Press reviews

Insulin resistance, a key factor in the development of type 2 diabetes and other metabolic disorders, is often linked to obesity, dyslipidemia, and hypertension. Recently, extracellular vesicles (EVs)—membrane-bound particles released by cells—have emerged as critical players in intercellular communication. By transporting proteins, lipids, and messenger RNAs, these vesicles facilitate the transmission of biological signals between cells and influence various pathophysiological processes, including the regulation of insulin sensitivity. This study investigates their role in modulating insulin resistance.  

What role do extracellular vesicles play in insulin resistance?

This research compared EVs from participants with and without insulin resistance (IR and non-IR) and evaluated their impact on insulin signaling in adipose tissue and the liver using murine models. The findings revealed that EVs from IR participants induced insulin resistance in mice, whereas EVs from non-IR participants did not. Furthermore, the study identified active phosphatases, PTP1B and PP2A, within the EVs from IR participants as key regulators of insulin resistance. Inhibiting PTP1B restored IRS1 and AKT signaling in adipocytes, while inhibiting PP2A reduced the development of insulin resistance in both adipocytes and hepatocytes.  

When vesicles take the lead: a revolution against insulin resistance

This research highlights the pivotal role of phosphatases carried by IR EVs in insulin resistance. PTP1B and PP2A emerge as potential therapeutic targets to combat insulin resistance and prevent metabolic complications, particularly in adipose and hepatic tissues. These findings pave the way for targeted therapeutic approaches, offering new hope in the fight against metabolic disorders associated with insulin resistance.  

Polycystic ovary syndrome (PCOS) is a common hormonal disorder in women of reproductive age, characterized by chronic inflammation, elevated oxidative stress, and abnormalities in cell death mechanisms (apoptosis). These biological imbalances contribute to issues such as irregular ovulation, hormonal disturbances, and other PCOS symptoms.

In this context, astaxanthin (ASX), a potent antioxidant, is being investigated for its potential to reduce inflammation and improve cellular function by modulating endoplasmic reticulum stress and apoptosis. These effects may enhance ovarian function and provide new therapeutic avenues for women with PCOS.  

What are the effects of astaxanthin on inflammation and cellular stress in PCOS?

This study involved 56 women with PCOS, divided into two groups:

• ASX Group: 12 mg of astaxanthin daily.
• Placebo Group.

 
Over eight weeks, the study aimed to evaluate the impact of ASX on inflammatory markers (TNF-α, IL-18, IL-6, CRP) and the expression of genes related to endoplasmic reticulum stress and apoptosis in peripheral blood mononuclear cells (PBMCs).  

Key findings include:

• Reduction in inflammatory markers: The ASX group showed a significant decrease in TNF-α, IL-18, and IL-6 levels compared to the placebo group. No significant change was observed for CRP.
• Impact on endoplasmic reticulum stress: ASX reduced the expression of several genes associated with endoplasmic reticulum stress, such as CHOP, ATF4, XBP1, and DR5, indicating improved cellular stress regulation.
• No significant improvement in clinical symptoms: Despite positive biological effects, no significant changes were observed in clinical symptoms such as hirsutism, hair loss, or menstrual cycle regularity.

 

Astaxanthin: a hopeful ally against inflammation in PCOS

The findings suggest that ASX may have a beneficial role in modulating inflammatory and apoptotic processes in women with PCOS. However, while these effects highlight a potential pathway for addressing the biological symptoms of the condition, no significant clinical improvements were observed.

These results emphasize the need for further research, particularly on dosage and treatment duration, to confirm the efficacy of ASX in managing PCOS.

Adverse childhood experiences (ACEs) are well-established risk factors for the development of depressive disorders in adulthood. Early trauma disrupts psychobiological and physiological mechanisms, increasing vulnerability to mental health issues later in life. Recent research highlights the central role of inflammation as a biological response to stress and trauma in the pathophysiology of depression. Prolonged inflammation may induce changes in the brain that influence mood and behavior. This study investigates the mediating role of inflammation in the relationship between ACEs and depression.  

Inflammation: A Key Mediator?  

A total of 22 studies were analyzed to evaluate the link between ACEs, inflammatory markers, and depressive symptoms in adulthood. Inflammation was measured through markers such as C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α).  

The findings indicate that CRP, IL-6, and composite inflammation levels significantly mediate the association between ACEs and adult depression.

