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Hemostasis Analyzers Market Size To Surpass US$ 10.02 Billion By 2033, The Brainy Insights
The Brainy Insights
The hemostasis analyzers market is evolving towards more user-friendly devices that offer high accuracy and timely results. The North America region emerged as the largest market for the hemostasis analyzers market, with a market share of 35.9% in 2023.
Newark, Aug. 26, 2024 (GLOBE NEWSWIRE) -- The global hemostasis analyzers market is anticipated to grow from USD 4.08 billion in 2023 to USD 10.02 billion by 2033, at a CAGR of 9.4% during the forecast period 2024-2033 Global hemostasis analyzers market is witnessing a considerable growth owing to increasing incidence of hemotological diseases across the globe. The market is now moving toward high robustness of devices, integrated analyzing software, a wide variety of ranges in these analyzers, and increased precision of results with reduced analysis time.
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Key Insights on Hemostasis Analyzers Market
The clinical laboratory analyzers segment led the hemostasis analyzers market with a market share of 69.9% in 2023.
The product segment is divided into clinical laboratory analyzers and point-of-care testing analyzers. The clinical laboratory analyzers segment led the hemostasis analyzers market with a market share of 69.9% in 2023. The clinical laboratory analyzers offers hospitals and healthcare professionals the laboratory testing tools to deliver appropriate medical care.
The prothrombin time segment accounted for the major market share of 36% in 2023.
The test type segment includes prothrombin time, fibrinogen, activated partial thromboplastin time, activated clotting time, D dimer, platelet function, anti-factor xa, heparin & protamine dose-response test for ACT, and others. The prothrombin time segment accounted for the major market share of 36% in 2023. The prothrombin time is routinely used to evaluate the effects of test articles on blood coagulation in general toxicology studies. Thus, extensive use of prothrombin time likely to drive the market growth over the forecast years.
The optical technology held the major market share of 31.2% in 2023.
The technology segment includes mechanical, optical, electrochemical, and other technologies. The optical technology held the major market share of 31.2% in 2023. This is mainly due to rising combination of immunological, chromogenic with optical photo technique, which has led to the development of high performance, multipurpose optical hemostasis analyzers.
Diagnostics centre dominated the market with a market share of 37.2% in 2023.
Story continues
The end-user segment is divided into diagnostic centres, hospitals, point of care, and others. Diagnostics centre dominated the market with a market share of 37.2% in 2023. The growth is mainly due to rise in advanced facilities and growing professional staffs in the diagnostic centres.
Scope of the Report:
Report Metrics
Details
Market size available for years
2024–2033
Base year considered
2022
Forecast period
2024–2033
Market Size in 2023
$4.08 Billion
Projected Market Value in 2033
$10.02 Billion
CAGR
9.4% From 2024 to 2033
Segments covered
Product, Technology, Test Type, End-User, Regions
Geographies covered
North America, Asia Pacific, Europe, Middle East and Africa, and Latin America
Companies covered
Siemens AG, Thermo Fisher Scientific Inc., Roche Diagnostics, Alere Inc., Sysmex Corporation, Nihon Kohden Corporation, DiagnosticaStago, Helena Laboratories, Instrumentation Laboratory, International Technidyne Corporation, Grifols
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The global hemostasis analyzers market is witnessing substantial growth, driven by the increasing prevalence of hematological diseases worldwide. Hemostasis analyzers are essential laboratory devices that aid medical practitioners in diagnosing and treating patients with blood clotting and bleeding disorders. These analyzers measure the mechanisms of clotting deficiencies associated with conditions such as thrombocytopenia, thromboembolic disease, impaired liver function, hemophilia, and more.
Hemostasis analyzers, also known as coagulation analyzers, utilize either mechanical or optical clot detection, with some advanced models capable of performing both. The market is evolving towards more user-friendly devices that offer high accuracy and timely results. Additionally, there is a growing emphasis on enhanced bioinformatics and integrated software that works seamlessly across multiple platforms and analyzers.
Currently, the market trends are focused on the development of robust devices with integrated analyzing software, a wide variety of analyzer options, and increased precision in results with reduced analysis times. However, the high cost of advanced hemostasis analyzers may pose a challenge to market growth in the coming years.
Despite these challenges, the demand for hemostasis analyzers continues to rise, underscoring the critical need for effective diagnostic tools in managing blood-related health conditions.
Regional Segmentation Analysis:
The regions analyzed for the market include North America, Europe, South America, Asia Pacific, and Middle East and Africa. The North America region emerged as the largest market for the hemostasis analyzers market and held the market share of 35.6% in the year 2020. This is mainly contributed to the factors such as highly advanced healthcare industry and favourable healthcare resources. In addition to this, growing ageing population and rising occurrence of CVD's such as deep vein thrombosis (DVT) and pulmonary embolism (PE), boosting the growth of the market in the region. The Europe region is anticipated to hold the prominent market share in the global hemostasis analyzers market, owing to increasing ageing population and increasing incidences of hemotological diseases across the region.
