Search Results (210)

Background: COVID-19-associated coagulopathy (CAC) is a complex condition, with high rates of thrombosis, high levels of inflammation markers and hypercoagulation (increased levels of fibrinogen and D-Dimer), as well as extensive microthrombosis in the lungs and other organs of the deceased. It resembles, without being identical, other coagulation disorders such as sepsis-DIC (SIC/DIC), hemophagocyte syndrome (HPS) and thrombotic microangiopathy (TMA). Platelets (PLTs), key regulators of thrombosis, inflammation and immunity, are considered an important risk mediator in COVID-19 pathogenesis. Platelet index MPV/PLT ratio is reported in the literature as more specific in the prognosis of platelet-related systemic thrombogenicity. Studies of MPV/PLT ratio with regards to the severity of COVID-19 disease are limited, and there are no references regarding this ratio to the outcome of COVID-19 disease at specific time points of hospitalization. The aim of this study is to evaluate the relationship of COVID-19 mortality with the red cell distribution width–coefficient of variation (RDW-CV), platelets and MPV/PLT ratio parameters. Methods: Values of these parameters in 511 COVID-19 hospitalized patients were recorded (a) on admission, (b) as mean values of the 1st and 2nd week of hospitalization, (c) over the total duration of hospitalization, (d) as nadir and zenith values, and (e) at discharge. Results: As for mortality (survivors vs. deceased), statistical analysis with ROC curves showed that regarding the values of the parameters on admission, only the RDW-CV baseline was of prognostic value. Platelet parameters, absolute number and MPV/PLT ratio had predictive potential for the disease outcome only as 2nd week values. On the contrary, with regards to disease severity (mild/moderate versus severe/critical), only the MPV/PLT ratio on admission can be used for prognosis, and to a moderate degree. On multivariable logistic regression analysis, only the RDW-CV mean hospitalization value (RDW-CV mean) was an independent and prognostic variable for mortality. Regarding disease severity, the MPV/PLT ratio on admission and RDW-CV mean were independent and prognostic variables. Conclusions: RDW-CV, platelets and MPV/PLT ratio hematological parameters could be of predictive value for mortality and severity in COVID-19 disease, depending on the hospitalization timeline. Full article

Platelets play critical roles in haemostasis and thrombosis. The platelet activation process is driven by agonist-induced rises in cytosolic [Ca²⁺]_i, where the patterns of Ca²⁺ responses are still incompletely understood. In this study, we developed a number of techniques to model the [Ca²⁺]_i curves of platelets from a single blood donor. Fura-2-loaded platelets were quasi-simultaneously stimulated with various agonists, i.e., thrombin, collagen, or CRP, in the presence or absence of extracellular Ca²⁺ entry, secondary mediator effects, or Ca²⁺ reuptake into intracellular stores. To understand the calibrated time curves of [Ca²⁺]_i rises, we developed two non-linear models, a multilayer perceptron (MLP) network and an autoregressive network with exogenous inputs (NARX). The trained networks accurately predicted the [Ca²⁺]_i curves for combinations of agonists and inhibitors, with the NARX model achieving an R² of 0.64 for the trend prediction of unforeseen data. In addition, we used the same dataset for the construction of a partial least square (PLS) linear regression model, which estimated the explained variance of each input. The NARX model demonstrated that good fits could be obtained for the nanomolar [Ca²⁺]_i curves modelled, whereas the PLS model gave useful interpretable information on the importance of each variable. These modelling results can be used for the development of novel platelet [Ca²⁺]_i-inhibiting drugs, such as the drug 2-aminomethyl diphenylborinate, blocking Ca²⁺ entry in platelets, or for the evaluation of general platelet signalling defects in patients with a bleeding disorder. Full article

