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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Out of 6586 live born babies, 736 babies with jaundice were studied from 1st July 1996 to 30th June, 1997, in a city based medical college nursery. Physiological jaundice was present in 8.92% of all live born babies and accounted for 79.89% of babies with jaundice. Breast milk jaundice and prematurity were next common causes responsible for 5.29% each of all cases with neonatal jaundice. Septicaemia caused jaundice in 4.75% cases. Among the babies with jaundice appearing between day 4 and day 7 of life, breast milk jaundice was the commonest cause occurring in 49.25% cases. The last entity surfaced probably due to exclusive breastfeeding recently initiated in the baby friendly hospital nursery.
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PMID:A new look on neonatal jaundice. 1245 86

Growth hormone deficiency (GHD) may be classified into partial isolated GHD (partial IGHD), severe IGHD or multiple pituitary hormone deficiency (MPHD) by the severity of GHD or associated with deficiency of one or more other anterior pituitary hormones during provocative tests. Morphological alterations on magnetic resonance imaging (MRI) in patients with GHD include pituitary hypoplasia, absence or interruption of pituitary stalk, and absence or ectopic posterior lobe. This study investigated the auxological, clinical severity, and anatomical characteristics of the pituitary hypothalamic region by MRI and correlated their relationships. We evaluated these parameters in 45 Taiwanese children with GHD (31 males and 14 females), aged from 3.13 to 17.91 years (10.5+/-2.5), who were divided into diagnostic subgroups of partial IGHD (18 patients), severe IGHD (13 patients), and MPHD (14 patients). We found that BA-CA, peak GH, IGF-I, IGF-I SDS, and height SDS were significantly different among these three groups. The partial IGHD group had significantly higher IGF-I than the MPHD group. There was no significant difference in prematurity, cesarean delivery, birth order, neonatal jaundice, and target height among these three groups. On MRI, patients with MPHD had significantly smaller pituitary height (PHt) SDS (p = 0.0012) and higher frequency of pituitary hypoplasia, pituitary stalk interruption, and ectopic posterior lobe (p = 0.026, 0.008, 0.005, respectively) than the other two groups. Furthermore, PHt SDS was correlated not only with peak GH (r = 0.40, p = 0.0058), but also with basal IGF-I SDS (r = 0.49, p = 0.0007) and body height SDS (r = 0.44, p = 0.025). In conclusion, morphological alterations on MRI of the hypothalamic-pituitary area are correlated with the severity of hypopituitarism. Meticulous evaluation of auxological, clinical and MRI findings can help evaluation of the severity of hypopituitarism and facilitate appropriate treatment in children with GHD.
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PMID:Auxological, clinical and MRI findings in Taiwanese children with growth hormone deficiency. 1557 Sep 89

An audit of neonatal care at Modilon Hospital, Madang was performed using obstetric and neonatal data for the five years 1995-1999. The overall perinatal mortality rate (PNMR) was 51.1 per 1000 total births with an early neonatal mortality rate (ENNMR) of 12.7 and a stillbirth rate (SBR) of 38.5. 839 neonates aged 0-28 days were admitted to the Special Care Nursery. The male to female ratio was 1.3:1. 186 babies (22%) died. The case fatality rate was higher in males than females (p<0.001). Babies born at health centres or born before arrival had a significantly higher fatality rate than hospital-born babies (p<0.001). The case fatality rate was highest in babies born preterm and declined with increasing birthweight from less than 1000 to 3999 g. The major recorded causes of admission were neonatal sepsis, prematurity, neonatal jaundice, birth asphyxia, respiratory distress and meconium aspiration syndrome. 60% of deaths occurred within 48 hours of admission, 32% between 48 hours and 7 days and 8% at 7 days or older. The proportion of deaths occurring during the afternoon and night shifts was significantly higher than that during the morning shift (p<0.001). This was most likely to be related to staffing levels. The major causes of death were prematurity or low birthweight (27%), sepsis (23%) and birth asphyxia (17%). Other causes of death included congenital abnormalities, meconium aspiration and meningitis. Antenatal care is still not universally available for Papua New Guinean women. Home delivery of high-risk mothers is commonplace, and women delivering in hospital often present in established labour. Perinatal and neonatal problems are therefore frequent. Newborn babies have the right to the best available care. This can only be provided if hospitals and health facilities understand the basic requirements of neonatal care and provide designated space, adequate staffing and proper equipment.
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PMID:Neonatal outcome at Modilon Hospital, Madang: a 5-year review. 1645 Jul 79