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Competitive Analysis:
Major players in the global hemostasis analyzers market are Siemens AG, Thermo Fisher Scientific Inc., Roche Diagnostics, Alere Inc., Sysmex Corporation, Nihon Kohden Corporation, DiagnosticaStago, Helena Laboratories, Instrumentation Laboratory, International Technidyne Corporation, and Grifols among others.
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COVID's Inflammation Linked To Long-Term Brain Effects
Summary: New research uncovers how COVID-19 may cause neuroinflammation, leading to persistent neurological symptoms even after recovery.
The study found elevated levels of pro-inflammatory cytokines and significant changes in cerebrospinal fluid among hospitalized patients, highlighting the brain's vulnerability to the virus.
These findings suggest that neuroinflammation could play a key role in the cognitive decline seen in "long COVID," stressing the need for ongoing monitoring and targeted therapies for survivors.
Key Facts:
Source: D'Or Institute
COVID-19 is primarily known for its effects on the respiratory system, but its consequences go far beyond that.
A recent study, published in the journal Brain, Behavior, & Immunity – Health and conducted at the D'Or Institute for Research and Education (IDOR), revealed molecular changes that may underlie the neurological symptoms exhibited by some patients affected by the disease, highlighting the importance of better understanding these still poorly known potential consequences of COVID-19.
COVID-19 Remains a Public Health Challenge
COVID-19 continues to be a concerning disease even after the end of its pandemic phase. In the first half of 2024 alone, it was responsible for over 3,000 deaths in Brazil. Additionally, scientific literature has been extensively documenting the deleterious effects of the infection even after patients have recovered, a condition now known as "long COVID."
Long COVID refers to a range of persistent symptoms that remain or emerge after the acute phase of the disease. Even after recovering from respiratory symptoms, patients may continue to face significant challenges, especially concerning neurological health. A significant portion of COVID-19 survivors, even those who had mild cases, may experience cognitive decline and difficulty concentrating for extended periods after the infection. This makes it important to study how the disease affects the brain even in the acute phase, as this may provide clues about these neurological sequelae.
During the infection, the most common neurological symptoms are headaches, fatigue, loss of smell, and even more severe complications such as strokes and encephalitis. Investigating these manifestations is crucial, as we still know little about the mechanisms leading to these complications and how they develop.
How the Study Was Conducted
Seeking biomarkers that could provide clues about neuroinflammatory processes in COVID-19, IDOR researchers analyzed data from patients confirmed to have COVID-19 who were hospitalized in theRede D'Or network between April and November 2020.
The sample included 35 patients aged between 26 and 87 years, divided between moderate and severe cases, all of whom presented significant neurological symptoms during the acute COVID-19 infection. The data were collected from medical records and included imaging exams (MRI and CT scans), blood tests, and cerebrospinal fluid (CSF) analysis—a fluid that surrounds the brain and spinal cord. Ten CSF samples from uninfected patients served as a control group.
Findings Reveal Significant Brain Inflammation
The analysis revealed that most patients had at least one comorbidity, with 65.7% having two or more. About 85.7% of patients exhibited neurological symptoms at the time of hospital admission, a clinical picture that was even more pronounced than respiratory symptoms.
Imaging exams showed that 28.6% of patients had focal or diffuse brain changes associated with COVID-19, including demyelinating lesions, encephalitis, and stroke.
Blood tests indicated that 66% of patients showed signs of an exacerbated inflammatory response. Proteomic analyses of the CSF revealed an altered protein pattern compared to the controls, with 116 significantly dysregulated proteins related to the immune system and metabolic processes.
Pro-Inflammatory Cytokines Are Associated with Disease Severity
The levels of two pro-inflammatory cytokines, IL-6 and TNFα, were elevated in the CSF of COVID-19 patients, with IL-6 being particularly higher in severe cases. These cytokines are associated with the severity of the disease and the changes observed in imaging exams.
Dr. Fernanda Aragão, a postdoctoral researcher at IDOR and the study's first author, comments that the research is one of the first to connect imaging exams and neurological symptoms with neuroinflammatory biomarkers capable of reflecting the severity of acute disease, a complication that remains difficult to predict.
Despite the severity distinction found from these biomarkers, the researcher emphasizes that neuroinflammation is independent of disease severity and may be one of the main causes of neurological disorders associated with COVID-19. She points out that even patients with milder cases showed significant changes in the CSF, suggesting that the body's inflammatory response may affect the brain in ways not yet fully understood.
