Browsing by Author "Baudrand, Rene"

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    An Ultrasound Model to Discriminate the Risk of Thyroid Carcinoma
    (ELSEVIER SCIENCE INC, 2011) Miguel Dominguez, Jose; Baudrand, Rene; Cerda, Jaime; Campusano, Claudia; Fardella, Carlos; Arteaga, Eugenio; Cruz, Francisco; Solar, Antonieta; Arias, Tatiana; Mosso, Lorena
    Rationale and Objectives: Thyroid nodules are common on ultrasonographic examination and are mostly benign. Ultrasound characteristics may help discriminate thyroid carcinoma (TC) from benign nodules. The aims of this study. were to identify ultrasonographic characteristics associated with IC and to validate a previously proposed model based on the presence of three ultrasonographic characteristics.,
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    Classic and nonclassic apparent mineralocorticoid excess syndrome
    (Endocrine Society, 2020) Carvajal, Cristián A.; Tapia-Castillo, Alejandra; Vecchiola, Andrea; Baudrand, Rene; Fardella, Carlos
    © 2020 Endocrine Society. All rights reserved.Context: Arterial hypertension (AHT) is one of the most frequent pathologies in the general population. Subtypes of essential hypertension characterized by low renin levels allowed the identification of 2 different clinical entities: aldosterone-mediated mineralocorticoid receptor (MR) activation and cortisol-mediated MR activation. Evidence Acquisition: This review is based upon a search of Pubmed and Google Scholar databases, up to August 2019, for all publications relating to endocrine hypertension, apparent mineralocorticoid excess (AME) and cortisol (F) to cortisone (E) metabolism. Evidence Synthesis: The spectrum of cortisol-mediated MR activation includes the classic AME syndrome to milder (nonclassic) forms of AME, the latter with a much higher prevalence (7.1%) than classic AME but different phenotype and genotype. Nonclassic AME (NC-AME) is mainly related to partial 11βHSD2 deficiency associated with genetic variations and epigenetic modifications (first hit) and potential additive actions of endogenous or exogenous inhibitors (ie, glycyrrhetinic acid-like factors [GALFS]) and other factors (ie, age, high sodium intake) (second hit). Subjects with NC-AME are characterized by a high F/E ratio, low E levels, normal to elevated blood pressure, low plasma renin and increased urinary potassium excretion. NCAME condition should benefit from low-sodium and potassium diet recommendations and monotherapy with MR antagonists. Conclusion: NC-AME has a higher prevalence and a milder phenotypical spectrum than AME. NC-AME etiology is associated to a first hit (gene and epigene level) and an additive second hit. NC-AME subjects are candidates to be treated with MR antagonists aimed to improve blood pressure, end-organ damage, and modulate the renin levels.
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    Higher Dehydroepiandrosterone Levels in Prepubertal Children Born Very Preterm
    (KARGER, 2018) Mericq, Veronica; Martinez Aguayo, Alejandro; Iniguez, German; Poggi, Helena; D'Apremont, Ivonne; Moore, Rosario; Arancibia, Monica; Garcia, Hernan; Peredo, Soledad; Trincado, Claudia; Sifaqui, Sofia; Tomas Ossa, Jose; Fardella, Carlos; Carvajal, Cristian; Campino, Carmen; Baudrand, Rene; Solari, Sandra; Allende, Fidel
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    Increased urinary glucocorticoid metabolites are associated with metabolic syndrome, hypoadiponectinemia, insulin resistance and beta cell dysfunction
    (ELSEVIER SCIENCE INC, 2011) Baudrand, Rene; Campino, Carmen; Carvajal, Cristian A.; Olivieri, Oliviero; Guidi, Giancesare; Faccini, Giovanni; Sateler, Javiera; Cornejo, Javiera; San Martin, Betty; Dominguez, Jose M.; Cerda, Jaime; Mosso, Lorena M.; Owen, Gareth I.; Kalergis, Alexis M.; Fardella, Carlos E.
    Metabolic syndrome (MetS) may have increased cortisol (F) production caused by 11 beta-hydroxysteroid dehydrogenase 1 (11 beta-HSD1) in liver and adipose tissue and/or by HPA axis dysregulation. F is then mainly metabolized by liver reductases into inactive tetrahydrometabolites (THMs). We measured THM levels in patients with or without MetS and evaluate the correlation between THMs and anthropometric and biochemical parameters. We recruited 221 subjects, of whom 130 had MetS by ATP III. We evaluated F, cortisone (E), adipokines, glucose, insulin and lipid profiles as well as urinary (24 h) F. E and THM levels. beta Cell function was estimated by the HOMA Calculator. We observed that patients with MetS showed higher levels of THMs, HOMA-IR and leptin and lower levels of adiponectin and HOMA-beta but no differences in F and E in plasma or urine. THM was associated with weight (r = +0.44, p < 0,001), waist circumference (r = +0.38, p < 0.01). glycemia (r = +0.37, p < 0.01), and triglycerides (r = +0.18, p = 0.06) and negatively correlated with adiponectin (r = -0.36, p < 0.001), HOMA-beta (r = -0.21, p < 0.001) and HDL (r = -0.29, p < 0.01). In a logistic regression model, THM levels were associated with hypertension, hyperglycemia and dyslipidemia. We conclude that MetS is associated with increased urinary THMs but not with F and E levels in plasma or urine. Increased levels of THM, reflecting the daily cortisol production subsequently metabolized, are correlated with hypoadiponectinemia, hypertension, dyslipidemia, insulin resistance and beta cell dysfunction. A subtle increased in glucocorticoid production may further account for the phenotypic and biochemical similarities observed in central obesity and Cushing's syndrome. (C) 2011 Elsevier Inc. All rights reserved.
