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Physical activity is essential for weight control, for limiting onset and complications of chronic disorders and for preventing impaired insulin sensitivity. Little is known about the glycaemic adaptations of physically active subjects, especially elite and professional athletes. Thus, we evaluated the glycaemic control in elite and professional cyclists by assessing fasting plasma glucose (FPG) and glycated haemoglobin (HbAlc). The study population consisted of 47 male professional road cyclists, 72 male elite road cyclists and 58 male sedentary blood donors. A significant difference was observed for FPG between sedentary controls (96 ± 8 mg/dL) and either elite (91 ± 8 mg/dL; p <0.001) or professional cyclists (89 ± 8 mg/dl; p <0.001). Athletes showed a consistent trend towards higher HbAl c values, reaching statistical significance between sedentary individuals and professional cyclists (5.2 ±0.3% versus 5.4 ± 0.2%; p = 0.017). In multiple linear regression analysis, the intensity of physical exercise is inversely correlated with FPG (r=-0.320; p<0.001) and directly correlated with HbAlc (r=0.190; p=0.006). These results demonstrate a significant association between intensity of the training regimen and both FPG and HbA1c, highlighting the need for establishing the appropriate critical difference for the measurement of FPG and HbA1c according to the training and exercise workload. [ABSTRACT FROM AUTHOR]

This article is a commentary celebrating the 50th anniversary of Seminars in Thrombosis and Hemostasis (STH), a journal that first published in 1974. The commentary focuses on the historical significance of a paper titled "Description of an in vitro platelet function analyzer–PFA-100," which was published in a supplementary issue of STH in 1995 and is one of the most highly cited papers in the journal's history. The paper describes the PFA-100, an instrument that has since evolved into the PFA-200 and has been widely used for various purposes in the field of hemostasis. The commentary also mentions the impact of the PFA-100 on research and its potential applications in different areas, such as screening for von Willebrand disease and monitoring platelet function in animals. The article concludes by acknowledging the 30th anniversary of the PFA-100 in 2024 and its significant contributions to the hemostasis community. [Extracted from the article]

The latest issue of Seminars in Thrombosis and Hemostasis (STH) is a compilation of articles covering various topics related to thrombosis and bleeding. It includes reviews on neonates with intrauterine growth restriction, pediatric presentations of the antiphospholipid syndrome, genetic variations in tissue factor-dependent disease, heterozygous factor XIII deficiency, and the use of global hemostasis assays in patients with myeloproliferative neoplasms. The document also features reviews on the role of CD36 in platelet activation, laser-induced blood coagulation in surgery, detecting blood clots in ECMO circuits, post-COVID venous thrombosis, and the effects of SARS-CoV-2 spike protein variants on platelets. Commentaries on various topics and the republishing of historical papers are also included. [Extracted from the article]

Thrombophilia is a complex disease process, clinically manifesting in various forms of venous thromboembolism. Although both genetic and acquired (or environmental) risks factors have been reported, the presence of a genetic defect (antithrombin [AT], protein C [PC], protein S [PS]) is considered three of the major contributing factors of thrombophilia. The presence of each of these risk factors can be established by clinical laboratory analysis; however, the clinical provider and laboratory personnel must understand the testing limitations and shortcomings associated with the assays for these factors to be able to ensure an accurate diagnosis. This article will describe the major pre-analytical, analytical, and post-analytical issues associated with the various types of assays and discuss evidence-based algorithms for analyzing AT, PC, and PS in plasma. [ABSTRACT FROM AUTHOR]

