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BACKGROUND: The commercialization of herbal products made in fictitious laboratories in Mexico has generated various problems, from the increase in cases of iatrogenic Cushing's syndrome, to the report of cases in other geographical latitudes of that syndrome. CLINICAL CASES: This paper reports a case series of Cushing's syndrome due to consume of complements such as Artri King or Ortiga ajo rey, among others, clinically proven and by the determination of serum cortisol, serum ACTH and urinary cortisol in 24 hours. CONCLUSIONS: The diagnosis of iatrogenic Cushing's syndrome should always be suspected in patients with chronic pain, who report having consumed "miracle" products; an exhaustive questioning directed towards these is enough to suspect the etiological association, which should be corroborated by measuring cortisol levels, ACTH and urinary cortisol to verify the exogenous nature of the glucocorticoid overdose. [ABSTRACT FROM AUTHOR]

Introducción: los glucocorticoides (GC) han sido ampliamente utilizados en el tratamiento de patologías oculares debido a sus efectos antiinflamatorios y anti-angiogénicos. Se ha sugerido que el mecanismo de acción antiangiogénico de los GC puede estar relacionado con la enzima fosfatidilinositol-3-cinasa (PI3K), la cual desempeña un papel crucial en la angiogénesis mediada por el receptor nicotínico de acetilcolina alfa 7 (α7-nAChR). La PI3K es una enzima lipoproteica heterodimérica compuesta por las subunidades; reguladora (p85) y catalítica (p110). Objetivo: esta revisión examina la evidencia de la interrelación entre los GC, y la vía de señalización de PI3K activada por α7-nAChR en la angiogénesis “in vitro”. Metodología: se realizó una revisión bibliográfica utilizando los motores de búsqueda PubMed y Web of Science, relacionando los conceptos “endothelial cell”, “α7-nAChR”, “PI3K”, y “glucocorticoid”. Resultados: se seleccionaron 30 artículos que informaron sobre la expresión de α7-nAChR y PI3K en células endoteliales humanas. Además, del efecto de dexametasona sobre las subunidades de PI3K y Akt en modelos humano, murino y porcino. A partir de estos hallazgos, se propuso un mecanismo mediante el cual los GC ejercen su efecto antiangiogénico a través de la modulación en la expresión de la subunidad inhibitoria p85 de PI3K activada por α7-nAChR en células endoteliales humanas. Conclusión: los antecedentes evidencian que dexametasona, ejerce su mecanismo de acción anti-angiogénico mediante el incremento de la expresión de la subunidad inhibitoria p85 de PI3K activada por α7-nAChR. Estos hallazgos podrían contribuir a explicar la posible falla terapéutica en el área oftalmológica en pacientes fumadores.

Das von Josef Fried erfundene Verfahren zur Einführung von 9a-Fluorsubstituenten in Glucocorticoide wirderläutert und ein kurzer Einblick in das Leben dieses bedeutenden Synthetikers und Wirkstoffforschers gegeben.

Background: Pre-and post-traumatic hypothalamic–pituitary–adrenal (HPA) axis markers have been studied to predict posttraumatic stress disorder (PTSD) risk, but its acute reactivity cannot be measured in real-life settings. Experimental paradigms can depict the cortisol response to stimuli that simulate traumatic events. Objective: To review experimental studies on the cortisol response to traumatic stimuli and the correlation between cortisol and PTSD symptoms. Method: Experimental, (un-)published studies in German or English from any year were eligible if they confronted non-traumatized humans with traumatic stimuli, assessed cortisol before, during or after stimulus presentation and subsequent PTSD symptoms. The literature was searched via PubMed, PubPsych, PsychINFO, PsycArticle, Web of Science, EMBASE, ProQuest and ClinicalTrials.gov up to 16th February 2021. Risk of bias was assessed with the Cortisol Assessment List. Multilevel-meta-analyses were conducted under the random effects model. The standardized mean change (dSMC) indicated the cortisol response. Coefficient r indicated the correlations between cortisol and PTSD symptoms. Results: 14 studies, investigating 1004 individuals, were included. A cortisol response was successfully induced between 21 and 40 min post-presentation onset (kobservations = 25, dSMC = 0.15 [.03;.26]). Cortisol was not associated with overall or cluster-level PTSD symptoms. On a symptom-level, higher pre-presentation onset cortisol was correlated with lower state tension (k = 8, r = −.18 [−.35; −.01]), higher state happiness (k = 8, r = −.34 [−.59; −.03], variable inverted) and lower state anger (k = 9, r = −.14 [−.26; −.01]). Higher post-presentation onset cortisol was correlated with higher state happiness (k = 16, r = −.20 [−.33; −.06]) and lower state sadness (k = 17, r = −.16 [−.25; −.05]), whereas cortisol response was positively correlated with state anxiety (k = 9, r =.16 [0.04; 0.27]). Conclusions: Experimental paradigms effectively induce a cortisol response. Higher basal cortisol, higher cortisol, as measured after traumatic stimulus presentation, and a lower cortisol response were associated with more adaptive emotional reactions. These markers did not predict longer-term PTSD symptoms. Experimental trauma paradigms successfully induced a cortisol response. Cortisol was predictive for single state, emotion-related symptoms, but not overall PTSD symptoms. Trauma paradigms shed light into the immediate post-trauma period that is hard to capture in real life, but the gap between experimental and naturalistic settings is difficult to overcome. [ABSTRACT FROM AUTHOR]

