Anatomía patológica y correlaciones anatomoclínicas de la acromegalia / Pathology and anatomoclinical correlations of acromegaly

Aproximadamente el 95% de los casos de exceso de secreción de hormona de crecimiento es debido a la presencia de un adenoma hipofisario secretor de hormona de crecimiento. Gracias a los hallazgos histológicos y a las técnicas de inmunohistoquímica y microscopia electrónica se han identificado 8 diferentes lesiones hipofisarias relacionadas con la acromegalia. En relación con su estructura, la inmensa mayoría de los adenomas se engloba en 2 tipos celulares relacionados, los de células densamente y escasamente granuladas. Hay controversia acerca de la implicación pronóstica y del abordaje terapéutico de los pacientes con diferentes tipos de afección histológica. En diversos estudios se han intentado relacionar estos diferentes patrones --distribución de filamentos de queratina, presencian de células foliculares, mutaciones relacionadas con cambios ultraestructurales--, con la actividad clínica y la evolución tumoral, con resultados variables. A continuación exponemos una revisión de los conocimientos disponibles hasta el momento acerca de las correlaciones entre histología, clínica y respuesta terapéutica de los adenomas hipofisarios secretores de hormona de crecimiento (AU)

More than 95% of patients with acromegaly harbor a GH-secreting pituitary adenoma. The introduction of sophisticated morphologic procedures, such as hystopathology, immunocytochemistry and electron microscopy has shed light on structural characteristics of pituitary adenomas. As a result, the pituitary lesions of patients with acromegaly are now divided into eight different types. Among them, densely granulated somatotroph adenomas and sparsely granulated somatotroph adenomas are the most frecuent and represent two morphologically distinct types of GH producing adenoma. However, the correlations between clinical characteristics, treatment and prognosis of these different morphologically variants are still unclear. Several studies have correlated distinct profiles as cytoqueratin distribution, folicular cells and mutations related with ultraestructural changes, acromegaly activity and tumor progression. Data were controversial. This review deals with the morphologic features and their correlations with hystology, clinical characteristics and terapeutic response of growth hormone-producing tumors of the human pituitary (AU)

The incidence and pathogenesis of hyperlipidaemia in 16 consecutive acromegalic patients.

Serum lipids were analyzed in 16 patients with active acromegaly. Of these 62.5% had hyperlipidaemia defined as exceeding and 90% fiducial limits of normal controls. The mean serum cholesterol (5.50 mmol/l) and triglyceride (4.09 mmol/l) levels of the patients were significantly higher than those of age-matched normal controls. Type V hyperlipoproteinaemia was observed in two cases and type III hyperlipoproteinaemia in one. There was no difference in the incidence of diabetes between the normolipidaemic (n = 6) and hyperlipidaemic (n = 10) groups. Serum levels of growth hormone in hypercholestelaemic patients (n = 3) were significantly higher than those of normolipidaemic patients and combined hyperlipidaemic patients (n = 5 tended to have higher levels of growth hormone than normolipidaemic patients. In cases developing type III or type V hyperlipoproteinaemia, the activity of hepatic triglyceride lipase of lipoprotien lipase was decreased, but in increased when serum GH levels fell after therapy for acromegaly. It is suggested that 1) growth hormone may play some role on the pathogenesis of hyperlipidaemia associated with acromegaly, and 2) growth hormone has an inhibitory effect on H-TGL and LPL, and so hyperlipoproteinaemia in some cases of acromegaly might be caused by low H-TGL or LPL activity resulting from high growth hormone levels.