However, these results do not account for certain confounding factors, such as body mass index (BMI), which can also influence inflammation levels. High body fat levels are often associated with low-grade chronic inflammation.  

Inflammation: The Key to Understanding and Treating Trauma-Linked Depression  

These findings suggest that inflammation is a critical mechanism linking childhood trauma to depressive symptoms. Elevated inflammatory markers in response to prolonged stress or trauma act as biological mediators, amplifying the effects of ACEs on depression development. While inflammation plays a significant role, other metabolic and psychobiological factors also contribute to this relationship.  

This study paves the way for therapeutic interventions targeting inflammation, particularly in cases of depression linked to childhood trauma.    

The use of pesticides in agriculture, while essential for pest control, poses a major public health challenge, particularly in developing countries. Excessive or improper use of these chemicals can lead to acute health symptoms such as headaches, nausea, and respiratory issues, predominantly affecting farmers. Despite the availability of recommended safety practices for handling pesticides, many farmers remain exposed to significant risks.  

Safety Practices and Acute Symptoms: A Status Report  

This study investigated pesticide safety practices and the prevalence of acute health symptoms among farmers in several developing countries.  

The analysis revealed that adherence to safe pesticide use practices is low, with an average of only 43.1% across the countries studied. Significant variations were observed, ranging from 12.5% in Tanzania to 87.2% in Iran. The findings also indicated that safety practices are influenced by factors such as better knowledge, positive attitudes towards pesticides, higher education levels, and more than five years of experience in their use.  

Regarding health symptoms, the study showed that, on average, 30.36% of farmers reported acute health symptoms related to pesticide exposure, with substantial differences between countries. The lowest rate of symptoms was observed in Ethiopia (1.59%), while the highest rate was reported in Kuwait (55.76%). 

Pesticide Safety: Balancing Best Practices and Surprising Symptoms  

The results highlight a significant gap in safety practices and a high prevalence of acute health symptoms among farmers in developing countries. This underscores the urgent need for tailored intervention measures, such as pesticide safety training, the distribution of personal protective equipment, and targeted educational programs. Educating farmers and improving their knowledge play a central role in enhancing safety and reducing health risks.

Systemic sclerosis is a rare and complex autoimmune disease characterized by widespread blood vessel damage, abnormal immune system activation, and excessive connective tissue fibrosis. These dysfunctions lead to severe complications affecting multiple organs, including the skin, lungs, heart, and kidneys.  

Angiogenesis, a key process that facilitates the formation of new blood vessels from existing ones, plays a central role in this pathology. This mechanism is often impaired in systemic sclerosis, resulting in inefficient vascularization and exacerbating tissue damage.  

Vascular endothelial growth factor (VEGF), a crucial cytokine regulating angiogenesis, has attracted significant attention as a potential biomarker. Abnormally high VEGF levels in systemic sclerosis suggest its involvement in disease progression, making it a promising target for future diagnostic and therapeutic approaches.  

VEGF: a key marker in systemic sclerosis?  

This study investigates circulating VEGF levels in patients with systemic sclerosis and their association with clinical manifestations. Key findings include:

• Patients with systemic sclerosis exhibit significantly higher VEGF concentrations compared to healthy individuals.
• A correlation was observed between VEGF levels and the severity of clinical manifestations, particularly digital ulcers, capillary abnormalities, and skin fibrosis.
• Although VEGF generally promotes angiogenesis, in this specific context, it appears to contribute to inefficient and disorganized vascularization, exacerbating existing vascular abnormalities.

When VEGF becomes a compass for systemic sclerosis  

The results suggest that VEGF could serve as a useful biomarker not only for assessing the activity of systemic sclerosis but also for predicting its clinical progression. Its central role in the disease's pathophysiology also makes it an especially promising target for developing new therapeutic strategies. These approaches would aim to restore functional vascularization while correcting existing abnormalities.  

These discoveries pave the way for innovative targeted treatments that could address vascular abnormalities and slow the progression of this debilitating disease, thereby improving patients' quality of life.

Leprosy, a chronic infectious disease caused by Mycobacterium leprae and Mycobacterium lepromatosis, remains a major public health challenge today. Despite advancements in treatment through multidrug therapy (MDT), the persistence of the disease, active transmission cases, and associated stigma continue to hinder eradication efforts. In this context, prophylactic and therapeutic vaccines are emerging as promising tools, offering a critical complementary approach to accelerate the elimination of this ancient disease.