Copyright of Nouveau Praticien Vétérinaire Canine & Féline is the property of EDP Sciences and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Minas Gerais Medical Journal / Revista Médica de Minas Gerais is the property of Associacao Medica de Minas Gerais and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Osteoarthritis is a complex degenerative disease with several factors contributing to joint damage. Objective: To compare the potential effect of hyaluronic acid (HA) and triamcinolone acetonide (TA), alone or combined, on the in vitro chondrogenic differentiation process of mesenchymal stem cells (MSCs). Methods: MSCs were divided into four groups: Control, HA, TA, and HA/TA combined. Each treatment group was cultured for 14 days in chondrogenic differentiation medium. The chondrogenic differentiation potential was assessed by histology and immunohistochemistry. Results: The HA and HA/TA-treated MSCs presented histological characteristics similar to native chondrocytes. The extracellular matrix (ECM) of TA-treated MSCs was compact and organized. Glycosaminoglycan staining was intense in Control, moderate in TA, slight in HA/TA, and undetectable in HA. Type II collagen immunoreactivity was high in the TA-treated ECM and MSCs. Conclusions: Histological analysis shows that HA influences morphological development similar to chondrocytes of the MSCs, but with low expression of specific cartilage molecules. The TA promotes formation of a compact and organized ECM. [ABSTRACT FROM AUTHOR]

La hiperglucemia inducida por glucocorticoides es un escenario frecuente al cual se enfrenta el clínico durante su práctica hospitalaria diaria, constituyendo un reto en el abordaje y control del estado metabólico de estos pacientes, con el fin de disminuir su morbimortalidad asociada. Presentamos el caso clínico de una paciente de género femenino de 69 años con antecedente de diabetes mellitus tipo 2 y linfoma no Hodgkin, hospitalizada para inicio de ciclo quimioterapéutico, durante el cual se documentan hiperglucemias sostenidas de difícil manejo. La paciente recibió tratamiento con esquema basalbolo y un bolo adicional de insulina NPH titulado según las dosis y tipo de glucocorticoide aplicado, alcanzando adecuado control metabólico. Se realiza una revisión de la literatura respecto a la hiperglucemia inducida por glucocorticoides, su abordaje y tratamiento, y las recomendaciones existentes en cuanto al uso de insulina NPH como esquema adicional correctivo.

Résumé Le syndrome de Cushing est le plus souvent d'origine iatrogénique, dû à la prise au long cours de glucocorticoïdes ou l'administration d'un traitement associant un glucocorticoïde et des médicaments modifiant la pharmacocinétique de celui-ci. Les professionnels de santé doivent demeurer vigilants lors de la délivrance et du suivi médicamenteux. Summary Cushing's syndrome is in most cases iatrogenic in origin, due to the prolonged intake of glucocorticoids or the administration of a treatment combining a glucocorticoid and medicines altering its pharmacokinetics. Health professionals must remain vigilant when dispensing medicines and monitoring their intake. [ABSTRACT FROM AUTHOR]

Antecedentes: las cabalgatas culturales suponen para los equinos un gran esfuerzo donde se someten a desafíos fisiológicos y ambientales, la concentración de cortisol y el nivel de deshidratación del animal son indicadores del proceso de homeorrexis y descompensación. Objetivo: evaluar la concentración de cortisol sérico y el grado de estrés hídrico en equinos durante dos cabalgatas culturales en los municipios de Granada y Acacias del departamento del Meta. Métodos: se seleccionaron 44 animales a conveniencia, aceptados a las cabalgatas, para evaluar en dos tiempos diferentes, tiempo 0 (T0, una hora antes de iniciar la cabalgata) y tiempo 1 (T1, 15 minutos después de terminar la cabalgata), la humedad de las mucosas, tiempo de llenado capilar, turgencia de la piel y retracción del globo ocular y establecer el grado de hidratación - deshidratación de los équidos; se tomaron muestras de sangre por venopunción yugular para determinar el volumen medio de eritrocitos mediante tubos de microhematocrito, las proteínas plasmáticas totales usando el método de Biuret y la concentración de cortisol a través del inmunoensayo de Elisa competitiva. Los datos fueron analizados en estadística descriptiva (expresados en mediana - Me - y rangos máximos y mínimos) y sometidos a las pruebas de Shapiro Wilks, Wilcoxon y Spearman con IC = 95 %. Este estudio contó con la aprobación del comité de bioética de la Universidad de los Llanos según acta N° 001 de 03 de agosto del 2023. Resultados: la concentración de cortisol T0 y T1 Me 5,72 [rangos 1,52 - 21,6 μl/dl] y Me 17,1 [rangos 1,41 - 36.7 μl/dl], respectivamente, con un aumento significativo en el T1 p < 0,001 y no se correlaciona con la edad, ni el sexo (Spearman, p > 0,05); no se obtuvieron diferencias significativas para status hídrico - grados de deshidratación (p = 0,140) sin embargo se evidenció un incremento significativo (p < 0,001) del microhematocrito (T0 Me 44,5 % [rangos 16-79 %] y T1 Me 49 % [rangos 13 - 115 %]) y de las PPT en T1 (T0 Me 5,89 [rangos 3,19 - 7,99 g/dl] ;T1 Me 6,22 [rangos 2,80 - 12,8 g/dl]). Conclusiones: las cabalgatas culturales afectan el bienestar animal al originar un importante aumento del cortisol sérico siendo este un biomarcador de estrés, y ocasionan un incremento en parámetros sanguíneos relacionados con el grado de deshidratación del animal, sin generar cambios significativos en el estatus hídrico. [ABSTRACT FROM AUTHOR]

