Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2011 Jul;23(7):598-602.
doi: 10.1097/MEG.0b013e328346e205.

Adenosine deaminase activity in patients with Crohn's disease: distinction between active and nonactive disease

Affiliations

Adenosine deaminase activity in patients with Crohn's disease: distinction between active and nonactive disease

Irit Maor et al. Eur J Gastroenterol Hepatol. 2011 Jul.

Abstract

Background: Crohn's disease (CD) is a common chronic inflammatory bowel disease. During the disease a cascade of immunologic events occur including mucosal influx of inflammatory cells like neutrophils. Adenosine deaminase (ADA) is important in inflammatory responses and serves as a marker of activated leukocytes.

Materials and methods: In this study, we investigated the activity of total ADA (tADA) and its isoenzymes, ADA1 and ADA2, in serum and neutrophils derived from 20 active patients with CD, 20 patients in remission, as well as in 15 healthy controls.

Results: Patients with active disease had significantly (P<0.001) higher levels of tADA in serum (22.9±4.9 U/l) than patients in remission or healthy controls (14.0±3.4 U/l and 13.2±2.4 U/l respectively). ADA2, the main isoenzyme in the serum was higher in active patients by 60% as compared with patients in remission and healthy controls (19.7±1.9 U/l, 12.3±1.2 U/l, and 12.2±0.9 U/l respectively). We did not find a significant difference in these parameters between healthy controls and stable patients. There was a positive correlation (R=0.516) between tADA activity and C-reactive protein levels in patients with CD. Enhanced activity in tADA was also detected in neutrophils that were obtained from all patients with CD as compared with healthy controls (15.3±2.9 U/g, 14.1±2.3 U/g, and 9.4±2.9 U/g protein, respectively). This is mainly due to a significant increment (up to 51%) in ADA1 activity, the main isoenzyme in the neutrophils (84% out of the tADA). The cause of this increment remains to be elucidated.

Conclusion: The results obtained in this study demonstrated elevated levels of tADA and ADA2 in patients with active disease. As the patient improves and becomes clinically stable these levels decrease, approaching normal values. tADA and ADA2 can be used as markers of inflammation, and provide a supportive indicator of CD activity.

PubMed Disclaimer