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Parámetros hematológicos y biomarcadores predictores de gravedad en Síndrome Inflamatorio Pediátrico Multisistémico asociado a SARS-CoV-2
(2021)
Patricia Verdugo
;
Patricia Álvarez
;
Patricia Aroca
;
Vicente Enrique Montes-nogales
;
POLI HARLOWE, MARIA CECILIA BERTA
<jats:p>El síndrome inflamatorio multisistémico pediátrico asociado a SARS-CoV-2 (MIS-C) se caracteriza por un estado hiperinflamatorio producto de una tormenta de citoquinas, evidenciado en alteraciones del laboratorio hematológico y proteínas de fase aguda.Objetivo: Describir las características clínicas y de laboratorio de pacientes hospitalizados por MIS-C e identificar marcadores predictores de gravedad.Pacientes y Método: Estudio retrospectivo de 32 pacientes. El grupo se dividió en crítico y no crítico según presentación clínica y tipo de terapia utilizada. En ellos se estudiaron aspectos clínicos y de laboratorio que incluyeron hemograma completo, pruebas de coagulación y biomarcadores. Resultados: 18/32 hombres, mediana de edad 6,8 años. Las manifestaciones más frecuentes fueron cardiovasculares (84,3%), digestivas (84%) y mucocutáneas (59%). El grupo de los críticos incluyó 15 pacientes, 12 hombres con mediana de edad de 8,9 años y los no críticos 17 pacientes; 6 hombres, con mediana de edad de 5,4 años. Los parámetros de laboratorio al ingreso en el grupo global mostraron aumento de la proteína C reactiva, dímero-D, leucocitos, neutrófilos, ferritina y fibrinógeno. La albúmina y la natremia en cambio se encontraban disminuidas. El grupo crítico se caracterizó por tener al ingreso: trombocitopenia, hipoalbuminemia, prolongación del tiempo de protrombina y elevación de la ferritina. Al deterioro hubo acentuación de la trombocitopenia, ascenso mayor de la proteína C reactiva junto a elevación de los neutrófilos.Conclusión: El hemograma, la proteína C reactiva y la albuminemia al ingreso resultaron ser de alto valor en la identificación de pacientes con riesgo de agravamiento clínico.</jats:p>
20Scopus© Citations 10
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miRNA Landscape in Pathogenesis and Treatment of Vogt–Koyanagi–Harada Disease
(2021)
Fabian Vega-Tapia
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Mario Bustamante
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Rodrigo A. Valenzuela
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Cristhian A. Urzua
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Loreto Cuitino
<jats:p>miRNAs, one of the members of the noncoding RNA family, are regulators of gene expression in inflammatory and autoimmune diseases. Changes in miRNA pool expression have been associated with differentiation of CD4<jats:sup>+</jats:sup> T cells toward an inflammatory phenotype and with loss of self-tolerance in autoimmune diseases. Vogt–Koyanagi–Harada (VKH) disease is a chronic multisystemic pathology, affecting the uvea, inner ear, central nervous system, and skin. Several lines of evidence support an autoimmune etiology for VKH, with loss of tolerance against retinal pigmented epithelium-related self-antigens. This deleterious reaction is characterized by exacerbated inflammation, due to an aberrant T<jats:sub><jats:italic>H</jats:italic></jats:sub>1 and T<jats:sub><jats:italic>H</jats:italic></jats:sub>17 polarization and secretion of their proinflammatory hallmark cytokines interleukin 6 (IL-6), IL-17, interferon γ, and tumor necrosis factor α, and an impaired CD4<jats:sup>+</jats:sup> CD25<jats:sup><jats:italic>high</jats:italic></jats:sup> FoxP3<jats:sup>+</jats:sup> regulatory T cell function. To restrain inflammation, VKH is pharmacologically treated with corticosteroids and immunosuppressive drugs as first and second line of therapy, respectively. Changes in the expression of miRNAs related to immunoregulatory pathways have been associated with VKH development, whereas some genetic variants of miRNAs have been found to be risk modifiers of VKH. Furthermore, the drugs commonly used in VKH treatment have great influence on miRNA expression, including those miRNAs associated to VKH disease. This relationship between response to therapy and miRNA regulation suggests that these small noncoding molecules might be therapeutic targets for the development of more effective and specific pharmacological therapy for VKH. In this review, we discuss the latest evidence regarding regulation and alteration of miRNA associated with VKH disease and its treatment.</jats:p>
4Scopus© Citations 7
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Proteomic Analysis of Niemann-Pick Type C Hepatocytes Reveals Potential Therapeutic Targets for Liver Damage
(2021)
Elisa Balboa
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Tamara Marín
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Juan Esteban Oyarzún
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Pablo S. Contreras
;
Robert Hardt
<jats:p>Niemann-Pick type C disease (NPCD) is a lysosomal storage disorder caused by mutations in the NPC1 gene. The most affected tissues are the central nervous system and liver, and while significant efforts have been made to understand its neurological component, the pathophysiology of the liver damage remains unclear. In this study, hepatocytes derived from wild type and Npc1−/− mice were analyzed by mass spectrometry (MS)-based proteomics in conjunction with bioinformatic analysis. We identified 3832 proteins: 416 proteins had a p-value smaller than 0.05, of which 37% (n = 155) were considered differentially expressed proteins (DEPs), 149 of them were considered upregulated, and 6 were considered downregulated. We focused the analysis on pathways related to NPC pathogenic mechanisms, finding that the most significant changes in expression levels occur in proteins that function in the pathways of liver damage, lipid metabolism, and inflammation. Moreover, in the group of DEPs, 30% (n = 47) were identified as lysosomal proteins and 7% (n = 10) were identified as mitochondrial proteins. Importantly, we found that lysosomal DEPs, including CTSB/D/Z, LIPA, DPP7 and GLMP, and mitocondrial DEPs, AKR1B10, and VAT1 had been connected with liver fibrosis, damage, and steatosis in previous studies, validiting our dataset. Our study found potential therapeutic targets for the treatment of liver damage in NPCD.</jats:p>