RESUMEN Y CONCLUSIONES 1. Se presentan 28 casos de tiroiditis sub-aguda, 4 en hombres y 24 en mujeres, atendidos en Consulta Privada durante un lapso de 11 años; de ellos 26 fueron tratados mediante drogas con acción glucocorticoide. 2. Se emplearon : a) prednisona per os, a dosis decreciente de 10 a 2.5 mg cada 8 horas durante 10 a 30 días, en 14 casos; b) dexametasona per os, a dosis decreciente de 0.4 a 0.1 mg cada 8 horas durante 13 días, en 1 caso; c) acetato del éster de 6-metil-prednisolona por vía intramuscular, a dosis única de 40 mg. 3. En 20 pacientes con tiempo de evolución de la enfermedad menor de 50 días, se obtuvo mejoría definitiva en todos ellos: 12 mediante prednisona y 8 mediante acetato de 6-metil-prednisolona. 4. En 6 pacientes con tiempo de evolución de la enfermedad mayor de 50 días, se obtuvo solamente mejoría transitoria, mediante prednisona, dexametasona o acetato de 6-metilprednisolona; 5 de ellos presentaron franca recidiva, controlable mediante glucocorticoide distinto al empleado como primer agente terapéutico. 5. El autor considera como el método de elección en el tratamiento actual de la tiroiditis subaguda en fase inicial o de daño progresivo tiroidiano auto-inmune, la administración intra-muscular de 40 mg de acetato del éster de 6-metilprednisolona, en una sola dosis.

The noninvasive nature of sample collection makes analysis of fecal hormone concentrations useful for examining endocrine responses in free-living wild animals. Glucocorticoid hormones (i.e., cortisol and corticosterone) are frequently measured as an indicator of activation of the endocrine stress axis. However, many factors may influence glucocorticoid concentrations in feces, and the influence of prey glucocorticoids on concentrations in the feces of predators is rarely considered. We tested whether cortisol consumption influenced concentrations of glucocorticoid metabolites in feces of captive Arctic foxes ( Vulpes lagopus (Linnaeus, 1758)) by adding cortisol (5 mg cortisol per kg fox body mass) to the foxes' diet. Food supplemented with supraphysiological concentrations of cortisol increased fecal glucocorticoid metabolite concentrations of Arctic foxes by 97% in males and 51% in females, compared with controls. In addition, fecal metabolite concentrations in nontreatment samples were higher for females (22.2 ± 3.3 ng·g−1, mean ± SE) than males (13.3 ± 1.5 ng·g−1), suggesting female Arctic foxes may have higher baseline cortisol concentrations or females may be more sensitive to captivity or relocation. These results indicate that prey cortisol can influence measurement of glucocorticoid metabolites in carnivore feces and suggest caution may be needed when interpreting such measurements in wild carnivores. [ABSTRACT FROM AUTHOR]

Introduction: The accumulation of visceral fat affects the metabolism of hormones and some nutrients, but these mechanisms remain unclear. Objective: To assess the influence of cortisol on the metabolism of zinc in morbidly obese women. Method: Cross-sectional, case-control study involving 80 women aged between 20 and 59 years. The participants were divided into two groups: experimental (morbidly obese, n = 40) and control (normal weight, n = 40). Zinc concentrations were determined by atomic absorption spectroscopy and serum and urinary cortisol by chemiluminescence method. Results: Zinc intake was significantly different between groups. Mean plasma zinc was lower in obese compared to control group. Mean values for erythrocyte zinc were 44.52 ± 7.84 μg/gHb and 40.17 ± 6.71 μg/gHb for obese and control groups, respectively. Urinary excretion of this mineral was higher in obese compared to control subjects (p < 0.05). Mean values for plasma cortisol were 9.58 ± 4.86 μg/dL for obese and 9.89 ± 5.61 μg/dL for control groups. Mean values for urinary cortisol were 163.00 ± 100.35 μg/dL and 109.71 ± 34.88 μg/dL for obese and control groups, respectively (p > 0.05). The correlation analysis between cortisol and zinc was not significant (p > 0.05). Conclusions: Obese patients have hypozincemia and high erythrocyte zinc levels. The correlation between zinc parameters and cortisol concentration showed no influence of this hormone on zinc metabolism.

