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Coronary aneurysms are typically defined as sections of a coronary artery where the diameter is more than 1.5 times that of an adjacent normal segment. In rare circumstances, these aneurysms can become exceedingly large, leading to the classification of giant coronary artery aneurysms. Despite their occurrence, there is no clear consensus on the precise definition of giant coronary artery aneurysms, and their etiology remains somewhat ambiguous. Numerous potential causes have been suggested, with atherosclerosis being the most prevalent in adults, accounting for up to 50% of cases. In pediatric populations, Kawasaki disease and Takayasu arteritis are the primary causes. Although often discovered incidentally, coronary artery aneurysms can lead to severe complications. These complications include local thrombosis, distal embolization, rupture, and vasospasm, which can result in ischemia, heart failure, and arrhythmias. The optimal approach to medical, interventional, or surgical management of these aneurysms is still under debate and requires further clarification. This literature review aims to consolidate current knowledge regarding coronary artery aneurysms' pathophysiology, emphasizing their definition, causes, complications, and treatment strategies. Recent research has begun to explore the molecular mechanisms involved in the formation and progression of coronary artery aneurysms. Various molecules, such as matrix metalloproteinases (MMPs), inflammatory cytokines, and growth factors, play crucial roles in the degradation of the extracellular matrix and the remodeling of vascular walls. Elevated levels of MMPs, particularly MMP-9, have been associated with the weakening of the arterial wall, contributing to aneurysm development. Inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukins (IL-1β and IL-6) have been implicated in promoting inflammatory responses that further degrade vascular integrity. Additionally, growth factors such as vascular endothelial growth factor (VEGF) may influence angiogenesis and vascular remodeling processes. Understanding these molecular pathways is essential for developing targeted therapies aimed at preventing the progression of coronary artery aneurysms and improving patient outcomes. [ABSTRACT FROM AUTHOR]

Hemophilia, which is a rare disease, results from congenital deficiencies of coagulation factors VIII and IX, respectively, leading to spontaneous bleeding into joints, resulting in hemophilic arthropathy (HA). HA involves complex processes, including synovial proliferation, angiogenesis, and tissue remodeling. Despite ongoing research, factors contributing to HA progression, especially in adults with severe HA experiencing joint pain, remain unclear. Blood markers, particularly collagen-related ones, have been explored to assess joint health in hemophilia. For example, markers like CTX-I and CTX-II reflect bone and cartilage turnover, respectively. Studies indicate elevated levels of certain markers post-bleeding episodes, suggesting joint health changes. However, longitudinal studies on collagen turnover and basement membrane or endothelial cell markers in relation to joint outcomes, particularly during painful episodes, are scarce. Given the role of the CX3CL1/CX3XR1 axis in arthritis, other studies investigate its involvement in HA. The importance of different inflammatory and bone damage biomarkers should be assessed, alongside articular cartilage and synovial membrane morphology, aiming to enhance understanding of hemophilic arthropathy progression. [ABSTRACT FROM AUTHOR]

Navigating through antithrombotic therapy in patients with both hemophilia and cardiovascular pathology presents a complex scenario with inherent challenges and opportunities. The presence of hemophilia, characterized by impaired blood clotting, adds a layer of complexity to the management of cardiovascular conditions requiring antiplatelet therapy and anticoagulation. Striking a delicate balance between the necessity for antithrombotic treatment to prevent cardiovascular events and the heightened risk of severe bleeding in individuals with hemophilia demands a nuanced and carefully considered approach. The challenges revolve around identifying an optimal therapeutic strategy that effectively mitigates cardiovascular risks without exacerbating bleeding tendencies. In hemophilic patients with cardiovascular disease, the decision to use antiplatelet therapy requires careful consideration of the individual's bleeding risk profile, considering factors such as the severity of hemophilia, history of bleeding episodes, and concurrent medications. The goal is to provide effective antithrombotic treatment while minimizing the potential for excessive bleeding complications. Conventional anticoagulants like warfarin pose difficulties due to their potential to increase the risk of bleeding. On the other hand, emerging options like novel direct oral anticoagulants (DOACs) present an opportunity, offering predictable pharmacokinetics and user-friendly administration. However, a comprehensive exploration of their safety and efficacy in hemophilic patients is imperative. Achieving the right equilibrium between preventing cardiovascular events and minimizing bleeding risk is pivotal in selecting the most effective therapeutic option for individuals with hemophilia and cardiovascular pathology. A multidisciplinary approach, integrating the expertise of hematologists and cardiologists, becomes essential to customize treatments and address the intricacies of this medical challenge. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases, among which includes coronary artery disease, represent one of the most important causes of mortality and morbidity worldwide. Research aimed at determining the risk factors involved recognizes a group of "traditional" risk factors, but also more recent studies identified over 100 "novel" ones which may have a role in the disease. Among the latter is the thrombophilia profile of a patient, a pathology well-established for its involvement in venous thromboembolism, but with less studied implications in arterial thrombosis. This paper reviews the literature, explaining the pathophysiology of the thrombophilia causes associated most with coronary thrombosis events. Results of several studies on the subject, including a meta-analysis with over 60,000 subjects, determined the significant involvement of factor V Leiden, prothrombin G20210A mutation, plasminogen activator inhibitor–1 and antiphospholipid syndrome in the development of coronary artery disease. The mechanisms involved are currently at different stages of research, with some already established and used as therapeutic targets. [ABSTRACT FROM AUTHOR]

