwrthgyrff gwaed a biopsïau coluddol, gyda chymorth profion genetig. Nid yw cadarnhau'r diagnosis yn rhwydd. Yn aml, mae'r gwrthgyrff yn y gwaed yn negyddol[16] ac mae nifer o bobl ond yn dangos newidiadau coluddol bychain gyda fili arferol.[17] Gall pobl ddangos symptomau eithafol a chael eu archwilio am flynyddoedd cyn y cyflawnir y diagnosis.[18] Yn fwyfwy, mae'r diagnosis yn cael ei wneud ar bobl nad ydynt yn dangos symptomau o ganlyniad i sgrînio.[19] Nid yw'r dystiolaeth ynghylch effeithiau sgrînio, fodd bynnag, yn ddigonol i benderfynu a yw'n ddefnyddiol ai peidio.[20] Tra bod y clefyd yn cael ei achosi tan anoddefgarwch parhaol i brotinau gwenith, nid yw'n ffurf o alergedd gwenith.

Yr unig driniaeth effeithiol sy'n hysbys yw'r deiet di-glwten llym gydol oes, sy'n arwain at adfer y mucosa coluddol, yn gwella symptomau ac yn lleihau'r risg o ddatblygu cymhlethdodau yn achos y rhan fwyaf o bobl.[21] Os nad yw'n cael ei drin, gall arwain at ganserau, megis lymffoma coluddol a chynnydd bychan yn y risg o farwolaeth gynnar.[22] Mae cyfraddau yn amrywio rhwng gwahanol ranbarthau'r byd, o cyn lleied a 1 mewn 300 i gynifer a 1 mewn 40, gyda'r cyfartaledd rhwng 1 mewn 100 ac 1 mewn 170 o bobl.[23] Mewn gwledydd datblygiedig, amcangyfrifir bod 80% o achosion heb gael eu hadnabod, fel arfer am nad oes cwynion gastrogolyddol ac oherwydd ymwybyddiaeth isel o'r cyflwr.[24] Mae'r clefyd ychydig yn fwy cyffredin ymhlith menywod na dynion.[25] Mae'r term "coeliac" yn tarddu o'r Groeg κοιλιακός (koiliakós, "abdomenol") a chafodd ei gyflwyno yn y 19eg ganrif mewn cyfieithiad o'r hyn a ystyrir yn gyffredinol fel disgrifiad o'r hen Roeg o glefyd Aretaeus o Cappadocia.[26][27]

Cyfeirnodau[golygu | golygu cod y dudalen]

  1. "Celiac Disease". Mehefin 2015. Archifwyd o'r gwreiddiol ar 13 Mawrth 2016. http://www.niddk.nih.gov/health-information/health-topics/digestive-diseases/celiac-disease/Pages/facts.aspx. Adalwyd 17 Mawrth 2016.
  2. Newnham ED (2017). "Coeliac disease in the 21st century: paradigm shifts in the modern age". J Gastroenterol Hepatol 32 Suppl 1: 82–85. doi:10.1111/jgh.13704. PMID 28244672. Archifwyd o'r gwreiddiol ar 16 Mawrth 2017. http://onlinelibrary.wiley.com/doi/10.1111/jgh.13704/full. "Presentation of CD with malabsorptive symptoms or malnutrition is now the exception rather than the rule"Free to read
  3. "Subclinical celiac disease and gluten sensitivity". Gastroenterol Hepatol Bed Bench 4 (3): 102–8. 2011. PMC 4017418. PMID 24834166. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4017418.
  4. "Diagnosis and classification of celiac disease and gluten sensitivity". Autoimmun Rev 13 (4–5): 472–6. 2014. doi:10.1016/j.autrev.2014.01.043. PMID 24440147.
