miércoles, 26 de julio de 2017

Síndrome de Cushing / Cushing syndrome



Julio 24, 2017. No. 2759






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Síndrome de Cushing
Medicina y Laboratario, 2009
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MANEJO DE PACIENTES CON SÍNDROME DE CUSHING.
Marcos M. Lima-Martínez, José Zerpa, Yorly Guerrero, Jenny Rivera, Marly Vielma
Rev Venez Endocrinol Metab 2013; 11(3):147-156
RESUMEN
El exceso crónico de glucocorticoides se acompaña de una amplia variedad de signos y síntomas conocidos como síndrome de Cushing. Esta condición, ocurre con mayor frecuencia por causas iatrogénicas cuando los glucocorticoides son usados como terapia antiinflamatoria por tiempo prolongado. El mecanismo patogénico del Cushing endógeno puede dividirse en dependiente o independiente de ACTH. A pesar de los avances en el diagnóstico y tratamiento de esta patología, el síndrome de Cushing continúa siendo un reto para el clínico. En este artículo, basado en niveles de evidencia científica y en la experiencia clínica de la Unidad de Endocrinología del IAHULA, se presenta el protocolo de manejo del Síndrome de Cushing, el cual incluye criterios diagnósticos, manejo clínico y tratamiento de esta condición. Palabras Clave: Síndrome de Cushing, cortisol, ACTH, hipófisis
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Diferenciación del hipercortisolismo patológico / neoplásico (síndrome de Cushing) del hipercortisolismo fisiológico / no neoplásico (antes conocido como síndrome de pseudo-Cushing).
DIAGNOSIS OF ENDOCRINE DISEASE: Differentiation of pathologic/neoplastic hypercortisolism (Cushing's syndrome) from physiologic/non-neoplastic hypercortisolism (formerly known as pseudo-Cushing's syndrome).
Eur J Endocrinol. 2017 May;176(5):R205-R216. doi: 10.1530/EJE-16-0946. Epub 2017 Feb 8.
Abstract
Endogenous hypercortisolism (Cushing's syndrome) usually implies the presence of a pathologic condition caused by either an ACTH-secreting neoplasm or autonomous cortisol secretion from a benign or malignant adrenal neoplasm. However, sustained or intermittent hypercortisolism may also accompany many medical disorders that stimulate physiologic/non-neoplastic activation of the HPA axis (formerly known as pseudo-Cushing's syndrome); these two entities may share indistinguishable clinical and biochemical features. A thorough history and physical examination is often the best (and sometimes only) way to exclude pathologic/neoplastic hypercortisolism. The presence of alcoholism, renal failure, poorly controlled diabetes and severe neuropsychiatric disorders should always raise suspicion that the presence of hypercortisolism may be related to physiologic/non-neoplastic Cushing's syndrome. As late-night salivary cortisol and low-dose dexamethasone suppression have good sensitivity and negative predictive value, normal studies exclude Cushing's syndrome of any form. However, these tests have imperfect specificity and additional testing over time with clinical follow-up is often needed. When there is persistent diagnostic uncertainty, secondary tests such as the DDAVP stimulation test and the dexamethasone-CRH test may provide evidence for the presence or absence of an ACTH-secreting tumor. This review will define and characterize the numerous causes of physiologic/non-neoplastic hypercortisolism and provide a rational clinical and biochemical approach to distinguish it from pathologic/neoplastic hypercortisolism (true Cushing's syndrome).
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La mejor práctica actual en el manejo de pacientes después de la cirugía hipofisaria.
Current best practice in the management of patients after pituitary surgery.
Ther Adv Endocrinol Metab. 2017 Mar;8(3):33-48. doi: 10.1177/2042018816687240. Epub 2017 Mar 1.
Abstract
Sellar and parasellar masses are a common finding, and most of them are treated surgically via transsphenoidal approach. This type of surgery has revolutionized the approach to several hypothalamic-pituitary diseases and is usually effective, and well-tolerated by the patient. However, given the complex anatomy and high density of glandular, neurological and vascular structures in a confined space, transsphenoidal surgery harbors a substantial risk of complications. Hypopituitarism is one of the most frequent sequelae, with central adrenal insufficiency being the deficit that requires a timely diagnosis and treatment. The perioperative management of AI is influenced by the preoperative status of the hypothalamic-pituitary-adrenal axis. Disorders of water metabolism are another common complication, and they can span from diabetes insipidus, to the syndrome of inappropriate antidiuretic hormone secretion, up to the rare cerebral salt-wasting syndrome. These abnormalities are often transient, but require careful monitoring and management in order to avoid abrupt variations of blood sodium levels. Cerebrospinal fluid leaks, damage to neurological structures such as the optic chiasm, and vascular complications can worsen the postoperative course after transsphenoidal surgery as well. Finally, long-term follow up after surgery varies depending on the underlying pathology, and is most challenging in patients with acromegaly and Cushing disease, in whom failure of primary pituitary surgery is a major concern. When these pituitary functioning adenomas persist or relapse after neurosurgery other treatment options are considered, including repeated surgery, radiotherapy, and medical therapy.
KEYWORDS: Cushing disease; diabetes insipidus; hypopituitarism; hypothalamic hormones; hypothalamic neoplasms; hypothalamo-hypophyseal system; pituitary hormones; pituitary neoplasms

XIV Congreso Virtual Mexicano de Anestesiología 2017
Octubre 1-Diciembre 31, 2017
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