Leprosy Vaccines: A Promising Strategy?

This study reviewed 12 randomized clinical trials assessing the efficacy of leprosy vaccines, divided into 8 prophylactic and 4 therapeutic studies. Key findings include:

• A significant reduction in infection risk was observed, with a combined relative risk of 0.61.
• Vaccines based on BCG, alone or combined with other components (e.g., Mycobacterium indicus pranii), showed varying protective effects depending on the populations studied (age, region).

Worth noting: Relative risk compares the likelihood of an event (such as disease) between two groups, indicating how many times higher or lower the risk is in one group versus another.

• Clinical severity scores, such as the Ramu score, significantly improved after administering therapeutic vaccines like Mycobacterium w.
• However, results on the bacterial index were inconsistent, suggesting a limited impact on active bacterial load.

Worth noting: The Ramu score is a clinical tool used to evaluate the severity of leprosy, considering criteria such as skin lesions, affected nerves, and internal organ involvement.

Promising Vaccines to Close a Millennia-Old Chapter

The findings indicate that leprosy vaccines, whether prophylactic or therapeutic, provide significant protection and improve clinical outcomes. However, the heterogeneity of studies, particularly in vaccination protocols and control groups, limits the generalization of conclusions.

The COVID-19 pandemic significantly impacted mental health and eating behaviors in the general population. Social restrictions, economic uncertainty, and isolation exacerbated dysfunctional eating behaviors, including binge eating, overeating, and body image concerns.

This study examines the evolution of eating disorders and dysfunctional eating behaviors during the first two waves of the pandemic.

Did the COVID-19 Pandemic Really Affect Eating Behaviors?

To address this uncertainty, 186 studies involving 406,076 participants were selected and analyzed. The following parameters were studied: predominant symptoms, weight changes, and psychosocial factors.

These findings reveal that body image concerns (52%), binge eating episodes (40%), and overeating (40%) were among the most frequent behaviors during this period. Similarly, weight gain was more common than weight loss (33% vs. 20%), reflecting significant changes in eating habits. Finally, a significant correlation was observed between psychological distress (stress, anxiety, depression) and eating behaviors, particularly overeating and body image concerns.

Meals Under Pressure: When the Pandemic Disrupts Our Plates and Minds

This study highlights the pandemic's negative impact on eating behaviors, revealing marked disparities based on gender, age, and cultural contexts. These results underscore the urgency of developing targeted strategies to prevent and mitigate these behaviors, especially during public health crises. Future studies should explore long-term impacts, identify the most vulnerable groups, and evaluate suitable therapeutic interventions, such as psychological support or dietary rehabilitation programs. 

Metabolic and psychological disorders, such as stress and obesity, share complex biological mechanisms regulated by the gut-brain axis. Chronic stress disrupts this balance by altering gut microbiota and reducing the production of key molecules like short-chain fatty acids (SCFAs), which exacerbates inflammation and stress responses.

Low-calorie diets present a promising opportunity to restore this balance by modulating the microbiota and improving stress management. However, their effects on bacterial diversity remain ambiguous. This study investigates the combined impact of caloric restriction and a clinical psychological intervention (CPI) on gut microbiota and mental well-being in overweight or stressed women.

Fewer Calories, Less Stress: Could the Microbiota Hold the Key?

In this study, 41 women were randomly divided into two dietary groups:

• Very Low-Calorie Diet (VLCD)
• F.X. Mayr Diet (FXM), including magnesium supplementation.

Each group was further split into those receiving or not receiving CPI. Blood and stool samples were analyzed before and after two weeks of caloric restriction.

Key findings from the study include:

• Microbial Diversity

Caloric restriction led to a reduction in alpha diversity, indicating a decrease in bacterial species richness. Beta diversity changes, reflecting differences between individuals, were influenced by several factors such as diet type, age, and body mass index.

Taxonomic Changes
Some SCFA-producing bacterial genera, such as Faecalibacterium and Roseburia, significantly decreased following caloric restriction. The FXM diet uniquely increased Oscillibacter, a bacterium associated with psychological improvements, suggesting specific beneficial effects.

• Mental Well-Being
  

Significant improvements in perceived stress scores and other psychological indices were observed, particularly in the FXM group. Conversely, CPI had a negligible effect on the microbiota compared to caloric restriction, reaffirming that diet plays a pivotal role in modulating the microbiota and mental well-being.

