{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,16]],"date-time":"2026-01-16T00:11:40Z","timestamp":1768522300509,"version":"3.49.0"},"reference-count":29,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2010,9,20]],"date-time":"2010-09-20T00:00:00Z","timestamp":1284940800000},"content-version":"vor","delay-in-days":262,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical Laboratory Analysis"],"published-print":{"date-parts":[[2010,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Celiac disease (CD) is a genetically based chronic inflammatory disorder of the small bowel induced by the dietary gluten and possibly other environmental cofactors. The objective of this study was to investigate the relation of adenosine deaminase (ADA), a cytoplasmic enzyme involved in the catabolism of purine bases, as an index of altered immune response, with adult CD patients. ADA has been shown to increase in several inflammatory conditions, but there is no literature data indicating an alteration in CD. Serum levels of ADA were investigated in newly diagnosed 20 CD patients. ADA levels were compared in patients with CD and in healthy controls. Correlation analysis was also performed between ADA and other serum markers of CD (anti\u2010gliadin and anti\u2010endomysial antibodies) Mean serum ADA levels were significantly elevated in CD patients compared with control group. ROC curve analysis suggested that the optimum ADA level cut\u2010off point for CD was 12.27\u2009U\/l. At a cut\u2010off value of 12.27\u2009U\/l, the sensitivity was 80% and specificity was 100%. There was no statistically significant correlation between ADA and anti\u2010gliadin and anti\u2010endomisium antibodies. Serum ADA levels elevated significantly in CD patients, suggesting a partial role in activated T\u2010cell response in the disease pathophysiology. ADA can be used as a supportive diagnostic marker in patients with CD. J. Clin. Lab. Anal. 24:323\u2013326, 2010. \u00a9 2010 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcla.20410","type":"journal-article","created":{"date-parts":[[2010,9,21]],"date-time":"2010-09-21T01:45:00Z","timestamp":1285033500000},"page":"323-326","source":"Crossref","is-referenced-by-count":9,"title":["Elevated adenosine deaminase levels in celiac disease"],"prefix":"10.1002","volume":"24","author":[{"given":"Basak","family":"Cakal","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yavuz","family":"Beyazit","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Seyfettin","family":"Koklu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Erdem","family":"Akbal","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ibrahim","family":"Biyikoglu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gulsen","family":"Yilmaz","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2010,9,20]]},"reference":[{"key":"e_1_2_5_2_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra010852"},{"key":"e_1_2_5_3_2","first-page":"687","article-title":"Contribution of the MHC region to the familial risk of celiac disease","volume":"36","author":"Bevan S","year":"1999","journal-title":"J Med Genet"},{"key":"e_1_2_5_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/nm0797-797"},{"key":"e_1_2_5_5_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bi.47.070178.003255"},{"key":"e_1_2_5_6_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2141.1977.tb08825.x"},{"key":"e_1_2_5_7_2","doi-asserted-by":"crossref","first-page":"5448","DOI":"10.1016\/S0021-9258(17)33080-6","article-title":"Human adenosine deaminase. 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