Scopus© Citations 9 1
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Association between spontaneous internal carotid artery dissection and perivascular adipose tissue attenuation on computed tomography angiography
(2023)
Kevin Cheng
;
Andrew Lin
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STECHER GUZMAN, XIMENA PATRICIA
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Tomas Bernstein
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Paulo Zuñiga
<jats:sec><jats:title>Background:</jats:title><jats:p> Spontaneous cervical artery dissection (sCAD) is a leading cause of ischemic stroke in young patients. Studies using high-resolution magnetic resonance imaging and positron emission tomography have suggested vessel wall inflammation to be a pathogenic factor in sCAD. Computed tomography (CT) attenuation of perivascular adipose tissue (PVAT) is an established non-invasive imaging biomarker of inflammation in coronary arteries, with higher attenuation values reflecting a greater degree of vascular inflammation. </jats:p></jats:sec><jats:sec><jats:title>Objectives:</jats:title><jats:p> We evaluate the CT attenuation of PVAT surrounding the internal carotid artery (PVAT<jats:sub>carotid</jats:sub>) with and without spontaneous dissection. </jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p> Single-center prospective observational study of 56 consecutive patients with CT-verified spontaneous dissection of the internal carotid artery (ICA). Of these patients, six underwent follow-up computed tomography angiography (CTA). Twenty-two patients who underwent CTA for acute neurological symptoms but did not have dissection formed the control group. Using semi-automated research software, PVAT<jats:sub>carotid</jats:sub> was measured as the mean Hounsfield unit (HU) attenuation of adipose tissue within a defined volume of interest surrounding the ICA. </jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p> PVAT<jats:sub>carotid</jats:sub> was significantly higher around dissected ICA compared with non-dissected contralateral ICA in the same patients (−58.7 ± 10.2 vs −68.9 ± 8.1 HU, p < 0.0001) and ICA of patients without dissection (−58.7 ± 10.2 vs −69.3 ± 9.3 HU, p < 0.0001). After a median follow-up of 89 days, there was a significant reduction in PVAT<jats:sub>carotid</jats:sub> around dissected ICA (−57.5 ± 13.4 to −74.3 ± 10.5 HU, p < 0.05), while no change was observed around non-dissected contralateral ICA (−71.0 ± 4.4 to −74.1 ± 4.1 HU, p = 0.19). ICA dissection was an independent predictor of PVAT<jats:sub>carotid</jats:sub> following multivariable adjustment for age and the presence of ICA occlusion. </jats:p></jats:sec><jats:sec><jats:title>Conclusion:</jats:title><jats:p> PVAT<jats:sub>carotid</jats:sub> is elevated in the presence of sCAD and may decrease following the acute event. </jats:p></jats:sec>
3 1Scopus© Citations 5
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Non-Canonical WNT/Wnt5a Pathway Activity in Circulating Monocytes of Untreated Psoriatic Patients: An Exploratory Study of Its Association with Inflammatory Cytokines and Cardiovascular Risk Marker-ADAMTS7
(2023)
Claudio Karsulovic
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Khanty Loyola
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CABRERA MORAGA, RAUL ALEJANDRO
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Claudio Perez
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Lia Hojman
<jats:p>The leading cause of death in psoriasis is cardiovascular disease. The determinants that induce the increase in this risk are not known. The systemic inflammatory process is dependent on lymphocytes and monocytes, as has been proposed. However, adaptation modules such as mTOR have recently been mentioned as having a role. Other factors, such as WNT and its non-canonical WNT5a-inducing pathway, are relevant in inflammation, cell migration, and neoangiogenesis. Thus, we studied circulating monocytes from untreated severe psoriatic patients and characterized inflammatory cytokines, chemokines, mTOR activity, and the cardiovascular risk marker ADAMTS7. Peripheral blood from ten severely psoriatic patients (Psoriasis severity index greater than 10) was extracted and age- and sex-matched with healthy subjects. Surface and intracellular flow cytometry were performed for cytokine, chemokine receptors, and mTOR activity. ADAMTS7 was measured using ELISA. Psoriatic patients had a higher frequency of WNT5a+ cells in monocytes, which also had higher levels of IL-1β, IL-6, CXCR3, CCR2, and phosphorylated S6R protein. We found that M1 monocytes are dominant in the WNT5a+ cell group, and intracellular levels of WNT5a were also augmented. Levels of WNT5a were correlated with ADAMTS7, a blood marker related to the pathogenesis of atheromatosis. WNT5a could be relevant to the cardiovascular risk of psoriatic patients considering its association with higher levels of inflammatory cytokines, chemokine receptors and the pro-atherogenic profile of circulating monocytes.</jats:p>
Scopus© Citations 2 4

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