Determination of adenosine deaminase (ADA) activity is one of the most promising markers in diagnosing of tuberculous pleural effusion. ADA has two main isoenzymes: ADA1 and ADA2.The ADA2 is the predominant isoform in tuberculous pleural effusion, suggesting its important role as a diagnostic marker.This study was conducted to determine the diagnostic value of ADA and ADA2 measurement in tuberculous pleural effusion. Total ADA and ADA2 isoenzyme activities were measured in 93 case of pleural effusion, including tuberculosis (26males/5females), malignancy (22males/8females), empyema and para-pneumonic (11males/4females), transudate (6males/4females), rheumatoid arthritis and idiopathic (4males/3females). ADA levels were determined by Giusti and Galanti methods. ADA2 was measured with a potent inhibitor of ADA1 isoenzyme. Total ADA and ADA2 activities in tuberculous exudates were 96.6±29.1 and 74.4±29 U/L, respectively. With diagnostic thresholds of 46 and 42 U/L, the sensitivities of ADA and ADA2 for tuberculous exudates were 100% and 97%; their specificities 82 and 88%; and their efficiencies 88% and 93.5%, respectively. All tuberculous exudates, 2 neoplastic, 8 para- infective (including 4 empyemas) and one rheumatoid arthritis had total ADA levels >46 U/L; of these, only one lymphoma and one rheumatoid arthritis had ADA2/ADA activity ratio >50%. Considering simultaneous criteria of total ADA more than 46U/L, ADA2 >42 U/L and ADA2/ADA more than 50%, we had only two false positive results, rising the specificity up to 96%. 1. ADA2 is a more efficient diagnostic marker for Tuberculous pleural effusion compared with total ADA.2. Overall, diagnostic value of ADA would be enhanced by the determination of its isoenzymes, especially for distinguishing between the tuberculous and para-infective effusions. (Tanaffos 2005; 4(15): 37-42)

Adenosine deaminase is an enzyme which catalyses adenosine to Inosine. The determination of adenosine deaminase in body fluids is important for the diagnosis of tuberculosis. There are contradictory reports about the diagnostic value of serum adenosine deaminase in pulmonary tuberculosis. This study was set up to investigate the diagnostic value of serum adenosine deaminase and its isoenzymes activities on pulmonary tuberculosis. In this descriptive study, blood samples were obtained from 26pulmonary tuberculosis patients (group 1), 17 suspected tuberculosis with negative in both smear and culture tests (group 2), and 67 healthy subjects (group 3). Total ADA and ADA2 determination was carried out by kinetic method and EHNA Inhibitor, respectively. ADA and ADA2 activities are as follow: 19.35±5.04, 13.35±5.34 (group 1) 17.24±6.20, 11.47±3.92 (group 2) and 13.96±4.25, 7.36±2.91(group 3). The mean differences of ADA and ADA2 activity between group 1 and 2 with group 3 was meaningful. The sensitivity and specificity for ADA and ADA2 tests were (26.9%, 94 %) and (50%, 97 %) respectively. The PPV for ADA and ADA2 were 63.6% and 86.7% and the NPV were 76.8% and 83.3%, respectively. This study indicated that the assessment of these enzymes in serum to some extend can be a useful method for differentiation of healthy subjects from respiratory disease, but these tests do not have enough sensitivity to assist in the diagnoses of tuberculosis patients from other respiratory diseases.

Aim of Study: Adenosine deaminase (ADA) specifications (EC3.5.4.4) is an enzyme is involved in purine metabolism that breaks adenosine and deoxy-adenosine and produce inosine and deoxy-inosine and ammonia. The highest levels are of adenosine deaminase activity in monocytes and lymphocytes. High serum ADA activity with increased serum levels of AST, ALT and immunoglobulins were reported in variety of diseases including hepatitis. We aimed to investigate the activity of total ADA in serum of patients with hepatitis B and were determined molecular weight ADA1 and ADA2 isozymes in serum and RBC of hepatitis patients.
We were defining experiments by electrophoresis on SDS-PAGE, for isozymes of ADA; ADA1 and ADA2 in serum and red blood cells. ADA1 molecular weight was estimated at about 35 KDa and ADA2 about 110 KDa. The total ADA activity was measured by the modified Ellis method in 37 patients with hepatitis B and 40 healthy controls in the age range (20-60 years).
The normal values for serum ADA in humans have been studied by various workers and found in serum samples to be in the range of 0-15 U/L, whiles in our analysis total ADA (tADA) enzyme activity is in controls and patients with hepatitis B, respectively, 13.35 ± 1.62 and 27.05 ± 8.49. Our results indicated that tADA level was higher in patients with hepatitis B than those of corresponding controls (P Therefore, the serum ADA level could be used as an index along with other parameters in follow up of patients with hepatitis B.

