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Clinical and Applied... 2021Coagulation activation has been reported in several cohorts of patients Coronavirus Disease 2019 (COVID-19). However, the true burden of systemic coagulopathy in... (Meta-Analysis)
Meta-Analysis
Coagulation activation has been reported in several cohorts of patients Coronavirus Disease 2019 (COVID-19). However, the true burden of systemic coagulopathy in COVID-19 remains unknown. In this systematic review and meta-analysis, we performed a literature search using PubMed, EMBASE, and Cochrane Database to identify studies that reported the prevalence of systemic coagulopathy using established criteria in patients with COVID-19. The primary outcome was the prevalence of systemic coagulopathy (disseminated intravascular coagulation [DIC] and/or sepsis-induced coagulopathy [SIC]). Pooled prevalences and 95% confidence intervals [CIs] were calculated using random-effects model. A total of 5 studies including 1210 patients with confirmed COVID-19 were included. The pooled prevalence of systemic coagulopathy was 7.1% (95%CI: 3.2%,15.3%, I = 93%). The pooled prevalence of DIC (N = 721) and SIC (N = 639) were 4.3% (95%CI 1.7%, 10.4%, I = 84%) and 16.2% (95%CI: 9.3%, 26.8%, I = 74%), respectively. Only 2 studies reported the prevalence of elevated D-dimer levels with the pooled prevalence of 84.6% (95%CI: 52.0%,96.5%, I = 94%). Average D-dimer and fibrinogen levels were remarkably increased, while platelet counts, PT, and aPTT ratios were minimally affected in COVID-19. The estimated prevalence of systemic coagulopathy in patients with COVID-19 was low despite D-dimer elevation in most patients. Relatively low systemic coagulopathy in COVID-19 may contribute to the high incidence of thrombosis rather than bleeding in patients with COVID-19.
Topics: COVID-19; Disseminated Intravascular Coagulation; Female; Fibrin Fibrinogen Degradation Products; Humans; Male; Platelet Count; Prevalence; SARS-CoV-2; Sepsis; Thrombosis
PubMed: 33443456
DOI: 10.1177/1076029620987629 -
Thrombosis and Haemostasis May 2021Immature platelets are larger and may be more thrombogenic than mature platelets. This systematic review included studies on the association between mean platelet...
BACKGROUND
Immature platelets are larger and may be more thrombogenic than mature platelets. This systematic review included studies on the association between mean platelet volume (MPV), immature platelet count (IPC), and immature platelet fraction (IPF) and the risk of major cardiovascular events (MACEs) in patients with acute coronary syndrome (ACS) or stable coronary artery disease (CAD).
METHODS
The literature search included studies in PubMed, Embase, Web of Science, and Cochrane Library. The review was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. Effect estimates that included multivariate adjusted odds ratios, relative risks, or hazard ratios were extracted.
RESULTS
Forty-two studies were identified. High MPV was positively associated with MACE in 20 of 26 studies of patients with ACS, four of five studies in patients with stable CAD, and in all six studies comprising a combined population with ACS and stable CAD. Using continuous models of MPV in patients with ACS, effect estimates varied from 0.90 (95% confidence interval [CI]: 0.95-1.03) to 1.66 (95% CI: 1.32-2.09). The strength of these associations was broadly similar among patients with stable CAD and in combined populations. Five studies investigated IPC or IPF as exposures and all reported positive associations with MACE among patients with ACS, stable CAD, or in combined populations.
CONCLUSION
This review demonstrated clear evidence for positive associations between measures of immature platelets and subsequent risk of MACE in acute and stable ischemic heart disease patients.