Semin Thromb Hemost 2020;46(3):379-3824Thachil J, Srivastava A. SARS-2 coronavirus-associated hemostatic lung abnormality in COVID-19: is it pulmonary thrombosis or pulmonary embolism? Semin Thromb Hemost 2020;46(7):789-79538Horowitz NA, Brenner B. thrombosis and hemostasis issues in cancer patients with COVID-19. 2021, 47, 05, 467 - 476 52 Favaloro E. J., Lippi G. Maintaining hemostasis and preventing thrombosis in coronavirus disease 2019 (COVID-19)-part I. Semin Thromb Hemost. Semin Thromb Hemost 2020;46(7):796-8038Fernández-Capitán C, Barba R, Díaz-Pedroche MDC, Sigüenza P, Demelo-Rodriguez P, Siniscalchi C, Pedrajas JM, Farfán-Sedano AI, Olivera PE, Gómez-Cuervo C, Llamas P, Villares P, Sanchez O, López-Reyes R, Catella J, Bikdeli B, Weinberg I, Tafur AJ, Jiménez D, Monreal M. presenting characteristics, treatment patterns, and outcomes among patients with venous thromboembolism during hospitalization for COVID-19. [Extracted from the article]

Snake venoms have evolved primarily to immobilize and kill prey, and consequently, they contain some of the most potent natural toxins. Part of that armory is a range of hemotoxic components that affect every area of hemostasis, which we have harnessed to great effect in the study and diagnosis of hemostatic disorders. The most widely used are those that affect coagulation, such as thrombin-like enzymes unaffected by heparin and direct thrombin inhibitors, which can help confirm or dispute their presence in plasma. The liquid gold of coagulation activators is Russell's viper venom, since it contains activators of factor X and factor V. It is used in a range of clotting-based assays, such as assessment of factor X and factor V deficiencies, protein C and protein S deficiencies, activated protein C resistance, and probably the most important test for lupus anticoagulants, the dilute Russell's viper venom time. Activators of prothrombin, such as oscutarin C from Coastal Taipan venom and ecarin from saw-scaled viper venom, are employed in prothrombin activity assays and lupus anticoagulant detection, and ecarin has a valuable role in quantitative assays of direct thrombin inhibitors. Snake venoms affecting primary hemostasis include botrocetin from the jararaca, which can be used to assay von Willebrand factor activity, and convulxin from the cascavel, which can be used to detect deficiency of the platelet collagen receptor, glycoprotein VI. This article takes the reader to every area of the diagnostic hemostasis laboratory to appreciate the myriad applications of snake venoms available in diagnostic practice. [ABSTRACT FROM AUTHOR]

The inflammatory process is strongly involved in the pathophysiology of venous thromboembolism (VTE) and has a significant role in disease prediction. Inflammation most probably represents a common denominator through which classical and nonclassical risk factors stimulate thrombotic process. Inflammation of the venous wall promotes the release of tissue factor, inhibits the release of anticoagulant factors, and hampers endogenous fibrinolysis. Systemic inflammatory response also inhibits restoration of blood flow in the occluded vessel. Recent studies indicate that increased inflammatory response ("cytokine storm") is related to prothrombotic state and thromboembolic events in patients with coronavirus disease 2019 (COVID-19). The growing evidence of involvement of inflammation in the pathogenesis of VTE indicates the importance of anti-inflammatory treatment and prevention of VTE. While aspirin was shown to be effective in prevention of recurrent venous thrombosis after treatment with anticoagulant drugs, some other anti-inflammatory drugs like nonsteroidal anti-inflammatory agents may have prothrombotic effect, thus potentially increasing the risk of VTE. Recently, new specific anti-inflammatory drug inhibitors of inflammatory markers that have been shown to be involved in the pathogenesis of VTE are being searched. As thrombogenesis is based on activation of coagulation provoked by inflammation, then prevention and treatment of VTE should include both anticoagulant and anti-inflammatory agents. Combined treatment is related to increased risk of bleeding complications, therefore subtherapeutic doses of both drugs should be used to improve the efficacy of management of VTE without increasing the risk of bleeding. [ABSTRACT FROM AUTHOR]