Oscillibacter, Faecalibacterium & Co.: In Search of the Perfect Menu for Mind and Body

This study highlights the potential of the FXM diet to favorably modulate gut microbiota, enhance mental well-being, and reduce stress. However, the loss of beneficial bacteria such as Faecalibacterium and Subdoligranulum raises concerns about the long-term effects of low-calorie diets.

These findings encourage the development of targeted dietary approaches, combined with in-depth analysis of specific microbes, to create innovative strategies for optimizing mental and metabolic health.

Post-traumatic stress disorder (PTSD) is a debilitating mental health condition that develops following major trauma. Recent research has highlighted the role of gut microbiota and inflammatory biomarkers in the development of this disorder through the gut-brain axis. This study examines the connections between gut microbiota composition, inflammatory biomarkers, and PTSD.

Do Gut Microbiota and Inflammation Truly Play a Role in PTSD?

To address this question, 15 studies were analyzed: 9 focusing on inflammatory biomarkers and 6 on gut microbiota composition. Key findings include:

• Systemic Inflammation: Patients with PTSD exhibit elevated levels of pro-inflammatory cytokines (IL-6, IL-1β, and TNF-α), indicating a chronic inflammatory state.
• Gut Microbiota Diversity and Composition: Although the reduction in alpha diversity was not statistically significant, two studies reported a marked decrease in Lachnospiraceae, a group of bacteria known for producing short-chain fatty acids (SCFAs). These bacteria are critical for maintaining intestinal integrity and modulating inflammation.
• Specific Correlations: Alterations in the gut microbiota, particularly the reduction of Lachnospiraceae, were associated with specific PTSD symptoms, such as hypervigilance and cognitive impairments.

Revolutionizing PTSD Management: Gut Microbiota at the Core of Therapeutic Solutions

The findings underscore the crucial role of the gut-brain axis in the pathophysiology of PTSD. Imbalances in gut microbiota may not only exacerbate inflammatory responses through increased intestinal permeability and pro-inflammatory cytokine release but also directly influence behavior via neurotransmitter production. This study emphasizes the importance of identifying gut microbiota-targeted interventions, such as probiotics or prebiotics, to modulate inflammatory responses and improve PTSD symptoms.

Low-grade systemic inflammation plays a key role in brain activity and mental disorders, particularly among individuals with metabolic syndrome (MetS). Recent research highlights the potential of the gut microbiota in modulating inflammation through the production of short-chain fatty acids (SCFAs) derived from microbial fermentation of dietary fibers. This study explores the effects of a diverse prebiotic fiber blend on inflammation, gut microbiota, and psychological symptoms in patients with MetS.

Can Prebiotic Fibers Improve Metabolic Syndrome Symptoms?

In this study, 60 adults with MetS were randomly divided into two groups:

• Prebiotic Group (n = 40): Daily consumption of 10 g of diverse prebiotic fibers combined with nutritional counseling.
• Control Group (n = 20): Nutritional counseling only.

The intervention lasted for 12 weeks. The results showed a significant reduction in high-sensitivity C-reactive protein (hs-CRP), a key marker of inflammation, in the treated group compared to the control group. An improvement in self-reported psychological symptoms, including perceived stress, anxiety, and depression, was also observed. Additionally, an increase in beneficial gut bacteria (Bifidobacterium and Parabacteroides), associated with SCFA production, was noted. However, no difference was observed in gut microbiota diversity between the groups at the end of the study.

Strengthening the Gut-Brain Axis with Prebiotic Fibers

This study reveals a significant correlation between systemic inflammation (measured by hs-CRP) and psychological disorders such as stress, anxiety, and depression. Gastrointestinal symptoms also emerged as key determinants of these psychological variations, illustrating the critical role of the gut-brain axis in mental health. These findings provide strong evidence for the integration of prebiotic fibers into nutritional management strategies aimed at reducing systemic inflammation and improving mental well-being in patients with MetS.  

Norovirus is one of the leading causes of acute gastroenteritis worldwide, responsible for frequent outbreaks and significant morbidity, particularly among children, the elderly, and immunocompromised individuals. Its rapid transmission through the fecal-oral route, often via contaminated food or human contact, makes it a major public health concern.  

The emergence of the GII.4 Sydney variant in 2012, characterized by its heightened transmissibility and partial evasion of preexisting immunity, marked a turning point in the global epidemiology of norovirus. Understanding its impact on infection prevalence and its implications for outbreak management has become a critical focus.  