Adenosine Deaminase (ADA) has been found to be involved in autoimmune disease progression.

We aimed to evaluate the diagnostic value of serum ADA activity in Autoimmune Liver Disease (AILD).

The study included 50 AILD patients, 33 viral hepatitis patients, and 60 healthy subjects. The serum levels of total Adenosine Deaminase (tADA) and its isoenzymes (ADA1 and ADA2) were determined. The Receiver Operating Characteristic (ROC) curve analysis was used to evaluate the diagnostic performance of serum ADA activity.

Our results showed that the serum tADA and ADA2 levels were significantly higher in AILD patients (tADA: 19 (IQR 14 - 24) U/L; ADA2: 16 (IQR 10 - 19) U/L) than in healthy controls (tADA: 9 (IQR 7 - 11) U/L; ADA2: 7 (IQR 6 - 9) U/L), while there was no significant difference in serum ADA1 activity between AILD and healthy subjects. Based on the ROC curves analysis, the optimal cutoff values of serum tADA and ADA2 activity were 11.5 and 9.5 U/L, respectively. At this level, the highest diagnostic values of tADA (specificity: 83.3%; sensitivity: 88%) and ADA2 (specificity: 85.0%; sensitivity: 82%) were obtained. Moreover, our results showed no significant difference in serum tADA, ADA1, and ADA2 levels between AILD and viral hepatitis patients (P = 0.049; P = 0.29; P = 0.054).

Serum ADA activity can be used to distinguish AILD patients from healthy subjects, but it cannot be used in the differential diagnosis of AILD and viral patients.

Global initiative for Chronic Obstructive Pulmonary Disease (Gold) has defined COPD as a disease characterized by airflow limitation that is not fully reversible. COPD is a subset of obstructive lung diseases which also includes cystic fibrosis, bronchitis and asthma. Adenosine deaminase (ADA, E.C.3.5.4.4) converts adenosine to inosine. ADA has two isoenzymes; ADA1 and ADA2. In COPD patients the serum level of ADA increases which can be regarded as a result of reduction in ADA activity. In this study we evaluated the level of ADA and its isoenzymes in COPD patients and healthy subjects. Martial and This was a case control study. ADA activity in 30 COPD patients with age range of 20-60 years whose disease had been confirmed by a pulmonologist in Ekbatan Hospital, was compared to the activity of the same enzyme in 60 healthy subjects consisting of 30 non smoker and 30 smoker subjects as control groups. Data were introduced into SPSS version.13 software and analyzed by Kruskall-Wallis and two-way ANOVA tests. ADA activity in the COPD and smoker control groups was significantly lower than that of non smoker group (18.99±7 and 22.99±6.7 U/L, respectively). Regarding ADA2 serum level, the difference between patient group and non smoker control group was significant (P<0.05). Activity of ADA1 isoenzyme in the study groups did not show any significant differences. In general ADA activity was decreased in COPD patients. Decreased ADA activity together with increased adenosine level may play an important role in producing pulmonary damage in COPD patients

Aim and Background. To compare the diagnostic efficiency of adenosine deaminase, isoenzyme adenosine deaminase-2 and concentration of interferon-γ in patients with tuberculous pleural effusion. Materials and Methods. The prospective study was done on 114 patients who were divided into 3 groups: tuberculous, non-tuberculous infectious pleurisy, and malignant effusion. The adenosine deaminase, adenosine deaminase-2 and interferon-γ were analyzed by receiver operating characteristic curves. Results. There was increase of all three markers in tuberculous pleural effusion but not in nontuberculous effusion. The cut-off values for adenosine deaminase, adenosine deaminase-2 and interferon-γ were 40, 26 U/l. and 299 pg/ml respectively. Adenosine deaminase, adenosine deaminase-2 activities were significantly higher in tuberculous effusion than in malignant pleural effusion (more than 5 times) and in non-tuberculous infectious pleurisy (more than 4 times). The median of interferon- γ concentration in pleural fluid of tuberculous patients was 1514.2 pg/ml (931.2-2187.5pg/ml) which was 10 times more than the median values of other groups of patients. There was no significant difference between patients with malignant effusion and those with non-tuberculous pleural effusion. Conclusions. ADA and ADA2 in pleural is a marker for diagnostic of pleural effusion and all three markers had higher diagnostic yield for tuberculous effusion with 95% sensitivity.

