Prevalence and risk factors of severe postpartum hemorrhage: a retrospective cohort study.

BACKGROUND: Although maternal deaths are rare in developed regions, the morbidity associated with severe postpartum hemorrhage (SPPH) remains a major problem. To determine the prevalence and risk factors of SPPH, we analyzed data of women who gave birth in Guangzhou Medical Centre for Critical Pregnant Women, which received a large quantity of critically ill obstetric patients who were transferred from other hospitals in Southern China. METHODS: In this study, we conducted a retrospective case-control study to determine the prevalence and risk factors for SPPH among a cohort of women who gave birth after 28 weeks of gestation between January 2015 and August 2019. SPPH was defined as an estimated blood loss ≥1000 mL and total blood transfusion≥4 units. Logistic regression analysis was used to identify independent risk factors for SPPH. RESULTS: SPPH was observed in 532 mothers (1.56%) among the total population of 34,178 mothers. Placenta-related problems (55.83%) were the major identified causes of SPPH, while uterine atony without associated retention of placental tissues accounted for 38.91%. The risk factors for SPPH were maternal age < 18 years (adjusted OR [aOR] = 11.52, 95% CI: 1.51-87.62), previous cesarean section (aOR = 2.57, 95% CI: 1.90-3.47), history of postpartum hemorrhage (aOR = 4.94, 95% CI: 2.63-9.29), conception through in vitro fertilization (aOR = 1.78, 95% CI: 1.31-2.43), pre-delivery anemia (aOR = 2.37, 95% CI: 1.88-3.00), stillbirth (aOR = 2.61, 95% CI: 1.02-6.69), prolonged labor (aOR = 5.24, 95% CI: 3.10-8.86), placenta previa (aOR = 9.75, 95% CI: 7.45-12.75), placenta abruption (aOR = 3.85, 95% CI: 1.91-7.76), placenta accrete spectrum (aOR = 8.00, 95% CI: 6.20-10.33), and macrosomia (aOR = 2.30, 95% CI: 1.38-3.83). CONCLUSION: Maternal age < 18 years, previous cesarean section, history of PPH, conception through IVF, pre-delivery anemia, stillbirth, prolonged labor, placenta previa, placental abruption, PAS, and macrosomia were risk factors for SPPH. Extra vigilance during the antenatal and peripartum periods is needed to identify women who have risk factors and enable early intervention to prevent SPPH.

Delineation of the molecular basis of borderline hemoglobin A2 in Chinese individuals.

BACKGROUND: The "gray zone" of borderline hemoglobin A2 (Hb A2) may be present in a large section of the population, especially in countries where thalassemia is common. However, very little is currently known of the molecular basis of borderline Hb A2 in Chinese individuals. METHOD: In this study, we performed a comprehensive analysis of the globin genotypes and KLF1 gene mutations associated with borderline Hb A2 in 165 Chinese subjects. RESULT: Fifteen (9.1%) were positive for a molecular defect in the α-,ß-globin genes, of whom, α-thalassemia mutations and α-globin gene triplication were found in eleven cases, accounting for about 73.3% of these globin gene defects. Twenty (12.1%) were positive for a molecular defect in the KLF1 gene. Eight different mutations were identified, six of which are here reported for the first time. The most common is the G176AfsX179 mutation, accounting for 50% of the total. CONCLUSIONS: The molecular characterization of borderline Hb A2 in Chinese individuals is significantly different than in Italian population. Our data is conductive to provision of genetic counseling for Chinese individuals with borderline Hb A2.

[Analysis of the phenotype-genotype relationship of Hb Constant Spring].

OBJECTIVE: To analyze the genotype-phenotype correlations in the Hb Constant Spring (HbCS) carriers, and to investigate the effect of HbCS on hematologic parameters. METHODS: Complete blood cell count and hemoglobin electrophoresis analyses were performed in 125 HbCS cases. The α-and ß-thalassemia mutations were determined by reverse dot-blotting and Gap-PCR. RESULTS: The presence of the SEA deletion or Hb Quong Sze (HbQS) with HbCS leads to HbH-CS disease. There was significant difference between HbH-CS and αCSα/-α, HbH-CS and αCSα/αα in the hematological parameters. The genotype of αCSα/-α or αα/αCSα had slight effect on hematological parameters. When the Hb Constant Spring mutation co-existed with heterozygous ß-thalassemia, the hematological characteristics of ß-thalassemia was presented. Only 57.6% of carriers with HbCS were detected by hemoglobin electrophoresis. CONCLUSION: The cases with co-existence of HbCS trait and other α-thalassemia trait, or ß-thalassemia trait, showed variation in their red blood cell parameters. For such compound heterozygotes for HbCS and other α- or ß-thalassaemia mutations, which were usually misdiagnosed in clinical screening by hemoglobin electrophoresis, accurate diagnose can be made by molecular diagnosis.

[Analysis of hematological characteristics on the 79 co-inheritance of α-thalassemia and ß-thalassemia carriers in Guangxi].

OBJECTIVE: To investigate the hematological characteristics of co-inheritance of α-thalassemia (α-thal) and ß-thalassemia (ß-thal) and to survey the incidence of co-inheritance of α-thal and ß-thal in Guangxi. METHODS: DNA samples from 370 primary and middle school students who were ß-thal carriers in Guangxi were further processed for the α-goblin gene mutation screening, and were grouped based on the genotype of ß- and α-goblin gene. The hematological indexes to the different groups were compared by One-way ANOVA. RESULTS: Of the total 370 ß-thal carriers, 79 were found to carry α-thal, which gave a frequency of 21.35% for ß-thal carriers and 1.36% for coincidence of these two common disorders in the local population. As expected, the 79 patients presented very variable α-globin alterations in combination with ß-globin mutations, showing 31 genotype combined with the coincidence of both Hb disorders. Except the genotypes of 3 ß-thal heterozygotes combined with ααα(anti3.7) triplication and 2 ß-thal carriers with IVS-II-654(C→T)/N combined-α(3.7)/αα presented the phenotype of thalassemia intermedia, and other 74 carriers with co-inheritance of α-thal and ß-thal all presented the phenotype of ß-thal trait. There were significant differences between ß-thal heterozygotes and the carriers with a co-inheritance of both ß+α(0) thal in MCH, MCV and Hb. In addition, there existed significant difference between the carriers with a co-inheritance of both ß+α(+) thal and a co-inheritance of both ß+α(0) thal in MCV, MCH and Hb. CONCLUSION: Compared to that of ß-thal heterozygotes, the carriers with a co-inheritance of α-thal and ß-thal had slighter phenotype with hematological characteristics. It's difficult to distinguish the double heterozygotes with the co-inheritance of α-thal and ß-thal from ß-thal heterozygotes by hematological indexes, the molecular diagnosis should be performed.