"This study reveals that neuroinflammation is a common factor in neurological cases of the disease, even in patients with diverse conditions, whether moderate or severe. Identifying these inflammatory markers that connect COVID-19 severity and neuroimaging changes could be very important for developing therapies aimed at both treating acute COVID-19 infections and addressing the persistent effects of what is known as long COVID," adds the author.
Implications for Long-Term Treatment and Monitoring
These findings highlight the need for long-term monitoring of patients who have had COVID-19, especially those at risk of developing persistent neurological complications. Better understanding these mechanisms can help develop more effective treatment and prevention strategies in the future.
IDOR's research provides valuable insights into the neurological impacts of COVID-19 and paves the way for future studies to explore these findings more deeply and in larger populations.
Thus, continued investigation into the neurological consequences of COVID-19 is presented as a crucial investment, especially with the evolution of new variants and the implementation of vaccination programs, to ensure that the long-term effects of the pandemic are adequately understood and addressed.
Author: Maria Eduarda Ledo de AbreuSource: D'Or InstituteContact: Maria Eduarda Ledo de Abreu – D'Or InstituteImage: The image is credited to Neuroscience News
Original Research: Open access."Changes in neuroinflammatory biomarkers correlate with disease severity and neuroimaging alterations in patients with COVID-19 neurological complications" by Fernanda Aragão et al. Brain, Behavior, and Immunity Health
Abstract
Changes in neuroinflammatory biomarkers correlate with disease severity and neuroimaging alterations in patients with COVID-19 neurological complications
COVID-19 induces acute and persistent neurological symptoms in mild and severe cases. Proposed concomitant mechanisms include direct viral infection and strain, coagulopathy, hypoxia, and neuroinflammation. However, underlying molecular alterations associated with multiple neurological outcomes in both mild and severe cases are majorly unexplored.
To illuminate possible mechanisms leading to COVID-19 neurological disease, we retrospectively investigated in detail a cohort of 35 COVID-19 mild and severe hospitalized patients presenting neurological alterations subject to clinically indicated cerebrospinal fluid (CSF) sampling. Clinical and neurological investigation, brain imaging, viral sequencing, and cerebrospinal CSF analyses were carried out.
We found that COVID-19 patients presented heterogeneous neurological symptoms dissociated from lung burden. Nasal swab viral sequencing revealed a dominant strain at the time of the study, and we could not detect traces of SARS-CoV-2's spike protein in patients' CSF by multiple reaction monitoring analysis.
Patients presented ubiquitous systemic hyper-inflammation and broad alterations in CSF proteomics related to inflammation, innate immunity, and hemostasis, irrespective of COVID-19 severity or neuroimaging alterations.
Elevated CSF interleukin-6 (IL6) correlated with disease severity (sex-, age-, and comorbidity-adjusted mean Severe 24.5 pg/ml, 95% confidence interval (CI) 9.62–62.23 vs. Mild 3.91 pg/mL CI 1.5–10.3 patients, p = 0.019).
CSF tumor necrosis factor-alpha (TNFα) and IL6 levels were higher in patients presenting pronounced neuroimaging alterations compared to those who did not (sex-, age-, and comorbidity-adjusted mean TNFα Pronounced 3.4, CI 2.4–4.4 vs.
Non-Pronounced 2.0, CI 1.4–2.5, p = 0.022; IL6 Pronounced 33.11, CI 8.89–123.31 vs Non-Pronounced 6.22, CI 2.9–13.34, p = 0.046). Collectively, our findings put neuroinflammation as a possible driver of COVID-19 acute neurological disease in mild and severe cases.
Fibrin Fuels Thromboinflammation And Brain Damage In COVID-19
Uncovering the molecular interactions between fibrin and the SARS-CoV-2 spike protein, researchers pave the way for targeted therapies that could curb the devastating effects of long COVID.Fibrin drives thromboinflammation and neuropathology in COVID-19. Image Credit: Juan Gaertner / Shutterstock
In a recent study published in the journal Nature, a large team of researchers in the United States provided evidence that fibrin plays a pivotal role in driving thromboinflammation (the harmful interaction between clotting and inflammation) and neuropathology in Coronavirus disease 2019 (COVID-19). They also explored the potential of fibrin-targeting immunotherapy as a treatment for both acute COVID-19 and long COVID-19.
BackgroundLong COVID has become a significant public health concern, with coagulation and neurological complications arising during acute infection and persisting into the post-acute phase, contributing to morbidity and mortality. These issues affect patients across all age groups, including those with mild or breakthrough infections. Persistent and resistant blood clots, despite adequate anticoagulation, suggest underlying mechanisms that are not yet fully understood. The interaction between hypercoagulability, immune response, and neurological complications in COVID-19 highlights the need for further research to uncover the precise mechanisms driving these complications and to develop effective treatments.