Neonatal jaundice, a physiologic condition reflecting the interplay between developmentally modulated changes in bilirubin production and metabolism, affects virtually all newborn infants. Usually, it is an entirely benign process that is resolved at the end of the first week of life without treatment or sequelae. However, in a small percentage of neonates, unconjugated hyperbilirubinemia can pose a neurotoxic risk especially in the presence of aggravating conditions such as a diminished albumin binding capacity and/or affinity, acidosis, displacing drugs and prematurity. Although neuronal cells are considered the main target for unconjugated bilirubin (UCB) toxicity, circulating cells are also affected during neonatal hyperbilirubinemia. Moreover, the UCB ability to cause hemolysis shall further aggravate neonatal jaundice through a vicious circle. In this review, we summarize the most relevant data obtained by our group regarding UCB toxicity and the role of some risk factors for kernicterus. In order to improve the risk assessment of neurotoxicity it is essential to understand the underlying mechanisms of UCB pathophysiology.
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PMID:Bilirubin toxicity to human erythrocytes: a review. 1688 10

This study was undertaken to know the pattern of jaundice prevalent among the babies admitted at the Neonatal Intensive Care Unit (NICU) of the B. P. Koirala Institute of Health Sciences (BPKIHS). A total of 293 neonates including 201 (68.6%) males and 92 (31.4%) females were admitted over a period of one year (15th June 2001 to 14th June 2002). Prematurity (30.0%), birth asphyxia (29.0%), neonatal septicemia (25.9%) and respiratory distress (23.9%) were the most common reasons for admission to the NICU. There were 42 cases of neonatal jaundice, among which babies born to primigravidae (59.5%), exceeded those born to multigravidae (40.5%). Pathological jaundice was found in 64.3% of the admitted cases of neonatal jaundice. Prematurity (33.3%) and neonatal septicemia (25.9%) were the most common causes of pathological jaundice, while prematurity with neonatal septicemia (14.8%), ABO incompatibility (11.1%), Rh incompatibility (7.4%) and prematurity, neonatal septicemia and ABO incompatibility combined (7.4%) accounted for the remaining cases of jaundice. A more detailed study related to the pathogenesis of jaundice among neonates is needed for the prevention of this disease in them.
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PMID:Overview of cases and prevalence of jaundice in neonatal intensive care unit. 1701 6

We believe that the syndrome of bilirubin-induced neurologic dysfunction [BIND] represents a spectrum of neurologic manifestations among vulnerable infants who have experienced an exposure to bilirubin of lesser degree than generally described in previous publications. Clinical neuro-motor manifestations extend to a range of subtle processing disorders with objective disturbances of visual-motor, auditory, speech, cognition, and language among infants with a previous history of moderate-to-severe hyperbilirubinemia of varied duration. Confounding effects include prematurity, hemolysis, perinatal-neonatal complications, altered bilirubin-albumin binding, severity and duration of bilirubin exposure, and the individual vulnerability of the infant related to genetic, family, social, and educational predilection, regardless of the cause of neonatal jaundice. Tools to better assess BIND specific domains of multisensory processing disorders, identified by pyschometric, audiologic, speech, language and visual-motor, and neuromotor examination would allow for prospective surveillance of infants at risk for the syndrome.
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PMID:The clinical syndrome of bilirubin-induced neurologic dysfunction. 2164 82

Hyperbilirubinaemia is common in the newborn period, and while the vast majority of babies are unaffected, significant neurological impairment remains a risk associated with extremely high levels of bilirubin. There is concern internationally that the number of babies affected by severe neonatal hyperbilirubinaemia may be increasing. This review describes the most current published data pertaining to the incidence and causes of severe neonatal hyperbilirubinaemia in order to determine whether concern regarding the possible re-emergence of kernicterus in Australia is warranted. Seven incidence studies conducted internationally between 1988 and 2005 identify an estimated incidence of severe neonatal jaundice of between 7.1 and 45 per 100,000 births and of kernicterus at 0.4-2.7. Major pathophysiological causes or associations include ABO and other blood group incompatibility, glucose-6-phoshate-dehydrogenase deficiency, infection and haemolysis of other causes including spherocytosis. Other factors associated with poor outcomes include prematurity, male gender, ethnicity, breastfeeding and early hospital discharge. The management of severe neonatal jaundice requires multifaceted risk quantification in addition to the availability of adequate surveillance, particularly in the context of early hospital discharge. It is of concern that currently there is a paucity of incidence data in Australia relating to this potentially devastating yet generally preventable condition. Therefore, a surveillance study has been initiated through the Australian Paediatric Surveillance Unit. It is anticipated that these data will accurately define the incidence in Australia and hopefully guide strategies to prevent a condition that we may have prematurely considered to be of historical interest only.
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PMID:Severe neonatal jaundice: is it a rare event in Australia? 2207 56