Hypercortisolims is an infrequent disease with multi-systemic compromise and increases morbility and mortality. Cardiovascular disease is one of the most common complications associaded with Cushing syndrome. The prognosis of this disease is affected by the difficulties associated with its diagnosis and treatment. Clearly, Cushing syndrome is still a clinical challenge. Cushing syndrome can be classified in ACTH dependent or ACTH independent. ACTH-dependent causes are more frequent, however, ACTH independent causes are responsible of less than 15% of Cushing`s syndrome and are secondary to adrenal tumors. Three cases of adrenal Cushing are reported with a review of the main clinical points of Cushing syndrome [ABSTRACT FROM AUTHOR]

Objetivo. El objetivo del estudio fue realizar una descripción histológica e histoquímica del proceso de cicatrización de la pythiosis cutánea en equinos tratados con acetonida de triamcinolona. Materiales y métodos. Se Realizó un estudio de tipo descriptivo, no probabilístico en animales de conveniencia con pythiosis cutánea. Fueron utilizados 24 equinos con pythiosis, siendo aplicado 50 mg de acetonida de triamcinolona vía intramuscular a un grupo de 12 animales (GT) y en otro grupo no fue aplicado tratamiento (GC). Se realizaron biopsias de tejidos para evaluación histológica e histoquímica, en las coloraciones de hematoxilina eosina (H&E), tricrómico de Gómori (TG), picrosirius red/polarization (PR/P) y plata metanamina de Grocott (GMS). Resultados. Se observó que en el GT el proceso inflamatorio fue disminuyendo progresivamente, evidenciado en la disminución de la capa fibrino leucocitaria, PMN y de los fenómenos de Splendore Hoepli, así como mayor angiogénesis, epiteliogénesis y aumento de la cantidad de fibroblastos y fibras colágenas generales, así mismo en el cambio progresivo de colágeno tipo III a colágeno tipo I al final del proceso, además de que la presencia de hifas intralesionales de Pythium insidiosum disminuyó a la segunda semana. Ninguno de los animales del GC presentó mejoría en las características histológicas e histoquímicas de la pythiosis y se mantuvieron iguales al primer día durante todo el estudio. Conclusiones. La acetonida de triamcinolona es una buena alternativa terapéutica en el tratamiento de las heridas granulomatosas por pythiosis en equinos con 100% de recuperación clínica y demostrada con las constataciones histológicas e histoquímicas.

