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.

Heparin-induced thrombocytopenia (HIT), even rare, is a life-threatening, immune-mediated complication of heparin exposure. It is considered the most severe non-bleeding adverse reaction of heparin treatment and one of the most important adverse drug reactions. The pathophysiological basis of HIT results from the formation of an immunocomplex consisting of an auto-antibody against platelet factor 4 (PF4) - heparin complex, which binds to the surface of platelets and monocytes, provoking their activation by cross-linking FcgIIA receptors. Platelets and monocyte activation, leads to the generation of catastrophic arterial and venous thrombosis, with a mortality rate of 20%, without early recognition. The definitive diagnosis of HIT i.e., clinical and laboratory evidence, can not be done at the onset of symptoms because laboratory results may not be available for several days. Thus, the initial approach is to predict the likelihood of HIT, because in highly suspected patients immediate heparin cessation and initiation of alternative anticoagulation treatment are crucial for the prevention of the devastating thrombotic sequelae. Herein, we describe the pathophysiology, the clinical manifestations, the diagnostic approach, and the management of patients with HIT.

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.

Venous thromboembolism (VTE) is a typical complication in patients with lung cancer. Khorana score is an established tool for thromboembolic risk stratification of ambulatory patients with cancer undergoing outpatient chemotherapy. The aim of this study was to evaluate the predictive value of the Khorana score for VTE and death in patients with lung adenocarcinoma during first-line or adjuvant chemotherapy. Medical records of 130 patients with lung adenocarcinoma receiving first-line or adjuvant chemotherapy were retrospectively studied during the time period June 2013 to May 2015. Venous thromboembolism occurred in 13 (10.0%) patients. Thromboembolic events were significantly correlated with reduced survival during treatment period (hazard ratio [HR]: 3.24; 95% confidence interval [CI]: 1.11-9.49; P = .032). The VTE rates did not present statistically significant difference between different Khorana score groups (P = .96). In univariate analysis, the risk of death during treatment period (median: 16 weeks) was 3.75 times higher in high-risk versus intermediate-risk patients (HR: 3.75, 95% CI: 1.36-10.36; P = .001) and had 2.25 times higher per point increase in the Khorana score (HR: 2.25, 95% CI: 1.36-3.73; P = .002); the above results were also reproduced in multivariate analysis. Khorana score represents a valuable tool for identifying patients with cancer in low thromboembolic risk but does not preserve its predictive value for higher risk individuals. Khorana score is an independent risk factor for death in patients with lung adenocarcinoma receiving first-line or adjuvant chemotherapy.

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.

Purpose: Considering the high prevalence of lung cancer, our purpose was to summarize the existing literature to identify the several factors that contribute to the increased risk of venous thromboembolism (VTE) in patients with lung cancer and to analyze the current recommendations for thromboprophylaxis and treatment of VTE in those patients. Methods: We searched the Medline and EMBASE databases from February 1985 to February 2014 to identify retrospective and prospective randomized controlled studies that investigate one or more risk factors for VTEs in patients with lung cancer. Results: A VTE is a major complication for patients diagnosed with lung cancer. The risk factors for VTE events in patients with lung cancer consist of cancer-related (histological type and stage of cancer), treatment-related (surgery, chemotherapy, angiogenic agents, and supportive care agents), and patient-related factors (comorbidities, immobility, performance status, and prior thrombosis). Low-molecular-weight heparins are recommended for long-term treatment of cancer-associated thrombosis. Duration of anticoagulant therapy beyond 6 months should be based on individual clinical evaluation. Thromboprophylaxis for patients with lung cancer during hospitalization and immediate postoperative period is well established. Conclusions: Efforts to assess thrombotic risk in patients with lung cancer may improve therapeutic and preventive strategies in the future, with final goal to minimize the burden and consequences of thrombotic events in patients with lung cancer.