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    Insulin Resistance Parameters in Children Who Were Born Very Preterm and Adequate for Gestational Age
    (KARGER, 2018) Garcia, Hernan; Poggi, Helena; Arancibia, Monica; Peredo, Soledad; Trincado, Claudia; Moore, Rosario; D'Apremont, Ivonne; Andrade, Daniela; Sifaqui, Sofia; Ossa, J. T.; Campino, Carmen; Carvajal, Cristian; Fardella, Carlos; Baudrand, Rene; Solari, Sandra; Allende, Fidel; Martinez Aguayo, Alejandro
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    Mineralocorticoid receptor modulation by dietary sodium influences NAFLD development in mice
    (ELSEVIER ESPANA, 2021) Cabrera, Daniel; Rao, Isabel; Raasch, Fabiola; Solis, Nancy; Pizarro, Margarita; Freire, Mariela; De Urturi, Diego Saenz; Ramirez, Carolina A.; Triantafilo, Nicolas; Leon, Jonathan; Riquelme, Arnoldo; Barrera Martínez, Francisco; Baudrand, Rene; Aspichueta, Patricia; Arrese, Marco; Arab, Juan P.
    Introduction and Objectives: Nonalcoholic-fatty-liver disease (NAFLD) is considered the hepatic manifestation of metabolic syndrome (MetS). Mineralocorticoid receptor (MR) activation is associated with increased risk of MetS but few studies have assessed the role of liver MR on NAFLD. We aimed to evaluate the effect of MR modulation by sodium intake in liver injury in experimental models of NAFLD.
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    Overexpression of 11 beta-Hydroxysteroid Dehydrogenase Type 1 in Hepatic and Visceral Adipose Tissue is Associated with Metabolic Disorders in Morbidly Obese Patients
    (SPRINGER, 2010) Baudrand, Rene; Carvajal, Cristian A.; Riquelme, Arnoldo; Morales, Mauricio; Solis, Nancy; Pizarro, Margarita; Escalona, Alex; Boza, Camilo; Perez, Gustavo; Dominguez, Angelica; Arrese, Marco; Fardella, Carlos E.
    The enzyme 11-beta-hydroxysteroid dehydrogenase type 1 (11 beta-HSD1) catalyzes intracellular glucocorticoid reactivation by conversion of cortisone to cortisol in different tissues and have been implicated in several metabolic disorders associated with obesity. The aim of this study was to evaluate the 11 beta-HSD1 expression in liver, visceral adipose tissue (VAT), and subcutaneous adipose tissue (SAT) in morbidly obese patients undergoing bariatric surgery and its correlations with clinical, anthropometric, and biochemical variables.
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    Overexpression of 11 beta-hydroxysteroid dehydrogenase type 1 in visceral adipose tissue and portal hypercortisolism in non-alcoholic fatty liver disease
    (WILEY, 2012) Candia, Roberto; Riquelme, Arnoldo; Baudrand, Rene; Carvajal, Cristian A.; Morales, Mauricio; Solis, Nancy; Pizarro, Margarita; Escalona, Alex; Carrasco, Gonzalo; Boza, Camilo; Perez, Gustavo; Padilla, Oslando; Cerda, Jaime; Fardella, Carlos E.; Arrese, Marco
    Background: The enzyme 11 beta-hydroxysteroid-dehydrogenase type 1 (11 beta HSD1) catalyses the reactivation of intracellular cortisol. We explored the potential role of 11 beta-HSD1 overexpression in visceral adipose tissue (VAT) in non-alcoholic fatty liver disease (NAFLD) assessing sequential changes of enzyme expression, in hepatic and adipose tissue, and the occurrence of portal hypercortisolism in obese mice. 11 beta-HSD1 expression was also assessed in tissues from obese patients undergoing bariatric surgery. Methods: Peripheral and portal corticosterone levels and liver histology were assessed in ob/ob mice at two time points (8-12 weeks of age). 11 beta-HSD1 tissue expression was assessed in by RT-pcr in ob/ob mice and in 49 morbidly obese patients. Results: Portal corticosterone serum levels were higher in obese mice with a 26% decrease between 8 and 12 weeks of age (controls: 78.3 +/- 19.7 ng/ml, 8-week-old ob/ob: 167.5 +/- 14.5 ng/ml and 12-week-old ob/ob: 124.3 +/- 28 ng/ml, P < 0.05). No significant differences were found in peripheral corticosterone serum levels. Expression of 11b-HSD1 was lower in the liver [-45% at 8 weeks and -35% at 12-weeks (P = 0.0001)] and highly overexpressed in VAT in obese mice, compared to controls (128-fold higher in 8-week-old ob/ob and 41-fold higher in 12-week-old ob/ob, P < 0.01). No significant differences were seen in the expression of 11 beta-HSD1 in subcutaneous adipose tissue. In multivariate analysis, human 11 beta-HSD1 expression in VAT (OR: 1.385 +/- 1.010-1.910) was associated with NAFLD. Conclusion: Murine NAFLD is associated with portal hypercortisolism and 11 beta-HSD1 overexpression in VAT. In humans, 11 beta-HSD1 VAT expression was associated with the presence of NAFLD. Thus, local corticosteroid production in VAT may contribute to NAFLD pathogenesis.
