METHODS: This cross-sectional retrospective study conducted in Kelantan involved 104 newly diagnosed female BC patients from 2015 to 2016 who underwent chemotherapy. For statistical analysis, chi-square was used to compare between CIA and non-CIA groups. In addition, simple and multiple logistic regression were used to determine the association of the CIA.
RESULTS: Our study revealed that 34.6% (n=36) of patients had mild anaemia, and 59.6% (n=62) had normal haemoglobin at pre-chemotherapy. The prevalence of anaemia increased from 40.4% to 77% at the end of our study. About 30.8% of patients received PRBC transfusion during chemotherapy with mean haemoglobin before the first transfusion of 7.9 g/dl. CIA was observed in 54.8% of cases. There was no significant association between CIA concerning the patient characteristic, cancer characteristic, or cancer treatment.
CONCLUSION: We concluded that a significant proportion (40.4%) of BC patients was anaemic even before chemotherapy, with the red blood cell requirements up to 30.8% throughout chemotherapy. A larger prospective study is needed to determine the predictors for the CIA and subsequently improve patient management.
CASE REPORT: A case of unusual severe HDFN due to anti-D alloimmunisation in undiagnosed RhD negative primigravida Malay woman is reported here. This case illustrates the possibility of an anamnestic response from previous unknown sensitisation event or the development of anti-D in mid trimester. The newborn expired due to hydrops fetalis and severe anaemia. Antenatally, the mother was identified as RhD positive and thus there was no antenatal antibody screening, antepartum anti-D prophylaxis or close fetal monitoring for HDFN.
DISCUSSION: The thorough antenatal ABO and RhD blood grouping with antibody screening is mandatory as part of prevention and early detection of HDFN especially due to anti-D alloimmunisation. Improper management of RhD negative women might lead to severe HDFN including in primigravida.
CASE REPORT: A 3-month-old baby boy was presented with neonatal anaemia and mild hepatomegaly. Full blood count revealed severe hypochromic microcytic anaemia. There was an abundance of HbH inclusion bodies in his red blood cells. High-performance liquid chromatography showed a reduced HbA2 level with the presence of pre-run peak. Capillary electrophoresis showed the presence of HbH and Hb Barts. Molecular analysis found a common α0-thalassaemia (--SEA) in one allele and mutation in codon 125 in the other allele.
DISCUSSION: Non-deletional HbH disease due to a combination of deletional and non-deletional mutations may present with severe clinical manifestations than those with deletion mutations, which warrants accurate diagnosis using molecular techniques.
METHODS: For this cross-sectional study, patient blood samples that showed a positive peak in zone 2 of CE were selected. Hemoglobin and DNA of the samples were investigated to ascertain the presence and levels of non-deletional and deletional α thalassemia. The results were statistically analyzed.
RESULTS: Of the 137 samples investigated, 118 (86.1%) were positive for termination codon Hb CS mutation. Heterozygous Hb CS was found in 92 (67.2%), compound heterozygous Hb CS in 22 (16.1%), and homozygous Hb CS in four (2.9%) samples. The ranges of Hb CS level for heterozygous Hb CS, compound heterozygous Hb CS, and homozygous Hb CS were within 0.2-2.7%, 0.3-2.2%, and 4.5-5.5%, respectively. Significant hematological differences in the Hb level, mean cell volume, mean cell hemoglobin, red cell distribution width, red blood cell count, and Hb CS level were observed between heterozygous, homozygous, and compound heterozygous Hb CS.
CONCLUSIONS: In view of the overlapping prevalence range of Hb CS level for heterozygous and compound heterozygous Hb CS, only Hb CS level within the range 4.5-5.5% was helpful in the diagnosis of homozygous Hb CS.