Cancer patients are characterized by hypercoagulable state and an increased rate of thrombotic events, the most common being venous thromboembolism. Several hemostatic pathways that are significantly implicated in mechanisms of thromboembolic disease are also involved in growth, invasion, and metastatic spread of malignant cells as well in tumor-induced neo-angiogenesis. This close connection between cancer and the hemostatic system has prompted numerous studies on the role of alterations in the level plasma biomarkers of the different compartments of hemostasis in predicting cancer prognosis. In this review, we collect the results of several exemplificative studies that have evaluated clotting activation biomarkers in relation to different cancer outcomes with a final emphasis on current research and forthcoming directions in this field. [ABSTRACT FROM AUTHOR]

The serine protease thrombin, a naturally derived enzyme, plays a key role in hemostasis by converting fibrinogen to fibrin and activating coagulation factor XIII whereby the fibrin clot is stabilized. Furthermore, thrombin activates platelets through protease-activated receptors on the platelet surface. Conversely, thrombin also exerts anticoagulant effects, enhancing the protein C activity while complexed with thrombomodulin. During recent years, it has become evident that thrombin has significant effects beyond hemostasis, as it contributes also to modulation of the endothelium, promotes inflammation and angiogenesis, and plays a role in tumor progression. Yet, due to the very short half-life and almost immediate inhibition in fluid phase by antithrombin, thrombin itself remains elusive, and only indirect measurement of thrombin generation is possible. This review provides a description of structure and mechanisms of action of thrombin both in physiological and pathological processes. Furthermore, it summarizes laboratory tests that measure in vivo or ex vivo thrombin generation, and presents knowledge on the value of these biomarkers in bleeding disorders, cardiopulmonary bypass surgery, and thromboembolic risk assessment in different patient populations. Finally, this review outlines further perspectives on using thrombin generation biomarkers for research purposes and in clinical practice. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD), encompassing acute myocardial infarction, ischemic stroke, and peripheral artery occlusive disease, is still the first cause of death and disability in Western countries. More specifically, compared with the reference HDL-C value (i.e., 56mg/dL), the pooled risk of all-cause death was 1.21 (95% confidence interval [95% CI], 1.09-1.36) higher for subjects in the highest HDL-C category, with a pooled hazard ratio of 1.03 (95% CI, 1.01-1.05) for each 10mg/dL increase of HDL-C concentration above the reference value. A similar trend was noted for cancer mortality, with a pooled hazard ratio of 1.02 (95% CI, 0.98-1.05) for each 10mg/dL increase above the reference HDL-C value and, even more surprisingly, for CVD mortality, with a pooled hazard ratio of 1.06 (95% CI, 1.01-1.10) for each 10mg/dL increase above the reference HDL-C value. More specifically, subjects with high values of HDL-C levels (i.e., >80mg/dL) had a nearly twofold higher risk of both all-cause (hazard ratio [HR], 1.96; 95% CI, 1.42-2.71) and CVD (HR, 1.71; 95% CI, 1.09-2.68) mortality compared to those with values in the range between 40 and 60mg/dL. [Extracted from the article]

To understand better the adaptation response of the cardiovascular system (CVS) to self-contained underwater breathing apparatus (SCUBA) diving, Galectin-3 (Gal-3) and specific CVS biomarkers were measured in plasma of 16 male recreational divers before and after (30 min, 3 and 6 h) diving (total time of 30 min at 30 m depth) undertaken a after long non-dive period. The one-time SCUBA dive caused a significant increase in Gal-3, N-terminal prohormone of brain natriuretic peptide (NT-proBNP), high-sensitivity troponin-I (hs-TnI), and myoglobin immediately after diving. Whereas Gal-3 and myoglobin dropped down to the basal levels during the recovery period, NT-proBNP and hs-TnI concentration continued to increase. An immediate increase of vascular endothelial growth factor, detected immediately after diving, was followed by a significant decrease and return to the basal level, 3 and 6 h after diving, respectively. After a significant initial decrease, endothelin-1 increased during the recovery period, but did not return to the basal level. The observed changes in these biomarkers reflect comprehensive, but transient adaptation of CVS and muscular system to the specific environmental conditions during the SCUBA dive. Whether the recurrent activation of these adaption mechanisms due to repetitive dives has positive or negative effects on CVS remains to be elucidated. [ABSTRACT FROM AUTHOR]

