Authors Experimental group Control group Results Conclusions RPL Nelen et al. [69 ] 123 RPL patients 104 normal women Increased fasting Hct (≥18.3 mmol/L) and afterload Hct (≥61.5 mmol/L) were both associated with RPL. Increased Hct was a risk factor for RPL. Raziel et al. [35 ] 36 nonpregnant RPL patients 40 parous women HHct was found in 31% of the RPL patients. Patients with RPL were more likely to have HHct. Zammiti et al. [34 ] 350 RPL patients 200 normal women The tHct levels were similar between the two groups. There was no association between the risk of RPL and tHct levels. Creus et al. [36 ] 60 RPL patients 30 fertile females There was no significant difference in the Hct levels between the two groups. RPL was not associated with HHct. Chakraborty et al. [68 ] 126 RPL patients with PCOS 117 normal women without PCOS There was a significant difference in Hct expression between the experimental group and the control group (70.63% vs. 57.26%; HHct could increase the possibility of RPL. Zarfeshan Fard et al. [70 ] 50 RPL patients 50 women having at least two normal pregnancies The expression of Hct was higher in the experimental group ( The 677CT genotype may be a risk marker for abortion, and the C allele protected women from RPL. Lin et al. [71 ] 403 RPL patients 342 normal females The expression of Hct was higher in the experimental group relative to that in the control group. MTHFR 677CT and MTRR 66AG gene mutations increased Hct expressions. PE Raijmakers et al. [72 ] 20 PE patients 10 healthy nonpregnant females and 10 normotensive pregnant females PE patients had higher Hct levels than normotensive pregnant women (13.3 vs. 8.4 mmol/L; Mild HHct may not be a risk marker for PE. HHct in PE was related to the changes of plasma volume instead of MTHFR gene mutation. Mao et al. [40 ] 62 PE patients 30 normal pregnant women Both the mild and severe PE patients exhibited higher Hct levels compared to controls. The Hct-ADMA-NO pathway was involved in the cause of PE and associated with the severity of PE. Kulkarni et al. [73 ] 49 PE patients 57 normotensive pregnant women Despite there being no difference in folic acid and vitamin B12 levels between the two groups, the Hct levels were higher in the experimental group. The reduction of DHA in PE was related to HHct. Laskowska et al. [41 ] 62 early-onset PE and 53 late-onset PE patients 65 normotensive pregnant women There were increased expressions of Hct in the serum of patients with PE, especially in the early-onset PE population. The expression level of Hct was related to the severity of PE and could indicate early symptoms of PE. Şanlıkan et al. [74 ] 30 severe PE and 24 mild PE patients 60 normal pregnant women Hct levels in the control group were lower compared to those in the experimental group. A significant difference did not exist in Hct expression between the mild and severe PE patients. Hct was significantly increased in PE patients, but it was not related to the severity of this disease. Wadhwani et al. [75 ] 62 PE patients 126 normotensive pregnant women PE patients had higher Hct levels compared with controls in the second trimester, third trimester, and during delivery. Increased Hct expressions occurred in PE patients from the first trimester to delivery. Maru et al. [76 ] 64 mild PE, 50 severe PE, and 32 eclampsia patients 68 healthy pregnant women Hct greater than 8 mmol/L was associated with severe PE, and maternal complications tended to occur among these women. Hct was usable as one of the predictors for PE. Serrano et al. [77 ] 2978 PE patients 4096 normal pregnant females The OR for PE was 1.16 (95% CI: 1.05-1.27) for 1SD enhancement in log-Hct. HHct was one of the high-risk factors for PE.
