[Immunohistochemistry for pituitary hormones and Ki-67 in growth hormone producing pituitary adenomas]. / Evaluación por inmunohistoquímica de la expresión de hormonas hipofisiarias y del marcador de proliferación celular Ki-67 en tejido de adenomas causantes de acromegalia.

BACKGROUND: Growth hormone (GH) producing adenomas, frequently express several hormones. This condition could confer them a higher proliferative capacity. Ki-67 is a nuclear protein antigen that is a marker for proliferative activity. AIM: To measure the immunohistochemical hormone expression in pituitary adenomas, excised from patients with acromegaly. To determine if the plurihormonal condition of these adenomas is associated with a higher proliferative capacity, assessed through the expression of Ki-67. MATERIAL AND METHODS: Forty one paraffin embedded surgical samples of pituitary adenomas from patients with acromegalia were studied. Immunohistochemistry for GH, prolactin (PRL), follicle stimulating hormone (FSH), luteinizing hormone (LH), thyroid stimulating hormone (TSH), adrenocorticotropin (ACTH) and for the expression of Ki-67 was carried out. RESULTS: All samples were positive for GH. Twenty seven had positive staining for PRL, 12 had positive staining for glycoproteic hormones and 11 for PRL and one or more glycoproteic hormones. Mean staining for Ki-67 was Z.6+/-3.3%. There were no differences in the expression of this marker between mono or plurihormonal tumors. The expression was neither associated with extrasellar extension. CONCLUSIONS: Half of GH producing pituitary adenomas are plurihormonal. There are no differences in the expression of Ki-67 between mono and plurihormonal adenomas.

Evaluación por inmunohistoquímica de la expresión de hormonas hipofisiarias y del marcador de proliferación celular Ki-67 en tejido de adenomas causantes de acromegalia / Immunohistochemistry for pituitary hormones and Ki-67 in growth hormone producing pituitary adenomas

Background: Growth hormone (GH) producing adenomas, frequently express several hormones. This condition could confer them a higher proliferative capacity. Ki-67 is a nuclear protein antigen that is a marker for proliferative activity. Aim: To measure the immunohistochemical hormone expression in pituitary adenomas, excised from patients with acromegaly. To determine if the pluríhormonal condition of these adenomas is associated with a higher proliferative capacity, assessed through the expression of Ki-67. Material and methods: Forty one paraffin embedded surgical samples of pituitary adenomas from patients with acromegalia were studied. Immunohistochemistry for GH, prolactin (PRL), follicle stimulating hormone (FSH), luteinizing hormone (LH), thyroid stimulating hormone (TSH), adrenocorticotropin (ACTH) and for the expression of Ki-67 was carried out. Results: All samples were positive for GH. Twenty seven had positive staining for PRL, 12 had positive staining for glycoproteic hormones and 11 for PRL and one or more glycoproteic hormones. Mean staining for Ki-67 was Z.6±3.3 percent. There were no differences in the expression of this marker between mono or pluríhormonal tumors. The expression was neither associated with extrasellar extensión. Conclusions: Half of GH producing pituitary adenomas are pluríhormonal. There are no differences in the expression of Ki-67 between mono and plurihormonal adenomas.

Hipertensión arterial de origen endócrino: II Parte. Enfermedades endócrinas sin mecanismo directo de hipertensión / Arterial hypertension of endocrine origin: II Part. Endocrine diseases without direct mechanism of hypertension

Se analiza la frecuencia de hipertensión arterial en diversas afecciones endocrinas tales como acromegalia; hipotiroidismo; hipertiroidismo primario; diabetes mellitus; obesidad y excesos de estrógenos. En cada caso se discuten los posibles mecanismos fisiopatológicos involucrados

Hipertensión arterial de origen endocrino: Parte I. Introducción, enfermedades endocrinas con mecanismo directo de hipertensión / Arterial hypertension of endocrine origin: Part I. Introduction, endocrine diseases with direct mechanism of hypertension

Se analizan los efectos de las hormonas en la regulación de la presión arterial, resaltando que algunas tienden a aumentarlas y otras a disminuirlas. Se separan las hipertensiones endocrinas en que las hormonas juegan un rol directo, produciendo aumento tensional, entre las que destacan afecciones de la corteza y la médula suprarrenal y aquéllas en que el factor hormonal representaría un mecanismo indirecto, o discutible. Entre los hipermineralocorticoidismos, el más relevante es el hiperaldosteronismos primario con sus 3 formas: adenoma, hiperplasia e hiperaldosteronismos suprimible con dexametasona. Se analizan sus síntomas, las etapas del diagnóstico y la terapia de cada caso. Otras formas de hipertensión por mineralocorticoides incluyen algunos hiperaldosteronismos secundarios y los defectos enzimáticos suprarrenales de la 17 hidroxilasa y la 11 hidroxilasa. La hipertensión del síndrome de Cushing se debería a varios mecanismos, que incluyen el efecto mineralocorticoide del cortisol, alteraciones del sistema renina-angiotensina y aumento de la reactividad vascular. En el feocromocitoma resalta la tríada sintomática cefalea, palpitaciones y sudoración. Entre los exámenes de laboratorio la medición de catecolaminas plasmáticas parece ser el índice más sensible, seguido de las metanefrinas, ácido vanilil mandélico y catecolaminas libres urinarias. La preparación preoperatoria reviste especial importancia