Mondelli Valeria, Dazzan Paola, Gabilondo Andrea, Tournikioti Kalliopi, Walshe Muriel, Marshall Nicolette, Schulze Katja K, Murray Robin M, McDonald Colm, Pariante Carmine M
Division of Psychological Medicine, Institute of Psychiatry, King's College London, London, UK.
Psychoneuroendocrinology. 2008 Aug;33(7):1004-12. doi: 10.1016/j.psyneuen.2008.05.010. Epub 2008 Jul 21.
Hypothalamic-pituitary-adrenal (HPA) axis hyperactivity has been demonstrated in both schizophrenia and bipolar disorder, but the mechanisms underlying this abnormality are still unclear. Enlarged pituitary volume has been recently reported in patients with first episode psychosis and been interpreted as a consequence of an increased activation of the HPA axis. The aim of this study was to assess the contribution of familial liability to pituitary volume in schizophrenia and bipolar disorder. Pituitary volume may be an indirect measure of HPA axis activity.
MRI brain scans and measurements of pituitary volumes were obtained for 183 subjects: 26 patients with established schizophrenia or schizoaffective disorder, 44 of their unaffected first-degree relatives (22 familial schizophrenia, 22 non-familial schizophrenia), 29 patients with established bipolar disorder, 38 of their unaffected first-degree relatives, and 46 healthy comparison subjects.
We found a significantly larger pituitary volume (effect size=0.7) in unaffected relatives of patients with schizophrenia compared with controls (p=0.002); the pituitary was even larger in relatives of patients with familial schizophrenia (effect size=0.8, p=0.005). We did not find a significant difference in pituitary volume when comparing the relatives of bipolar patients with controls. Among patients, those with schizophrenia who were receiving prolactin-elevating antipsychotics had an increased pituitary volume compared with controls (effect size=1.0, p=0.006).
These results suggest that the larger pituitary volume previously reported in first episode schizophrenia could be partly due to a genetic susceptibility to over-activate the HPA axis.
下丘脑 - 垂体 - 肾上腺（HPA）轴功能亢进在精神分裂症和双相情感障碍中均有体现，但这种异常背后的机制仍不清楚。最近有报道称首发精神病患者的垂体体积增大，并被解释为HPA轴激活增加的结果。本研究的目的是评估家族易感性对精神分裂症和双相情感障碍患者垂体体积的影响。垂体体积可能是HPA轴活动的间接指标。
对183名受试者进行了脑部MRI扫描并测量了垂体体积：26名确诊为精神分裂症或分裂情感性障碍的患者，其44名未受影响的一级亲属（22名家族性精神分裂症患者亲属，22名非家族性精神分裂症患者亲属），29名确诊为双相情感障碍的患者，其38名未受影响的一级亲属，以及46名健康对照者。
我们发现，与对照组相比，精神分裂症患者未受影响的亲属垂体体积显著更大（效应量 = 0.7，p = 0.002）；家族性精神分裂症患者亲属的垂体体积更大（效应量 = 0.8，p = 0.005）。将双相情感障碍患者的亲属与对照组进行比较时，我们未发现垂体体积有显著差异。在患者中，正在接受可升高催乳素的抗精神病药物治疗的精神分裂症患者与对照组相比，垂体体积增大（效应量 = 1.0，p = 0.006）。
这些结果表明，先前报道的首发精神分裂症患者垂体体积较大可能部分归因于过度激活HPA轴的遗传易感性。
