Adenosine deaminase (ADA) in Rheumatoid Arthritis in patients (RA) Huda Th. Al-Marsomi J Fac Med Baghdad Vol. 51, No. 2, 2009 198 Adenosine Deaminase (ADA) in Rheumatoid Arthritis in patients (RA) Huda Th. Al-Marsomi* PhD Summary: Background: Rheumatoid Arthritis (RA) is heterogenous syndrome. Because the diversity of disease processes and formation of complex lymphoid microstructures that indicate the multiple T cell activation pathways are involved .affected patients have major abnormalities in the T cell pool with clonally expanded CD4 + T cell that lose expression of the CD28null molecule and lack the ability for profiliration. Adenosine deaminase (ADA) is an indicator of the proliferation and differenation of lymphocyte, in particularly the T cell subcells. Patients and Methods: Total ADA levels were measured in the sera of RA patients and healthy group according to Giusti (1981). Results: The mean value of ADA was lower in patients with RA than control group with no significant differences. Conclusion: the lower value of ADA (which involved in the proliferation of lymphocyte) in RA patients may results from the predominance of CD4 + T cells in the peripheral blood Key words: RA, ADA, IR. Introduction: Rheumatoid Arthritis (RA) is a sever chronic inflammatory auto-immune disorder of mysterious etiology, characterized by inflammation of synovial membrane, principally affecting peripheral joints in asymmetric fashion , extra-articular manifestations also occur, so RA is a disease of an aberrant immunresponse (IR) in a genetically predisposed host, Both humoral and cellular IR are important in this disease(1,2).In RA patients have abnormalities in T cell function that are not restricted to the T cell participating in the synovial infiltrates . One aberration is the expansion of selected CD4 T cell to large colonel population. In patients with sever RA, the CD4 +CD28null T cells were initially identified(3,4) .Adenosine deaminase (ADA) (Adenosine aminohydrolase, EC (3.5.4.4)) is the enzyme that irreversibly catalyzes the deamination of adenosine and deoxyadenosine to inosine and deoxyinosine respectively and ammonia(5) . ADA is involved in the proliferation and differenation of lymphocyte, particularly the Tcell subtype, which was found to play a crucial role in the metabolism of the immune system cells and it is essential for the proper development of both T and B lymphocyte in mammals(6). The aim of this study is to investigate the ADA level among RA patients as indicator of IR. *Department of Microbiology, College of Medicine, Al-Nahrin University. Patients and Methods: The study included two groups: a. Rheumatoid Arthritis (RA) patients: Blood samples were collected from thirty patients, their ages ranged from (30-60) years who were attending to AL – Kadhmia teaching hospital from march to august in 2005 and diagnosed by doctors to be infected with RA( before any treatment),all patients have symptoms for two to six months. b .Healthy control group: fifteen individuals from blood bank donors, who have no history of clinical evidence of RA or other clinical disease. Sera were separated and stored at -20 ºC until use. Total ADA levels were measured in the serum of each patient by the method described by Giusti ( 1981) (7). The method is based on measuring the rate of ammonia consumption at 620 nm following the reaction. Results: As shown in table 1 results indicated that their were no significant differences between RA patients (14.63±2.4 U/L) and control group (18.9± 2.15 U/L). Original Article Fac Med Baghdad 2009 Vol. 51 No. 2 Received June 2008 Accepted Jan. 2009 Adenosine deaminase (ADA) in Rheumatoid Arthritis in patients (RA) Huda Th. Al-Marsomi J Fac Med Baghdad Vol. 51, No. 2, 2009 199 Table-1: Mean± SD of serum adenosine deaminase (ADA) level in U/L among RA patients and control group. t=3.09, P<0.05, SD=Standard deviation Discussion: RA is the most common inflammatory arthritis, affecting about 1% of the general population world wide (8) . Pathogenesis of RA is till not fully understood , There is evidence that CD4 +T cells play a central role in initiating , perpetuating and precipitating chronic inflammation in synovial tissue(1,9). Another role of activated CD4 +T cells is stimulation of B cells to differentiate into plasma cells producing RF (Rheumatoid Factor) and other autoantibodies(2,10). ADA enzyme is one of the most essential immune enzymes. It is function gives a clear picture of the immune status of the body. It was found to play a critical role in proper development of the T- and B-lymphocytes in mammals( 10,11). In this study, no significant difference was found regarding the mean value of serum ADA among RA patients when compared with the control group and this may be because those in RA patients had marked difficulties in repopulating the T cell compartment. In RA patients, Peripheral CD4+T cells counts remained depressed to lymphopenic levels for an extended period also T cell have a limited prolifirative life span and chronic immune activation could lead to accumulation of clonally expanded senescents cell (CD4+CD28null) which generally characterized by a limited or complete lack of proliferation that agreement with our resultas as that ADA a marker for cell proliferation. It will be of interest to measure ADA level in synovial tissue before and after treatment and compare it with ADA level in serum to get more information about association between the immune response and ADA level as parameter to response to treatment . References: 1. Anderson, R.J; Rheumatoid arthritis, Clinical and laboratory Features.In: Keppel, J.H; Crofford, L.J; Ston, J.H.et al .Primer on the Rheumatic Disease.12thedit.Atlanta Georgia-Arthritis Foundation .2001:218-225. 2. Helen, ch. ,Mansel, H. ,Siraj, M. and Neil, S.:Joints and muscles. In: Essentials of clinical Immunology 5thed.Blackwell publishing.U.S.A.;2006:p.180-183. 3. Abbe,N.V., Eduardo,D., Cornelia,M.W. and Jorg,J.G. :Biology of T lymphocytes. Rheum Dis Clin N Am ,2004;(30 ) 135-157. 4. Cornella,M.W.,Bryl,E.,Jorg, J.G.; The role of T cells in Rheumatoid Arthritis. Archivum immunologiae et therapiexperimentalis,2000;48:429-435 . 5.Dinjens,W.N.M., Tenkate,J. and Bosman,F.T.:Distribution of adenosine deaminase complexing protein (ADCP) in human tissue. J Histochem Cytochem ,1989;(37)1869-1875. 6.Ammann, A.J.:Immunodeficiency disease. In : Stites, D.P.; Stobo, J.and wells, J.V.editors. Basic and Clinical Immunology.6thed. USA Appleton&Lange; 1987; p.339-341. 7. Giusti, G.:Adenosine deaminase.In: Bergmeyer, H.V. Ed. Methods of Enzymatic Analysis.2nded . Florid: Verlag Chemise International; 1981.2 p.1092-1099. 8. Al-Rawi, Z.S., AL-Azzawi, AJ., Al-Ajili, F.M., Al- WakilR.:Rheumatiod arthritis in population samples in Iraq. Ann Rheum Dis,1978; 37:73-75. 9.Kathleen ,B.and Mason,I,:Pathomechanisms in rheumatoid arthritis-time for a string theory? .The Journal of Clinical Investigation ,2006 ;116(4):869- 871. 10. AL-Ubaide, A.H.; AL-Jeboori, T.I. &Juma, A, S.ADAlevel in patients with hydatid disease (Echinococcus granulosis).Iraqi J Med Sci, 2003; 2(1):25-28. 11.Juma, A., AL-Jeboori, T.I., Tawfiq, M.S. &Fadhil, R.S.:ADA Activity in the serum of patients with Schistosoma haematobium & those with bladder carcinoma. Iraqi J Med Sci, 2003; 2(3):24-28. Group Mean ±SD RA patients 14.63±2.4/L Control group 18.9±2.15U/L