RESUMEN
Cyanoacrylate adhesive closure (CAC) systems are widely used to treat varicose veins. In terms of efficacy and safety, these nonthermal, non-tumescent methods are noninferior to endovenous thermal ablation techniques. However, no published studies have compared products that use CAC systems. VenaSeal® (Medtronic, Santa Rosa, CA, USA) and VenaBlock® (Invamed) are the most commonly used CAC-based products worldwide. This study aimed to focus on the efficacy of these two commonly used products, with little emphasis on safety. Published full-text articles on the VenaBlock® and VenaSeal® systems were searched. Data for each product were evaluated by comparing them with each other in terms of effectiveness. In total, 1882 extremities from 11 studies using VenaBlock® and 524 extremities from eight studies using VenaSeal® were included and compared. Both devices were effective, and their cumulative recanalization-free survival rates were similar (P=0.188) at the 6-, 12-, 24-, 36-, and 60-month follow-ups. Both products improved the venous clinical severity score (VCSS) and quality of life (QoL) scores. VenaBlock® and VenaSeal® are effective in terms of cumulative recanalization-free survival rates, and no significant difference was found between the two groups (P=0.188). Both significantly improve the VCSS and QoL scores. CAC is feasible for the treatment of varicose veins.
RESUMEN
Chronic subdural hematoma (c-SDH) is a frequent and serious neurological disease. It develops due to hemorrhage to the subdural space, mainly caused by head trauma. The middle meningeal artery (MMA) plays a critical role in the supply of blood to c-SDH. The decision on the type of treatment for c-SDH depends mainly on clinical and imaging evaluation. In cases in which patients are critically ill, the hematoma must be evacuated immediately. For this purpose, surgery is generally accepted as the mainstay of treatment. Among surgical techniques, twist-drill craniotomy, burr-hole craniotomy, and craniotomy are the three most used. The recurrence rate of c-SDH after surgery is an important problem with a rate of up to 30%. The technical success classification embolization of MMA (EMMA) has emerged as an effective and safe option for the treatment of c-SDH, especially those that recur. EMMA is commonly used as an adjunct to surgery or less frequently alone. The technical success of EMMA has been a promising minimal invasive strategy as an alternative or adjunctive therapy to surgical methods. Polyvinyl alcohol is the most widely used among various embolizing agents, including n-butyl cyanoacrylate, coil, and gelatin sponge. EMMA has been shown to prevent the formation or recurrence of c-SDH by eliminating blood flow to the subdural space. Complication rates are low. The large-scale comparative prospective will ensure efficacy and safety. This article aims to highlight the current information about EMMA in patients with c-SDH.
RESUMEN
Abdominal aortic aneurysm (AAA) is an enlargement of the aorta greater than 50% in diameter. Although up to 80% of cases result in mortality if the aneurysm ruptures, patients are often diagnosed too late, as most cases are asymptomatic. The current treatment for AAA is still surgery as there are currently no effective drug treatments. Knowledge of the pathophysiological mechanisms is essential for the development of new preventive and therapeutic approaches. However, the molecular mechanisms are complex and remain unclear. Apoptosis of vascular smooth muscle cells, the major cellular component of the aorta, and degeneration of the extracellular matrix, the skeleton of the aortic wall, are hallmarks of AAA pathology. Inflammation, mainly through macrophage cells, has been recognized as a central factor in the development of AAA. Macrophage cells also orchestrate other pathways and immune cells involved in this process. Macrophages do not exist as pure populations at aneurysm sites. M1 macrophages are pro-inflammatory and weaken the aortic wall during AAA development. M2 macrophages, in contrast, are involved in anti-inflammatory reactions and aorta tissue repair. The balancing effect on AAA progression makes M1/M2 macrophages therapeutic targets to control inflammation and destruction of the aortic wall. An early diagnosis is also important to allow for early interventions. This review article, based on the available data, aims to evaluate the role of an immunotherapeutic approach in controlling AAA development by briefly discussing the immunological mechanisms.
RESUMEN
Endovascular strategies play a vital role in the treatment of peripheral arterial disease (PAD). However, luminal loss or restenosis after endovascular intervention remains a significant challenge. The main underlying mechanisms are negative vascular remodeling and elastic recoil in balloon angioplasty. During stenting, the main reason for this complex is neointimal proliferation. Endothelial cell injury due to endovascular intervention initiates a series of molecular events, such as overexpression of growth factors, cytokine secretion, and adhesion molecules. These induce platelet activation and inflammatory processes, which trigger the proliferation and migration of vascular smooth muscle cells into the intima, resulting in neointimal hyperplasia. During this process, PAD progression is mainly caused by chronic inflammation, in which macrophages play a central role. Of the current strategies, drug release interventions aim to suppress restenosis using antiproliferative drugs, such as sirolimus and paclitaxel, during drug release. These drugs inhibit vascular reendothelialization and reduce late in-stent restenosis. For this reason, immunotherapy can be considered an important alternative. Interventions that polarize macrophages to the M2 subtype are particularly important, as they shape the immune response in an anti-inflammatory direction and contribute to tissue repair. However, there are several challenges to overcome, such as localizing antiproliferative or polarizing agents only to areas of vascular injury. This review discusses, based on the early study observations, immunotherapeutic approaches to prevent restenosis after endovascular intervention for the treatment of PAD.
RESUMEN
Leishmaniasis is a serious parasitic disease caused by Leishmania spp. transmitted through sandfly bites. This disease is a major public health concern worldwide. It can occur in 3 different clinical forms: cutaneous, mucocutaneous, and visceral Leishmaniasis (CL, MCL, and VL, respectively), caused by different Leishmania spp. Currently, licensed vaccines are unavailable for the treatment of human Leishmaniasis. The treatment and prevention of this disease rely mainly on chemotherapeutics, which are highly toxic and have an increasing resistance problem. The development of a safe, effective, and affordable vaccine for all forms of vector-borne disease is urgently needed to block transmission of the parasite between the host and vector. Immunological mechanisms in the pathogenesis of Leishmaniasis are complex. IL-12-driven Th1-type immune response plays a crucial role in host protection. The essential purpose of vaccination is to establish a protective immune response. To date, numerous vaccine studies have been conducted using live/attenuated/killed parasites, fractionated parasites, subunits, recombinant or DNA technology, delivery systems, and chimeric peptides. Most of these studies were limited to animals. In addition, standardization has not been achieved in these studies due to the differences in the virulence dynamics of the Leishmania spp. and the feasibility of the adjuvants. More studies are needed to develop a safe and effective vaccine, which is the most promising approach against Leishmania infection.