Academic Unit of Diabetes and Endocrinology, University of Sheffield, Sheffield, UK.
Neuroendocrinology. 2010;92 Suppl 1:82-5. doi: 10.1159/000314316. Epub 2010 Sep 10.
Active Cushing's syndrome is associated with insulin resistance induced by the high and prolonged circulating level of glucocorticoids. In endogenous Cushing's syndrome the overall incidence of diabetes mellitus and insulin resistance is very likely to be under-reported as not all patients are actively investigated with glucose tolerance tests. Whilst it is common clinical experience that management of diabetes mellitus is necessary in patients with Cushing's syndrome there is a dearth of literature-based evidence to support which regimes are the most effective. Therefore, a pragmatic approach is necessary on an individualized patient basis, whereby patients are stratified according to the severity of their impaired glucose homeostasis. The most effective means of control of diabetes mellitus in a patient with active Cushing's syndrome is to lower the levels of circulating cortisol. This may initially be achieved by using adrenal steroidogenesis blockade with drugs including metyrapone, ketaconazole, or, on occasion, mitotane. The rapid action of metyrapone is particularly suitable in this circumstance. Despite this, diabetes-specific therapy is often necessary and metformin and PPAR-γ agonists may be of use, but in the acute setting insulin therapy is frequently needed. Definitive management directed against source driving Cushing's syndrome is often highly effective at either reducing the severity of diabetes, or allowing its complete resolution. Patients experiencing diabetes mellitus in the context of exogenously administered glucocorticoids may well require insulin therapy for the period that the high levels of steroids are being administered. Despite resolution of Cushing's syndrome after definitive treatment patients may continue to exhibit insulin resistance. This and other cardiovascular risk factors require ongoing and long-term attention.
活性库欣综合征与糖皮质激素的高浓度和长时间循环有关，导致胰岛素抵抗。在内源性库欣综合征中，糖尿病和胰岛素抵抗的总体发生率很可能被低估，因为并非所有患者都接受葡萄糖耐量试验进行积极检查。虽然在库欣综合征患者中，糖尿病的管理是必要的，这是常见的临床经验，但缺乏基于文献的证据来支持哪种治疗方案最有效。因此，有必要根据个体患者的情况采取务实的方法，根据患者糖稳态受损的严重程度对患者进行分层。控制活性库欣综合征患者糖尿病的最有效方法是降低循环皮质醇水平。这最初可以通过使用包括米托坦、酮康唑或偶尔使用美替拉酮在内的药物来阻断肾上腺类固醇生成来实现。美替拉酮的快速作用在这种情况下特别适用。尽管如此，通常仍需要糖尿病特异性治疗，二甲双胍和过氧化物酶体增殖物激活受体-γ激动剂可能有用，但在急性情况下，胰岛素治疗通常是必需的。针对库欣综合征病因的明确治疗通常在降低糖尿病严重程度或使其完全缓解方面非常有效。在接受外源性糖皮质激素治疗的情况下出现糖尿病的患者，在高剂量类固醇治疗期间可能需要胰岛素治疗。尽管在明确治疗后库欣综合征得到解决，但患者可能仍然存在胰岛素抵抗。这种情况和其他心血管危险因素需要持续和长期关注。