This study quantifies the prevalence of norovirus gastroenteritis following the emergence of the GII.4 Sydney variant and highlights its public health implications to guide effective global surveillance and vaccination strategies.  

How Do Norovirus and Its GII.4 Sydney Variant Impact Global Health?  

Based on 48 analyses conducted between 2012 and 2020, this study reveals that norovirus is implicated in 18% of acute gastroenteritis cases globally. The GII.4 Sydney variant predominates during outbreaks, underscoring its virulence and transmissibility. The data also show higher virus prevalence in Asia and Africa compared to Europe and North America, reflecting disparities in surveillance, immunity, and healthcare infrastructure. Additionally, the study highlights that children under five years old are particularly affected, emphasizing the need for targeted interventions in this vulnerable population.  

A Global Burden Exacerbated by the GII.4 Sydney Variant  

This study underscores the significant global burden of norovirus, magnified by the dominance of the GII.4 Sydney 2012 variant. These findings provide a solid foundation for developing public health strategies, including strengthened surveillance systems and vaccine research. However, norovirus remains a major challenge, particularly in resource-limited regions where its impact is most severe. 

Oxidative stress and inflammation are two key mechanisms involved in the development of many chronic diseases, including cardiovascular diseases, diabetes, cancers, and neurodegenerative disorders. Oxidative stress, driven by an excess of free radicals, damages cells, while chronic inflammation exacerbates metabolic and vascular imbalances.  

Polyphenols, particularly flavonoids found in dark chocolate and cocoa, have antioxidant and anti-inflammatory properties. They neutralize free radicals, reduce oxidative damage to cells, and modulate pro-inflammatory cytokines, thereby improving endothelial function. These molecules hold promising potential for preventing chronic diseases or mitigating pathological processes associated with them.

This study explores the effects of dark chocolate and cocoa consumption on specific markers of oxidative stress and inflammation to better understand their role in a nutritional prevention strategy.  

Can Dark Chocolate Really Reduce Oxidative Stress and Inflammation?  

This study analyzed 33 randomized controlled trials involving 1,379 adult participants. The specific biomarkers examined included:

• Malondialdehyde (MDA), an indicator of lipid peroxidation;
• Nitric oxide (NO), a key marker of vascular health;
• Inflammatory markers such as C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α).

 
The doses of flavonoids studied were variable, with subgroups established to examine the effects of high doses (>450 mg/day) and intervention durations ranging from 2 to 12 weeks.  

The analysis revealed that consuming flavonoid-rich dark chocolate was notably associated with improved oxidative stress. This included a significant reduction in MDA levels and a marked increase in NO levels, reflecting enhanced vascular and endothelial function. However, the impact on inflammatory markers was limited. No significant reduction in CRP, IL-6, or TNF-α levels was observed across the studies, except in participants with unhealthy baseline conditions, where more pronounced anti-inflammatory effects were detected. Finally, benefits were most evident with high flavonoid doses (>450 mg/day) and shorter intervention durations (≤4 weeks).  

A Touch of Cocoa for Health  

This study highlights the potential of polyphenol-rich dark chocolate to reduce oxidative stress, particularly through increased NO and decreased MDA levels. Although its effects on inflammation are modest, they appear more significant in at-risk populations. These findings support the integration of dark chocolate into a functional nutritional approach to prevent chronic diseases. However, further studies are needed to better understand the underlying biological mechanisms and define optimal doses to maximize benefits.  

Polyphenols found in cocoa, particularly in dark chocolate, are known for their antioxidant properties and health benefits. Several studies suggest that their consumption can enhance cognitive performance, reduce mental fatigue, and maintain focus during prolonged tasks. In this context, this study investigates the effects of consuming cocoa polyphenol-rich dark chocolate on brain activity.  

Can Dark Chocolate Influence Brain Activity During Cognitive Tasks?

For this study, 26 healthy participants aged 30 to 49 were selected. Each participant consumed two types of chocolate in a crossover design: one rich in polyphenols (635 mg) and one low in polyphenols (211.7 mg). Brain activities were measured during two sessions of cognitive tasks (continuous effort and attentional selectivity) at 25 and 50 minutes post-ingestion. Analyses focused on the activation of the dorsolateral prefrontal cortex (DLPFC) and inferior parietal cortex (PPC), regions involved in efficient cognitive resource utilization.  