Gynecological malignancies (ovarian, endometrial, and cervical cancers), including disseminated intravascular coagulation (DIC), often provoke systemic coagulopathy. In recent years, tumor-derived, tissue factor–positive microparticles (TF⁺ MPs) have emerged as potent drivers of cancer-associated thrombosis and possibly DIC. These small (0.1–1 µm) membrane vesicles bud from cancer cell surfaces and carry procoagulant factors (phosphatidylserine and TF) on their surface. We review how TF⁺ MPs are generated by tumor cells and amplify the extrinsic coagulation cascade, potentially triggering DIC in patients with advanced gynecologic cancers. Clinical studies have linked el evated TF⁺ MP levels and activity to venous thromboembolism (VTE) in cancer, and small case series suggest dramatically high MP–TF activity in cancer-related DIC. We summarize evidence that TF⁺ MPs from ovarian tumors carry exceptionally high TF procoagulant activity (median ~80 pg/mL), and nearly all patients with cancer-associated VTE or DIC have MP–TF levels above normal. This review discusses diagnostic implications (e.g., measuring MP–TF activity as a biomarker) and treatment strategies (through the reduction in tumors, anticoagulation, and experimental TF inhibitors) in this setting. We also identify gaps in knowledge (standardized MP assays, prospective studies) and propose future directions (targeting MP formation or TF signaling). Two summary tables highlight recent studies of TF⁺ MPs in gynecologic cancer and their clinical outcomes. Illustrative figures depict the TF⁺ MP-triggered coagulation cascade and a conceptual framework for clinical management. Understanding TF⁺ MPs in gynecological cancer could improve the prediction and management of DIC and related thromboses. Full article

Background: Kidney transplantation is the treatment of choice for pediatric patients with end-stage kidney disease. However, transplantation in children weighing < 15 kg remains challenging due to limited donor availability and higher surgical and medical risks. We report our 35-year single-center experience in this population, focusing on perioperative and long-term outcomes. Methods: We retrospectively analyzed kidney transplants performed from 1987 to 2023 in children weighing < 15 kg. Data on demographics, donor type, complications, immunosuppression, and outcomes at 2, 5, and 10 years (including survival, graft function, rejection, infections, and urological issues) were collected. Outcomes were compared between deceased and living donors and between recipients weighing < 10 kg and ≥10 kg. Results: Ninety-six transplants were included (mean age 3.3 years; mean weight 11.1 kg), 80 from deceased and 16 from living donors. Most patients (69.8%) had been treated with peritoneal dialysis. Median follow-up was 120 months. Patient survival was 95.8%; graft survival was 78.1%. Eight grafts (8.3%) were lost to renal vein thrombosis, all in deceased-donor recipients (p = 0.60). Preserved renal function (eGFR > 60 mL/min/1.73 m²) declined from 80.4% at 2 years to 66.0% at 5 years and 18.0% at 10 years. Graft survival at 10 years was significantly lower in children < 10 kg vs. ≥10 kg (49.6% vs. 80.3%, p = 0.003). CAKUT was associated with higher urological complication rates (p = 0.017). No significant differences emerged between living and deceased donor groups. Conclusions: Transplantation in children < 15 kg is feasible with good outcomes, but those <10 kg present lower graft survival at 10 years. Multidisciplinary assessment and center experience are key to optimizing results. Full article

Background/Objectives: Hepatic artery thrombosis (HAT) is a serious vascular complication in patients undergoing orthotopic liver transplantation (OLT). It is associated with a high risk of graft loss, re-transplantation (re-OLT), and mortality. This study aimed to evaluate the incidence and management of HAT, analyzing potential risk factors. The secondary objectives included quantifying 90-day postoperative morbidity and mortality rates. Methods: In this retrospective, observational, single-center study, data from liver transplant donors and recipients who underwent OLT between 2004 and 2024 were analyzed. HAT was classified as early (e-HAT, ≤30 days) or late (l-HAT, >30 days). Univariate statistical analysis was performed to identify the risk factors associated with HAT occurrence. Multivariate analysis was not performed due to the small number of HAT events, which would increase the risk of model overfitting. Results: In the 20 year study period, a total of 532 OLTs were performed, including 37 re-OLTs. The rates of major morbidity, reoperation, and mortality within 90 days were 44.5%, 22.3%, and 7.1%, respectively. HAT occurred in 2.4% of cases (e-HAT: 1.6%; l-HAT: 0.7%). Among e-HAT cases, 66.6% were asymptomatic and identified through routine postoperative Doppler ultrasound. All e-HAT cases were surgically treated, with a re-OLT rate of 33.3%. Three l-HAT cases required re-OLT. Overall, the HAT-related mortality and re-OLT rates were 7.6% and 46.1%, respectively. At a follow-up of 86 months, the rate of graft loss was 9.2%, and the rate of post-OLT survival was 77%. Patients who developed HAT had a higher donor-to-recipient body weight ratio and longer warm ischemia times (WITs). Additionally, patients undergoing re-OLT had a higher risk of developing HAT. Conclusions: Although the incidence of HAT is low, its clinical consequences are severe. Early Doppler ultrasound surveillance is crucial for detecting e-HAT and preventing graft loss. A high donor-to-recipient body weight ratio, a prolonged warm ischemia time, and re-OLT seem to be associated with a high risk of HAT. Full article

