Heyderman R S, Klein N J, Shennan G I, Levin M
Infectious Diseases Unit, Hospitals for Sick Children, London.
Arch Dis Child. 1991 Nov;66(11):1296-9. doi: 10.1136/adc.66.11.1296.
A deficiency of prostacyclin (PGI2) production by the vascular endothelium might underline the severe vasoconstriction and intravascular thrombosis that characterise meningococcal shock. The effect on PGI2 synthesis by human umbilical vein endothelial cells (HUVEC) in culture was examined in sera from children with meningococcal shock, healthy adults, and children with other febrile illnesses. In comparison with adult controls, PGI2 synthesis was reduced when HUVEC were incubated with the sera from 10 of 13 patients with meningococcal shock. A similar defect was observed with only four of 20 sera from children with other febrile illnesses. The effect of sera from patients with meningococcal shock on HUVEC was reversible with normal serum, and seems to be due to the absence of a factor necessary for PGI2 production rather than an inhibitor. These findings suggest that a deficiency of PGI2 may have a role in the pathogenesis of meningococcal shock and that exogenous PGI2 may be of therapeutic benefit.
血管内皮细胞产生前列环素（PGI2）不足可能是脑膜炎球菌性休克所具有的严重血管收缩和血管内血栓形成的潜在原因。研究了脑膜炎球菌性休克患儿、健康成年人以及患有其他发热性疾病患儿的血清对培养的人脐静脉内皮细胞（HUVEC）合成PGI2的影响。与成年对照组相比，当HUVEC与13例脑膜炎球菌性休克患者中10例患者的血清一起孵育时，PGI2合成减少。在患有其他发热性疾病患儿的20份血清中，仅4份观察到类似缺陷。脑膜炎球菌性休克患者血清对HUVEC的影响可被正常血清逆转，且似乎是由于缺乏PGI2产生所需的一种因子而非抑制剂所致。这些发现提示，PGI2缺乏可能在脑膜炎球菌性休克的发病机制中起作用，外源性PGI2可能具有治疗益处。