FUNDAMENTO: Cronicamente, os glicocorticóides induzem alterações cardiometabólicas adversas, incluindo resistência à insulina, diabete, dislipidemia, esteatose hepática e hipertensão arterial. OBJETIVOS: Avaliar o efeito da prática regular de exercício físico aeróbio sobre as alterações cardiometabólicas induzidas por administração crônica de dexametasona (Dex - 0,5 mg/kg/dia i.p) em ratos. MÉTODOS: Ratos Wistar machos (n = 24) foram divididos em quatro grupos: Grupo controle; Grupo treinado; Grupo tratado com Dex e Grupo tratado com Dex e treinado. O treinamento físico (iniciado 72 horas após a primeira dose de Dex) foi realizado 3 vezes por semana, até o final do tratamento. Ao final desse período, realizaram-se as seguintes avaliações bioquímicas: glicemia em jejum, teste de tolerância à glicose e análise do perfil lipídico no sangue que incluiu colesterol total (CT), LDL-c, HDL-c, VLDL-c e triglicerídeos (TG). O peso do músculo gastrocnêmio, análise histopatológica do fígado e os índices cardiometabólicos (CT/HDL-c, LDL-c/HDL-c e TG/HDL-c) também foram avaliados. RESULTADOS: Observou-se hiperglicemia, menor tolerância à glicose, elevação do CT, LDL-c, VLDL-c e TG, diminuição do HDL-c, presença de esteatose hepática, hipotrofia muscular e elevação dos índices CT/HDL-c, LDL-c/HDL-c e TG/HDL-c nos animais tratados com Dex. O exercício físico reduziu a hiperglicemia, melhorou a tolerância à glicose, reduziu a dislipidemia e preveniu a esteatose hepática , a hipotrofia muscular e reduziu os índices CT/HDL-c, LDL-c/HDL-c e TG/HDL-c. Entretanto, não houve efeito significante do treinamento físico sobre o HDL-c. CONCLUSÃO: O exercício físico aeróbio tem efeito protetor contra as alterações cardiometabólicas induzidas pelo uso crônico de glicocorticóides.FUNDAMENTO: Crónicamente, los glucocorticoides inducen alteraciones cardiometabólicas adversas, incluyendo resistencia a la insulina, diabetes, dislipidemia, esteatosis hepática e hipertensión arterial. OBJETIVOS: Evaluar el efecto de la práctica regular de ejercicio físico aeróbico sobre las alteraciones cardiometabólicas inducidas por administración crónica de dexametasona (Dex - 0,5 mg/kg/día i.p) en ratones. MÉTODOS: Se dividieron ratones Wistar machos (n = 24) en cuatro grupos: Grupo control; Grupo entrenado; Grupo tratado con Dex y Grupo tratado con Dex y entrenado. El entrenamiento físico (iniciado 72 horas después de la primera dosis de Dex) se realizó 3 veces por semana, hasta el final del tratamiento. Al final de ese período, se realizaron las siguientes evaluaciones bioquímicas: glicemia en ayunas, test de tolerancia a la glucosa y análisis del perfil lipídico en sangre que incluyó colesterol total (CT), LDL-c, HDL-c, VLDL-c y triglicéridos (TG). También se evaluaron, el peso del músculo gastrocnemio, análisis histopatológico del hígado y los índices cardiometabólicos (CT/HDL-c, LDL-c/HDL-c y TG/HDL-c). RESULTADOS: Se observó hiperglicemia, menor tolerancia a la glucosa, elevación de CT, LDL-c, VLDL-c y TG, disminución del HDL-c, presencia de esteatosis hepática, hipotrofia muscular y elevación de los índices CT/HDL-c, LDL-c/HDL-c y TG/HDL-c en los animales tratados con Dex. El ejercicio físico redujo la hiperglicemia, mejoró la tolerancia a la glucosa, redujo la dislipidemia y previno la esteatosis hepática, la hipotrofia muscular y redujo los índices CT/HDL-c, LDL-c/ HDL-c ye TG/HDL-c. Con todo, no hubo efecto significativo del entrenamiento físico sobre el HDL-c. CONCLUSIÓN: El ejercicio físico aeróbico tiene efecto protector con las alteraciones cardiometabólicas inducidas por el uso crónico de glucocorticoides.BACKGROUND: Chronically, glucocorticoids induce adverse cardiometabolic alterations including insulin resistance, diabetes, dyslipidemia, liver steatosis and arterial hypertension. OBJECTIVES: To evaluate the effect of regular practice of aerobic exercise on cardiometabolic alterations induced by chronic administration of dexamethasone (Dex - 0.5 mg/kg/day ip) in rats. METHODS: Male Wistar rats (n = 24) were divided in four groups: Control group; Trained group; Treated with Dex group and Treated with Dex and trained group. The exercise training (initiated 72 hours after the first dose of Dex) was carried out three times a week until the end of the treatment. At the end of this period, the following biochemical assessments were performed: fasting glycemia, oral glucose tolerance test and analysis of the blood lipid profile that included total cholesterol (TC), LDL-c, HDL-c, VLDL-c and triglycerides (TG). The weight of the gastrocnemius muscle, the histopathological analysis of the liver and cardiometabolic indices (TC/HDL-c, LDL-c/HDL-c and TG/HDL-c) were also performed. RESULTS: Hyperglycemia, lower glucose tolerance, increased TC, LDL-c, VLDL-c, TG, CT/HDL-c, LDL-c/HDL-c and TG/HDL-c, decreased HDL-c, presence of liver steatosis and muscular hypotrophy were observed in the animals treated with Dex. The exercise training reduced hyperglycemia, improved glucose tolerance, decreased dyslipidemia and prevented liver steatosis, muscular hypotrophy and reduced CT/HDL-c, LDL-c/HDL-c and TG/HDL-c ratios. However, there was no significant effect on HDL-c. CONCLUSION: The aerobic exercise training have a protective effect against the cardiometabolic alterations induced by the chronic use of glucocorticoids.

Copyright of Revue de Médecine Vétérinaire is the property of Ecole Nationale Veterinaire de Toulouse and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Recently, topical dexamethasone-induced ocular hypertension and a consequent loss of retinal ganglion cells (RGCs) have been described in mice. This has been proposed as a model of steroid-induced glaucoma. In this study, we set up and evaluated a similar model in rats. Results: Ten-week old Sprague Dawley (SD) rats (N = 12) were used to evaluate the effect of topical 0.1% dexamethasone (50 µl) administered 3 times daily for 4 weeks. Sodium chloride (0.9%) was used in another group of rats (N = 12) that served as the controls. After 1 week, we observed a progressive decrease in body weight in the dexamethasone-treated rats compared both to the pre-treatment baseline and the vehicle-treated rats. In contrast to earlier work that showed elevated Intraocular pressure (IOP) following dexamethasone instillation in mice, IOP in the rats unexpectedly fell to 11.3 ± 1.3 mmHg in the treated eyes, compared to 14.8 ± 2.4 mmHg in the untreated eyes, after 3 weeks of topical dexamethasone (P = 0.032). Blood tests performed after 4 weeks of treatment showed a 3.3-fold increase in both plasma cholesterol (P < 0.001) and alanine transaminase (P = 0.019) in the dexamethasone-treated rats compared to the control rats. Meanwhile, topical steroid did not induce changes in either plasma blood glucose or glycated hemoglobin (HbA1c). We also did not detect changes in the expression of RGC markers (with real-time PCR) following the treatment. Conclusions: In contrast to mice, which previously showed increased IOP following the topical administration of dexamethasone, the rats displayed a paradoxical reduction in IOP following a similar treatment. This was accompanied by a loss of body weight without affecting the level of blood glucose. [ABSTRACT FROM AUTHOR]

