Thoracic ectopic kidney is a rare anomaly, the rarest of all renal ectopia types (p = 0.005%). Herein, we describe a case of thoracic ectopic kidney in an 83-year-old black man who, upon seeking medical attention, presented a clinical profile consistent with pulmonary emphysema. A chest X-ray was ordered, and the results showed evidence of a mass, which was then diagnosed (through computed tomography) as renal ectopia. The majority of thoracic ectopic kidney cases present as an intrathoracic tumor seen on chest X-rays ordered for reasons other than suspicion of this anomaly and do not require special treatment.
INTRODUCTIONAsthma is a chronic inflammatory disease of the airways that affects approximately 300 million people worldwide. In the United States, between 2001 and 2003, asthma exacerbations caused 4,210 deaths, 504,000 hospitalizations and 1.8 million emergency room visits. 1 Since the mid-1990s, inhaled corticosteroids have been tested for managing asthma exacerbations in emergency-room settings. They have systemic corticosteroid-sparing potential and avoid the need for venipuncture, which is sometimes a difficult procedure. [2][3][4] These drugs exert vasoconstrictor effects on the mucosa by reducing neuronal reuptake of noradrenaline at the neuromuscular junctions of mucosal vessels, thus reducing secretions and facilitating the delivery of beta-2 agonists to their target receptors. Their onset of action is rapid, with peak vasoconstriction occurring in 30 minutes and lasting up to 90 minutes after inhalation. 5,6 Ciclesonide is a prodrug that is activated at the site of action (bronchial cells and lining fluid of the bronchus) by bronchial esterases. These convert ciclesonide to desisobutyryl ciclesonide, which has 100-fold greater affinity for the glucocorticoid receptor than ciclesonide itself. 7Because of this peculiar property, common side effects such as hoarseness, dysphonia, oral candidiasis and suppression of the hypothalamic-pituitary-adrenal axis are much less frequent with ciclesonide than with other high-dose inhaled corticosteroids, as it is inactive outside the lung. [7][8][9][10][11] The anti-inflammatory action of intravenous corticosteroids occurs via a genomic mechanism.This reduces expression of proinflammatory mediators such as interleukins 12 and upregulates
Background: Current guidelines for management of acute asthma exacerbations advocate the administration of short-acting bronchodilators and systemic corticosteroids. The use of inhaled corticosteroids for this purpose has been tested since the 1990s, but the optimal agent, dose, and strategy have yet to be defined. Within the context, we designed a double-blind, randomized clinical trial aiming to compare high doses of inhaled ciclesonide to systemic corticosteroids in the treatment of acute asthma exacerbations in the emergency department. Methods: This double-blind, randomized clinical trial enrolled 58 patients with a clinical diagnosis of bronchial moderate and severe asthma by GINA(Global Initiative for Asthma) criteria who presented to the emergency department with peak flow <50% of predicted. Patients were randomized into two groups. Over the course of 4 hours, one group received 1440 mcg inhaled ciclesonide plus hydrocortisone-identical placebo (ciclesonide + placebo group), while the other received 500 mg intravenous hydrocortisone plus ciclesonide-identical placebo (hydrocortisone + placebo group). Both groups received short-acting bronchodilators (fenoterol hydrobromide and ipratropium bromide) as recommended by GINA. The research protocol included spirometry, rigorous and frequent clinical evaluation (dyspnea, accessory muscle use, wheezing, respiratory effort), and vital signs and ECG monitoring. Data were obtained at baseline, 30, 60, 90, 120, 180, and 240 minutes. We compared data from baseline to hour 4 between and within groups. Results: Overall, 31 patients received ciclesonide + placebo and 27 received hydrocortisone + placebo. Inhaled ciclesonide was as effective as intravenous hydrocortisone in improving clinical parameters (Borg-scored dyspnea, p=0.95; sternocleidomastoid muscle use, p=0.55; wheezing, p=0.55; respiratory effort, p=0.95) and spirometric parameters (forced vital capacity, p=0.50; forced expiratory volume in the first second, p=0.83; peak expiratory flow, p=0.51).Conclusions: Inhaled ciclesonide was non-inferior to systemic hydrocortisone for management of acute asthma exacerbations, improving both clinical and spirometric parameters.Trial registration: RBR-6XWC26 - Registro Brasileiro de Ensaios Clínicos (http://www.ensaiosclinicos.gov.br/rg/RBR-6xwc26/). Date of registration: 05/01/2016 'retrospectively registered'.
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