Insel Beverly J, Brown Alan S, Bresnahan Michaeline A, Schaefer Catherine A, Susser Ezra S
Mailman School of Public Health of Columbia University Epidemiology, 722 W. 168 St., NY 10032, USA.
Schizophr Res. 2005 Dec 15;80(2-3):331-42. doi: 10.1016/j.schres.2005.06.005. Epub 2005 Jul 11.
Predicated on a maternal immune response to paternally inherited foreign fetal blood antigens, we hypothesized that maternal-fetal blood incompatibility increases susceptibility to schizophrenia in the offspring. The relation between schizophrenia and maternal-fetal blood incompatibility, arising from the D antigen of the Rhesus (Rh) and the ABO blood group antigens, was examined in a cohort of live-births.
The data were drawn from the Prenatal Determinants of Schizophrenia Study, a cohort of births occurring between 1959 and 1967 to women enrolled in a Kaiser Permanente Plan-Northern California Region (KP). Adult offspring belonging to the KP from 1981 to 1997 were followed for the incidence of schizophrenia spectrum disorder (SSD). Cox proportional hazards regression was the primary analytic technique.
Among second and later born offspring, the adjusted incidence rate ratio (RR(adj)) of SSD was 1.80 (95% CI=0.71-4.58) for the Rh incompatible offspring compared with the Rh compatible offspring; with the males exhibiting higher rate ratio (RR(adj)=2.37; 95% CI=0.82-6.86) than the females (RR(adj)=0.93 95% CI=0.12-7.01). Among all offspring, the RR(adj) for ABO incompatibility was lower and the elevated rate ratio was similarly limited to the males (RR(adj)=1.68; 95% CI=0.76-3.70). For Rh and/or ABO incompatibility, the RR(adj) was 1.57 (95% CI=0.87-2.82). A statistically significant result was detected only for the male offspring (RR(adj)=2.22; 95% CI=1.10-4.47).
Although the results should be interpreted with caution given the few events of SSD, the findings extend the line of evidence that maternal-fetal blood incompatibility is a risk factor for schizophrenia spectrum disorder; with the strongest evidence to date implicating that the susceptibility pertains only to male offspring.
基于母体对父系遗传的外来胎儿血液抗原的免疫反应，我们推测母胎血型不相容会增加后代患精神分裂症的易感性。在一组活产队列中，研究了精神分裂症与由恒河猴（Rh）D抗原和ABO血型抗原引起的母胎血型不相容之间的关系。
数据来自精神分裂症产前决定因素研究，该队列研究对象为1959年至1967年间在凯撒永久医疗计划北加利福尼亚地区（KP）登记的妇女所生的婴儿。对1981年至1997年属于KP的成年后代进行随访，观察精神分裂症谱系障碍（SSD）的发病率。Cox比例风险回归是主要的分析技术。
在二胎及以后出生的后代中，Rh血型不相容的后代与Rh血型相容的后代相比，SSD的调整发病率比（RR(adj)）为1.80（95%CI=0.71-4.58）；男性的发病率比（RR(adj)=2.37；95%CI=0.82-6.86）高于女性（RR(adj)=0.93，95%CI=0.12-7.01）。在所有后代中，ABO血型不相容的RR(adj)较低，发病率升高同样仅限于男性（RR(adj)=1.68；95%CI=0.76-3.70）。对于Rh和/或ABO血型不相容，RR(adj)为1.57（95%CI=0.87-2.82）。仅在男性后代中检测到具有统计学意义的结果（RR(adj)=2.22；95%CI=1.10-4.47）。
尽管鉴于SSD事件较少，结果应谨慎解释，但这些发现扩展了证据链，表明母胎血型不相容是精神分裂症谱系障碍的一个风险因素；迄今为止最有力的证据表明易感性仅与男性后代有关。