The analysis showed that consuming polyphenol-rich chocolate was associated with reduced cerebral effort and improved efficiency in utilizing cognitive resources. Conversely, although the differences in brain activity were notable, no significant improvements were observed in cognitive performance (reaction times or accuracy rates). Similarly, participants reported comparable levels of fatigue with both types of chocolate, with no notable differences.  

Dark Chocolate: A Natural Brain Booster

This study highlights that consuming cocoa polyphenol-enriched dark chocolate significantly enhances the efficiency of brain activity during continuous and demanding cognitive tasks, reducing the mental effort required to mobilize cognitive resources. These findings support the potential of cocoa polyphenols as a dietary supplement to promote mental performance and sustain cognitive functions. Further research is now needed to explore the underlying biological mechanisms, determine optimal doses, and investigate their long-term impact on cognitive performance. 

Menopause is often associated with an increase in depressive symptoms, affecting up to 35% of postmenopausal women. These issues, often exacerbated by hormonal fluctuations, sleep disorders, or age-related body changes, negatively impact quality of life and lead to increased healthcare costs. In this context, it is crucial to identify effective and accessible approaches to manage these symptoms, particularly through nutritional interventions.

This study evaluates the impact of daily dark chocolate consumption on depression and sleep quality in menopausal women aged 45 to 65. Additionally, it explores potential effects on anthropometric parameters such as body mass index (BMI), weight, and waist circumference to assess possible implications for overall physical health.  

Dark Chocolate: A Natural Solution for Depression in Menopausal Women?

Sixty menopausal women with mild to moderate depressive symptoms were selected and randomly divided into two groups:

• Group 1: Daily consumption of 12 g of dark chocolate (78% cocoa).
• Group 2: Daily consumption of 12 g of milk chocolate.

The intervention lasted eight weeks, with evaluations using the Beck Depression Inventory-II (BDI-II) to measure depression and the Pittsburgh Sleep Quality Index (PSQI) to assess sleep quality. Anthropometric parameters were also recorded.

The study revealed a significant reduction in depression scores in the group consuming dark chocolate, with an adjusted mean difference of -2.3 (p = 0.003) and a moderate effect size (Cohen's d = -0.54). However, no significant improvement was observed between the two groups regarding overall sleep quality or its subdomains. Similarly, measurements of weight, BMI, and circumferences (waist and hips) showed no significant differences between the groups after the intervention.  

Dark Chocolate: A Small Treat with Big Benefits

This study suggests that daily consumption of dark chocolate rich in polyphenols can be an effective complementary method to reduce depressive symptoms in menopausal women. However, no effects were observed on sleep quality or physical health indices. These findings highlight the potential of functional foods in nutritional recommendations, though further research is needed to clarify the mechanisms of action, optimal dosages, and intervention duration.  

The COVID-19 pandemic, caused by SARS-CoV-2, has led to millions of deaths worldwide. Among its major complications is an associated coagulopathy, characterized by hypercoagulation and thromboembolic disorders. These abnormalities, linked to an excessive inflammatory response, manifest as thromboses, pulmonary embolisms, or strokes, and represent a significant factor in the mortality of critically ill patients. This study aimed to establish the association between coagulation parameters and mortality in COVID-19 patients, highlighting potential biomarkers to assess risk and guide clinical care.

Which coagulation markers are associated with mortality?

A meta-analysis of 48 studies, including 6,969 participants, compared deceased patients to survivors. The main parameters analyzed included platelet count, prothrombin time (PT), D-dimer, INR, fibrinogen, and activated partial thromboplastin time (aPTT).

The results revealed significant thrombocytopenia in deceased patients, characterized by a lower average platelet count compared to survivors. Furthermore, levels of D-dimer, PT, and INR were significantly higher in deceased patients, indicating a hypercoagulable state. In contrast, fibrinogen and aPTT did not show significant differences between the two groups.

COVID-19 and coagulation parameters: a crucial link to mortality

This study emphasizes the critical role of coagulation parameters, such as D-dimer and PT, in assessing the severity and mortality risk in COVID-19 patients. Thrombocytopenia, already recognized as a marker of severity, is also confirmed as a reliable indicator of poor prognosis. These findings support the integration of systematic coagulation testing into clinical monitoring to quickly identify high-risk patients and optimize therapeutic strategies, particularly with anticoagulant use.