Résumé Un certain nombre de médicaments agissent au niveau de l’axe hypophyso-surrénalien. Les hormones glucocorticoïdes sont indiquées dans le traitement glucocorticoïde de substitution au cours de l’insuffisance surrénale, les hormones minéralocorticoïdes dans le traitement minéralocorticoïde substitutif au cours de l’insuffisance corticosurrénale et les anticortisoliques dans certaines pathologies bien précises. Summary A certain number of medicines act on the hypothalamic-pituitary-adrenal axis. Glucocorticoid hormones are indicated for glucocorticoid replacement therapy in cases of adrenal insufficiency, mineralocorticoid hormones for mineralocorticoid replacement therapy for corticoadrenal insufficiency and anti-cortisols for some specific pathologies. [ABSTRACT FROM AUTHOR]

Résumé La bronchopneumopathie chronique obstructive diminue fortement la qualité de vie des patients. La stratégie de prise en charge est aussi bien non-médicamenteuse, avec l’arrêt du tabac, que médicamenteuse. Les bronchodilatateurs inhalés sont au cœur de la thérapie. Le pharmacien doit favoriser l’observance. Summary Chronic obstructive pulmonary disease significantly affects patients’ quality of life. The treatment strategy involves both non-pharmacological therapies, including smoking cessation, as well as drug-based therapies. Inhaled bronchodilators are at the heart of the therapy. The pharmacist must encourage compliance. [ABSTRACT FROM AUTHOR]

The long noncoding RNA (lncRNA) GAS5 has been found to act as a decoy for the glucocorticoid receptor (GR), thus implicating GAS5 as a potential regulator of glucocorticoid sensitivity and resistance. Airway smooth muscle (ASM) cells and airway epithelial cells (AEC) play an important role in the pathogenesis and persistence of asthma and other chronic airways diseases. These airway structural cell types are also important cellular targets of the anti-inflammatory actions of glucocorticoids. In this study, we sought to examine the relevance of GAS5 to glucocorticoid sensitivity and resistance in ASM and AEC. We provide the first evidence that pro-inflammatory mediators up-regulate GAS5 levels in both airway epithelial and smooth muscle cells, and that decreasing GAS5 levels can enhance glucocorticoid action in AEC. [ABSTRACT FROM AUTHOR]

Copyright of Canadian Journal of Physiology & Pharmacology is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Diabetes mellitus is a major health problem worldwide for being one of the most common non-communicable diseases, as well as for the severity of its complications. Cortisol is hyper secreted in chronic form during diabetes and in some emotional states such as stress, contributing to increased blood glucose and thus making metabolic control unmanageable. Objective: To determine the behavior of serum cortisol levels in diabetic patients treated with floral therapy. Subjects and methods: We studied 200 type 2 diabetic outpatients without clinical diabetic foot, divided into two groups: a study group that received floral treatment and a control group receiving placebo treatment. The patients studied were of either sex, aged between 40 and 78 years old, with over 10 years of evolution of the disease, to whom cortisol levels determinations and serum glucose levels were performed on an empty stomach. Determinations were performed before and after floral and placebo treatment. Results: When initiating treatment, high levels of cortisol in serum and metabolic lack of control were found in all patients. After treatment, the study group that received floral treatment significantly decreased both cortisol levels and their serum glucose. These results were not found in the group that received placebo. Conclusions: The role of normocortisolemia levels in type 2 diabetic individuals is important to maintain metabolic control; this has been achieved by using a floral treatment. Among natural therapies, floral stands out as a therapy that uses energy pathways to achieve harmonization of emotional states. [ABSTRACT FROM AUTHOR]

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Glucocorticoid (GC) excess alters glucose homeostasis and promotes modifications in murinometric and anthropometric parameters in rodents and humans, respectively. β-hydroxy-β-methylbutyrate (HMB), a leucine metabolite, has been proposed as a nutritional strategy for preventing muscle wasting, but few data regarding its effects on glucose homeostasis are available. Here, we analyzed whether the effects of GC excess on glucose homeostasis may be attenuated or exacerbated by the concomitant ingestion of HMB. Adult Wistar rats (90-days-old) were assigned to four groups: (1) vehicle treated (Ctl), (2) dexamethasone (DEX) treated (Dex), (3) HMB treated (Hmb), and (4) DEX plus HMB treated (DexHmb). Dex groups received DEX (1 mg·kg body weight (BW)−1, intraperitoneal) for 5 consecutive days. HMB groups ingested HMB (320 mg·kg BW−1, oral gavage) for the same 5 days. HMB ingestion did not attenuate the effects of DEX on food intake and body weight loss, changes in masses of several organs, insulin resistance, and glucose intolerance ( p > 0.05). In fact, in DexHmb rats, there was increased fasting glycemia and exacerbated glucose intolerance with the main effect attributed to DEX treatment ( p < 0.05). HMB exerted no attenuating effect on plasma triacylglycerol levels from DexHmb rats, but it seems to attenuate the lipolysis induced by β-adrenergic stimulation (20 μmol·L−1 isoproterenol) in fragments of retroperitoneal adipose tissue from DexHmb rats. Therefore, HMB does not attenuate the diabetogenic characteristics of GC excess. In fact, the data suggest that HMB may exacerbate GC-induced glucose intolerance. [ABSTRACT FROM AUTHOR]

