874
Correspondence
small; of the eight women with preeclampsia, the two with low platelets had negative cytotoxicity values just like the controls, and the study patients seem to be a heterogeneous group. Second, if the authors believe in their postulate and conclusions, how can they explain the increase in the cytotoxic activity of the serum in the normal patients post partum? Finally, in spite of the statistically significant differences between the predelivery and postdelivery values in the normal and preeclamptic patients, how could the authors draw theoretical conclusions in a clinical context without having a normal range for chromium 51 releaseltotal 51Cr when all the values were in a narrow range of 0.32 and 0.45. In my opinion the vascular damage in patients with preeclampsia is secondary to the failure to increase the intravascular volume, characteristic of normal pregnancies.1.2 The authors failed to prove that there is an association between a cytotoxic factor in the serum and preeclampsia when compared with normal pregnant patients. I believe that the authors were measuring "Cr release from human umbilical vein endothelial cells exposed to pregnant and puerperal serum, and they proved that the latter releases it. Emeric P. Frohlich, MRCOG Department of Obstetrics and Gynaecology University of the Witwatersrand and]. G. Strijdom Hospital Private Bag XO 1 Auckland Park 2006, South Africa REFERENCES 1. Redman CWG. Maternal plasma volume and disorders of pregnancy. Br Med J 1984;288:955-6. 2. Frohlich EP. A hypothesis of the pathogenesis of preeclampsia. Med Hypotheses [In press).
Reply To the Editors: We are glad that Dr. Frohlich found our article interesting and are equally pleased that he feels our hypothesis (endothelial cell injury that is secondary to blood-borne agents causes the pathophysiologic changes of preeclampsia) has not been proved. This would certainly be premature on the basis of our limited and preliminary data. The principle of the scientific method is to present and test hypotheses. We feel that our hypothesis has "passed" an initial test on the basis of the data we presented. We are of course aware of the heterogeneous nature of the preeclamptic women in our study. This is unfortunately the nature of advanced preeclampsia, and it was our purpose to initially test only patients in whom the diagnosis of preeclampsia was certain. The fact that the cytotoxicity indices were not positive in all patients with preeclampsia is likely to be due to the heterogeneity of the disease, although it may also be due to the insensitivity of the 51Cr release assay. When we began this study, we were concerned that nonspecific immunemediated endothelial injury by heterologous sera might
March 1990 Am J Obstet Gynecol
mask the effect of preeclampsia. For this reason we chose to use the patients as their own controls, comparing predelivery and postdelivery sera by the cytotoxicity assay. The nonspecific effects of sera on allogeneic endothelial cells explain our failure to define a "normal range" for the results. However, on the basis of the data presented and our subsequent experiments, cytotoxicity indices for normal pregnant women consistently have values
Correspondence
small; of the eight women with preeclampsia, the two with low platelets had negative cytotoxicity values just like the controls, and the study patients seem to be a heterogeneous group. Second, if the authors believe in their postulate and conclusions, how can they explain the increase in the cytotoxic activity of the serum in the normal patients post partum? Finally, in spite of the statistically significant differences between the predelivery and postdelivery values in the normal and preeclamptic patients, how could the authors draw theoretical conclusions in a clinical context without having a normal range for chromium 51 releaseltotal 51Cr when all the values were in a narrow range of 0.32 and 0.45. In my opinion the vascular damage in patients with preeclampsia is secondary to the failure to increase the intravascular volume, characteristic of normal pregnancies.1.2 The authors failed to prove that there is an association between a cytotoxic factor in the serum and preeclampsia when compared with normal pregnant patients. I believe that the authors were measuring "Cr release from human umbilical vein endothelial cells exposed to pregnant and puerperal serum, and they proved that the latter releases it. Emeric P. Frohlich, MRCOG Department of Obstetrics and Gynaecology University of the Witwatersrand and]. G. Strijdom Hospital Private Bag XO 1 Auckland Park 2006, South Africa REFERENCES 1. Redman CWG. Maternal plasma volume and disorders of pregnancy. Br Med J 1984;288:955-6. 2. Frohlich EP. A hypothesis of the pathogenesis of preeclampsia. Med Hypotheses [In press).
Reply To the Editors: We are glad that Dr. Frohlich found our article interesting and are equally pleased that he feels our hypothesis (endothelial cell injury that is secondary to blood-borne agents causes the pathophysiologic changes of preeclampsia) has not been proved. This would certainly be premature on the basis of our limited and preliminary data. The principle of the scientific method is to present and test hypotheses. We feel that our hypothesis has "passed" an initial test on the basis of the data we presented. We are of course aware of the heterogeneous nature of the preeclamptic women in our study. This is unfortunately the nature of advanced preeclampsia, and it was our purpose to initially test only patients in whom the diagnosis of preeclampsia was certain. The fact that the cytotoxicity indices were not positive in all patients with preeclampsia is likely to be due to the heterogeneity of the disease, although it may also be due to the insensitivity of the 51Cr release assay. When we began this study, we were concerned that nonspecific immunemediated endothelial injury by heterologous sera might
March 1990 Am J Obstet Gynecol
mask the effect of preeclampsia. For this reason we chose to use the patients as their own controls, comparing predelivery and postdelivery sera by the cytotoxicity assay. The nonspecific effects of sera on allogeneic endothelial cells explain our failure to define a "normal range" for the results. However, on the basis of the data presented and our subsequent experiments, cytotoxicity indices for normal pregnant women consistently have values