This study was done to assess the prevalence of neonatal jaundice, underlying risk factors and efficacy of phototherapy, which would be of value in identifying and implementing strategies to prevent morbidity and mortality from this condition. A retrospective study was carried out in 86 neonates admitted to neonatal intensive care unit at Nepal Medical College Teaching Hospital, Attarkhel, Kathmandu from May, 2005 to April 2008. All of the newborns who developed hyperbilirubinemia and required phototherapy and/or exchange blood transfusion (EBT) were included in this study. Case records were evaluated for details of maternal and babies birth history and clinical examinations. The initiation of phototherapy and/or EBT were done by using standard guidelines. Out of total of 820 NICU admissions, 86 (10.5%) had significant hyperbilirubinemia. Amongst them 59.3% were male and 40.7% female. Septicemia, prematurity and ABO incompatibility were observed in 33.7%, 23.2% and 13.9% cases respectively. Phototherapy was required in 95.5% and EBT in 4.6% cases. In our study, septicemia, prematurity and ABO incompatibility were found to be the most common risk factors of neonatal jaundice. The data showed, phototherapy as an effective procedure in management of neonatal hyperbilirubinemia.
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PMID:Overview of neonatal hyperbilirubinemia at Nepal Medical College Teaching Hospital. 2280 17

Neonatal jaundice is a leading cause of hospitalization in the first week of life worldwide. If inappropriately managed, it may result in significant bilirubin-induced mortality and disability. We set out to describe the epidemiology of neonatal hyperbilirubinemia as well as the practices and challenges in the care of infants with significant neonatal hyperbilirubinemia (SNH) in Nigeria, as basis for policy intervention and research priorities. We systematically searched PubMed, Scopus, EMBASE, Cumulative Index to Nursing and Allied Health Literature, WHO Library Database, African Index Medicus, African Journals Online, and local journals for studies published between January 1960 and December 2014. We included studies, without restriction on methodological design that provided evidence on the incidence/prevalence, etiological /risk factors and adverse outcomes of hyperbilirubinemia, care-seeking practices, diagnosis and treatment, as well as follow-up evaluation of infants with SNH in Nigeria. A total of 558 studies were identified from all sources out of which 198 (35.5%) were finally selected. SNH accounted for about one in five neonatal admissions and has been associated consistently with substantial case fatality and neuro-developmental sequelae such as cerebral palsy and auditory impairments, especially among out-born babies. Glucose-6-phosphate dehydrogenase (G6PD) deficiency, prematurity/low birth weight, infection, and ABO incompatibility were most frequently, and Rhesus disease rarely, associated with SNH. Late presentation at appropriate health facilities was common and resulted in high rates of acute bilirubin encephalopathy (ABE), kernicterus and avoidable exchange transfusions. Uniform practice guidelines, including developmental assessment and surveillance of infants with SNH, were rare at all levels of healthcare delivery. In summary, since 1960, SHN persists as a major contributor to neonatal mortality and developmental disabilities in Nigeria. The underpinning maternal, perinatal and neonatal factors as well as systems-based constraints are not insurmountable. Systematic and sustained interventions are warranted to curtail the disproportionate and perennial burden of this condition in this population.
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PMID:The burden and management of neonatal jaundice in Nigeria: A scoping review of the literature. 2675 12

Background: Autism spectrum disorders (ASD) are complex psychiatric disorders, with gene environment interaction being in the basis of their etiology. The association of perinatal complications and ASD is well established. Recent findings suggested that oxidative stress and polymorphism in genes encoding antioxidant enzymes might be involved in the development of ASD. Glutathione transferases (GSTs) have an important role in the antioxidant defense system. We aimed to establish whether the predictive effects of prenatal and perinatal complications (as possible oxidative stress inducers) on ASD risk are dependent on GST polymorphisms. Methods: The study included 113 ASD cases and 114 age- and sex group-matched healthy controls. All participants were genotyped for GSTA1, GSTM1, GSTT1, and GSTP1 polymorphisms. The questionnaire regarding prenatal and perinatal risk factors and complications was administered for all the subjects in the study. Results: The evaluated perinatal complications as a group significantly increased the risk of ASD [odds ratio (OR) = 9.415; p = 0.000], as well as individual perinatal complications, such as prematurity (OR = 11.42; p = 0.001), neonatal jaundice (OR = 8.774; p = 0.000), respiratory distress syndrome (OR = 4.835; p = 0.047), and the use of any medication during pregnancy (OR = 2.413; p = 0.03). In logistic regression model, adding GST genotypes did not modify the significant effects found for prematurity and neonatal jaundice as risk factors in ASD. However, there was a significant interaction of GST genotype with medication use during pregnancy and the use of tocolytics during pregnancy, which was predictive of ASD risk only in carriers of GSTM1-null, as opposed to carriers of GSTM1-active genotype. Conclusion: Specific perinatal complications may be significant risk factors for ASD. GSTM1 genotype may serve as a moderator of the effect of some prenatal factors on the risk of ASD such as using medication during pregnancy. It may be speculated that different oxidative stress-related genetic and environmental factors could lead to development of ASD. Apart from etiological mechanisms, possible therapeutic implications in ASD are also discussed.
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PMID:Autism Spectrum Disorders and Perinatal Complications-Is Oxidative Stress the Connection? 3168 Oct 27


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