About the studyC57BL/6 and K18-hACE2 mice were utilized in this study, obtained from Jackson Laboratory and other sources, and housed under standard conditions. Mice aged 3 to 7 months of both sexes were used for experiments conducted in an Association for Assessment and Accreditation of Laboratory Animal Care (AAALAC)-accredited Animal Biosafety Level 3 (ABSL3) facility at Gladstone Institutes, following institutional guidelines.
Human citrated plasma and Peripheral Blood Mononuclear Cells (PBMCs) were commercially sourced, with no human participants directly involved. The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) recombinant trimeric spike protein was produced in Chinese Hamster Ovary (CHO) cells, purified, and used in various assays.
Fibrin polymerization in human plasma was assessed by measuring turbidity after initiating clotting with thrombin and calcium chloride. Scanning electron microscopy (SEM) analyzed fibrin clots formed on silicon wafers, followed by image processing with National Institutes of Health (NIH) Images.
ELISA plates coated with fibrinogen or fibrin were used to study the specific binding interactions of the spike protein, detected with specific antibodies. Additional methods included peptide arrays, epitope mapping, alanine scanning, structural modeling, and docking studies to explore the precise regions within fibrinogen and spike that mediate their interaction.
In vivo experiments involved injecting labeled spike protein and fibrinogen into mice, followed by tissue imaging. Resistance of fibrin clots to plasmin digestion, reactive oxygen species (ROS) detection in macrophages, and various immunoassays were performed. Data analysis ensured statistical rigor, supporting the study's robust conclusions.
Study resultsGiven the higher frequency and severity of abnormal blood clots in COVID-19 patients compared to other respiratory infections, it was hypothesized that SARS-CoV-2 might directly bind to fibrinogen, promoting clot formation and altering clot structure and function. A solid-phase binding assay confirmed the specific interaction between fibrinogen/fibrin and the SARS-CoV-2 spike protein, identifying key binding sites on both molecules. This included the spike S1(N501Y) mutant, which enhances viral transmission and binding to Angiotensin-Converting Enzyme 2 (ACE2). The affinity of the spike for fibrin was lower than for ACE2, yet fibrinogen was found to co-immunoprecipitate with the spike protein and co-localized with spike in the lungs of infected mice. This suggests that fibrin and spike interact both in solution and within tissues.
To further explore the binding regions, a custom fibrinogen peptide array identified key binding sites in the fibrinogen Bβ and γ chains, mapping these to specific regions on the spike protein. Computational docking provided models that demonstrated a close association between these binding sites, confirming the interaction at a molecular level.
Subsequent tests revealed that spike protein alters fibrin clot structure and increases clot turbidity, indicating denser and more resistant clots, as observed in thromboembolic diseases and in COVID-19 patients. Additionally, the spike delayed the degradation of fibrin by plasmin, further suggesting that the spike contributes to the formation of fibrinolysis-resistant clots. This resistance to degradation could be a key factor in the persistence of inflammation and clot-related complications in long COVID. Spike also enhanced fibrin-induced inflammation, as shown by increased ROS release from macrophages.
Mutagenesis studies pinpointed the interaction between spike and a specific epitope on the fibrinogen γ-chain, which is crucial for binding the CD11b receptor involved in immune activation. Blocking this specific epitope with a monoclonal antibody, 5B8, not only inhibited the fibrin-spike interaction but also reduced spike-enhanced ROS release, indicating a potential therapeutic mechanism to mitigate both clot formation and inflammation. In vivo, co-injection of fibrinogen and spike into the mouse brain increased fibrin-induced microglial reactivity, underscoring the pro-inflammatory role of fibrin in the presence of SARS-CoV-2 spike protein.
ConclusionsTo summarize, the study reveals that fibrinogen plays a central role in driving thromboinflammation and neuropathology in COVID-19, not merely as a consequence of systemic inflammation but as an active participant in the disease process. Fibrinogen's interaction with the SARS-CoV-2 spike protein leads to abnormal clot formation, hyperinflammation, and direct effects on microglia in the brain, contributing to the neurological symptoms observed in COVID-19. The 5B8 anti-fibrin antibody was found to block many of these pathological effects, providing dual protection by reducing both thromboinflammation and neurodegeneration. Fibrin's suppression of NK cell activity further highlights its role in modulating the immune response, potentially impairing viral clearance and exacerbating disease severity. This mechanism could be significant in both acute and long COVID, where persistent fibrin deposition may contribute to ongoing inflammation and cognitive decline. The study also points to the potential for fibrin-targeting therapies to reduce thromboinflammation and protect against neurological damage in COVID-19 without compromising normal hemostasis, offering a promising therapeutic avenue for patients suffering from the long-term effects of COVID-19.
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