Sepsis is associated with high morbidity and mortality, and short-term mortality remains above 30% despite relevant supportive and antibiotic treatments. The aim of this systematic review was to summarize and discuss the current evidence of the association of an increased number of circulating immature platelets with disease severity and mortality in patients with sepsis or septic shock. The review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement and was registered at the PROSPERO database (registration number: CRD42018104326). A systematic literature search was performed in PubMed, Web of Science, Scopus, and Embase on June 20, 2018, without time restrictions. The included studies were quality-assessed by the National Institutes of Health's Quality Assessment Tools. In total, 14 studies were included. The parameters used for the determination of platelet maturity were mean platelet volume, immature platelets fraction, reticulated platelet percentage, and absolute immature platelets count. Nine studies reported significantly increased immature platelet markers in nonsurvivors of septic shock compared with survivors, as well as in patients with severe sepsis or septic shock compared with patients without severe sepsis and septic shock. Six of these nine studies demonstrated that increased immature platelet markers were predictors of mortality and/or disease severity (area under the receiver operating curve: 0.599–0.886). This review suggests that an increased number of circulating immature platelets is associated with increased disease severity and mortality in patients with sepsis and septic shock. Larger studies are needed to confirm whether immature platelets should be routinely monitored to support the prediction of disease severity and mortality in septic patients. [ABSTRACT FROM AUTHOR]

Objective  The aim of this study was to assess the utility of early postnatal platelet indices in the prediction of hemodynamically significant patent ductus arteriosus (hsPDA) and its response to pharmacological treatment in preterm infants. Study Design  The medical records of 971 infants with gestational age < 30 weeks and birth weight < 1,500 g were analyzed retrospectively. Infants with hsPDA comprised the study group and those without hsPDA comprised the control group. Complete blood count results were recorded, and red cell distribution width-to-platelet ratio (RPR) and platelet mass were calculated. Results  A total of 481 infants, 169 in the hsPDA group and 312 in the control group, were included. In terms of platelet indices, the hsPDA group showed significantly lower mean platelet volume (MPV) and platelet mass, whereas RPR was significantly higher (p  < 0.05, respectively). Multiple logistic regression analysis showed that RDS (relative ratio [RR]: 2.39; 95% confidence interval [CI]: 1.45–3.93; p  < 0.001), MPV < 7.85 (RR: 3.71; 95% CI: 2.29–6.01; p  < 0.001), and RPR > 0.070 (RR: 5.33; 95% CI: 3.28–8.65; p  < 0.001) were independent risk factors for hsPDA. Conclusion  Low MPV and platelet mass and high RPR in the first hours of life are risk factors for hsPDA and hsPDA refractive to pharmacological treatment with ibuprofen in preterm infants. [ABSTRACT FROM AUTHOR]

