Iron parameters in pregnant women with beta-thalassaemia minor combined with iron deficiency anaemia compared to pregnant women with iron deficiency anaemia alone demonstrate the safety of iron supplementation in beta-thalassaemia minor during pregnancy.

In patients with beta-thalassaemia intermedia or major, hepcidin induces iron overload by continuously promoting iron absorption. There have been no studies in pregnant women with beta-thalassaemia minor combined with iron deficiency anaemia (IDA), examining whether hepcidin is inhibited by GDF15, as may occur in patients with beta-thalassaemia intermedia or major, or whether the iron metabolism characteristics and the effect of iron supplementation are consistent with simple IDA in pregnancy. We compared and analysed routine blood parameters, iron metabolism parameters, the GDF15 levels, and the hepcidin levels among four groups, namely the beta-thalassaemia (ß) + IDA, ß, IDA, and normal groups. In addition, the ß + IDA and IDA groups received iron supplementation for four weeks. We found no statistically significant correlation between hepcidin and GDF15 in any group, but a positive correlation was observed between hepcidin and ferritin. After iron supplementation, the routine blood parameters and iron metabolism parameters in the ß + IDA group were improved, and the hepcidin content was significantly increased. These results suggest that in pregnant women with beta-thalassaemia minor, hepcidin functions normally to maintain iron homeostasis, and that iron supplementation is effective and safe.

Comparison of Two Strategies for Prophylactic Donor Lymphocyte Infusion in Patients With Refractory/Relapsed Acute Leukemia.

Prophylactic donor lymphocyte infusion (pDLI) could reduce relapse in patients with refractory/relapsed acute leukemia (RRAL) undergoing allogeneic hematopoietic stem cell transplantation (allo-HSCT), but optimal timing of pDLI remains uncertain. We compared the outcomes of two strategies for pDLI based on time from transplant and minimal residual disease (MRD) status in patients with RRAL. For patients without grade II-IV acute graft-versus-host disease (aGVHD) on day +60, pDLI was given on day +60 regardless of MRD in cohort 1, and was given on day +90 unless MRD was positive on day +60 in cohort 2. A total of 161 patients with RRAL were enrolled, including 83 in cohort 1 and 78 in cohort 2. The extensive chronic GVHD (cGVHD) incidence in cohort 2 was lower than that in cohort 1 (10.3% vs. 27.9%, P = 0.006) and GVHD-free/relapse-free survival (GRFS) in cohort 2 was superior to that in cohort 1 (55.1% vs. 41.0%, P = 0.042). The 2-year relapse rate, overall and leukemia-free survival were comparable between the two cohorts (29.0% vs. 28.2%, P = 0.986; 63.9% vs. 64.1%, P = 0.863; 57.8% vs. 61.5%, P = 0.666). Delaying pDLI to day +90 based on MRD for patients with RRAL undergoing allo-HSCT could lower extensive cGVHD incidence and improve GRFS without increasing incidence of leukemia relapse compared with pDLI on day +60.

[Association of P450-2E1 and GSTM1 genetic polymorphisms with susceptibility to antituberculosis drug-induced hepatotoxicity].

OBJECTIVE: To observe the relationship between the genetic polymorphism of P450-2E1 and the risk for antituberculosis drug-induced hepatotoxicity in a Chinese population. METHODS: Blood samples and clinical data were collected from 85 patients with antituberculosis drug-induced hepatotoxicity and 100 tuberculosis patients without hepatotoxicity as the control. DNA was extracted from the blood samples, and the frequencies of P450-2E1 RsaI genotypes were analyzed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The relationship between the polymorphisms of P450-2E1 RsaI and the antituberculosis drug-induced hepatotoxicity was analyzed. Predisposing factors for antituberculosis drug-induced hepatitis, such as gender, age, and polymorphism of P450-2E1 RsaI were evaluated by using logistic regression analysis. RESULTS: The frequencies of the 3 gene types P450-2E1 RsaI c1/c1, c1/c2, and c2/c2 were 75% (64/85), 20% (17/85) and 5% (4/85) respectively in patients with antituberculosis drug-induced hepatotoxicity, and 61% (61/100), 30% (30/100), and 9% (9/100) respectively in the controls. A statistical difference was found between the cases and the controls (chi(2) = 4.284, P < 0.05, OR = 2.016, 95%CI = 1.058 - 3.842). Logistic regression analysis showed that the polymorphism of P450-2E1 RsaI remained a significant independent risk factor for antituberculosis drug-induced hepatotoxicity after adjustment for age, gender and body mass index. CONCLUSION: Polymorphisms of P450-2E1 were found to be significantly associated with the risk of antituberculosis drug-induced hepatotoxicity, and the c1/c1 genotype was one of the risk factors.