The Similarities and Differences of Biological Markers in Bipolar Disorders and Paranoid Schizophrenia

尿β -苯乙胺（PEA）是情感性障碍和偏执型精神分裂症的生物学标志物之一，在快速循环双相情感障碍中进行了检测。在躁狂转变为抑郁之前发现尿PEA增加。这一发现表明PEA在快速循环的转换机制中起着生物触发器的作用，特别是在从躁狂到抑郁的转换中。其次，我们研究了PEA在精神分裂症中的作用。精神分裂症分为偏执型和非偏执型两种。尿PEA排泄增加仅在偏执型精神分裂症中发现。发现血小板单胺氧化酶（MAO）活性与尿PEA排泄之间的关系。这些结果表明PEA在双相情感障碍和精神分裂症中起着不同的作用。我们之前报道抑郁症患者丙咪嗪的平均最大结合位点（Bmax）明显低于健康对照组。重度抑郁症患者Bmax值与17项汉密尔顿抑郁量表总分呈显著负相关，双相情感障碍患者Bmax值与总分呈显著负相关。在这项研究中，我们研究了血小板帕罗西汀在双相情感障碍中的结合。但与健康对照组相比，帕罗西汀结合Bmax没有显著降低。讨论了内源性抑制剂作用于丙咪嗪结合位点的假设。然后，我们研究了对照组和抑郁症患者，以确定内源性抑制剂的活性是否作用于丙咪嗪结合。对照组和抑郁症患者血清对丙咪嗪和帕罗西汀的抑制活性相似。

Urinary beta-phenylethylamine ( PEA ), one of biological markers in both affective disorder and paranoid schizophrenia, was examined in rapid cycler bipolar disorder. Increase in urinary PEA was found preceding the switch from mania to depression. This finding suggests that PEA plays the role of a biological trigger in the switch mechanism of a rapid cycler, especially in the switch from mania to depression. Secondary, we studied the role of PEA in schizophrenia. Schizophrenia was divided into two types : paranoid and non-paranoid. Increased urinary PEA excretion was found only in paranoid schizophrenia. A relationship between platelet monoamine oxidase (MAO) activity and urinary PEA excretion was found. These results suggest that PEA plays different roles in bipolar disorder and schizophrenia.We previously reported the mean maximum number of binding sites (Bmax) of imipramine in depressed patients was significantly lower than that in healthy controls. A significant negative correlation was found between the Bmax values and total scores of the 17-item Hamilton depression rating scale in major depression, but not in bipolar disorder. In this study, we investigated platelet paroxetine binding in bipolar disorder. But, the Bmax of paroxetine binding was not significantly decreased compared to that of healthy controls. The hypothesis that endogenous inhibitors acting on imipramine binding sites was discussed. Then, we studied controls and depressed patients to conform whether the activity of endogenous inhibitors acting on imipramine binding. But inhibition activities of the imipramine and paroxetine by serum from controls and depressed patients were similar.