Role of creatine kinase isoenzyme-BB and magnesium in the asphyxiated newborn infants

Birth asphyxia is the single most important cause of neurological morbidity in newborn infants. Damage to brain cells produces measurable amounts of creatine kinase isoenzyme [CK-BB] in the serum that is why CK-BB has attracted attention as a possible predictor of the extent of brain damage. One of the mechanisms that appear to be particularly relevant to the problem of birth asphyxia is the release of glutamate N-methyl-D-aspartate [NMDA] which is a glutamate receptor subtype that appears to be the most important in brain injury. NMDA receptor is coupled to Ca [2+] channel and its activation opens the Ca [2+] channels. Mg [2+] acts as a gate at the NMDA channel by blocking the Ca [2+] entry within the NMDA channel. Taken together, Mg [2+] acts as an important therapeutic approach to limit brain injury. The aim of this study is to assess the value of total CK and CK-BB as a marker of birth asphyxia, also, to examine the relationship between CK-BB and perinatal asphyxia both prior to the administration of Mg [2+] and after it, in order to evaluate the neuroprotective role of Mg [2+]. In the present study, the mean blood level of CK-BB at 6 h of life in the asphyxiated groups 11[98 +/- 7.3] and III [85 +/- 5.8] and at 24 h of life in group II [105 +/- 8.3] and group III [55 +/- 5.6] was significantly higher than that of the controls [p < 0.01]. At 24 h of age there was a statistical significant [p < 0.01] decrease in the level of CK-BB in group III [Mg [2+] treated] when compared to group II [no Mg [2+] treatment]. Therefore, CK-BB might be useful as an early marker of brain damage in the asphyxiated infants. The outcome of the patients with perinatal asphyxia was better in group III who received Mg [2+] [22% died] than in group II who did not received Mg [2+] [46% died] and this pointed to the neuroprotective role of Mg [2+]

PCR detection of minimal residual disease in pediatric acute lymphoblastic leukemia

Over the last four decades acute lymphoblastic leukemia [ALL] of childhood has turned from a fatal to curable disease. Nevertheless, about 30% of children relapse after initial remission. Achievement of complete remission is an essential step in maintaining prolonged remission. Minimal residual disease [MRD] is usually present in most patients after completion of therapy, and multitude of techniques for its detection have been developed over the last decade. In the present study we optimized a PCR amplification of immunoglobulin heavy chain [IgH] gene rearrangements to investigate MRD in children with ALL at diagnosis and after remission. This technique seemed to be simple, reliable and more sensitive than other techniques. One year follow up of the patients after induction of remission, PCR showed a higher percentage of maintained remission among patients with negative PCR amplification of IgH gene rearrangements also provide reliable marker for relapse detection in B lineage ALL. These results will help to adopt more effective therapeutic protocols to achieve molecular remission rather than the morphological one used now a day