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Fetal Haemoglobin (fetal + haemoglobin)
Selected AbstractsMaternal serum alpha-fetoprotein, fetal middle cerebral artery blood flow velocity and fetal haemoglobin in pregnancies at risk of fetal anaemiaPRENATAL DIAGNOSIS, Issue 2 2006Jose L. Bartha Abstract Objectives To evaluate the relationships between maternal serum alpha-fetoprotein (MSAFP) levels and both middle cerebral artery (MCA) peak systolic velocity and fetal haemoglobin in women at risk of fetal anaemia. Methods Forty-one measurements of MSAFP were carried out in 22 women at risk of fetal anaemia (16 alloimmunised patients and 6 cases of parvovirus infection) who were monitored by using MCA Doppler measurements. The relationships between MSAFP (MoM) and both MCA peak systolic velocity (z -scores) and fetal haemoglobin (MoM) were studied. Results There were significant correlations between MSAFP and both MCA Doppler measurements (r = 0.56, p = 0.00017) and fetal haemoglobin (n = 13, r = ,0.71, p = 0.006). MSAFP was higher in cases with fetal anaemia (n = 10) than in those with normal haemoglobin levels (n = 3) (1.7 ± 0.4 vs 0.8 ± 0.1 MoM; p = 0.006). In cases of alloimmunised pregnancies with fetal anaemia, MSAFP elevations preceded the presence of increased MCA Doppler velocity by 2.7 weeks (range 0,9 weeks). Conclusion MSAFP is significantly correlated with both MCA Doppler measurements and fetal haemoglobin. Elevations of MSAFP may appear earlier than MCA Doppler abnormalities in cases of fetal anaemia associated with red blood cell alloimmunisation. Copyright © 2006 John Wiley & Sons, Ltd. [source] Derivated fetal haemoglobin as a marker for red cell age in the human fetus reflecting stimulated or impaired red blood cell productionPRENATAL DIAGNOSIS, Issue 7 2001Margriet Huisman Abstract We have determined whether derivated fetal haemoglobin (dHbF, consisting of glycated and acetylated HbF) can be used as a cell age marker for fetal red blood cells (RBCs). Cord blood was obtained between 19 and 39 weeks of gestation from 28 alloimmunised anaemic fetuses (23 RhD+ and 5,Kell) and from 20 non-anaemic fetuses and newborns (controls). Density gradient centrifugation was applied to 36 samples (20 RhD+, 15 controls and 1,Kell) to obtain fractions of increasing cell age. Blood samples were used for measurements of mean cellular volume (MCV), mean cell haemoglobin (MCH), mean corpuscular haemoglobin concentration (MCHC), pyruvate kinase activity (PK) and derivated fetal haemoglobin (dHbF) by cation-exchange HPLC. Reticulocytes were counted only in the whole blood samples. In all density gradient separated RBC fractions, the values for MCV, MCH and PK activity decreased and those of MCHC and dHbF increased with increasing density (equivalent to increasing cell age). The mean density was lower for RBCs of the anaemic RHD group (1.072±0.007,g/ml) than for the non-anaemic controls (1.077±0.005,g/ml) (p<0.05) The RBC density of the Kell sensitised fetus did not differ from those of the controls. In the control group, the values of the cell age markers in whole blood changed significantly with the gestational age, showing an increase of mean age of the erythrocyte population. The best linear relationship was found for dHbF (y=6.28+0.17*weeks; r=0.84; p<0.001). In the anaemic RhD+ fetuses, the RBC age markers did not change with gestational age; the dHbF percentages were lower, and the MCV, MCH, PK values and the reticulocyte counts were higher than in the controls (0.05 A new method to determine the feto-placental volume based on dilution of fetal haemoglobin and an estimation of plasma fluid loss after intrauterine intravascular transfusionBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 10 2002M. Hoogeveen Objectives (1) To calculate the feto-placental volume (FPV), using the haematocrit (Ht) values and the percentages of fetal haemoglobin (HbF), before and after red blood cell transfusion. (2) To estimate the transfusion-induced loss of plasma fluid. Design Retrospective analysis of data of 42 anaemic fetuses at the first transfusion [gestational age (GA) 19,36 weeks]. Setting Department of Obstetrics, Leiden University Medical Centre, The Netherlands. Sample Fifteen hydropic and 27 non-hydropic fetuses. Methods Donor blood volume (Vdonor) and Ht (Htdonor), fetal pre- and post-transfusion Ht values (Htinitial, Htfinal) and percentages of HbF (HbFinitial and HbFfinal) were used to calculate the FPV. The total red cell volume after transfusion (RCVfinal) and Htfinal were used to estimate the plasma fluid loss. Main outcome measures Feto-placental blood volume and loss of plasma fluid. Results The equations that use Htfinal over-estimate the FPV when the formula does not account for the difference between donor and post-transfusion Ht (FPVHt= 21.36 * GA , 390; r= 0.89). FPV is under-estimated (FPVHt= 9.90 * GA , 172; r= 0.84) when the blood volume increases with a volume less than the added donor blood volume. The calculation of FPV, using HbF percentages and the initial fetal RCV, is independent of volume changes (FPVHbF= 15.10 * GA , 279; r= 0.85). Comparing