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Summary: Background and aim: In 1999, 80% of French neonatal centers used corticosteroids, mainly betamethasone (BMT), to prevent or treat bronchopulmonary dysplasia (BPD) [Lee SK, McMillan DD, Ohlson A, et al. Variations in practice and outcomes in the canadian NICU Network 1996–1997. Pediatrics 2000;106:1070–9]. As many data suggested a low risk–benefit ratio, an updated assessment of this use was necessary [Desnoulez L, Empana J, Anceschi M, et al. Prise en charge de l’immaturité pulmonaire en néonatologie : enquête sur les pratiques européennes. Arch Pediatr 2005;12:4–9; Halliday HL, Ehrenkranz RA, Doyle LW. Early postnatal (less than 96h) corticosteroids for preventing chronic lung disease in preterm infants. Cochrane Database Syst Rev 2003:CD001146; Yeh TF, Lin YJ, Lin HC, et al. Outcomes at school age after postnatal dexamethasone therapy for lung disease of prematurity. N Engl J Med 2004;350:1304–13; Lin YJ, LKin CH, Wu JM, et al. The effects of early postnatal dexamethasone therapy on pulmonary outcome in premature infants with respiratory distress syndrome: a 2-year follow-up study. Acta Paediatr 2005;94:310–16]. Methods: Questionnaires addressing the use of and indications for corticosteroids were sent to all French neonatal centers. Results: The study was conducted over 5 months (July to November 2006). Of 202 questionnaires sent out, 186 (92%) were completed. Of these 186 centers, 147 (79%) had a standard protocol for corticosteroid use, covering systemic and inhaled steroids (76 units), only systemic steroid therapy (30 units) and only inhaled steroids (41 units). Systemic corticosteroids were used in 106 centers for hemodynamic purposes in 42 cases (40%), prevention of BPD in 1 case (1%), early treatment of BPD (day 4 to day 21) in 23 cases (22%) and late treatment of BPD (after day 21) in 74 cases (70%). Hemisuccinate hydrocortisone (HSHC) was the only corticoid used for hemodynamic failure. The steroid used for early treatment of BPD was BMT (21 out of 23). The duration of treatment was less than 4 days in 10 centers (43%). The steroid most often used for late treatment was BMT (67 out of 74). The duration of treatment was less than 4 days in 29 centers, between 4 and 8 days in 22 centers, and longer than 8 days in 26 centers. Among 117 centers administering corticosteroids by inhalation, 74% used budesonide. Use of corticosteroids was higher in teaching hospitals (86%) than in others (49%), likely due to the immaturity of the neonates hospitalized in these centers. Conclusion: We showed a still frequent use of corticosteroids in preterm infants in France but only after the fourth day of life to treat BPD and not as a prevention therapy. We also found a marginal use of DXM in accordance with both short-term and long-term adverse side effects, suggesting an unbalanced risk–benefit ratio even though it has a beneficial effect on respiratory status. Our findings indicate the need for national recommendations and trials to assess oral BMT treatment in premature neonates with BPD. [Copyright &y& Elsevier]

Prolonged stress results in elevation of glucocorticoid (GC) hormones, which can have deleterious effects in the brain. The hippocampus, which has a high concentration of glucocorticoid receptors, is especially vulnerable to increasing levels of GCs. GCs have been suggested to endanger hippocampal neurons by exacerbating the excitotoxic glutamate-calcium-reactive oxygen species (ROS) cascade. In an effort to reveal the mechanisms underlying GC-mediated hippocampal neurotoxicity, we aimed to clarify the molecular pathway of GC-induced ROS increase by using organotypic hippocampal slice cultures. Assays for ROS, using 2′,7′-dichlorodihydrofluorescein diacetate fluorescence, showed that treatment of synthetic GC, dexamethasone (DEX) significantly enhanced ROS levels. Time course and dose response analyses indicated that peak amount of ROS was generated at 4 h after treatment with 50 µmol/L DEX. By contrast, other steroid hormones, progesterone and estradiol did not influence ROS production. N-acetyl-l-cysteine completely suppressed ROS produced by DEX. Propidium iodide staining exhibited prominent cell death in the hippocampal layer after 96 h of DEX treatment. RU486, a GC receptor antagonist, almost completely blocked the effect of DEX on ROS production and cell death, indicating that DEX-induced ROS overproduction and hippocampal death are mediated via GC receptors. Real-time reverse transcriptase PCR analysis demonstrated that after DEX treatment the level of glutathione peroxidase mRNA was decreased whereas that of NADPH oxidase mRNA was significantly enhanced. These findings suggest that excess GCs cause hippocampal damage by regulating genes involved in ROS generation. [ABSTRACT FROM AUTHOR]