Topics: Acute Coronary Syndrome; Blood Platelets; Humans; Myocardial Ischemia; Platelet Activation; Platelet Count; Risk
PubMed: 33302302
DOI: 10.1055/s-0040-1721386 -
BMC Medicine Nov 2020Antiretroviral therapy (ART) alters platelet reactivity, and as a consequence, patients living with HIV may be at an increased risk of cardiovascular disease (CVD). The... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Antiretroviral therapy (ART) alters platelet reactivity, and as a consequence, patients living with HIV may be at an increased risk of cardiovascular disease (CVD). The current evidence on platelet activation levels in patients with HIV remains inconclusive. We therefore aimed to systematically synthesise evidence on the association of platelet activation in HIV-infected patients on successful treatment.
METHODS
Electronic databases were searched from inception until November 2019. Studies were included if the primary or secondary outcome of the study was to assess platelet activation in HIV-infected patients on ART. The primary outcome of this review included the levels of platelet activation. The pooled effect estimates were calculated using a random-effects meta-analysis model.
RESULTS
We identified 30 studies comprising of 2325 participants. The pooled estimates showed elevated levels of platelet activation in treatment-naïve HIV-infected patients compared to uninfected controls (Hedges' g 2.00 [95%CI 1.05, 2.94]; z = 4.12, p < 0.0001). These remained elevated despite successful ART (Hedges' g 2.05 [95%CI 0.58, 3.52]; z = 2.71, p = 0.0067).
CONCLUSION
The levels of platelet activation are elevated in treatment-naïve HIV-infected patients, and these persist during successful ART. Further studies should assess the clinical relevance of monitoring the levels of platelet activation in HIV-infected patients on ART.
Topics: Anti-Retroviral Agents; Cardiovascular Diseases; HIV Infections; Humans; Platelet Activation
PubMed: 33203400
DOI: 10.1186/s12916-020-01801-9 -
CNS Spectrums Apr 2022Blood platelets, due to shared biochemical and functional properties with presynaptic serotonergic neurons, constituted, over the years, an attractive peripheral... (Review)
Review
BACKGROUND
Blood platelets, due to shared biochemical and functional properties with presynaptic serotonergic neurons, constituted, over the years, an attractive peripheral biomarker of neuronal activity. Therefore, the literature strongly focused on the investigation of eventual structural and functional platelet abnormalities in neuropsychiatric disorders, particularly in depressive disorder. Given their impact in biological psychiatry, the goal of the present paper was to review and critically analyze studies exploring platelet activity, functionality, and morpho-structure in subjects with depressive disorder.
METHODS
According to the PRISMA guidelines, we performed a systematic review through the PubMed database up to March 2020 with the search terms: (1) platelets in depression [Title/Abstract]"; (2) "(platelets[Title]) AND depressive disorder[Title/Abstract]"; (3) "(Platelet[Title]) AND major depressive disorder[Title]"; (4) (platelets[Title]) AND depressed[Title]"; (5) (platelets[Title]) AND depressive episode[Title]"; (6) (platelets[Title]) AND major depression[Title]"; (7) platelet activation in depression[All fields]"; and (8) platelet reactivity in depression[All fields]."
RESULTS
After a detailed screening analysis and the application of specific selection criteria, we included in our review a total of 106 for qualitative synthesis. The studies were classified into various subparagraphs according to platelet characteristics analyzed: serotonergic system (5-HT2A receptors, SERT activity, and 5-HT content), adrenergic system, MAO activity, biomarkers of activation, responsivity, morphological changes, and other molecular pathways.
CONCLUSIONS
Despite the large amount of the literature examined, nonunivocal and, occasionally, conflicting results emerged. However, the findings on structural and metabolic alterations, modifications in the expression of specific proteins, changes in the aggregability, or in the responsivity to different pro-activating stimuli, may be suggestive of potential platelet dysfunctions in depressed subjects, which would result in a kind of hyperreactive state. This condition could potentially lead to an increased cardiovascular risk. In line with this hypothesis, we speculated that antidepressant treatments would seem to reduce this hyperreactivity while representing a potential tool for reducing cardiovascular risk in depressed patients and, maybe, in other neuropsychiatric conditions. However, the problem of the specificity of platelet biomarkers is still at issue and would deserve to be deepened in future studies.
