Bolli G, De Feo P, Massi-Benedetti M, Compagnucci P, Cartechini M G, Santeusanio F, Brunetti P
J Clin Endocrinol Metab. 1982 Feb;54(2):447-9. doi: 10.1210/jcem-54-2-447.
In a gastrectomized woman with an adrenal pheochromocytoma we observed hypertensive crisis in association with postprandial hypoglycemic episodes. To assess whether hypoglycemia could be responsible for the hypertensive crises, we measured circulating catecholamines and glucagon during an insulin-induced blood glucose decrement carried out by an artificial endocrine pancreas. When the blood glucose level reached 36 mg/dl, a severe hypertensive crisis occurred. At this time, circulating catecholamines increased 2-fold (norepinephrine, from 2200 to 3568 pg/ml; epinephrine, from 950 to 1750 pg/ml), while no changes in glucagon were observed. Our observation suggests that in patients with pheochromocytoma, hypoglycemia may trigger a marked release of catecholamines independent of glucagon secretion. This response probably is mediated by activation of the sympathetic nervous system. Our results also suggest that the pancreatic A-cell response to blood glucose decrement is totally suppressed in patients with pheochromocytoma by the chronically high levels of circulating catecholamines. Thus, hypoglycemia may be added to the list of other well known factors which may provoke hypertensive emergencies in patients with pheochromocytoma.
在一名患有肾上腺嗜铬细胞瘤的胃切除女性患者中，我们观察到高血压危象与餐后低血糖发作相关。为了评估低血糖是否可能是高血压危象的原因，我们在人工内分泌胰腺诱导的胰岛素性血糖降低过程中测量了循环儿茶酚胺和胰高血糖素。当血糖水平降至36mg/dl时，发生了严重的高血压危象。此时，循环儿茶酚胺增加了2倍（去甲肾上腺素从2200pg/ml增至3568pg/ml；肾上腺素从950pg/ml增至1750pg/ml），而胰高血糖素未观察到变化。我们的观察表明，在嗜铬细胞瘤患者中，低血糖可能引发儿茶酚胺的显著释放，且与胰高血糖素分泌无关。这种反应可能是由交感神经系统的激活介导的。我们的结果还表明，嗜铬细胞瘤患者中，由于循环儿茶酚胺长期处于高水平，胰腺A细胞对血糖降低的反应被完全抑制。因此，低血糖可能被添加到其他已知的、可能诱发嗜铬细胞瘤患者高血压急症的因素列表中。
