Pressure ulcers related to prone positioning: a pandemic amidst a pandemic.

OBJECTIVE: To explore the epidemiology and risk factors associated with the development of pressure ulcers (PUs) in patients receiving prone positioning (PP) ventilatory therapy; to compare the inflammatory status of patients who develop PUs with those who do not; and to describe the experience and useful findings that have allowed us to improve the management of these patients to reduce the incidence of PUs. METHOD: An observational, descriptive and longitudinal study was conducted, where sociodemographic and laboratory data were collected from patients who were hospitalised and required PP ventilatory therapy in critical care areas (CCA) during the months of May-October 2020. RESULTS: From the total number of patients who required PP during their CCA stay (n=240), 202 (84.2%) developed a PU. The four most frequent areas where a PU appeared were: the head and neck (n=115); the pinna (n=21); the torso (n=21); and the lower limbs (n=21). Patients who developed PU were more frequently males with higher initial levels of creatinine phosphokinase and ferritin. The incidence for each month of follow-up decreased from 8.3% to 5.8%. CONCLUSION: Regardless of the intervention, a multidisciplinary approach is required to optimise the prevention and treatment of these wounds. While PUs are often the result of other medical conditions or poor health status in general, the vast majority of PUs are avoidable.

The Paradigm of the Inflammatory Radicular Cyst: Biological Aspects to be Considered.

Inflammatory radicular cysts (IRCs) are chronic lesions that follow the development of periapical granulomas (PGs). IRCs result from multiple inflammatory reactions led initially by several pro-inflammatory interleukins and growth factors that provoke the proliferation of epithelial cells derived from epithelial cell rests of Malassez present in the granulomatous tissue, followed by cyst formation and growth processes. Multiple theories have been proposed to help explain the molecular process involved in the development of the IRC from a PG. However, although multiple studies have demonstrated the presence of epithelial cells in most PGs, it is still not fully understood why not all PGs turn into IRCs, even though both are stages of the same inflammatory phenomenon and receive the same antigenic stimulus. Histopathological examination is currently the diagnostic gold standard for differentiating IRCs from PGs. Although multiple studies have evaluated the accuracy of non-invasive or minimally invasive methods in assessing the histopathological nature of the AP before the intervention, these studies' results are still controversial. This narrative review addresses the biological insights into the complex molecular mechanisms of IRC formation and its histopathological features. In addition, the relevant inflammatory molecular mediators for IRC development and the accuracy of non-invasive or minimally invasive diagnostic approaches are summarised. (EEJ-2022-03-041).

Cellular and molecular regulation of the programmed death-1/programmed death ligand system and its role in multiple sclerosis and other autoimmune diseases.

Programmed Cell Death 1 (PD-1) receptor and its ligands (PD-Ls) are essential to maintain peripheral immune tolerance and to avoid tissue damage. Consequently, altered gene or protein expression of this system of co-inhibitory molecules has been involved in the development of cancer and autoimmunity. Substantial progress has been achieved in the study of the PD-1/PD-Ls system in terms of regulatory mechanisms and therapy. However, the role of the PD-1/PD-Ls pathway in neuroinflammation has been less explored despite being a potential target of treatment for neurodegenerative diseases. Multiple Sclerosis (MS) is the most prevalent, chronic, inflammatory, and autoimmune disease of the central nervous system that leads to demyelination and axonal damage in young adults. Recent studies have highlighted the key role of the PD-1/PD-Ls pathway in inducing a neuroprotective response and restraining T cell activation and neurodegeneration in MS. In this review, we outline the molecular and cellular mechanisms regulating gene expression, protein synthesis and traffic of PD-1/PD-Ls as well as relevant processes that control PD-1/PD-Ls engagement in the immunological synapse between antigen-presenting cells and T cells. Also, we highlight the most recent findings regarding the role of the PD-1/PD-Ls pathway in MS and its murine model, experimental autoimmune encephalomyelitis (EAE), including the contribution of PD-1 expressing follicular helper T (TFH) cells in the pathogenesis of these diseases. In addition, we compare and contrast results found in MS and EAE with evidence reported in other autoimmune diseases and their experimental models, and review PD-1/PD-Ls-targeting therapeutic approaches.

[Adverse cutaneous reactions to drugs]. / Reacciones cutáneas adversas a medicamentos.

Adverse cutaneous reactions to drugs are any undesirable change in the structure or function of the skin. These are among the adverse side effects to common drugs. The most commonly implicated drugs are antibiotics and anticonvulsants. Cutaneous clinical manifestations are diverse ranging from mild or moderate reactions, such as urticaria and maculopapular rash, to severe cutaneous adverse reactions (SCAR), which are known due to their high morbidity and mortality (among these: Stevens-Johnson syndrome, toxic epidermal necrolysis (TEN), and drug reaction with eosinophilia and systemic symptoms (DRESS). The clinical pattern, etiology, prognosis and treatment differ among these skin reactions, which is why it is necessary a clear diagnosis based on a comprehensive clinical examination, skin biopsy, and specific laboratory tests. The therapeutic options depend on the clinical diagnosis. For all reactions, a symptomatic and adequate supportive therapy is necessary; in some cases, a systemic immunomodulatory therapy can be useful.

Las reacciones cutáneas adversas a medicamentos son cualquier cambio indeseable en la estructura o función de la piel. Estas figuran entre los efectos adversos secundarios a medicamentos más comunes. Los grupos de fármacos más frecuentemente implicados son los antibióticos y los anticonvulsivantes. Las manifestaciones clínicas cutáneas son diversas y abarcan desde las reacciones leves o moderadas, como es el caso de la urticaria y el exantema maculopapular, hasta las reacciones cutáneas adversas severas, que son conocidas por su alta morbilidad y mortalidad, por ejemplo, el síndrome de Stevens Johnson, la necrosis epidérmica tóxica (NET) y el síndrome de hipersensibilidad, denominado reacción a fármacos con eosinofilia y síntomas sistémicos (DRESS). El patrón clínico, la etiología, el pronóstico y el tratamiento difieren entre estas reacciones cutáneas, por lo que es necesario un diagnóstico claro basado en un examen clínico exhaustivo, biopsia de piel y estudios de laboratorio. Las opciones terapéuticas dependen del diagnóstico clínico. Para todas las reacciones es necesario un tratamiento adecuado de soporte; en algunos casos puede utilizarse terapia inmunomoduladora.