  5. "European Society for Pediatric Gastroenterology, Hepatology, and Nutrition guidelines for the diagnosis of coeliac disease". J Pediatr Gastroenterol Nutr 54 (1): 136–60. Jan 2012. doi:10.1097/MPG.0b013e31821a23d0. PMID 22197856. Archifwyd o'r gwreiddiol ar 3 Ebrill 2016. http://www.espghan.org/fileadmin/user_upload/guidelines_pdf/Guidelines_2404/European_Society_for_Pediatric_Gastroenterology_.28__1_.pdf. "Since 1990, the understanding of the pathological processes of CD has increased enormously, leading to a change in the clinical paradigm of CD from a chronic, gluten-dependent enteropathy of childhood to a systemic disease with chronic immune features affecting different organ systems. (...) atypical symptoms may be considerably more common than classic symptoms"
  6. "The Spectrum of Differences between Childhood and Adulthood Celiac Disease". Nutrients 7 (10): 8733–51. Hydref 22, 2015. doi:10.3390/nu7105426. PMC 4632446. PMID 26506381. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4632446. "Several additional studies in extensive series of celiac patients have clearly shown that TG2A sensitivity varies depending on the severity of duodenal damage, and reaches almost 100% in the presence of complete villous atrophy (more common in children under three years), 70% for subtotal atrophy, and up to 30% when only an increase in IELs is present. (IELs: intraepithelial lymphocytes)"
  7. Fasano A (Apr 2005). "Clinical presentation of celiac disease in the pediatric population". Gastroenterology 128 (4 Suppl 1): S68-73. doi:10.1053/j.gastro.2005.02.015. PMID 15825129.
  8. "Clinical and diagnostic aspects of gluten related disorders". World J Clin Cases 3 (3): 275–84. Mawrth 16, 2015. doi:10.12998/wjcc.v3.i3.275. PMC 4360499. PMID 25789300. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4360499.
  9. "Gluten-free diet in children: an approach to a nutritionally adequate and balanced diet". Nutrients 5 (11): 4553–65. Tachwedd 18, 2013. doi:10.3390/nu5114553. PMC 3847748. PMID 24253052. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3847748.
  10. "Coeliac disease". Lancet 373 (9673): 1480–93. Ebrill 2009. doi:10.1016/S0140-6736(09)60254-3. PMID 19394538.
  11. Pinto-Sánchez, María Inés; Causada-Calo, Natalia; Bercik, Premysl; Ford, Alexander C.; Murray, Joseph A.; Armstrong, David; Semrad, Carol; Kupfer, Sonia S. et al. (Ebrill 2017). "Safety of Adding Oats to a Gluten-free Diet for Patients with Celiac Disease: Systematic Review and Meta-analysis of Clinical and Observational Studies". Gastroenterology 153: 395–409.e3. doi:10.1053/j.gastro.2017.04.009.
  12. "Role of oats in celiac disease". World J Gastroenterol 21 (41): 11825–31. Tachwedd 7, 2015. doi:10.3748/wjg.v21.i41.11825. PMC 4631980. PMID 26557006. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4631980. "It is necessary to consider that oats include many varieties, containing various amino acid sequences and showing different immunoreactivities associated with toxic prolamins. As a result, several studies have shown that the immunogenicity of oats varies depending on the cultivar consumed. Thus, it is essential to thoroughly study the variety of oats used in a food ingredient before including it in a gluten-free diet."
  13. "Coeliac disease and autoimmune disease-genetic overlap and screening". Nat Rev Gastroenterol Hepatol 12 (9): 507–15. Medi 2015. doi:10.1038/nrgastro.2015.136. PMID 26303674. "The abnormal immunological response elicited by gluten-derived proteins can lead to the production of several different autoantibodies, which affect different systems."
  14. Nodyn:NICE
  15. "Age-related differences in celiac disease: Specific characteristics of adult presentation". World J Gastrointest Pharmacol Ther 6 (4): 207–12. Tachwedd 6, 2015. doi:10.4292/wjgpt.v6.i4.207. PMC 4635160. PMID 26558154. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4635160. "In addition, the presence of intraepithelial lymphocytosis and/or villous atrophy and crypt hyperplasia of small-bowel mucosa, and clinical remission after withdrawal of gluten from the diet, are also used for diagnosis antitransglutaminase antibody (tTGA) titers and the degree of histological lesions inversely correlate with age. Thus, as the age of diagnosis increases antibody titers decrease and histological damage is less marked. It is common to find adults without villous atrophy showing only an inflammatory pattern in duodenal mucosa biopsies: Lymphocytic enteritis (Marsh I) or added crypt hyperplasia (Marsh II)"
  16. "Systematic review: the use of serology to exclude or diagnose coeliac disease (a comparison of the endomysial and tissue transglutaminase antibody tests)". Aliment Pharmacol Ther 24 (1): 47–54. Gorffennaf 1, 2006. doi:10.1111/j.1365-2036.2006.02967.x. PMID 16803602. Archifwyd o'r gwreiddiol ar 4 Mai 2016. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2036.2006.02967.x/pdf.