Thrombophilia is a generic term that defines an increased propensity toward thrombosis and associated morbidity. Factor V Leiden (FVL; G1691A) and the prothrombin gene mutation (PGM; G20210A) comprise the most common genetic associations with thrombosis, and thus comprise the most commonly requested genetic thrombophilia investigations. This report describes an audit of local test findings that suggests growing futility in testing for FVL and PGM. Test requests for FVL and PGM were assessed for a recent period of 2.5 years (starting from 2016 to end of June 2018) from a large tertiary-level pathology provider. From a total of more than 10,000 thrombophilia-related test requests over the analysis period, 2,700 and 2,135 were, respectively, for FVL and PGM. The age ranges of patients varied across the full life span spectrum, but the peak investigation age range for the entire cohort was 30 to 39 years. Investigations were more often requested for females (> 70% of requests) than males, and the peak investigation age range for females (30–39 years) was earlier than males (50–59 years). However, proportionally more males than females were identified with FVL (15.4 vs. 6.6%) or PGM (10.4 vs. 4.3%), respectively. The age-related patterns of test ordering were also identified as closely aligned to birth patterns in females and thrombosis patterns in males. There has been a trend to annual reduction in detection of FVL mutation from a peak of more than 25% in 1996 to ∼10% in each year of the past decade, suggesting poorer patient selection. Of test-requesting indications, pregnancy/fetal morbidity was identified in 16.4% of all requests for females, and thromboembolism was identified in 21.4 and 18.0% of all requests for females and males, respectively. In terms of FVL identification, a heterozygous pattern was identified in 4.2% of women tested for pregnancy/fetal morbidity, but 11.7 and 15.1% of females and males, respectively, for thromboembolism. In comparison, the background rate of FVL detection in the general population in our geographical region is approximately 3 to 7%. Overall, better targeted patient selection for testing of FVL and PGM occurred in the male cohort based on higher relative capture of thrombophilia mutations than the female cohort. However, patient selection was not optimal in either the male or female cohorts, since the captured mutation rates were only marginally higher than the expected background population detection rate. Moreover, the decline in relative identification of FVL from overall test requests over time suggests deterioration of patient selection practices by referring physicians. Notably, tests requested in the setting of thromboembolism provided a higher likelihood of FVL detection than pregnancy/fetal morbidity. These data suggest some contemporary futility of genetic testing for FVL and PGM in the real world, and in particular, in females for indications around pregnancy/fetal morbidity, proposed to be related to poor patient selection in most instances. [ABSTRACT FROM AUTHOR]

This study compares the serological markers between runners who are hepatitis B virus carries (HBVc) and runners who are non-HBVc in a 100-km ultra-marathon race. Blood samples of 8 HBVc and 18 non-HBVc runners were drawn 1 week before, immediately following, and 24 h after the race. Samples were analyzed and compared between the 2 groups for liver function tests, muscle damage markers and oxidative stress cytokines. For HBVc runners, HBV-DNA (hepatitis B virus-deoxyribonucleic acid) levels were also evaluated for virus reactivation. The results demonstrate a statistically signifi cant increase in both immediate and 24-h post-race values for alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), creatine kinase (CK), high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), compared with pre-race values. No statistically signifi cant diff erence was observed between the 2 groups for the values of AST, LDH, CK, hs-CRP, IL-6 and TNF-α either before or after the race. There was also no statistically signifi cant change in the levels of HBV-DNA in HBVc runners. These findings suggest that HBVc runners do not have higher risks of liver function impairment, muscle breakdown and inflammatory response compared to non-HBVc runners in such endurance races. [ABSTRACT FROM AUTHOR]

The aim was to study the effects of scuba diving immersion on plasma antioxidant defenses, nitric oxide production, endothelin-1 and vascular endothelial growth factor levels. 9 male divers performed an immersion at 50 m depth for a total time of 35 min. Blood samples were obtained before diving at rest, immediately after diving, and 3 h after the diving session. Leukocyte counts, plasma 8oxoHG, malondialdehyde and nitrite levels significantly increased after recovery. Activities of lactate dehydrogenase, creatine kinase, catalase and superoxide significantly increased immediately after diving and these activities remained high after recovery. Plasma myeloperoxidase activity and protein levels and extracellular superoxide dismutase protein levels increased after 3 h. Endothelin-1 concentration significantly decreased after diving and after recovery. Vascular endothelial growth factor concentration significantly increased after diving when compared to pre-diving values, returning to initial values after recovery. Scuba diving at great depth activated the plasma antioxidant system against the oxidative stress induced by elevated pO2 oxygen associated with hyperbaria. The decrease in endothelin-1 levels and the increase in nitric oxide synthesis could be factors that contribute to post-diving vasodilation. Diving increases vascular endothelial growth factor plasma levels which can contribute to the stimulation of tissue resistance to diving-derived oxidative damage. [ABSTRACT FROM AUTHOR]