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A simple technique of intra-uterine transfusion of foetus in University Hospital, Kuala Lumpur

Kwi NK, Hing NK

Med J Malaysia, 1974 Jun;28(4):287-9.
PMID: 4278824
Matched MeSH terms: Erythroblastosis, Fetal/prevention & control*
Molecular Detection of Glycophorins A and B Variant Phenotypes and their Clinical Relevance

Hassan SN, Thirumulu Ponnuraj K, Mohamad S, Hassan R, Wan Ab Rahman WS

Transfus Med Rev, 2019 04;33(2):118-124.
PMID: 30910255 DOI: 10.1016/j.tmrv.2019.02.003

Crossover or conversion between the homologous regions of glycophorin A (GYPA) and glycophorin B (GYPB) gives rise to several different hybrid glycophorin genes encoding a number of different glycophorin variant phenotypes which bear low prevalence antigens in the MNS blood group system. GP.Mur is the main glycophorin variant phenotype which causes hemolytic transfusion reaction (HTR) and hemolytic disease of the fetus and newborn (HDFN) in East and Southeast Asians. The detection of glycophorin variant phenotypes using serological methods is limited to phenotyping reagents that are not commercially available. Moreover, the red blood cells used for antibody identification are usually of the GP.Mur phenotype. The current Polymerase Chain Reaction (PCR)-based methods and loop-mediated isothermal amplification (LAMP) are available alternatives to phenotyping that allow for the specific detection of glycophorin variant phenotypes. This review highlights the molecular detection method for glycophorins A and B variant phenotypes and their clinical relevance.

Matched MeSH terms: Erythroblastosis, Fetal/diagnosis; Erythroblastosis, Fetal/genetics
Anti-M induced severe haemolytic disease of foetus and newborn in a Malay woman with recurrent pregnancy loss

Mohd Nazri H, Noor Haslina MN, Shafini MY, Noor Shaidatul Akmal AR, Rapiaah M, Wan Zaidah A

Malays J Pathol, 2017 Apr;39(1):73-76.
PMID: 28413208 MyJurnal

Haemolytic disease of the foetus and newborn (HDFN) is caused by maternal red blood cells (RBC) alloimmunisation resulted from incompatibility of maternal and foetal RBCs. However, only a few HDFN attributed to anti-M were reported, varying from asymptomatic to severe anaemia with hydrops foetalis and even intrauterine death. A case of severe HDFN due to anti-M alloantibody from an alloimmunized grandmultiparous Malay woman with recurrent pregnancy loss is reported here. The newborn was delivered with severe and prolonged anaemia which required frequent RBC transfusions, intensive phototherapy and intravenous immunoglobulin administration. Although anti-M is rarely known to cause severe HDFN, a careful serological work-up and close assessment of foetal well-being is important, similar to the management of RhD HDFN. Alloimmunisation with anti-M type can lead to severe HDFN and even foetal loss.

Matched MeSH terms: Erythroblastosis, Fetal/blood*; Erythroblastosis, Fetal/diagnosis
Fulltext Haemolytic Disease of Foetus and Newborn and Haemolytic Transfusion Reaction Due to Kidd antibody in Hospital Umum Sarawak, Malaysia

Irni Mohd Yasin, Narazah Mohd Yusoff, Afifah Hassan, Muhammad Masrin Md. Zahrin

Journal of Biomedical and Clinical Sciences, 2017;2(202):26-27.
MyJurnal

Haemolytic Disease of Foetus and Newborn (HDFN) and Haemolytic Transfusion Reaction (HTR) may occur due to antibodies against Kidd antigen. In Malaysia, the prevalence of RBC alloimmunization due to Kidd antibody for cases of HDFN and HTR have been reported [1-2] however there is insufficient data in Hospital Umum Sarawak (HUS).The aim of this study is to determine whether Kidd alloimmunization causes HDFN and HTR. Indirectly categorize Kidd phenotype blood in regular blood donors.

Matched MeSH terms: Erythroblastosis, Fetal
Neonatal hyperbilirubinaemia

Sinniah D

Med J Malaya, 1971 Mar;25(3):211-4.
PMID: 4253249
Matched MeSH terms: Erythroblastosis, Fetal/epidemiology
Fulltext Alpha-chain thalassemia and hydrops fetalis in Malaya: report of five cases

Lie-Injo LE

Blood, 1962 Nov;20:581-90.
PMID: 13930509

Five cases of severe hydrops and erythroblastosis fetalis in association with a large amount of Hb “Bart’s,” all of Chinese origin, are described. The following characteristic clinical and hematologic symptoms were found. There were generalized hydrops, ascites and gross enlargement of the liver. The spleen, however, was not ahvays enlarged. The placenta was large and friable. Severe erythroblastosis of the blood was always found, with reticulocytosis, many target cells and thin cells. The MCV of the red cells was very high. The cells showed an interesting sickling phenomenon. No evidence of isoimmunization was found. In eight parents examined, no abnormal hemoglobin was detected, and alkali-resistant hemoglobin and hemoglobin A2 were not found to be increased. Their blood showed microcytosis of the red cells cxcept in one father and one mother. In this mother, however, the blood was examimied after a blood transfusion. It is thought probable that these were cases of homozygous alpha-chain thalassemia.