  17. "Systematic review: noncoeliac gluten sensitivity". Aliment Pharmacol Ther 41 (9): 807–20. Mai 2015. doi:10.1111/apt.13155. PMID 25753138. "Furthermore, seronegativity is more common in coeliac disease patients without villous atrophy (Marsh 1-2 lesions), but these ‘minor’ forms of coeliac disease may have similar clinical manifestations to those with villous atrophy and may show similar clinical–histological remission with reversal of haematological or biochemical disturbances on a gluten-free diet (GFD)."
  18. "Support for patients with celiac disease: A literature review". United European Gastroenterol J 3 (2): 146–59. Apr 2015. doi:10.1177/2050640614562599. PMC 4406900. PMID 25922674. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4406900.
  19. "Recent advances in coeliac disease". Gut 55 (7): 1037–46. 2006. doi:10.1136/gut.2005.075119. PMC 1856316. PMID 16766754. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1856316.
  20. US Preventive Services Task, Force.; Bibbins-Domingo, K; Grossman, DC; Curry, SJ; Barry, MJ; Davidson, KW; Doubeni, CA; Ebell, M et al. (28 Mawrth 2017). "Screening for Celiac Disease: US Preventive Services Task Force Recommendation Statement.". JAMA 317 (12): 1252–1257. doi:10.1001/jama.2017.1462. PMID 28350936.
  21. "Practical insights into gluten-free diets". Nat Rev Gastroenterol Hepatol 12 (10): 580–91. Hydref 2015. doi:10.1038/nrgastro.2015.156. PMID 26392070. "A lack of symptoms and/or negative serological markers are not reliable indicators of mucosal response to the diet. Furthermore, up to 30% of patients continue to have gastrointestinal symptoms despite a strict GFD.122,124 If adherence is questioned, a structured interview by a qualified dietitian can help to identify both intentional and inadvertent sources of gluten."
  22. "Celiac disease and non-celiac gluten sensitivity". BMJ 351: h4347. Hydref 2015. doi:10.1136/bmj.h4347. PMC 4596973. PMID 26438584. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4596973. "Celiac disease occurs in about 1% of the population worldwide, although most people with the condition are undiagnosed. It can cause a wide variety of symptoms, both intestinal and extra-intestinal because it is a systemic autoimmune disease that is triggered by dietary gluten. Patients with celiac disease are at increased risk of cancer, including a twofold to fourfold increased risk of non-Hodgkin’s lymphoma and a more than 30-fold increased risk of small intestinal adenocarcinoma, and they have a 1.4-fold increased risk of death."
  23. Fasano, A; Catassi, C (Rhagfyr 20, 2012). "Clinical practice. Celiac disease". The New England Journal of Medicine 367 (25): 2419–26. doi:10.1056/NEJMcp1113994. PMID 23252527.
  24. "Celiac disease from a global perspective". Best Pract Res Clin Gastroenterol 29 (3): 365–79. Jun 2015. doi:10.1016/j.bpg.2015.05.004. PMID 26060103.
  25. "Review article: safe amounts of gluten for patients with wheat allergy or coeliac disease". Aliment. Pharmacol. Ther. 23 (5): 559–75. Mawrth 2006. doi:10.1111/j.1365-2036.2006.02768.x. PMID 16480395.
  26. Adams F, translator (1856). "On The Cœliac Affection". The extant works of Aretaeus, The Cappadocian. London: Sydenham Society. pp. 350–1. Adalwyd 12 Rhagfyr 2009.  Check date values in: |access-date= (help)
  27. Losowsky MS (2008). "A history of coeliac disease". Dig Dis 26 (2): 112–20. doi:10.1159/000116768. PMID 18431060.

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