Platelet activation is a link in the pathophysiology of diseases prone to thrombosis and inflammation. Numerous platelet markers, including mean platelet volume (MPV), have been investigated in connection with both thrombosis and inflammation. This review considers MPV as a prognostic and therapeutic marker as well as the factors influencing its measurement. Established cardiovascular risk factors, such as smoking, hypertension, dyslipidemia, and diabetes, can influence MPV, depending on confounding factors. Low-grade inflammation is one such factor. Evidence, particularly derived from prospective studies and a meta-analysis, suggest a correlation between an increase in MPV and the risk of thrombosis. High MPV associates with a variety of established risk factors, cardio- and cerebrovascular disorders, and low-grade inflammatory conditions prone to arterial and venous thromboses. High-grade inflammatory diseases, such as active rheumatoid arthritis or attacks of familial Mediterranean fever, present with low levels of MPV, which reverse in the course of anti-inflammatory therapy. Lifestyle modification, antihypertensive, lipid lowering and diet therapies can also affect MPV values, but these effects need to be investigated in large prospective studies with thrombotic endpoints.

The platelet-to-lymphocyte ratio (PLR) has emerged as an informative marker revealing shifts in platelet and lymphocyte counts due to acute inflammatory and prothrombotic states. PLR has been extensively examined in neoplastic diseases accompanied by immune suppression and thrombosis, which can be predicted by combined blood cell counts and their ratios. Several large observational studies have demonstrated the value of shifts in PLR in evaluating the severity of systemic inflammation and predicting infections and other comorbidities, in inflammatory rheumatic diseases. The value of PLR as an inflammatory marker increases when its fluctuations are interpreted along with other complementary hematologic indices, particularly the neutrophil-to-lymphocyte ratio (NLR), which provides additional information about the disease activity, presence of neutrophilic inflammation, infectious complications, and severe organ damage in systemic lupus erythematosus. PLR and NLR have high predictive value in rheumatic diseases with predominantly neutrophilic inflammation (e.g., Behçet disease and familial Mediterranean fever). High PLR, along with elevated platelet count, is potentially useful in diagnosing some systemic vasculitides, particularly giant-cell arteritis. A few longitudinal studies on rheumatic diseases have demonstrated a decrease in PLR in response to anti-inflammatory therapies. The main limitations of PLR studies are preanalytical faults, inadequate standardization of laboratory measurements, and inappropriate subject selection. Nonetheless, accumulating evidence suggests that PLR can provide valuable information to clinicians who encounter multisystem manifestations of rheumatic diseases, which are reflected in shifts in platelet, lymphocyte, neutrophil, or monocyte counts. Interpretation of PLR combined with complementary hematologic indices is advisable to more accurately diagnose inflammatory rheumatic diseases and predict related comorbidities.

Review articles comprehensively covering a specific topic are crucial for successful research and academic projects. Most editors consider review articles for special and regular issues of journals. Writing a review requires deep knowledge and understanding of a field. The aim of this review is to analyze the main steps in writing a narrative biomedical review and to consider points that may increase the chances of success. We performed a comprehensive search through MEDLINE, EMBASE, Scopus, and Web of Science using the following keywords: review of the literature, narrative review, title, abstract, authorship, ethics, peer review, research methods, medical writing, scientific writing, and writing standards. Opinions expressed in the review are also based on personal experience as authors, peer reviewers, and editors.

The ongoing pandemic coronavirus disease 19 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a matter of global concern. Environmental factors such as air pollution and smoking and comorbid conditions (hypertension, diabetes mellitus and underlying cardio-respiratory illness) likely increase the severity of COVID-19.

The pathogenesis of Coronavirus disease 2019 (COVID-19) is gradually being comprehended. A high number of thrombotic episodes are reported, along with the mortality benefits of heparin. COVID-19 can be viewed as a prothrombotic disease. We overviewed the available evidence to explore this possibility. We identified various histopathology reports and clinical case series reporting thromboses in COVID-19. Also, multiple coagulation markers support this. COVID-19 can be regarded as a risk factor for thrombosis. Applying the principles of Virchow's triad, we described abnormalities in the vascular endothelium, altered blood flow, and platelet function abnormalities that lead to venous and arterial thromboses in COVID-19. Endothelial dysfunction, activation of the renin-angiotensin-aldosterone system (RAAS) with the release of procoagulant plasminogen activator inhibitor (PAI-1), and hyperimmune response with activated platelets seem to be significant contributors to thrombogenesis in COVID-19. Stratifying risk of COVID-19 thromboses should be based on age, presence of comorbidities, D-dimer, CT scoring, and various blood cell ratios. Isolated heparin therapy may not be sufficient to combat thrombosis in this disease. There is an urgent need to explore newer avenues like activated protein C, PAI-1 antagonists, and tissue plasminogen activators (tPA). These should be augmented with therapies targeting RAAS, antiplatelet drugs, repurposed antiinflammatory, and antirheumatic drugs.