Topics: Antidepressive Agents; Biomarkers; Blood Platelets; Depressive Disorder, Major; Humans; Serotonin
PubMed: 33092669
DOI: 10.1017/S1092852920001959 -
Clinical Transplantation Jan 2021Cardiac allograft vasculopathy (CAV) is mediated by endothelial inflammation, platelet activation and thrombosis. Antiplatelet therapy may prevent the development of... (Meta-Analysis)
Meta-Analysis
Cardiac allograft vasculopathy (CAV) is mediated by endothelial inflammation, platelet activation and thrombosis. Antiplatelet therapy may prevent the development of CAV. This systematic review and meta-analysis summarizes and appraises the evidence on the effect of antiplatelet therapy after heart transplantation (HT). CENTRAL(Ovid), MEDLINE(Ovid), Embase(Ovid) were searched from inception until April 30, 2020. Outcomes included CAV, all-cause mortality, and CAV-related mortality. Data were pooled using random-effects models. Seven observational studies including 2023 patients, mean age 52 years, 22% female, 47% with ischemic cardiomyopathy followed over a mean 7.1 years proved eligible. All studies compared acetylsalicylic acid (ASA) to no treatment and were at serious risk of bias. Data from 1911 patients in 6 studies were pooled in the meta-analyses. The evidence is very uncertain about the effect of ASA on all-cause or CAV-related mortality. ASA may reduce the development of CAV (RR 0.75, 95% CI: 0.44-1.29) based on very low certainty evidence. Two studies that conducted propensity-weighted analyses showed further reduction in CAV with ASA (HR 0.31, 95% CI: 0.13-0.74). In conclusion, there is limited evidence that ASA may reduce the development of CAV. Definitive resolution of the impact of antiplatelet therapy on CAV and mortality will require randomized clinical trials.
Topics: Allografts; Aspirin; Female; Heart Transplantation; Humans; Male; Middle Aged; Platelet Aggregation Inhibitors; Postoperative Complications
PubMed: 33068308
DOI: 10.1111/ctr.14125 -
The Pharmacogenomics Journal Feb 2021Non-variceal upper gastrointestinal bleeding (non-variceal UGIB) is a frequent and severe adverse drug reaction. Idiosyncratic responses due to genetic susceptibility to... (Review)
Review
Non-variceal upper gastrointestinal bleeding (non-variceal UGIB) is a frequent and severe adverse drug reaction. Idiosyncratic responses due to genetic susceptibility to non-variceal UGIB has been suggested. A systematic review was conducted to assess the association between genetic polymorphisms and non-variceal UGIB. Twenty-one publications and 7134 participants were included. Thirteen studies evaluated genetic polymorphism in patients exposed to non-steroidal anti-inflammatory drugs, low-dose aspirin, and warfarin. Eight studies present at least one methodological problem. Only six studies clearly defined that the outcome evaluated was non-variceal UGIB. Genetic polymorphisms involved in platelet activation and aggregation, angiogenesis, inflammatory process, and drug metabolism were associated with risk of non-variceal UGIB (NOS3, COX-1; COX-2; PLA2G7; GP1BA; GRS; IL1RN; F13A1; CDKN2B-AS1; DPP6; TBXA2R; TNF-alpha; VKORC1; CYP2C9; and AGT). Further well-designed studies are needed (e.g., clear restriction to non-variceal UGIB; proper selection of participants; and adjustment of confounding factors) to provide strong evidence for pharmacogenetic and personalized medicine.
Topics: Gastrointestinal Hemorrhage; Gastrointestinal Tract; Genetic Association Studies; Genetic Predisposition to Disease; Hemorrhage; Humans; Polymorphism, Genetic; Risk Factors
PubMed: 32948830
DOI: 10.1038/s41397-020-00185-6 -
The Annals of Pharmacotherapy Feb 2021To evaluate intravenous immune globulin (IVIG) for autoimmune heparin-induced thrombocytopenia (aHIT), including platelet recovery, IVIG dose, dosing weight, IVIG...
