Agostinis C., Batistelli S., Suárez Ayala S., López J., Pietrangelo C.
Las glándulas paratiroides se localizan en el cuello, en la cara posterior de la glándula tiroides. Tienen como función secretar PTH, la cual está regulada por la concentración extracelular de calcio. Se define como hiperparatiroidismo a la producción excesiva de PTH por las glándulas paratiroideas, siendo el 85 % aproximadamente de los casos producto de un adenoma; un 12 % debido a hiperplasia y menos del 1 % por carcinomas. El hiperparatiroidismo primario ectópico se presenta en el 10 % de los pacientes, de los cuales del 1 al 2 % corresponde a la localización mediastinal(1). Presentamos una paciente de 38 años, internada en nuestra institución por hipercalcemia sintomática, comprobándose niveles plasmáticos elevados de PTH. Se le realizó una gammagrafía con tecnecio 99 MIBI que evidenció una imagen hipercaptante a nivel de mediastino anterior. Fue intervenida quirúrgicamente, obteniendo como resultado de la anatomía patológica un adenoma paratiroideo.
The imbalance between energy intake and energy expenditure observed in malnourished or frankly undernourished women with functional hypothalamic amenorrhea triggers an increased activity of hypothalamic hormones and peripheral neuropeptides, at facilitating the availability of endogenous energy metabolites. Osteoporosis, immune depression, hypothalamic amenorrhea and increased cardiovascular risk can be interpreted as secondary effects of the homeosthatic adaptation reactions by central and peripheral hormones. The extent of somatotropic axis deficiency, hypoestrogenism and time of evolution condition the nature of coronary circulation alterations and myocardial structural and functional involvement. An unfavorable lipid profile (normal LDL/ low HDL and hypertriglyceridemia), the rise in peripheral markers of fibrinolytic and inflammatory processes, results in a proatherosclerotic and prothrombotic environment. A premature presence of atheroma plaques in carotid walls, intima media thickness and subsequent artery stiffness may be frequently observed. This makes blood flow difficult, leading to coronary ischemia and predisposition to stroke. Echocardiographic studies show a decrease in the muscle mass of the left ventricle walls and the interventricular septum. These structural changes correlate with a volume reduction in the post-stress systolic ejection fraction, which subsequently occurs at rest at rest.The reduction in diastolic filling volume can be observed if the course of the disease is relatively long, showing, a serious compromise of cardiac performance. Even if the incidence of supraventricular extrasystoles, atrial fibrillation and bradycardia is not statistically significant, the presence of such arrhythmias increases CVR and the possibility of potential sudden death.