Polymorphisms of TRIB1 genes for coronary artery disease and stroke risk: A systematic review and meta-analysis.

BACKGROUND AND AIMS: In recent years, the results of the association between Tribbles Pseudokinase 1 (TRIB1) gene polymorphism and the risk of coronary artery disease (CAD) and stroke are inconsistent. This study aimed to systematically review the literature on TRIB1 gene polymorphisms and susceptibility to coronary atherosclerotic heart disease (CAD) and stroke. METHODS: This study collected studies published until May 2022 through a systematic search of PubMed, Web of Science, and Google Scholar databases. After a systematic literature search, pooled odds ratio (OR) and their corresponding 95 % confidence interval (CI) were used to assess the strength of the association. RESULTS: We identified 6 studies on rs17321515, including 12,892 controls and 4583 patients, and 3 on rs2954029, including 1732 controls and 1305 patients. In different genetic models, the rs2954029 genetic polymorphism significantly increased the risk of CAD and stroke. In the codominant model, the AA genotype increased the risk of CAD and stroke (OR = 1.74, 95 % CI = 1.39-2.17, P < 0.001); the TA genotype also increased the prevalence of CAD and stroke risk (OR = 1.39, 95 % CI = 1.18-1.64, P < 0.001). Compared with the control group, the TT + TA genotype increased the risk of CAD and stroke in the dominant genetic model (OR = 1.46, 95 %CI = 1.25-1.71, P < 0.001), and in the recessive model, the TA + AA genotype increased the risk of CAD and stroke (OR = 1.41, 95 % CI = 1.15-1.72, P < 0.001). In addition, the TRIB1 rs17321515 polymorphism was not found to be associated with the risk of CAD and stroke, which may be related to other factors such as race. CONCLUSIONS: The rs2954029 A allele was significantly associated with an increased risk of CAD and stroke, according to the present meta-analysis. However, the association of rs17321515 polymorphism with susceptibility to CAD and stroke has not been found in this study.

Clinical verification of Lou type warfarin pharmacokinetic dosing algorithms equation.

Warfarin is the most commonly used oral anti-coagulant in clinic practice. However, it is difficult to recommend the correct dosage due to its narrow therapeutic window. The aim of the present study was to verify the clinical value of the Lou type equation, using pharmacogenetics­based warfarin dosing algorithms to appropriately predict the actual maintenance dose. A total of 87 Chinese Han patients who required treatment with warfarin were enrolled and randomly divided into the experimental and control groups. In the experimental group, the first 3 doses of warfarin were calculated according to the Lou type equation. While in the control group, these 3 treatments were performed following the doctors' recommendations. Then the dose of warfarin was gradually adjusted to the stable dose according to the changes in the international standardized ratio. At the end of the 50 day experimental period, there were a greater number of patients in the experimental group who exhibited a stable blood concentration of warfarin than those in the control group (83.35 and 64.4%, respectively). In addition, the mean and median times for patients to obtain a stable dose in the experimental group were significantly shorter than those in the control group (mean, 18.2±1.7 and 27.3±2.0 days; and median, 11.7±1.1 and 20.5±1.8 days, respectively). The adverse reaction rate of the experimental group (9.5%) was markedly lower than that of the control group (26.7%). The occurrence of adverse reactions in the experimental group was also significantly later when compared with the control group (43.9±1.6 and 38.6±1.5 days, respectively). Furthermore, there was no significant difference between the average predicted dose (3.4±1.1 mg/day) and the average actual dose (3.5±1.4 mg/day; P=0.313). In conclusion, using the Lou type warfarin pharmacokinetic dosing algorithm equation to administer warfarin markedly shortened the adjustment time of warfarin to reach a stable dose and reduced the adverse reactions rate, thus supporting clinical feasibility.