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Stress activates the synthesis and secretion of catecholamines and adrenal glucocorticoids, increasing their circulating levels. In vivo, hepatic 11β-hydroxysteroid dehydrogenase 1 (HSD1) stimulates the shift of 11-dehydrocorticosterone to corticosterone, enhancing active glucocorticoids at tissue level. We studied the effect of 3 types of stress, 1 induced by bucogastric overload with 200 mmol/L HCl causing metabolic acidosis (HCl), the second induced by bucogastric overload with 0.45% NaCl (NaCl), and the third induced by simulated overload (cannula), on the kinetics of hepatic HSD1 of rats and their influence on the activity of the gluconeogenic enzyme phosphoenolpyruvate carboxykinase, glycemia, and glycogen deposition. Compared with unstressed controls, all types of stress significantly increased HSD1 activity (146% cannula, 130% NaCl, and 253% HCl), phosphoenolpyruvate carboxykinase activity (51% cannula, 48% NaCl, and 86% HCl), and glycemia (29% cannula, 30% NaCl, and 41% HCl), but decreased hepatic glycogen (68% cannula, 68% NaCl, and 78% HCl). Owing to these results, we suggest the following events occur when stress is induced: an increase in hepatic HSD1 activity, augmented active glucocorticoid levels, increased gluconeogenesis, and glycemia. Also involved are the multiple events indirectly related to glucocorticoids, which lead to the depletion of hepatic glycogen deposits, thereby contributing to increased glycemia. This new approach shows that stress increments the activity of hepatic HSD1 and suggests that this enzyme could be involved in the development of the Metabolic Syndrome. [ABSTRACT FROM AUTHOR]

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Summary Olfactory stimuli modulate emotional conditions and the whole body immune system. Effects of odorant inhalation on cutaneous immune reaction were examined. Contact hypersensitivity to 2,4,6-trinitrochlorobenzene was elicited in C57BL/6 mice. The reaction was suppressed at both the induction and elicitation phases by exposure to an odorant, citralva. Topical application of citralva or lyral/lilial did not affect the reaction. The suppressive effect of citralva was more potent than that of another odorant, lyral/lilial. Citralva decreased the number of epidermal Langerhans cells, whereas lyral/lilial had a weak effect. Citralva but not lyral/lilial induced plasma corticosterone. Glucocorticoid receptor antagonist abrogated the suppressive effect of citralva on contact hypersensitivity. Serum interleukin-12 was downregulated by exposure to citralva or lyral/lilial. These data demonstrate that olfactory stimuli regulate the cutaneous immune system. [ABSTRACT FROM AUTHOR]

Background: There is no a unified opinion in the treatment of IgA nephropathy. This prospective cohort study was to explore the effectiveness and safety of tacrolimus for treatment of IgA (Immunoglobulin A) nephropathy patients., Methods: In this study, we assigned 50 patients with biopsy-proven IgA nephropathy in a 1:1.5 ratio to receive oral tacrolimus or full-dose glucocorticoid for 6 months. All the patients had 24-h urine protein excretion≥2.0g/24h and estimated glomerular filtration rate≥50mL/min/1.73m 2 . Primary endpoint was rate of complete remission., Results: After 6 months of treatment, seven participants achieved complete remission in the tacrolimus group and twelve participants in the glucocorticoid group, the complete remission rate was 35% and 40%, respectively. There were not significantly differences between two groups (P=0.7). However, the serum creatinine level from baseline was an increase of 13±13.5μmol/L in the tacrolimus group and a decrease of 8.2±20μmol/L in the glucocorticoid group. When patients stopped taking tacrolimus for 3 months, creatinine level can almost fall to normal level. Thus, patients with renal insufficiency have a high incidence in the tacrolimus group., Conclusions: Tacrolimus was noninferior to full-dose glucocorticoid in inducing proteinuria remission at 6 months. This suggested that those IgA nephropathy patients who are unwilling to full-dose glucocorticoid could consider tacrolimus, but need to pay attention to the impact on renal function., (Copyright © 2021 Elsevier España, S.L.U. All rights reserved.)

Dexamethasone is a synthetic glucocorticoid that has been associated with oxidative stress in central and peripheral tissues. p -Chloro-diphenyl diselenide (( p -ClPhSe) 2 ) is an antioxidant organoselenium compound. The present study evaluated whether nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap-1) signaling contributes to the ( p -ClPhSe) 2 antioxidant effects in the kidney of mice exposed to dexamethasone. Adult Swiss mice received dexamethasone (intraperitoneal) at a dose of 2 mg/kg or its vehicle for 21 days. After that, mice were treated with ( p -ClPhSe) 2 (intragastric) (1, 5, or 10 mg/kg) for 7 days. Samples of kidneys were collected for biochemical assays. ( p -ClPhSe) 2 at a dose of 1 mg/kg reversed the renal reactive oxygen species (ROS) and carbonyl protein (CP) levels increased by dexamethasone. ( p -ClPhSe) 2 at doses of 5 and 10 mg/kg was effective against the increase of thiobarbituric acid reactive substances, ROS, and CP, as well as the decrease of δ-aminolevulinic acid dehydratase activity and nonprotein sulfhydryl levels induced by dexamethasone. At 5 mg/kg, ( p -ClPhSe) 2 reduced the renal levels of 4-OH-2-HNE and heme oxygenase (HO-1), as well as modulated the Nrf2/Keap-1 signaling in mice exposed to dexamethasone. The present findings revealed that ( p -ClPhSe) 2 antioxidant effects were associated with the modulation of Nrf2/Keap-1 signaling pathway in the kidney of mice exposed to dexamethasone.

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