OBJECTIVE
To evaluate intravenous immune globulin (IVIG) for autoimmune heparin-induced thrombocytopenia (aHIT), including platelet recovery, IVIG dose, dosing weight, IVIG product used, and complications reported.
DATA SOURCES
PubMed and EMBASE were searched from inception through June 21, 2020. Search terms included , , , , , , and .
STUDY SELECTION AND DATA EXTRACTION
Patients administered IVIG for HIT and diagnosed by immunoassay (optical density ≥2) or positive activation assay were included.
DATA SYNTHESIS
Twenty-four cases were reviewed; 92% had persistent aHIT. Time to IVIG administration post-nonheparin anticoagulant initiation was 9 days (median). Most common IVIG cumulative dose was 2 g/kg (dosed as 1 g/kg/d for 2 consecutive days); 75% had a favorable platelet increase (≥50 × 10/L) within 5 days of initial IVIG dosing.
RELEVANCE TO PATIENT CARE AND CLINICAL PRACTICE
aHIT is characterized by critically low platelets, thrombosis, and a persistent delay in platelet recovery despite treatment with a nonheparin anticoagulant. An immunoassay and subsequent confirmatory activation assay (at low, high, and 0 IU/mL unfractionated heparin levels) is recommended to confirm diagnosis. Patients nonresponsive to nonheparin anticoagulants within 5 days of initiation should be evaluated for IVIG treatment (2 g/kg cumulative dose). More data are needed to clarify appropriate IVIG dosing weight, although based on current published literature, it is recommended to use actual body weight.
CONCLUSIONS
Data reported support use of IVIG as adjunctive therapy for patients with aHIT. Judicious IVIG use based on key clinical and laboratory findings is critical.
Topics: Anticoagulants; Autoimmunity; Blood Platelets; Female; Heparin; Humans; Immunoglobulins, Intravenous; Male; Middle Aged; Platelet Count; Thrombocytopenia; Thrombosis
PubMed: 32693627
DOI: 10.1177/1060028020943542 -
Panminerva Medica Mar 2023The recent Sars-CoV-2 pandemic (COVID-19) has led to growing research to explain the poor clinical prognosis in some patients. While early observational studies...
INTRODUCTION
The recent Sars-CoV-2 pandemic (COVID-19) has led to growing research to explain the poor clinical prognosis in some patients. While early observational studies highlighted the role of the virus in lung failure, in a second moment thrombosis emerged as a possible explanation of the worse clinical course in some patients. Despite initial difficulties in management of such patients, the constant increase of literature in the field is to date clarifying some questions from clinicians. However, several other questions need answer.
EVIDENCE ACQUISITION
We performed systematic research using Embase and PubMed, inserting the keywords and mesh terms relative to the new coronavirus and to VTE: "COVID-19," "SARS," "MERS," "coronavirus," "2019 n-CoV," venous thromboembolism," "pulmonary embolism," "deep vein thrombosis," "thromboembolism," "thrombosis." Boolean operators "AND," "OR," "NOT" were used where appropriate. We found 133 articles of interest but only 20 were selected, providing the most representative information.
EVIDENCE SYNTHESIS
A novel disease (COVID-19) due to severe acute respiratory syndrome coronavirus 2 (Sars-CoV-2) infection was responsible for thousands of hospitalizations for severe acute respiratory syndrome, with several cases of thrombotic complications due to excessive inflammation, platelet activation, endothelial dysfunction, and stasis. COVID-19 and hospitalizations for COVID-19 may carry several potential risk factors for thrombosis. Severe coagulation abnormalities may occur in almost all the severe and critical ill COVID-19 cases.
CONCLUSIONS
Despite a strong pathophysiological rationale, the evidence in literature is not enough to recommend an aggressive antithrombotic therapy in COVID-19. However, it is our opinion that an early use, even at home at the beginning of the disease, could improve the clinical course.
