JCEM：肾上腺偶发瘤患者内脏脂肪增加

内脏脂肪是一个重要的心血管危险因素。由于在肾上腺偶发瘤患者，内脏脂肪没有被系统的测量，为了验证内脏脂肪体积是否与地塞米松抑制后的血清皮质醇水平的切点有关，来自英国谢菲尔德大学医学与生物科学院的John Newell Price教授及其团队进行了一项研究，该研究发现在伴有肾上腺偶发瘤、且地塞米松抑制后血清皮质醇大于1.8ug/dl的患者，内脏脂肪增加。该研究结果在线发表在2013年4月30日的美国《临床内分泌代谢杂志》（The journal of clinical endocrinology & metabolism）上。
该研究是一项回顾性横断面研究，在谢菲尔德大学教学医院内分泌研究中心进行。诊断伴有肾上腺偶发瘤的73例女性患者和52例男性患者，以及9例显性库欣综合症患者参与这个研究。测量地塞米松抑制后的血清皮质醇水平和内脏脂肪比率：通过CT测量内脏脂肪–皮下脂肪（V:S）和内脏脂肪–脂肪总体积（V：TV）。
该研究结果表明，68例患者在地塞米松抑制后血清皮质醇高于1.8ug/dl（50nmol/l）患者与那些血清皮质醇低于1.8ug/dl患者相比，显示平均V:S和V:TV脂肪比率显著增加：女性，lnV:S,-0.45 vs -0.69[平均差0.24（95%可信区间[CI]0.08–0.41）；P=0.004]和V:TV，0.39 vs 0.34[平均差0.05（95%CI 0.02–0.09）；P=0.004]；男性lnV:S,0.64 vs 0.29[平均差0.35（95%CI 0.08–0.63）；P=0.01]和V:TV，0.65 vs 0.57[平均差0.08（95%CI 0.02–0.14）；P=0.02]。通过单因素方差分析（ANVOA）和事后分析（Fisher最小显著性差异法），在地塞米松抑制血清皮质醇分组[1.8–2.9ug/dl(50–82nmol/l)，3.0–5.0ug/dl(83–137nmol/l，＞5.0ug/dl(＞138nmol/l)和库欣综合征]之间的脂肪比率没有差异（平均V:TV分别为：0.38,0.40,0.40,0.41），但他们都与低于1.8ug/dl组患者（V:TV：0.34，P=0.03）有显著差异。
该研究发现，在伴有肾上腺偶发瘤、且地塞米松抑制后血清皮质醇大于1.8ug/dl的患者，内脏脂肪增加，并与在伴有显性库欣综合征患者发现结果相似。 
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• NEJM：晚期肾上腺癌联合化疗
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Visceral Fat Accumulation and Postdexamethasone Serum Cortisol Levels in Patients With Adrenal Incidentaloma.
Objective
Visceral fat is a significant cardiovascular risk factor. Because visceral fat has not been measured systematically in patients with adrenal incidentalomas, we have tested the hypothesis that visceral fat volume may be associated with cutoffs for serum cortisol levels post dexamethasone.
Design
This was a retrospective, cross-sectional study.Setting:The study was conducted at the Endocrine Investigation Unit, University Teaching Hospital.Participants:Seventy-three women and 52 men diagnosed with adrenal incidentalomas and 9 patients with overt Cushing's syndrome participated in this study.
Main Outcome Measures
The following was measured for serum cortisol level after dexamethasone suppression and visceral fat ratios: visceral-subcutaneous (V:S) and visceral-total volume (V:TV) measured by computed tomography.
Results
Sixty-eight patients with a postdexamethasone serum cortisol greater than 1.8 μg/dL (50 nmol/L) showed a significantly higher mean V:S and V:TV fat ratio compared with those whose serum cortisol was less than 1.8 μg/dL: women, lnV:S, -0.45 vs -0.69 [mean difference 0.24 (95% confidence interval [CI] 0.08-0.41); P = .004] and V:TV, 0.39 vs 0.34 [mean difference 0.05 (95% CI 0.02-0.09); P = .004]; men, lnV:S, 0.64 vs 0.29 [mean difference 0.35 95% CI 0.08-0.63); P = .01] and V:TV, 0.65 vs 0.57 [mean difference 0.08 (95% CI 0.02-0.14); P = .02]. By ANOVA and post hoc analysis (Fisher's least significant differences), there was no difference in fat ratios between the postdexamethasone serum cortisol groups [1.8-2.9 μg/dL (50-82 nmol/L), 3.0-5.0 μg/dL (83-137 nmol/L), > 5.0 μg/dL (>138 nmol/L) and Cushing's syndrome (mean V:TV: 0.38, 0.40, 0.40, 0.41, respectively)], but they all differed significantly from the less than the 1.8-μg/dL group (V:TV: 0.34, P = .03).
Conclusion
Visceral fat is increased in patients with adrenal incidentalomas and a postdexamethasone serum cortisol of greater than 1.8 μg/dL and is similar to that found in patients with overt Cushing's syndrome.