Background The prevalence of autism spectrum disorders(ASDs) has increased 10 times over the past half century,while paternal and maternal age at pregnancy has alsoincreased. Studies looking for an association between paternalor maternal age at pregnancy and ASDs in offspring have notbeen conclusive.Objective To assess for possible associations between paternaland maternal age at pregnancy and ASDs in offspring.Methods This case-control study had 50 case and 100control subjects, each case was matched for age and genderto two controls. Case subjects were obtained by consecutivesampling of patients aged 18 months to 7 years who visited theDevelopmental Behavioral & Community Pediatrics OutpatientClinic and private growth and development centers from Januaryto April 2013, while control group were children of the sameage range and same gender who visited pediatric outpatientclinic at Sanglah Hospital mostly due to acute respiratory tractinfection, without ASDs as assessed by the DSM-IV-TR criteria.We interviewed parents to collect the following data: maternaland paternal age at pregnancy, child’s birth weight, historyof asphyxia, hospital admission during the neonatal period,pathological labor, maternal smoking during pregnancy, paternalsmoking, and gestational age. Data analysis was performed withChi-square and Fisher’s exact tests.Results Multivariable analysis showed that higher paternal ageat pregnancy was associated with ASDs in offspring (OR 6.3;95%CI 2.0 to 19.3; P 0.001). However, there was no significantassociation between maternal age during pregnancy and theincidence of ASDs. Asphyxia and paternal smoking were alsoassociated with higher incidence of ASDs in the offspring (OR10.3; 95%CI 1.9 to 56.5; P 0.007 and OR 3.2; 95%CI 1.5 to 6.9;P 0.003, respectively).Conclusion'in offspring by 6.3 times. In addition, paternal smoking increased the risk of ASDs in offspring by 3.2 times and asphyxia increasedthe risk of ASDs in offspring by 10.3 times.
Acute myeloid leukaemia (AML) is a. malignant, clonally disease that involves proliferation of blasts in bone marrow, blood, or other tissue. The blasts most often show myeloid or monocytic differentiation. The incidence of AML increases with age, but when neonatal leukaemia does occur, it is paradoxically AML rather than ALL. All the signs and symptoms that present on patient with AML are caused by the infiltration of the bone marrow with leukaemic cells and resulting failure of normal haematopoiesis. Without the normal haematopoietic elements, the patient is at risk for developing life-threatening complications of anaemia, infection due to functional neutropenia, and haemorrhage due to thrombocytopenia. Organomegaly is seen in approximately half of patient with AML due to hepatic and sphlanic infiltration with leukaemic blasts. Prognosis of neonatal leukaemia is poor with the 6-month survival rate is only one third despite aggressive chemotherapy. It has higher mortality rate than any other congenital cancer. The researchers reported two of AML diagnosed cases in neonatal period. The first case, a one-day-old male was referred with respiratory distress and suspect Down syndrome with spontaneous petechiae. The second case, a 17-day-old female presented with bloody diarrhoea and history of hypothyroid. Dysmorphic face and hepatosplenomegalia were found in both of the physical examination. Their complete blood count revealed leukocytosis and thrombocytopenia. Peripheral blood smear revealed myeloblast 30% on the first case and 23% on the second case. Both immunophenotyping revealed the population of blast expressing myeloid lineage (CD33 and CD34).
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