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Use of an Advanced Hybrid Closed Loop System During Marathon Running: Case Examples and Clinical Implications
(Wiley, 2025-02-28)
María T. Onetto
;
Denise Montt‐Blanchard
;
Cari Berget
;
Kristel Strodhoff
;
Bruno Grassi
Maintaining glucose levels in the target range during aerobic training and athletic competition is especially difficult. The use of Automated Insulin Delivery (AID) technology is increasing, but exercise continues to be a challenge for persons with type 1 diabetes (T1D). In this case report series, we present 3 cases (C1, C2 and C3) of persons with T1D who used the MiniMed 780G during marathon races. We describe the strategies they used before, during and after the race to manage their glycaemia as well as the results of these strategies on their glycaemic control during the race.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>The Medtronic CareLink platform was employed to remotely access insulin pump settings and glycaemic outcomes. Race parameters were obtained from sport watches. Supplemental data were obtained through interviews.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Carelink data for Cases 1, 2, and 3 before the race were downloaded: Time in range (TIR) 70–180 mg/dL 89%, 76%, 82%; time above range (TAR) > 180 mg/dL, 9%, 20%, 16%; time below range (TBR) < 70 mg/dL, 1%, 4%, 1%, respectively. The breakfast insulin reduction percentages were −25%, 0%, and 0% for C1, C2, and C3, respectively. In all three cases, insulin dose reduction was applied to the pre‐race snack at percentages of −50%, −100% and −83%. The consumption of carbohydrates during the race was 0.39 g/kg/hour, 0.42 g/kg/hour, and 0.5 g/kg/hour, respectively. The total amount of carbohydrates consumed was 101 g, 120 g, and 115 g, respectively. Throughout the race, a temporary target was used for all cases.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>These cases provide insights for healthcare professionals who assist athletes with T1D using AID systems during prolonged physical activities. Highlighting the significance of specialised education, planning, and personalised approaches.</jats:p></jats:sec>
4
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IL-10 and IL-6/IL-10 as predictive biomarkers for treatment response in non-infectious uveitis
(Frontiers Media SA, 2025-05-13)
Rodrigo A. Valenzuela
;
Fabian Vega-Tapia
;
Nathaly Elizalde
;
Ivan Flores
;
Felipe M. Rojas
Uveitis, a group of heterogeneous diseases causing ocular inflammation, is a major contributor to vision loss globally. While systemic corticosteroids (CS) are the mainstay treatment, identifying CS-refractory patients remains a significant challenge. This study aimed to explore cytokine expression and Glucocorticoid Receptor (GR) levels as biomarkers for the early detection of CS-refractory cases in non-infectious uveitis. We assayed blood samples from 19 patients with non-infectious uveitis, for the expression of IL-6, IL-17A, TNF-α, IL-10 and GRα. The cohort included 11 refractory and 8 sensitive patients, categorized based on their clinical response to corticosteroids (prednisone 1 mg/kg/day). Blood draws were conducted at three time points (at baseline, day 7- and day 14 after CS initiation), and peripheral blood mononuclear cells (PBMCs) were isolated to measure cytokine and GRα transcript levels via real-time PCR. The expression levels of GRα and cytokines IL-6, IL-17A and TNF-α did not show significant changes between CS-sensitive and CS-refractory patients on the different days of treatment. However, IL-10 expression levels as the day14-to-day7 ratio were significantly higher in patients sensitive to CS therapy. A higher day14-to-day7 ratio was also found for the IL-6/IL-10, IL-17A/IL-10 and GRα/IL-10 ratios. ROC curve analysis demonstrated a robust predictive performance of IL-10 mRNA expression and the IL-6/IL-10 ratio for identifying CS-refractory patients. In conclusion, the expression of IL-10 and the IL-6/IL-10 ratio hold promise as early predictive biomarkers for CS treatment refractoriness in patients with non-infectious uveitis. These findings offer valuable insights into personalized treatment strategies, potentially leading to improved clinical outcomes.
Scopus© Citations 6 1
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The Latin American Society for Immunodeficiencies Registry
(2024)
Gisela Seminario
;
Maria Edith Gonzalez-Serrano
;
Carolina Sanchez Aranda
;
Anete Sevciovic Grumach
;
Gesmar Rodrigues Silva Segundo
Scopus© Citations 1 3
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Histiocitosis de Erdheim Chester como desafío diagnóstico ante un cuadro sistémico: Reporte de un caso
(2024)
Dominga García
;
Yorman Flores
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Maximiliano Vergara
;
Cristian Labarca Solar
Scopus© Citations 1
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Síndrome de hipertensión intracraneana como manifestación inhabitual del síndrome de Sjögren. Caso clínico
(2023)
Dominga García
;
Cristián Labarca
5
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¿Ha disminuido la colectomía por crisis de colitis ulcerosa?
(2023)
Nicolás Besser
;
Erika Chacón
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Andrés Iglesias
;
Manuel Álvarez-Lobos
;
Carolina Pavez
1
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Outcomes of hematopoietic stem cell gene therapy for Wiskott-Aldrich syndrome
(2023)
Roxane Labrosse
;
Julia I. Chu
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Myriam A. Armant
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John K. Everett
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Danilo Pellin
<jats:title>Abstract</jats:title> <jats:p>Wiskott-Aldrich syndrome (WAS) is a rare X-linked disorder characterized by combined immunodeficiency, eczema, microthrombocytopenia, autoimmunity, and lymphoid malignancies. Gene therapy (GT) to modify autologous CD34+ cells is an emerging alternative treatment with advantages over standard allogeneic hematopoietic stem cell transplantation for patients who lack well-matched donors, avoiding graft-versus-host-disease. We report the outcomes of a phase 1/2 clinical trial in which 5 patients with severe WAS underwent GT using a self-inactivating lentiviral vector expressing the human WAS complementary DNA under the control of a 1.6-kB fragment of the autologous promoter after busulfan and fludarabine conditioning. All patients were alive and well with sustained multilineage vector gene marking (median follow-up: 7.6 years). Clinical improvement of eczema, infections, and bleeding diathesis was universal. Immune function was consistently improved despite subphysiologic levels of transgenic WAS protein expression. Improvements in platelet count and cytoskeletal function in myeloid cells were most prominent in patients with high vector copy number in the transduced product. Two patients with a history of autoimmunity had flares of autoimmunity after GT, despite similar percentages of WAS protein–expressing cells and gene marking to those without autoimmunity. Patients with flares of autoimmunity demonstrated poor numerical recovery of T cells and regulatory T cells (Tregs), interleukin-10–producing regulatory B cells (Bregs), and transitional B cells. Thus, recovery of the Breg compartment, along with Tregs appears to be protective against development of autoimmunity after GT. These results indicate that clinical and laboratory manifestations of WAS are improved with GT with an acceptable safety profile. This trial is registered at clinicaltrials.gov as #NCT01410825.</jats:p>
12Scopus© Citations 30
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Annular elastolytic giant cell granuloma: an unusual presentation in non-sun-exposed areas
(2023)
Claudia Suárez
;
Gonzalo Hevia
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Catalina Silva-Hirschberg
;
Alex Castro
3
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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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Enfermedad relacionada a IgG4. Serie clínica de pacientes chilenos
(2022)
María C. Cuéllar
;
Miguel Gutiérrez
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Alejandra Herrera
;
Fabián Elgueta
;
Pamela Wurmann
Scopus© Citations 1 4

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