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    Perspective review: lessons from successful clinical trials and real-world studies of systemic therapy for metastatic pheochromocytomas and paragangliomas
    (SAGE PUBLICATIONS LTD, 2024) Jimenez, Camilo; Baudrand, Rene; Uslar, Thomas; Bulzico, Daniel
    Pheochromocytomas and paragangliomas (PPGLs) are orphan tumors with the potential to spread to distant organs such as the lymph nodes, the skeleton, the lungs, and the liver. These metastatic tumors exhibit high rates of morbidity and mortality due to their frequently large tumor burden, the progression of the disease, and the excessive secretion of catecholamines that lead to cardiovascular disease and gastrointestinal dysmotility. Several molecular drivers responsible for the development of PPGLs have been described over the last 30 years. Although therapeutic options are limited, substantial progress has been made in the recognition of effective systemic therapies for these tumors. Successful clinical trials with radiopharmaceuticals such as high-specific-activity meta-iodobenzylguanidine and tyrosine kinase inhibitors such as cabozantinib and sunitinib have been recently published. This review will discuss the results of these studies and their impact on current clinical practices. In addition, this review will provide valuable information on how to design clinical trials to treat patients with metastatic PPGLs with novel medications.
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    Plasminogen Activator Inhibitor-1 and Adiponectin Are Associated With Metabolic Syndrome Components
    (2022) Vecchiola, Andrea; Garcia, Killen; Gonzalez-Gomez, Luis M.; Tapia-Castillo, Alejandra; Artigas, Rocio; Baudrand, Rene; Kalergis, Alexis M.; Carvajal, Cristian A.; Fardella, Carlos E.
    BACKGROUND We aimed to study the associations of adipocytokines, endothelial damage markers, and high-sensitivity C-reactive protein (hs-CRP) with metabolic syndrome (MetS) components. METHODS This cross-sectional study included 202 subjects categorized into MetS and No-MetS according to Harmonizing Adult Treatment Panel III. RESULTS Subjects with MetS showed higher levels of proinflammatory molecules but significantly lower adiponectin levels than subjects with No-MetS. Among the studied adipocytokines, plasminogen activator inhibitor-1 (PAI-1) and adiponectin showed the strongest associations with most MetS components. PAI-1 was associated with MetS (odds ratio (OR) 1.107 (1.065-1.151), P < 0.0001), whereas adiponectin was inversely associated with MetS (OR 0.710 (0.610-0.825), P < 0.0001). Following adjustment by sex, age, body mass index, and 24-hour urinary sodium excretion in a multivariate analysis, the association of PAI-1 (OR 1.090 (1.044-1.137), P < 0.0001) and adiponectin (OR 0.634 (0.519-0.775), P < 0.0001) with MetS remained significant. Multivariate analyses supported a model in which systolic blood pressure (BP) could be predicted by PAI-1, hs-CRP, and matrix metalloproteinase 2 (R-2 = 0.125; P = 0.04); diastolic BP (R-2 = 0.218; P = 0.0001) and glucose (R-2 = 0.074; P = 0.0001) could be predicted by PAI-1; waist circumference could be predicted by PAI-1 and hs-CRP (R-2 = 0.28; P = 0.016). Receiver operating characteristic curve analysis showed that a PAI-1 concentration had the best sensitivity and specificity for discriminating subjects with MetS. CONCLUSION PAI-1 and adiponectin rendered the most robust associations with MetS components in a general population, indicating that unfavorable adipose tissue performance is a key contributor to these metabolic anomalies. Further prospective analyses should allow establishing whether these adipocytokines can anticipate the progress of MetS and cardiovascular risk.