جستجوی مقالات مرتبط با کلیدواژه « Plasminogen Activator Inhibitor » در نشریات گروه « پزشکی »

The study aimed to assess the diagnostic accuracy of some fibrinolytic parameters in the differential diagnosis between patients with unstable angina and musculoskeletal disorders.

This cross-sectional study included 119 patients with chest pain, and the provisional diagnosis “UA” was conducted in in 2021 in Bogomolets National Medical University. After a full set of diagnostic procedures, the authors formed four groups: patients with ischemic and non-cardiogenic chest pain without coronary artery disease history (1 & 2) or coronary artery disease history (3 & 4). Blood plasma tissue plasminogen activator and plasminogen activator inhibitor type 1 concentrations, tissue plasminogen activator/plasminogen activator inhibitor type 1, and plasminogen activator inhibitor type 1/tissue plasminogen activator ratios were analyzed.

Binary logistic models were assessed, receiver operating characteristic curves, calculated sensitivity, specificity, and positive likelihood ratio of each indicator. No diagnostic utility of tissue plasminogen activator concentration alone was revealed (p=0.68). Plasminogen activator inhibitor type 1 concentration and plasminogen activator inhibitor type 1/tissue plasminogen activator ratio demonstrated a moderate increase (by 28% and 26%) in the probability of UA (positive likelihood ratio= 4.66 (2.57, 8.45) and 3.87 (2.29, 6.55), sensitivity 87.3% and 88.7%, specificity 81.2% and 77.1% at cut-off point 0.343rel.units/ml and 1.775, respectively), while tissue plasminogen activator/plasminogen activator inhibitor type 1 raised the probability of MSD by 41% (positive likelihood ratio= 6.47 (3.29, 13.00), sensitivity 72.9%, specificity 88.7% at cut-off point 0.584).

PAI-1 concentration alone and tissue plasminogen activator /PAI-1 ratio but not tissue plasminogen activator alone have demonstrated promising results for differential diagnostic between ischemic and non-cardiogenic chest pain.

Recurrent pregnancy loss (RPL) defined by two or more failed pregnancies before 20 weeks of gestation. Several factors play a role in RPL including thrombophilic conditions which can be influenced by gene polymorphisms. Plasminogen activator inhibitor-1 (PAI-1) and angiotensin converting enzyme (ACE) genes are closely related to fibrinolytic process, embryonic development and pregnancy success.

The aim of this study was to investigate the relationship between RPL and common polymorphisms in ACE and PAI-1 genes.

In this case control study, 100 women with recurrent abortions (at least two) were selected as cases and 100 healthy women with two or more normal term deliveries without a history of abortion as controls. Total genomic DNA was isolated from blood leukocytes. The status of the PAI-1 4G/5G and ACE (D/I) polymorphism was determined by PCR-RFLP.

Homozygosity for PAI-1 4G polymorphism was seen in 17 cases (17%), and 5 controls (5%) (p=0.006) so patients with homozygote 4G mutation were significantly more prone to RPL in contrast to control group (OR: 4.63, % 95 CI: 1.55-13.84). In addition, 7 patients (7 %), and no one from the control group, were homozygote (I/I) for ACE polymorphism (p=0.034), suggesting no significant associations between ACE D allele or DD genotype and RPL.

Considering these results, because 4G/4G polymorphism for PAI-1 gene could be a thrombophilic variant leading to abortion, analysis of this mutation and other susceptibility factors are recommended in patients with RPL.

Preeclampsia is a hypertensive disorder of pregnancy, which is associated with increased maternal and prenatal morbidity and mortality. Oxidative stress associated with preeclampsia may be a consequence of reduced antioxidant defense pathways that might involve inadequate glutathione peroxidase (GPx) levels, perhaps linked to reduced selenium availability. The soluble FMS-like tyrosine kinase-1 (sFlt-1) that contributes to endothelial dysfunction may be partially responsible for the clinical manifestation of preeclampsia. Furthermore, elevated plasminogen activator inhibitor-1 (PAI-1) and decreased plasminogen activator inhibitor-2 (PAI-2) are found in preeclamptic women. Hence, the PAI1: PAI2 ratio maybe a predictor of preeclampsia.. The objective of this study was to evaluate the effects of selenium supplementation on sFlt-1, GPx activity and PAI1: PAI2 ratio in pregnant women.. A total of 125 high-risk pregnant women (with a familial history of hypertension, hyperlipidemia and other risk factors for preeclampsia) in the first trimesters of pregnancy were assigned to either selenium (n = 61) or placebo (n = 64) groups. The selenium group received 100 μg/day of selenium as a selenium-yeast tablet for six months. The placebo group received a placebo yeast tablet for the same period. At the beginning of the trial and at the end, blood samples were collected and the levels of sFlt-1, PAI-1, PAI2 and GPx were measured in blood serum and plasma.. Serum selenium concentrations were raised in the selenium group (P < 0.001) from the first to the third trimester, but was unchanged in the placebo group (P = 0.85). The results showed that sFlt-1 had significantly increased in both groups by the end of the gestation period, and selenium supplementation had no significant effect on the selenium group (P = 0.51). However, GPx activity was significantly increased in the selenium treatment group after supplementation compared to the control group (P < 0.001). The PAI1: PAI2 ratio was not significantly different between the two groups (P = 0.44).. Selenium intake during the second and third trimester of pregnancy increased GPx activity but did not have a significant effect on serum sFlt-1 levels or the ratio of PAI1: PAI2 in the serum..

Plasminogen activator inhibitor-1 (PAI-1) is a glycoprotein with inhibitory effects on the formation of plasmin from plasminogen by plasminogen activator. Thus, it prevents clot lysis in vessel walls. Several evidences prove the relationship between coronary artery disease and response to fibrinolytic therapy in patients with myocardial infarction with PAI-1 level. Opium addiction is one of the most important factors in causing myocardial infarction and cardiovascular events. This is due to it causing imbalance between coagulation and anticoagulation factors in the blood. This study was designed and implemented to determine the levels of PAI-I in opium-addicted patients with coronary artery disease in comparison with non addicts. In this case-control study, 160 patients with coronary heart disease, which was confirmed by angiography results, were enrolled. All of the patients had a medical history, their creatine levels and lipid profile were evaluated, morphine urine test was performed, and after that a blood sample was taken to determine the levels of PAI-1. Thus, the 80 patients who had a positive morphine urine test result formed the case group, and the control group was constituted of the 80 patients with negative morphine test results. The two groups were matched. Average level of PAI-1 in the control group was 2.4±2.6 and in the case group was 8.8 ± 9.1 and it was statistically significant (P < 0.001). The frequency of two vessel disease was higher in opium addicted patients than non-addicted patients and this was statistically significant (P = 0.030). However, the frequency of single vessel and three vessel disease was the same in the two groups. The two groups had no differences in age, lipid profile, and creatinine level. Moreover, females are at a higher risk of high PAI-1 levels. PAI-1 levels in opium addicted patients with coronary heart disease are higher than other patients. In these patients, the risk of atherosclerosis and myocardial infarction is higher than normal.