Adenosine deaminase (ADA) is involved in recurrent spontaneous abortion (RSA) while normal pregnancy is defined by suppressed cell-mediated immunity. This study aimed to determine the connection between single nucleotide polymorphism (SNP) G22A and protection against RSA. In this analytical case-control study, the allele frequency of ADA G22A gene polymorphism was determined in 113 participants including 50 women with RSA and 63 healthy pregnant women using RFLP-PCR to determine if there is a statistically significant difference in the frequency of ADA genotypes between the patient group and the control group. The frequency of ADA2/ADA2 (AA) genotype was significantly different between RSA patients and controls (P = 0.004) while no significant differences were identified in the genotype frequency of ADA1/ADA1 (GG) (OR = 0.678; P = 0.228) and ADA1/ADA2 (GA) (OR = 0.976; P = 0.943). SNP G22A in the ADA gene was associated with the protection against RSA. The frequency of ADA alleles in RSA patients was compared between the age groups, and the results indicated that the ADA2 (A) allele was associated with protection against RSA in patients aged 35 years or younger (P < 0.0001). The findings showed that women carrying the ADA*2 allele are protected against RSA.

Severe combined immunodeficiency (SCID) is a rare and mortal disorder with X-linked and autosomal recessive inheritance. Many genes is related to the disease including ADA, RAG1, RAG2, Artemis, CD45, JAK3, IL7R which have different clinical presentation and T and B lymphocytes profile. In this study, we investigated gene mutations in suspected patients referred to the Children Medical Center Hospital, Department of Allergy & Clinical Immunology. Blood tests for patients showed T-B- profile, so we selected the genes that were responsible in T and B cell maturation (ADA, RAG1 and RAG2). According to our possibilities, we studied ADA and RAG1 genes in patients. We did the test by PCR and Sequencing method. Also total ADA activity (tADA) and its isoenzymes (ADA1 and ADA2) were estimated in patients. Our investigation showed two mutations in ADA gene and three in RAG1 gene. In this study, we offer a new protocol for investigation of RAG1 gene. This is the first study on diagnosis of SCID patients through genetic investigation in Iranian patients.

Context: 

Diamond-Blackfan anemia (DBA) is a rare autosomal recessive disorder characterized by erythroblastopenia and pure red cell aplasia. The condition typically results from an abnormality in a ribosomal protein gene.

Cases of cytopenia have been linked to ADA2 deficiency caused by CECR1 mutations. In the current case study, a child presented with severe anemia requiring multiple RBC transfusions due to the condition going undiagnosed. After 8 years, the patient developed elevated ferritin levels, severe neutropenia, and a serious infection that complicated the clinical picture. Molecular analysis revealed homozygous variants (c.140G>T p.Gly47Val) in the ADA2 gene inherited from heterozygous parents.

This case represents the first documented instance in Iran, highlighting the importance of screening for congenital defects in seemingly healthy couples, especially emphasizing the need for prenatal diagnosis (PND) using molecular methods and genetic sequencing.

Chronic obstructive pulmonary disease (COPD) has been defined by the Global Initiativefor Chronic Obstructive Lung Disease (GOLD), as a disease state characterized by airflowlimitation which is not fully reversible. COPD consists of emphysema which is thedestruction and inflammation of the lung alveoli. Adenosine deaminase (ADA, E.C.3.5.4.4)converts adenosine to inosine. There are two isoenzymes of ADA in serum; ADA1 andADA2. It has been established that in COPD patients the adenosine levels increase, whichcan contribute to decrease of ADA activity. In this research we studied the ADA and itsisoenzyme activity in COPD patients.This descriptive analytical case-control study was performed on thirty patients who werehospitalized in the pulmonary wards with an acute exacerbation of COPD. ADA activity wasdetermined in 30 COPD patients, 30 nonsmokers and 30 smokers controls. All subjects were male. We used colorimetric (Giusti) method for measuring of ADA activity. The data were analyzed using SPSS 13 software and Kruskall-Wallis and two-way ANOVA tests.Total ADA activity in the COPD and smoker control groups was significantly lower thanin non smoker group (18.99 ± 7, 19.03 ± 9.1 and 22.95 ± 6.7 U/L, respectively). There was a significant difference for ADA2 between the three groups. Whereas the ADA1 activity in the three groups had no significant difference.Based on the obtained data, decrease of ADA activity may play an important role in theformation of pulmonary injury in COPD patients.