RCVfinal and Htfinal values showed that 31.1 ± 14.5% of the transfused volume was lost. Results of the hydropic fetuses did not differ from those of the non-hydropic fetuses. Conclusions FPV values based on Ht values are less reliable than those based on RCV and HbF findings. When, for practical reasons, Ht values have to be used, we propose an adapted equation for the calculation of the necessary volume of donor blood: Vdonor= FPVHbF* (Htfinal, Htinitial) / (Htdonor, 0.70 * Htfinal). [source] research paper: Role of the cold shock domain protein A in the transcriptional regulation of HBG expressionBRITISH JOURNAL OF HAEMATOLOGY, Issue 6 2010Raffaella Petruzzelli Summary Impaired switching from fetal haemoglobin (HbF) to adult globin gene expression leads to hereditary persistence of fetal haemoglobin (HPFH) in adult life. This is of prime interest because elevated HbF levels ameliorate ,-thalassaemia and sickle cell anaemia. Fetal haemoglobin levels are regulated by complex mechanisms involving factors linked or not to the ,-globin gene (HBB) locus. To search for factors putatively involved in the expression of the ,-globin genes (HBG1, HBG2), we examined the reticulocyte transcriptome of three siblings who had different HbF levels and different degrees of ,-thalassaemia severity although they had the same ,BA - and ,,B cluster genotypes. By mRNA differential display we isolated the cDNA coding for the cold shock domain protein A (CSDA), also known as dbpA, previously reported to interact in vitro with the HBG2 promoter. Expression studies performed in K562 and in primary erythroid cells showed an inverse relationship between HBG and CSDA expression levels. Functional studies performed by Chromatin Immunoprecipitation and reporter gene assays in K562 cells demonstrated that CSDA is able to bind the HBG2 promoter and suppress its expression. Therefore, our study demonstrated that CSDA is a trans-acting repressor factor of HBG expression and modulates the HPFH phenotype. [source] Laboratory correlates for a phase II trial of romidepsin in cutaneous and peripheral T-cell lymphomaBRITISH JOURNAL OF HAEMATOLOGY, Issue 2 2010Susan E. Bates Summary Romidepsin has shown promise in the treatment of T-cell lymphomas, and so we evaluated molecular endpoints gathered from 61 patients enrolled on a phase II trial of romidepsin in cutaneous and peripheral T-cell lymphoma at the National Institutes of Health. The endpoints included histone H3 acetylation and ABCB1 gene expression in peripheral blood mononuclear cells (PBMCs); ABCB1 gene expression in tumour biopsy samples; and blood fetal haemoglobin levels (HbF), all of which were increased following romidepsin treatment. The fold increase in histone acetylation in PBMCs at 24 h was weakly to moderately well correlated with the pharmacokinetic parameters Cmax and area under the curve (AUC)last (, = 0·37, P = 0·03 and , = 0·36, P = 0·03 respectively) and inversely associated with clearance (, = ,0·44; P = 0·03). Histone acetylation in PBMCs at 24 h was associated with response (P = 0·026) as was the increase in fetal haemoglobin (P = 0·014); this latter association may be due to the longer on-study duration for patients with disease response. Together, these results suggest that pharmacokinetics may be an important determinant of response to histone deacetylase inhibitors (HDIs) , the association with histone acetylation in PBMCs at 24 h is consistent with a hypothesis that potent HDIs are needed for a critical threshold of drug exposure and durable activity. [source] Are there clinical phenotypes of homozygous sickle cell disease?BRITISH JOURNAL OF HAEMATOLOGY, Issue 4 2004Neal Alexander Summary The distribution of clinical features was examined in subjects with homozygous sickle cell (SS) disease in the Jamaican Cohort Study to determine whether there is evidence of distinct clustering of symptoms or clinical phenotypes. A twofold model yielded groups that could be interpreted as painful crisis or leg ulcer phenotypes and 78% of patients were classified with 95% confidence into one of these. The painful crisis phenotype also manifested higher frequencies of dactylitis, meningitis/septicaemia, acute chest syndrome and stroke. Attempts to define a three-group model were less convincing although 43% of patients could be allocated with 95% confidence. The three-group model essentially divided subjects with the leg ulcer phenotype into subgroups with higher and lower frequencies of painful crisis, dactylitis, meningitis/septicaemia and acute chest syndrome. In the three-group model, the painful crisis phenotype had lower total haemoglobin, fetal haemoglobin, mean cell volume and higher reticulocytes but there was no apparent influence of alpha thalassaemia or beta globin haplotype. Both environmental and genetic factors are likely to contribute to most manifestations of SS disease and the evidence for different clinical phenotypes suggests that a search for associated genetic polymorphisms may provide insights into the mechanisms of clinical variability in SS disease. [source]
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