Background: Although contemporary stent technology has significantly evolved, a substantial number of patients present with stent failure (SF), the clinical expression of which is either in-stent restenosis (ISR) or stent thrombosis (ST). Methods: In this observational, single-center study, we aimed to compare the clinical characteristics, clinical presentation, angiographic findings and subsequent management of patients who underwent percutaneous coronary intervention (PCI) for SF, either ISR or ST, with patients who had PCI for de novo lesions. Results: Over a period of two years (September 2022–October 2024), 1120 patients underwent PCI, of whom 9% had SF. Of the 101 SF cases, the majority (76 cases, 75%) had ISR, while the rest (25 cases, 25%) had ST. Regarding baseline characteristics, patients who underwent PCI for SF had a higher incidence of diabetes mellitus (53% vs. 29%; p < 0.001), dyslipidemia (88% vs. 50%; p < 0.001) as well as prior coronary artery bypass grafting surgery (7.9% vs. 3.7%; p = 0.043), while they were less likely to be current smokers (33% vs. 52%; p < 0.001). SF PCI patients presented more frequently with unstable angina (17% vs. 8.9%; p = 0.010). A new stent was implanted in less than half of SF cases (i.e., stent implantation, 44% vs. 91%; p < 0.001). On the other hand, in the clinical setting of SF, drug-coated balloons (44% vs. 5.3%; p < 0.001) and plain balloon angioplasty (8.9% vs. 0.7%; p < 0.001) was applied more frequently compared with de novo lesions. Furthermore, the usage of cutting/scoring balloons and lithotripsy was significantly higher in the SF group (8.9% vs. 0.4% and 12% vs. 3%, respectively; p < 0.001 for both). Intracoronary imaging guidance was more commonly used in the SF group (33% vs. 13%; p < 0.001). Stent malapposition (44%) and neoatherosclerosis (67%) were the most common mechanisms of ST and ISR, respectively, as identified by intravascular imaging modalities. Finally, the success rates were comparable (96% vs. 98%; p = 0.150) between the two groups. Conclusions: Approximately one of ten patients underwent PCI because of the failure of a previously implanted stent. Use of intracoronary imaging is significantly higher in the clinical context of SF. While DES implantation remains the standard of practice for de novo lesions, DCBs are a popular alternative, especially for ISR cases. Interventional cardiologists who are involved in the treatment of SF cases should be familiar with interpreting intravascular imaging to guide the use of the adjunctive device required to ensure that optimal procedural results in SF cases are obtained. Full article

Thrombosis is a common complication in cancer patients, with a substantial impact on morbidity and mortality. Diffuse large B-cell lymphoma (DLBCL) and other aggressive lymphomas carry a high venous thromboembolism (VTE) risk. Extracellular vesicles (EVs) have gained attention in recent research as a new potential biomarker for VTE development. To determine the profile and association of EVs with VTE in patients with DLBCL, we conducted a prospective cohort study on 62 patients diagnosed with DLBCL. A total of 11 patients (17.7%) developed VTE. The concentrations of platelet-derived EVs (PEVs), E-selectin+ EVs, P-selectin+ EVs, tissue factor (TF)-positive/CD20+ EVs, TF−/CD19+ EVs, TF−/CD45+ EVs, and TF−/CD20+ EVs were significantly higher in DLBCL patients compared to healthy controls. In contrast, the concentration of TF− PEVs was significantly lower in DLBCL patients compared to healthy controls. No statistically significant differences were observed in the concentrations of the EV profiles among the DLBCL patients with and without VTE. Using Cox regression analysis, we found that none of the observed EV populations demonstrated an association with overall survival (OS). In conclusion, patients with DLBCL have elevated concentrations of distinct EV populations—in particular, PEVs, E-selectin EVs, P-selectin EVs, TF+/CD20+ EVs, and TF− DLBCL/B-cell EVs (CD19, CD20, CD45)—compared to healthy controls. DLBCL patients exhibit a specific EV profile, which is not significantly related to the risk of VTE and OS outcomes. Our data provide an intriguing insight into EV profiles in patients with DLBCL. Additional research is needed to elucidate these findings further. Full article

