Background: Antiphospholipid syndrome (APS) is a rare systemic autoimmune disease characterized by persistent antiphospholipid antibodies (aPL) in combination with recurrent thrombosis in the veins and/or arteries, obstetric morbidity, and various non-thrombotic associated complications. APS can be primary, as an isolated condition, or secondary in the context of another autoimmune disease, especially systemic lupus erythematosus. This comprehensive clinical review aims to summarize the current understanding of APS pathogenesis, diagnostic approaches, and treatment strategies for this unique clinical entity. Methods: A comprehensive review of the existing literature on APS was conducted, focusing on pathophysiological mechanisms, current diagnostic criteria, and therapeutic approaches. Results: APS pathogenesis involves complex interactions between aPL, phospholipid-binding proteins, and the coagulation cascade. Apart from the cardinal features of thrombosis and APS-related obstetric morbidity, APS is associated with a wide spectrum of clinical manifestations. Diagnosis remains challenging due to overlapping symptoms with other conditions, and clinicians should maintain a high index of suspicion in order to set the diagnosis. The recently published 2023 ACR/EULAR criteria although not definitive for clinical decision-making, these criteria offer clinicians a valuable tool to aid in determining whether further investigation for APS is warranted. Continued refinement of these criteria through ongoing feedback and updates is anticipated. Treatment strategies center on anticoagulation, but individualized approaches are necessary. Conclusions: Early diagnosis and multidisciplinary management of APS are critical to reducing morbidity and improving outcomes. Moreover, familiarization with the 2023 ACR/EULAR criteria is encouraged, recognizing that ongoing feedback and updates will contribute to their ongoing refinement and improvement. While VKAs remain the mainstay of treatment for most APS patients further research is needed to optimize treatment strategies and deepen our understanding of APS’s underlying disease mechanisms.

As the incidence of type 2 diabetes mellitus (T2DM) continues to increase globally, researchers are keen to investigate various interventions to mitigate its impact. Among these, vitamin D supplementation has attracted significant attention due to its influence on insulin secretion from the pancreas and insulin receptors in body cells. A substantial body of evidence indicates that vitamin D supplementation can reduce low-grade inflammation, a critical factor in developing insulin resistance. In addition, vitamin D aids in sustaining low resting concentrations of reactive oxygen species and free radicals, normalizes Ca²⁺ signaling, diminishes the expression of cytokines that are pro-inflammatory, and enhances the production of cytokines that are anti-inflammatory. This review discusses the effects of vitamin D on the glycemic control of individuals with T2DM and evaluates the impact of vitamin D supplementation on glycemic markers in this population. The investigation employs a comprehensive analysis of the existing literature with a special focus on recent studies published in the past decade. Based on the findings in the literature, it can be concluded that vitamin D supplementation alongside anti-diabetic medications may enhance glycemic control and potentially reduce the risk of diabetic complications. The evidence supports the notion that vitamin D supplementation can be a valuable addition to pharmacological agents for the management of T2DM, potentially enhancing glycemic control and overall health outcomes in affected individuals.

Superior vena cava syndrome (SVCS) is a clinical entity characterized by signs and symptoms arising from the obstruction or occlusion of the thin-walled superior vena cava (SVC) and can result in significant morbidity and mortality. Despite the rise of benign cases of SVCS, as a thrombotic complication of intravascular devices, it is most commonly seen secondary to malignancy as a consequence of thrombosis, direct invasion of tumor cells inside the vessel, or external compression. SVCS can be the initial presentation of a previously undiagnosed tumor in up to 60% of cases. Lung cancer and non-Hodgkin lymphoma (NHL) are responsible for up to 85%-90% of malignancy-related SVCS, while metastatic cancers account for approximately 10%. Herein, we review the pathophysiology, etiology, clinical presentation, diagnosis, and management of malignancy-related SVCS.

Hematopoietic stem cell transplantation-associated thrombotic microangiopathy (HSCT-TMA) and graft-versus-host disease (GvHD) represent life-threatening syndromes after allogeneic hematopoietic stem cell transplantation (allo-HSCT). In both conditions, endothelial dysfunction is a common denominator, and development of relevant biomarkers is of high importance for both diagnosis and prognosis. Despite the fact that soluble urokinase plasminogen activator receptor (suPAR) and growth differentiation factor-15 (GDF-15) have been determined as endothelial injury indices in various clinical settings, their role in HSCT-related complications remains unexplored. In this context, we used immunoenzymatic methods to measure suPAR and GDF-15 levels in HSCT-TMA, acute and/or chronic GVHD, control HSCT recipients, and apparently healthy individuals of similar age and gender. We found considerably greater SuPAR and GDF-15 levels in HSCT-TMA and GVHD patients compared to allo-HSCT and healthy patients. Both GDF-15 and suPAR concentrations were linked to EASIX at day 100 and last follow-up. SuPAR was associated with creatinine and platelets at day 100 and last follow-up, while GDF-15 was associated only with platelets, suggesting that laboratory values do not drive EASIX. SuPAR, but not GDF-15, was related to soluble C5b-9 levels, a sign of increased HSCT-TMA risk. Our study shows for the first time that suPAR and GDF-15 indicate endothelial damage in allo-HSCT recipients. Rigorous validation of these biomarkers in many cohorts may provide utility for their usefulness in identifying and stratifying allo-HSCT recipients with endothelial cell impairment.

Background: Endothelial dysfunction is a key player in stroke pathophysiology. The Endothelial Activation and Stress Index (EASIX) is a biomarker of endothelial injury validated in hematology, sepsis, and cardiovascular cohorts; however, its prognostic role in stroke remains unclear. This retrospective cohort study aims to provide preliminary evidence on the potential utility of EASIX levels as a biomarker for assessing stroke severity and predicting outcomes. Methods: We retrospectively studied 100 patients aged ≥ 18 years admitted with acute ischemic stroke (AIS) or transient ischemic attack (TIA) between January 2020 and July 2024. EASIX was calculated on admission as LDH × creatinine/platelets. Outcomes included in-hospital and 12-month mortality, stroke severity assessed by the NIHSS score, and disability assessed as a modified Rankin score (mRS). Results: Median age was 82 years; 56% were female. The in-hospital and 12-month mortality rates were 47.9% in patients with AIS and 17.2% in patients with TIA, respectively. Overall, EASIX was not associated with NIHSS, mRS, or mortality in the total cohort. Ιn the subgroup of patients with small vessel disease (n = 10), higher EASIX was associated with worse mRS at 12 months (β = 2.383, p = 0.02) and increased mortality (β = 0.653, p = 0.02). EASIX correlated positively with WBC (p < 0.001) and CRP (p = 0.01). Female sex was associated with lower EASIX values. Conclusions: EASIX was not associated with outcomes in the overall AIS/TIA cohort, but it demonstrated potential prognostic relevance in small vessel disease (SVD), which has not been reported previously in the literature. Further prospective research is warranted to validate the potential association between systemic endothelial stress and small vessel disease before the implementation of EASIX as a prognostic tool in patients with stroke due to SVD.