RESUMEN
Leprosy is an infectious disease caused by Mycobacterium leprae that affects the skin and nerves. The nerve damage in leprosy may be related to alterations in transcriptional factors, such as Krox-20, Oct-6, Sox-10. Thirty skin biopsies in leprosy patients and 15 non-leprosy skin biopsies were evaluated using RT-qPCR to assess Krox-20, Oct-6, and Sox-10 and these data was related with S-100 immunohistochemistry. Changes in gene expression were observed in the skin and dermal nerves of leprosy patients in Oct-6 and Sox-10. When comparing Oct-6 with S-100 IHC as diagnostic tests for leprosy, Oct-6 showed a sensitivity of 73.3%, and specificity of 100%, while S-100 IHC showed a sensitivity of 96.6% and specificity of 100%. Our data suggest Oct-6 could be an auxiliary biomarker specific to detecting changes in dermal nerves in leprosy and thus useful to health workers and pathologists with no expertise to observe nerve injuries in leprosy.
Asunto(s)
Lepra/diagnóstico , Factor 6 de Transcripción de Unión a Octámeros/genética , Adulto , Anciano , Anticuerpos Antibacterianos/sangre , Carga Bacteriana , Biomarcadores/metabolismo , Biopsia , Estudios Transversales , Proteína 2 de la Respuesta de Crecimiento Precoz/genética , Femenino , Humanos , Inmunoglobulina G/sangre , Inmunohistoquímica , Lepra/genética , Lepra/metabolismo , Lepra/patología , Masculino , Persona de Mediana Edad , Mycobacterium leprae/inmunología , Proteínas S100/metabolismo , Factores de Transcripción SOXE/genética , Sensibilidad y Especificidad , Piel/inervación , Piel/metabolismo , Piel/patología , Transcripción GenéticaRESUMEN
Resumen: la medición del cortisol total en sangre ha sido parte fundamental en el estudio del eje hipotálamo-hipófisis-adrenal y de sus alteraciones, tales como el síndrome de Cushing y la insuficiencia adrenal. El cortisol circula en plasma en su mayoría unido a proteínas, pero su fracción libre es la biológicamente activa y se puede medir en sangre, orina y saliva. La secreción de cortisol no es homogéneadurante el día, por el contrario, está regida por un ritmo circadiano, que a su vez, se puede ver afectado por diferentes estresores físicos y psicológicos. Por esta razón, se cuenta con pruebas como el cortisol en orina de 24 horas que permiteevaluar la producción diaria de cortisol. También es posible realizar pruebas funcionales como la supresión de cortisol con dexametasona para el estudio del síndrome de Cushing y la prueba de estímulo con la hormona adrenocorticotropa(ACTH) como parte del estudio de la insuficiencia adrenal. Esta revisión tiene como objetivo realizar una puesta al día sobre los diferentes métodos para medir el cortisol como parte del estudio del eje hipotálamo-hipófisis-adrenal, haciendo énfasis en su utilidad para el diagnóstico de condiciones patológicas endocrinas.
Abstract: Total cortisol measurement in blood has been a fundamental part in the study of the hypothalamic-pituitary-adrenal axis, and of its disorders, such as Cushing syndrome and adrenal insufficiency. Cortisol circulates in the plasma mainly bound to proteins, but the free fraction is the biologically activeone, which can be measure in blood, urine, and saliva. Cortisol secretion is not homogeneous throughout the day; instead, secretion is governed by a circadian rhythm that also can be affected by different physical and psychologicalstressors. For this reason, other tests such as 24-hour urinary cortisol are available, which evaluates the daily production of cortisol. Functional tests such as cortisol suppression with dexamethasone for the Cushings syndrome study and the ACTH stimulation test as part of adrenal insufficiency study can also be performed. This review aims to perform an update on the different cortisol measuring methods as part of the study of hypothalamic pituitary adrenal axis, emphasizing in their use to endocrine diseases diagnosis.
Asunto(s)
Humanos , Insuficiencia Suprarrenal , Síndrome de Cushing , Hidrocortisona , Saliva , Suero , Transcortina , OrinaRESUMEN
Vitronectin, a multifunctional glycoprotein, is involved in coagulation, inhibition of the formation of the membrane attack complex (MAC), cell adhesion and migration, wound healing, and tissue remodeling. The primary cellular source of vitronectin is hepatocytes; it is not known whether resident cells of airways produce vitronectin, even though the glycoprotein has been found in exhaled breath condensate and bronchoalveolar lavage from healthy subjects and patients with interstitial lung disease. It is also not known whether vitronectin expression is altered in subjects with asthma and COPD. In this study, bronchial tissue from 7 asthmatic, 10 COPD and 14 control subjects was obtained at autopsy and analyzed by immunohistochemistry to determine the percent area of submucosal glands occupied by vitronectin. In a separate set of experiments, quantitative colocalization analysis was performed on tracheobronchial tissue sections obtained from donor lungs (6 asthmatics, 4 COPD and 7 controls). Vitronectin RNA and protein expressions in bronchial surface epithelium were examined in 12 subjects who undertook diagnostic bronchoscopy. Vitronectin was found in the tracheobronchial epithelium from asthmatic, COPD, and control subjects, although its expression was significantly lower in the asthmatic group. Colocalization analysis of 3D confocal images indicates that vitronectin is expressed in the glandular serous epithelial cells and in respiratory surface epithelial cells other than goblet cells. Expression of the 65-kDa vitronectin isoform was lower in bronchial surface epithelium from the diseased subjects. The cause for the decreased vitronectin expression in asthma is not clear, however, the reduced concentration of vitronectin in the epithelial/submucosal layer of airways may be linked to airway remodeling.