Hemophilia patients have a deficiency in or dysfunction of clotting factors, which can lead to a bleeding tendency. However, paradoxically, some hemophilia patients may also be at an increased risk of developing thrombotic events such as deep vein thrombosis or pulmonary embolism. The pathophysiology of thrombosis in hemophilia patients is not fully understood, but it is thought to involve a complex interplay of various factors, including the severity of the hemophilia, the presence of other risk factors such as obesity, smoking, or the use of hormonal therapies, and the presence of certain genetic mutations that increase the risk of thrombosis. In addition, it has been suggested that the use of clotting factor replacement therapy, which is a standard treatment for hemophilia, may also contribute to the development of thrombosis in some cases. [ABSTRACT FROM AUTHOR]

Background: Enchondroma is the most common benign bone tumor of the hand. Surgical excision of the tumor using curettage is the treatment of choice. The management of the resulting defects is still a controversial topic in the literature. Methods: This retrospective study includes 15 patients diagnosed with solitary enchondroma in the hand bones: eight cases with type A, three cases with type B and four cases with type D according to Takigawa classification. The aim of this study was to compare the course and outcome in the three patient groups treated by curettage associated with natural consolidation of the bone defect, autologous bone graft or injectable synthetic bone substitute in association with plate and screw osteosynthesis. Results: Outcomes were assessed using the DASH score (mean score 2.5) and TAM score (excellent in all patients) with no significant functional differences between the three groups. Defects managed with k-IBS® injectable bone substitute were associated with shorter operating time, simpler surgical technique and less postoperative pain assessed by VAS score. Conclusion: The use of k-IBS® bone substitute is efficient and less technically demanding than autologous bone grafting. The Takigawa classification could be a good indicator for treatment choice. [ABSTRACT FROM AUTHOR]

Depression is the most common psychiatric disorder in the elderly, as well as one of the most common comorbidities in patients with hip fracture. Although many authors have confirmed that clinically recognized depressive symptomatology after hip fracture has a negative impact on functional outcomes and mortality, the role of depressive symptomatology evaluated at the time of admission remains insufficiently investigated. Depression can be assessed using the Geriatric Depression Scale. Predictor measurements of rehabilitation results that can interact with depression can be obtained. Linear multiple regression modeling can be used to evaluate the relationship between depression and functional outcome. The identified factors associated with the postoperative 1 and 2 year follow-up of a hip fracture should be incorporated into clinical strategies and postoperative nursing to provide muscle rehabilitation and good functional outcomes. In addition, the health care plan must ensure, before discharge, that the community in which older adults live provides nutritional education, cognitive screening and psychological support. Depression is a common disorder among orthopedic patients. A previous psychiatric diagnosis predisposes patients to depression following a trauma. The socio-economic status is also a predictive factor for increasing depression scores at 9 months after discharge. Patients with a greater sense of support from friends and family have an inverse correlation with depression. Reestablishing the quality of life the patient had before the fracture also seems to have a protective effect against depression. The severity of the trauma does not seem to affect the scores for the evaluation of depression. Psychiatric counseling can avoid associated psychiatric comorbidities in trauma patients. High levels of depressive symptomatology in elderly patients with hip fracture influence functional outcomes both in the short and the long term. We firmly support the introduction of the routine evaluation of this comorbidity. Failure to identify this associated pathology in patients with hip fracture represents a missed opportunity for eventual improvement in both early and late functional outcomes. [ABSTRACT FROM AUTHOR]

Dementia and hip fractures are two crucial problems in the elderly and the associations of these pathologies increase substantial morbidity and mortality. 178 patients with dementia (average age 81.5 years) were operated with an uncemented bipolar prosthesis for a displaced femoral neck fracture. They started rehabilitation sessions in the immediate postoperative period and were divided into two groups: group 1 - partial weight-bearing for 72 cases - and group 2 - total weightbearing for 106 cases. 17 patients were unable to walk and 6 died during hospitalization. 172 patients were discharged to a rehabilitation department (46.6%) or to their home with (31.9%) or without (21.5%) rehabilitation facilities. During follow-up, 103 out of 172 patients accepted a phone interview. After three months 55 patients had regained the pre-fracture level of independence (6 patients from group 1 and 49 patients from group 2; 81% were included in a rehabilitation program). The mortality at one year postoperative period was 26.21%; the majorities of these patients were included in group 1, were more than 80 years old and had more than 4 comorbidities (except dementia). The authors concluded that, for patients undergoing uncemented bipolar HA, immediate total weight-bearing and discharging to a rehabilitation facility showed a better recovery and return to the pre-fracture level, as well as a better one-year survival rate. [ABSTRACT FROM AUTHOR]

In medical practice, a particularly important therapeutic problem is the patient with traumatic injuries developing ethanol withdrawal during hospitalization. The management of such patients requires both a comprehensive approach in terms of therapy and a very delicate one regarding issues of medical ethics and social implications and costs. More medical schools, among which the ones in France, the US, the UK, etc., opt for the administration of alcoholic solutions, perfusable ones included, for preventing withdrawal symptoms. We consider that currently the relevant Romanian protocols are inappropriate as they ignore the fact that an addiction can be cured only if the patient is willing to and, even if this is the case, alcohol dependence is unlikely to be cured. Therefore, we believe that the preventive administration of certain alcoholic solutions in hospital would be beneficial both to the patient's evolution and to the prevention of the social implications of treating the alcohol withdrawal syndrome (AWS) in a trauma center or intensive care unit. [ABSTRACT FROM AUTHOR]