In this study, pharmacotherapies of abdominal compartment syndrome (ACS) and intra-abdominal hypertension (IAH) in animal studies were reviewed from the perspective of ACS/IAH as failed cytoprotection issues, as non-specific injuries, and from the point of view of the cytoprotection concept as resolution. Therefore, this review challenges the unresolved theoretical and practical issues of severe multiorgan failure, acknowledged significance in clinics, and resolving outcomes (i.e., open abdomen). Generally, the reported agents not aligned with cytoprotection align with current pharmacotherapy limitations and have (non-)confirmed effectiveness, mostly in only one organ, mild/moderate IAH, prophylactic application, and provide only a tentative resolution. Contrarily, stable gastric pentadecapeptide BPC 157 therapy, as a novel and relevant cytoprotective mediator having pleiotropic beneficial effects, simultaneously resolves many targets, resolving established disturbances, specifically compression/ischemia (grade III and grade IV), and decompression/advanced reperfusion. BPC 157 therapy rapidly activates collateral bypassing pathways, and, in ACS and IAH, and later, in reperfusion, there is a “bypassing key” (i.e., azygos vein direct blood flow delivery). This serves to counteract multiorgan and vessel failure, including lesions and hemorrhages in the brain, heart, lung, liver, kidney and gastrointestinal tract, thrombosis, peripherally and centrally, intracranial (superior sagittal sinus), portal and caval hypertension and aortal hypotension, occlusion/occlusion-like syndrome, advanced Virchow triad circumstances, and free radical formation acting as a membrane stabilizer and free radical scavenger. Likewise, not only in ACS/IAH resolving, but also in other occlusion/occlusion-like syndromes, this “bypassing key” could be an effect of the essential endothelial cytoprotective capacity of BPC 157 and a particular modulatory effect on the NO-system, and a rescuing impact on vasomotor tone. Full article

Background: Chronic kidney disease (CKD) and its advanced stage, end-stage renal disease (ESRD), affect millions worldwide and are associated with a paradoxical hemostatic imbalance—marked by both increased thrombotic and bleeding risks—which complicates anticoagulant use and demands clearer, evidence-based clinical guidance. Design: This study is a critical review synthesizing the current literature on anticoagulant therapy in CKD and ESRD, with emphasis on altered pharmacokinetics, clinical complications, and therapeutic adjustments. Data Sources: PubMed, Scopus, and Google Scholar were searched for articles discussing anticoagulation in CKD/ESRD, focusing on pharmacokinetics, clinical outcomes, and dosing recommendations. Study Selection: Studies examining the safety, efficacy, and pharmacokinetics of anticoagulants—including heparin, low-molecular-weight heparin (LMWH), warfarin, and direct oral anticoagulants (DOACs)—in CKD and ESRD populations were included. Data Extraction and Synthesis: Key findings were summarized to highlight the dose modifications, therapeutic considerations, and clinical challenges in managing anticoagulation in CKD/patients with ESRD. Emphasis was placed on balancing thrombotic and bleeding risks and identifying gaps in existing guidelines. Results: Patients with CKD and ESRD exhibit a paradoxical hypercoagulable state marked by platelet dysfunction, altered coagulation factors, and vascular endothelial damage. This condition increases the risk of thrombotic events, such as deep vein thrombosis (DVT) and pulmonary embolism (PE), while simultaneously elevating bleeding risks. Hemodialysis and CKD-associated variables further complicate the management of coagulation. Among anticoagulants, unfractionated heparin (UFH) is preferred due to its short half-life and adjustability based on activated partial thromboplastin time (aPTT). Low-molecular-weight heparins (LMWHs) offer predictable pharmacokinetics but require dose adjustments in CKD stages 4 and 5 due to reduced clearance. Warfarin necessitates careful dosing based on the estimated glomerular filtration rate (eGFR) to maintain an international normalized ratio (INR) ≤ 4, minimizing bleeding risks. Direct oral anticoagulants (DOACs), particularly Apixaban, are recommended for patients with eGFR < 15 mL/min or those on dialysis, although data on other DOACs in CKD remain limited. The lack of comprehensive guidelines for anticoagulant use in CKD and ESRD highlights the need for individualized, patient-centered approaches that account for comorbidities, genetics, and clinical context. Conclusions: Managing anticoagulation in CKD/ESRD is challenging due to complex coagulation profiles and altered pharmacokinetics. Judicious dosing, close monitoring, and patient-centered care are critical. High-quality randomized controlled trials are needed to establish clear guidelines and optimize therapy for this vulnerable population. Full article

