Komatani A, Sugai Y, Watanabe N, Yamaguchi K, Kawakatsu S
Department of Radiology, Yamagata University School of Medicine.
Kaku Igaku. 1998 Oct;35(8):715-20.
The discrepancy between 99mTc-hexamethyl-propyleneamine oxime (HMPAO) and 99mTc-ethyl cysteinate dimer (ECD) in Alzheimer's disease (AD) was investigated and compared with in cerebral ischemic disease (CID). The subjects were fourteen AD and thirty-one CID patients with clinically reasonable rCBF reduced lesion on 133Xe SPECT. The subjects did not include the cases of acute and subacute CID. These SPECT were performed within two weeks by ring-type dynamic SPECT (HEADTOME, Shimadzu, Japan). In the CID group, both of HMPAO and ECD SPECT could hardly detect the mildly reduced rCBF lesion on 133Xe SPECT but normal on X-CT. In the case of AD group, the rCBF-reduced lesion on 133Xe SPECT could be detected well by ECD SPECT, but the HMPAO hardly detected the reduced lesion. This discrepancy between HMPAO and ECD may be due to the difference of the retention mechanism. In the case of AD, the injury of esterase activity that participates with the ECD retention may be more notable than that of glutathione activity for the HMPAO retention. These results suggest suggest that the reduction of ECD or HMPAO density depends directly on the insufficiency of retention mechanism rather the than rCBF reduction. And the insufficiency of this retention mechanism depends on also type of the disease i.e. AD or CID.
研究了99m锝-六甲基丙烯胺肟（HMPAO）和99m锝-乙基半胱氨酸二聚体（ECD）在阿尔茨海默病（AD）中的差异，并与脑缺血性疾病（CID）进行比较。研究对象为14例AD患者和31例CID患者，这些患者在133氙单光子发射计算机断层扫描（SPECT）上有临床上合理的局部脑血流（rCBF）降低病变。研究对象不包括急性和亚急性CID病例。这些SPECT检查在两周内通过环形动态SPECT（HEADTOME，日本岛津公司）完成。在CID组中，HMPAO和ECD SPECT均难以检测到133氙SPECT上轻度降低的rCBF病变，但X线计算机断层扫描（X-CT）显示正常。在AD组中，ECD SPECT能很好地检测到133氙SPECT上rCBF降低的病变，但HMPAO几乎检测不到降低的病变。HMPAO和ECD之间的这种差异可能是由于滞留机制的不同。在AD病例中，参与ECD滞留的酯酶活性损伤可能比参与HMPAO滞留的谷胱甘肽活性损伤更明显。这些结果表明，ECD或HMPAO密度的降低直接取决于滞留机制的不足，而不是rCBF的降低。而且这种滞留机制的不足也取决于疾病类型，即AD或CID。
