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Serum adenosine deaminase activity and acute cerebral infarction: a retrospective case-control study based on 7913
Yanyan Ling1, Chuan Jiang1, Zhenzhen Xiao1
1Department of Neurology, Shandong Second Provincial General Hospital, Jinan 250000, China.
Insights
Serum adenosine deaminase (ADA) activity is significantly lower in patients with acute cerebral infarction (ACI). This finding suggests decreased ADA may play a role in ACI development and could be an adaptive response.
Area of Science:
- Biochemistry
- Neurology
- Enzymology
Background:
- Adenosine deaminase (ADA) deaminates adenosine to inosine, a pathway linked to uric acid (UA).
- Adenosine and UA are implicated in cerebrovascular events.
- The relationship between serum ADA activity and acute cerebral infarction (ACI) is not well understood.
Purpose of the Study:
- To investigate the association between serum ADA activity and ACI.
- To explore potential correlations between ADA levels and risk factors for ACI.
Main Methods:
- A cohort study including 7913 subjects (3968 ACI patients, 3945 controls).
- Serum ADA activity was measured using an automatic biochemistry analyzer.
Main Results:
- Serum ADA activity was significantly lower in ACI patients (10.10 ± 3.72 U/L) compared to controls (11.07 ± 2.85 U/L).
- Lower ADA concentrations were negatively correlated with ACI (OR = 1.161).
- Smoking and alcohol decreased ADA levels in ACI patients, while diabetes and hypertension increased them.
Conclusions:
- Reduced serum ADA concentrations are observed in ACI patients.
- Decreased ADA may contribute to ACI pathogenesis.
- Hypothesized that lower ADA activity is an adaptive mechanism to preserve adenosine levels and protect against ischemic brain injury.
Background:
Adenosine deaminase (ADA) is a key enzyme that catalyzes the deamination of adenosine into inosine, which eventually decomposes into uric acid (UA). A body of papers have reported that adenosine and UA are closely related to cerebrovascular events. However, the association between serum ADA activity and acute cerebral infarction (ACI) remains unclear.
Methods:
7913 subjects were enrolled, including 3968 ACI patients and 3945 controls, in this study. An automatic biochemistry analyzer was used to determine serum activity.
Results:
Serum ADA activity was found that was significantly decreased in patients with ACI (10.10 ± 3.72 U/L) compared to those without ACI (11.07 ± 2.85 U/L, p < 0.001). After Logistic regression analysis, ADA concentrations were negatively correlated with ACI (OR = 1.161, 95% CI: 1.140-1.183, p < 0.001). Smoking and alcohol consumption decreased serum ADA concentrations in patients with ACI, whereas diabetes and hypertension had the opposite effect.
Conclusions:
Serum ADA concentrations in patients with ACI are markedly decreased, suggesting that the decreased ADA concentrations may be involved in the pathogenesis of ACI. We hypothesized that decreased ADA activity may be an adaptive mechanism to maintain adenosine levels and protect against ischemic brain injury.
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