Browsing by Author "Anguita, Rodrigo"
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Item Association of retinal detachment with age 50 years or younger at onset in patients with acute retinal necrosis(2021) Urzúa, Cristhian; Knickelbein, Jared; Cuitino, Loreto; Moreno, Uriel; Anguita, Rodrigo; Velásquez, Víctor; Concha, Luz Elena; Morales, Sergio; Villarroel, Francisco; Sen, H Nida; Arellanes, LourdesBackground Due to the guarded prognosis of acute retinal necrosis (ARN), it is relevant to develop a strategy to earlycategorize those patients in a higher risk of worse outcomes. The purpose of this study is to describe clinical features andpredictive factors for retinal detachment (RD) in patients with ARN. Methods Retrospective observational case series of 34 adult patients (38 eyes) with ARN examined between January 2005 and July 2015 in the National Eye Institute (Bethesda, USA), the Department of Ophthalmology, University of Chile (Santiago, Chile), and APEC (CDMX, Mexico). Results A total of 16 males and 18 females with a mean age at presentation of 44.5±16.8 years were included. Twentyseven patients (79.4%) received intravenous acyclovir as frst-line treatment, and 7 patients received either oral antiviral (4 patients) or oral plus intravitreal antiviral (3 patients). All subjects were treated with prednisone, with a mean initial dose of 57.7±16.3 mg per day. Seventeen patients (50.0%) developed retinal detachment. An association of retinal detachment with age at onset was observed (p=0.04), with patients younger than 50 years presenting a higher risk (OR=14.86, p=0.0009). Additionally, patients in this higher risk group had more infammation in both anterior chamber and vitreous (p=0.04 and 0.03, respectively). No other predictive factor for retinal detachment was found in the present study. Conclusions RD represents an important complication in patients with ARN. Younger patients may be at higher risk of this complication, possibly secondary to the presence of a higher level of infammation.Item Glucocorticoid Receptor-α and MKP-1 as Candidate Biomarkers for Treatment Response and Disease Activity in Vogt-Koyanagi-Harada Disease(Elsevier Inc, 2019) Urzúa, Cristhian; Chen, Ping; Chaigne-Delalande, Benjamin; Liu, Baoying; Anguita, Rodrigo; Guerrero, Julia; Sabat, Pablo; Velásquez, Víctor; Sen, Nida; Lee, Richard; Goecke, AnnelisePurpose To investigate the potential of utilizing the expression of genes for glucocorticoid receptor (GR) and mitogen-activated protein kinase phosphatase-1 (MKP-1) as biomarkers of corticosteroid (CS) refractoriness and disease activity in patients with Vogt-Koyanagi-Harada (VKH) disease. Design Prospective cohort study. Methods Twenty VKH patients receiving their first cycle of CS treatment in the absence of additional systemic immunosuppressive therapy and a control group of fifteen healthy volunteers were recruited from the University of Chile (Santiago, Chile) and US National Institutes of Health (Bethesda, United States). Intraocular inflammation was clinically quantified at enrolment and all follow-up visits. CS refractoriness was defined as an ocular reactivation of VKH upon CS withdrawal at a daily oral prednisone dose of 10 mg or more. Quantitative Reverse transcription polymerase chain reaction (qRT-PCR) was performed to measure the mRNA levels of the alpha (α) and beta (β) isoforms of GR and MKP-1 in peripheral blood mononuclear cells (PBMC) after in vitro stimulation with either anti-CD3/anti-CD28 antibodies, lipopolysaccharide (LPS), or phytohemagglutinin (PHA), in the presence or absence of dexamethasone (Dex). Results After 6 hours of stimulation in the presence of Dex, PBMC from CS-refractory VKH patients had an impaired elevation in GRα expression (P = .03). Furthermore, inactive patients showed a significant Dex-induced upregulation of MKP-1 (P = .005). Conclusions In this pilot study, the expression of GR isoforms and MKP-1 corresponded with patients' clinical response to systemic CS treatment and disease activity, respectively. Hence, these candidate biomarkers have potential clinical utility in the early identification of CS refractoriness and subclinical inflammation in patients with VKH disease.