Background: Deep vein thrombosis (DVT) management remains challenging despite standard anticoagulation therapy. This study evaluated the comprehensive benefits of combining rivaroxaban with Aescuven (CAV) compared to rivaroxaban monotherapy (SAT) in DVT treatment. Methods: A retrospective analysis was conducted on DVT patients (2018–2023) using multi-method propensity score matching and ensemble weighting. Outcomes included improvement rate (IPR), daily improvement rate (DIR), cost-effectiveness ratio (CER), daily improvement cost (DIC), cost–LOS efficiency (CLE), and length of stay (LOS). Counterfactual analysis was implemented to estimate causal effects. Results: The CAV group demonstrated superior outcomes compared to SAT: IPR increased by 6.39 percentage points (95% CI: 5.61–7.39), DIC substantially reduced by 3323.38 CNY (95% CI: 2887.95–3758.81), and CLE improved by 136.97 CNY per day (95% CI: 122.31–151.64), with minimal LOS increase (0.15 days, 95% CI: 0.12–0.18). Network analysis revealed significant correlations between baseline coagulation parameters and treatment outcomes, particularly between APTT and economic benefits. Conclusions: The CAV regimen achieved significant clinical and economic advantages over standard monotherapy without substantially increasing resource utilization. These findings support integrating venoprotective agents into conventional anticoagulation strategies for optimized DVT management. Full article

Translational control is crucial for maintaining cellular homeostasis, yet the distinct features and regulatory requirements governing protein synthesis during erythropoiesis remain unclear. Here, we reveal that erythroid cells exhibit an extraordinarily high demand for protein synthesis, which is required for their differentiation but also implies the need for tight regulation to prevent excessive erythropoiesis. Notably, we identify significant phosphorylation of eukaryotic elongation factor 2 (eEF2) at threonine 56 during erythroid differentiation, which reduces protein synthesis and acts as a molecular brake to limit unchecked erythropoiesis. This is evidenced by elevated red blood cell counts in peripheral blood and increased incidence of blood hyperviscosity and thrombosis in eEF2_T56M mice, which are deficient in eEF2 phosphorylation. Mechanistic studies demonstrate that eEF2 phosphorylation selectively regulates the translation of a subset of proteins, including NFE2, which partially mediates the effects of eEF2 modification. Collectively, our findings highlight a previously unappreciated role for translational control in achieving efficient and balanced erythropoiesis, with eEF2 phosphorylation serving as a critical protective mechanism against hyperactive erythropoiesis and offering a potential therapeutic target for hematologic disorders such as polycythemia vera. Full article

In the vascular system, pathological conditions that cause hypoxia are associated with increased platelet activity and thrombosis. Using a platelet spreading assay, we show that severe hypoxia (i.e., 1%), venous (i.e., 5%), and, surprisingly, arterial (i.e., 12%) oxygen concentrations cause a significant reduction in platelet surface area coverage on fibrinogen in comparison to atmospheric oxygen condition (i.e., 21% oxygen), whilst adhesion and spreading on collagen and CRP were not affected. Importantly, the addition of thrombin or zinc restored full platelet spreading on fibrinogen, indicating that the inhibition of platelet spreading on fibrinogen was due to defective integrin activation. Analysis of integrin activation with FACs via PAC-1 staining supported a significant reduction in integrin activation in hypoxic conditions. Interestingly, a fibrinogen matrix prepared at 1%, 5%, or 12% oxygen failed to induce full platelet spreading, even when the experiments were performed at atmospheric oxygen concentration, indicating that the structure and activity of the fibrinogen coating is affected by oxygen. The effect of oxygen on different matrix proteins is critical to understand, as these data clearly demonstrate that collagen and CRP can support platelet activation at all O₂ concentrations, whilst fibrinogen mediated platelet activation and spreading is lost at physiological and pathological O₂ concentrations. These data have clear implications for thrombus formation data and highlight the role of oxygen in regulating platelet function. Full article

