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.

Objective Several investigations have documented an association between migraine and right‐to‐left shunt (RLS). However, whether there are specific clinical features that can distinguish between migraine patients with and without RLS is unclear. This study aims to explore whether there are specific clinical features that can distinguish between migraine patients with and without RLS, and to investigate the relationship between the degree of shunt and clinical parameters of headache. Methods In this study, we enrolled consecutive migraineurs who underwent a structured, standardized questionnaire for family and personal history and for detailed migraine features. RLS was diagnosed based on a contrast enhancement transcranial Doppler (c‐TCD) examination. Results Overall, 113 migraine with aura (MA) and 192 migraine without aura (MO) patients were included. Patients with MA and RLS (MARLS+) had a higher frequency for sensory aura symptoms than those with MA without RLS (MARLS−) (27.4% vs. 10.0%, p = .03). Patients with MO and RLS (MORLS+) presented with significantly younger initial age of migraine onset and experienced more severe pain intensity than those with MO without RLS (MORLS−) (mean ± SD, 25.6 ± 8.9 vs. 29.8 ± 12.7 years, p = .008 and 5.9 ± 1.4 vs. 5.3 ± 1.3, p = .006, respectively). There was no relationship between the degree of shunt and the clinical parameters of headache. Conclusions Our results indicate that MO patients presented with a younger initial age of migraine onset and that sensory aura symptoms in MA patients may predict the presence of RLS. However, we did not find support for relationship between the degree of shunt and clinical parameters of headache.

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.