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Serum adenosine deaminase activity and coronary artery disease: a retrospective case-control study based on 9929
Chao Xuan1, Qing-Wu Tian2, Shao-Yan Zhang2
1Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, 59, Haier Road, Qingdao 266101, China.
Insights
Serum adenosine deaminase (ADA) activity is lower in patients with coronary artery disease (CAD), especially myocardial infarction (MI). This finding suggests ADA may play a protective role in cardiovascular health.
Area of Science:
- Biochemistry
- Cardiology
- Metabolic Disorders
Background:
- Adenosine deaminase (ADA) is crucial for purine metabolism, converting adenosine to uric acid (UA).
- Both adenosine and UA are linked to cardiovascular events.
- The relationship between serum ADA activity and coronary artery disease (CAD) remains unclear.
Purpose of the Study:
- To investigate the correlation between serum ADA activity and the presence of CAD.
- To explore the role of ADA in cardiovascular disease pathogenesis.
Main Methods:
- A hospital-based retrospective case-control study involving 5212 CAD patients and 4717 matched controls.
- Serum ADA activity was measured using peroxidase assays on an automatic biochemistry analyzer.
Main Results:
- Serum ADA activity was significantly lower in CAD patients (10.08 ± 3.57 U/l) compared to controls (11.71 ± 4.20 U/l).
- Lower ADA activity negatively correlated with CAD presence (OR = 0.852, p < 0.001) after adjustments.
- Patients with myocardial infarction (MI) exhibited the lowest ADA activity (9.77 ± 3.80 U/l).
- Diabetes and hypertension were associated with increased ADA activity in CAD patients.
Conclusions:
- Serum ADA activity is significantly reduced in CAD patients, particularly those with MI.
- This suggests a potential compensatory mechanism involving adenosine levels to protect the cardiovascular system during CAD.
Background:
Adenosine deaminase (ADA) regulates purine metabolism through the conversion of adenosine to uric acid (UA). Adenosine and UA are closely associated with cardiovascular events, but the correlation between serum ADA activity and coronary artery disease (CAD) has not been defined.
Methods:
We performed a hospital-based retrospective case-control study that included a total of 5212 patients with CAD and 4717 sex- and age-matched controls. The serum activity of ADA was determined by peroxidase assays in an automatic biochemistry analyzer.
Results:
Serum ADA activity in the CAD group (10.08 ± 3.57 U/l) was significantly lower than that of the control group (11.71 ± 4.20 U/l, p < 0.001). After adjusting for conventional factors, serum ADA activity negatively correlated with the presence of CAD (odds ratio = 0.852, 95% confidence interval: 0.839-0.865, p < 0.001). Among the patients with CAD, serum ADA activity was lowest in patients with myocardial infarction (MI; 9.77 ± 3.80 U/l). Diabetes mellitus and hypertension increased the serum ADA activity in CAD patients.
Conclusions:
Serum ADA activity is significantly attenuated in patients with CAD, particularly in MI. We propose a mechanism by which the body maintains adenosine levels to protect the cardiovascular system in the event of CAD.
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