Matched MeSH terms: Erythroblastosis, Fetal*
Hb Bart's level in cord blood and deletions of alpha-globin genes

Lie-Injo LE, Solai A, Herrera AR, Nicolaisen L, Kan YW, Wan WP, et al.

Blood, 1982 Feb;59(2):370-6.
PMID: 6895707

The white blood cell DNA of 36 cord blood samples with Hb Bart's in the red blood cells was studied for alpha-globin gene deletions by hybridization of DNA fragments digested by the restriction endonucleases Eco RI, Hpa I, Bam HI, and Bgl II. All 16 DNA samples from cord blood with Hb Bart's below 3% and no other abnormal hemoglobin had one alpha-globin gene deletion (alpha thal2), except one which had two alpha-globin gene deletions (alpha thal1). Most of the alpha thal2 were of the rightward deletion alpha thal2 genotype. Two new types of alpha thal2 variation was found, probably due to a polymorphism somewhere in an area outside the alpha-globin gene. All 14 cases with Hb Bart's between 3.5% and 8.5% and no other abnormal hemoglobin had two alpha-globin gene deletions (alpha thal1), except one that did not have any alpha-globin gene deletion and one that had one alpha-globin gene deletion. Three DNA samples of cord blood with Hb Bart's accompanied by Hb CoSp did not have any alpha-globin gene deletion. Sixty-five DNA samples from cord blood without Hb Bart's or other abnormal hemoglobin had no alpha-globin gene deletions, except one that had one alpha-globin gene deletion (alpha thal2). Two of the 65 DNA samples were found to have triplicated alpha-globin gene loci.

Matched MeSH terms: Erythroblastosis, Fetal/blood
Gene mapping of Malaysian alpha thalassemias with alpha and zeta globin gene probes

Lie-Injo LE, Herrera AR, Lebo RV, Hassan K, Lopez CG

Am J Hematol, 1985 Mar;18(3):289-96.
PMID: 2983536

Restriction enzyme analysis of the alpha and zeta globin genes was carried out in four cases of Hb Bart's hydrops fetalis, in three patients with Hb H disease without Hb CoSp, in three patients with Hb H disease with Hb CoSp, in 47 individuals with alpha thalassemia trait, and in 47 normal individuals. All four cases of Hb Bart's hydrops fetalis resulted from deletions of alpha 1 and alpha 2 globin genes which did not extend to the psi zeta 1 and zeta 2 globin genes. The same type of deletion was observed in alpha thal1 carriers, but two newborns (one Malay and one of Chinese extraction) had a nondeletion type of alpha thal1 which was confirmed by quantitative alpha globin gene analysis. In addition, two other newborns diagnosed as alpha thal1 trait carriers (one Malay, one Chinese) were shown to have a deletion of both alpha globin genes by quantitative alpha globin gene analysis, but further testing with zeta globin gene probe failed to reveal an abnormal fragment length characteristic of an alpha globin gene deletion. We believe that this last condition is due to a large deletion which includes all alpha globin genes and all zeta globin genes on the same chromosome. On another front, Bgl II restriction analysis of all four Hb Bart's hydrops fetalis cases and the alpha thal1 trait carriers showed a 10.5-kb Bgl II restriction fragment, in the hydrops fetalis as a single band, while in the carriers this 10.5-kb fragment was accompanied by the usual normal 12.5-kb and 11.3-kb fragments. We report that this 10.5-kb fragment, previously thought to be specific for the Southeast Asian alpha thal1 gene deletion, is also common in normal individuals. Nevertheless, digestion with other enzymes can clearly differentiate the alpha thal1 and normal genotypes. We distinguish the findings in the alpha thalassemias from the extensive DNA polymorphism in the region of the alpha and zeta globin genes.

Matched MeSH terms: Erythroblastosis, Fetal/genetics
Severe anti-D haemolytic disease of fetal and newborn in rhesus D negative primigravida

Hassan MZ, Iberahim S, Abdul Rahman WSW, Zulkafli Z, Bahar R, Ramli M, et al.

Malays J Pathol, 2019 Apr;41(1):55-58.
PMID: 31025639

INTRODUCTION: Anti-D alloimmunisation may occur from the blood transfusion or fetomaternal haemorrhage which can lead to haemolytic disease of fetal and newborn (HDFN). The morbidity and mortality of HDFN related to anti-D is significantly reduced after introduction of anti-D prophylaxis and furthermore, anti-D HDFN in RhD negative primigravida is uncommonly seen.
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.

Matched MeSH terms: Erythroblastosis, Fetal