Topics: Humans; Anticoagulants; COVID-19; Disease Progression; SARS-CoV-2; Thrombosis; Venous Thromboembolism
PubMed: 32549531
DOI: 10.23736/S0031-0808.20.03999-3 -
Advances in Rheumatology (London,... Jun 2020Hydroxychloroquine and chloroquine, also known as antimalarial drugs, are widely used in the treatment of rheumatic diseases and have recently become the focus of...
Hydroxychloroquine and chloroquine, also known as antimalarial drugs, are widely used in the treatment of rheumatic diseases and have recently become the focus of attention because of the ongoing COVID-19 pandemic. Rheumatologists have been using antimalarials to manage patients with chronic immune-mediated inflammatory rheumatic diseases for decades. It is an appropriate time to review their immunomodulatory and anti-inflammatory mechanisms impact on disease activity and survival of systemic lupus erythematosus patient, including antiplatelet effect, metabolic and lipid benefits. We also discuss possible adverse effects, adding a practical and comprehensive approach to monitoring rheumatic patients during treatment with these drugs.
Topics: Antimalarials; Antiphospholipid Syndrome; Antirheumatic Agents; Arthritis, Rheumatoid; COVID-19; Chloroquine; Coronavirus Infections; Drug Eruptions; Drug Interactions; Female; Glucose; Heart Diseases; Humans; Hydroxychloroquine; Lipids; Lupus Erythematosus, Cutaneous; Lupus Erythematosus, Systemic; Male; Pandemics; Platelet Aggregation; Pneumonia, Viral; Pregnancy; Renal Insufficiency; Retinal Diseases; Sjogren's Syndrome
PubMed: 32517786
DOI: 10.1186/s42358-020-00134-8 -
Orthopaedic Journal of Sports Medicine Apr 2020Platelet-rich plasma (PRP) has wide applications in orthopaedic care. Its beneficial effects are attributed to the growth factor profile from the platelet secretome. In... (Review)
Review
BACKGROUND
Platelet-rich plasma (PRP) has wide applications in orthopaedic care. Its beneficial effects are attributed to the growth factor profile from the platelet secretome. In theory, these effects would be diminished by medications that inhibit platelet activation and/or the subsequent release of growth factors.
PURPOSE
To determine whether commonly used antiplatelets, nonsteroidal anti-inflammatory drugs (NSAIDs), or anticoagulant medications affect platelet growth factor release in PRP.
STUDY DESIGN
Systematic review; Level of evidence, 2.
METHOD
A systematic review of the literature related to antiplatelet, anti-inflammatory, and anticoagulant drugs was performed following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. We used the Downs and Black objective quality scoring system. The literature search consisted of PubMed and Cochrane Library databases. Search terms consisted of 1 item selected from "platelet-rich plasma," "platelet-derived growth factor," and "platelet-rich plasma AND growth factor" combined with 1 item from "antiplatelet," "aspirin," "anticoagulant," and "NSAID." Only studies published within the past 25 years were included.
RESULTS
A total of 15 studies met the inclusion criteria: 7 studies detected no significant decrease in growth factors or mitogenesis, whereas 6 detected a decrease with antiplatelet agents, 1 detected mixed results with an antiplatelet agent, and 1 had mixed results with an antiplatelet agent/vasodilator. In terms of PRP activation, all 3 studies assessing collagen, the 2 studies analyzing adenosine diphosphate alone, and the 1 study investigating arachidonic acid found a decrease in growth factor concentration.
CONCLUSION
Antiplatelet medications may decrease the growth factor release profile in a cyclooxygenase 1- and cyclooxygenase 2-dependent manner. Eight of 15 studies found a decrease in growth factors or mitogenesis. However, more studies are needed to comprehensively understand antiplatelet effects on the PRP secretome.
PubMed: 32426401
DOI: 10.1177/2325967120912841