Background/Objectives: Inhaled corticosteroids (ICS) affect oxidative stress and systemic inflammation, which might modify the risk of thrombosis in asthmatic patients exposed to particulate matter with an aerodynamic diameter smaller than 2.5 microns (PM_2.5). Therefore, we aim to know the systemic biomarkers of oxidative stress, inflammation, and coagulation in ICS-treated, well-controlled adult asthmatic patients after exposure to PM_2.5. Methods: This study was conducted to compare urinary biomarkers of oxidative stress, i.e., 8-hydroxydeoxyguanosine (8-OHdG), and blood biomarkers of inflammation and hypercoagulation, i.e., complete blood count (CBC), high-sensitivity C-reactive protein (hsCRP), fibrinogen, D-dimer, tumor necrosis factor-alpha (TNF-α), and interleukins (IL-6 and IL-8), between well-controlled adult asthmatic patients and healthy controls in low and high-pollution periods. Results: Forty-one ICS-controlled asthmatic patients and twenty controls were included. Urinary 8-OHdG, white blood cells and differential counts, platelets count, hsCRP, IL-6, and IL-8 in the asthma group were not significantly higher than controls during the same period. The D-dimer level of the asthma patients was significantly higher than the controls (p < 0.05). The median level of TNF-α levels during the pollution period in asthma patients was significantly higher than the non-pollution period with levels of 14.3 (9.3, 27.4) and 11.3 (7.8, 21.1) pg/mL, p = 0.041, respectively. Conclusions: During exposure to PM_2.5, serum TNF-α was increased while the other markers of oxidative stress and inflammation were not high in ICS-treated asthma. ICS might mitigate PM_2.5-induced systemic oxidative stress, inflammation, and hypercoagulation in asthma. Full article

Chronic inflammation is a pivotal driver in the progression of atherosclerosis, significantly contributing to the burden of cardiovascular disease (CVD). Patients with chronic inflammatory diseases, such as inflammatory bowel diseases (IBDs) (e.g., ulcerative colitis and Crohn’s disease), rheumatological disorders, as well as individuals with auto-immune diseases (such as systemic lupus erythematosus), present a higher risk of major adverse cardiac events (MACEs). Despite their elevated CVD risk, these populations remain underrepresented in cardiovascular research, leading to a critical underestimation of their cardiovascular risk (CVR) in clinical practice. Furthermore, even recent CVR scores poorly predict the risk of events in these specific populations. This narrative review examines the physiopathological mechanisms linking chronic inflammation, immunomodulation, atherosclerosis, thrombosis and cardiovascular events. We review data from epidemiological studies and clinical trials to explore the potential cardiovascular benefits of anti-inflammatory and immunomodulatory therapies. Despite existing evidence, significant gaps in knowledge remain. Future research is mandatory, focusing on innovative strategies for risk stratification and optimization, including lipidomics, proteomics, advanced inflammatory markers, microbiota profiling, and cardiovascular imaging. Addressing these unmet needs will enhance understanding of cardiovascular risk in chronic inflammatory diseases, enabling tailored interventions and better outcomes. Full article

Diabetes mellitus is a metabolic disorder associated with oxidative stress, inflammation, and coagulation disturbances, which contribute to microvascular and macrovascular complications. We evaluated the therapeutic effects of lavender oil (Lavandula angustifolia) in a streptozotocin (STZ)-induced rat model of type 1 diabetes mellitus (T1DM) with experimentally induced thrombosis. Sixty male Wistar rats were divided into control, thrombosis, diabetes, thrombosis–diabetes, and lavender oil pretreatment groups (100 and 200 mg/kg body weight [bw]). Lavender oil exhibited dose-dependent benefits, with the 200 mg/kg bw dose leading to significant reductions in proinflammatory cytokines (e.g., tumor necrosis factor α (TNF-α); regulated upon activation, normal T cell expressed and secreted (RANTES); and monocyte chemoattractant protein-1 (MCP-1)) and oxidative stress, along with improved glycemic control, the partial restoration of C-peptide levels, and the attenuation of matrix metalloproteinase 2 and 9 (MMP-2 and MMP-9) activity (p < 0.0001). Histopathological and coagulation analyses confirmed its organ-protective and antithrombotic effects, including reduced tissue damage, vascular inflammation, and thrombus formation, and prolonged bleeding and clotting times. Our findings suggest that lavender oil exhibits dose-dependent antioxidant, anti-inflammatory, hypoglycemic, and organ-protective effects, indicating its potential as a complementary therapy for managing inflammation in T1DM with or without thrombosis. Full article