A number of mediators are involved in the inflammatory processes that affect joints and vascular wall of patients with rheumatoid arthritis (RA). Tumour necrosis factor alpha (TNFa) is one such mediator, and it is widely regarded as an important target for anti-rheumatic treatment. Most recent studies show that anti-TNFa medication suppresses inflammation and reduces overall activity of RA. The aim of the current study was to investigate changes of mean platelet volume (MPV) in response to the 3-month anti-TNFa therapy in RA. Twenty-one RA patients without established cardiovascular disease were recruited for anti-TNFa therapy and underwent thorough clinical and laboratory evaluation at baseline, 2 weeks, and 12 weeks. Anti-TNFa therapy resulted in a significant (p = 0.01) increase in MPV over the duration of the study (7.7 +/- 0.9, 7.8 +/- 1.1, and 8.4 +/- 1.1 fL at baseline, 2 weeks, and 12 weeks, respectively). The results of the study expand perspectives of the use of MPV in conditions associated with high-grade inflammation, particularly RA, for monitoring anti-inflammatory treatment. More prospective studies with large numbers of patients are warranted to ascertain associations of high and low values of MPV with diverse markers of inflammation and vascular pathology.

Aspirin is well recognized as an effective antiplatelet drug for secondary prevention in subjects at high risk of cardiovascular events. However, most patients receiving long-term aspirin therapy still remain at substantial risk of thrombotic events due to insufficient inhibition of platelets, specifically via the thromboxane A2 pathway. Although the exact prevalence is unknown, estimates suggest that between 5.5% and 60% of patients using this drug may exhibit a degree of "aspirin resistance," depending upon the definition used and parameters measured. To date, only a limited number of clinical studies have convincingly investigated the importance of aspirin resistance. Of these, few are of a sufficient scale, well designed, and prospective, with aspirin used at standard doses. Also, most studies do not sufficiently address the issue of noncompliance to aspirin as a frequent, yet easily preventable cause of resistance to this antiplatelet drug. This review article provides a comprehensive overview of aspirin resistance, discussing its definition, prevalence, diagnosis, and therapeutic approaches. Moreover, the clinical implications of aspirin resistance are explored in various cardiovascular disease states, including diabetes mellitus, hypertension, heart failure, and other similar disorders where platelet reactivity is enhanced. (J Am Coll Cardiol 2008;51:1829-43)

Background: The coronavirus disease 2019 (COVID-19) pandemic has led to a large volume of publications, a barrage of non-reviewed preprints on various professional repositories and a slew of retractions in a short amount of time. Methods: We conducted an e-survey using a cloud-based website to gauge the potential sources of trustworthy information and misinformation and analyzed researchers', clinicians', and academics' attitude toward unpublished items, and pre-and post-publication quality checks in this challenging time. Results: Among 128 respondents (mean age, 43.2 years; M:F, 1.1:1), 60 (46.9%) were scholarly journal editors and editorial board members. Social media channels were distinguished as the most important sources of information as well as misinformation (81 [63.3%] and 86 [67.2%]). Nearly two in five (62, 48.4%) respondents blamed reviewers, editors, and misinterpretation by readers as additional contributors alongside authors for misinformation. A higher risk of plagiarism was perceived by the majority (70, 58.6%), especially plagiarism of ideas (64.1%) followed by inappropriate paraphrasing (54.7%). Opinion was divided on the utility of preprints for changing practice and changing retraction rates during the pandemic period, and higher rejections were not supported by most (76.6%) while the importance of peer review was agreed upon by a majority (80, 62.5%). More stringent screening by journal editors (61.7%), and facilitating open access plagiarism software (59.4%), including Artificial Intelligence (AI)-based algorithms (43.8%) were among the suggested solutions. Most (74.2%) supported the need to launch a specialist bibliographic database for COVID-19, with information indexed (62.3%), available as open-access (82.8%), after expanding search terms (52.3%) and following due verification by academics (66.4%), and journal editors (52.3%). Conclusion: While identifying social media as a potential source of misinformation on COVID-19, and a perceived high risk of plagiarism, more stringent peer review and skilled post-publication promotion are advisable. Journal editors should play a more active role in streamlining publication and promotion of trustworthy information on COVID-19.