Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is prevalent in Thailand. This condition can cause acute hemolysis during oxidative stress and also severe hyperbilirubinemia in the newborn in some populations. Our aim was to study the prevalence of G6PD deficiency in relation to neonatal jaundice. We performed quantitative red blood cell (RBC) G6PD assay in the cord blood of 505 male subjects. Observation of jaundice and determination of bilirubin level as well as work up for other causes of jaundice were made in the G6PD deficiency group compared to a G6PD normal group. Questionnaires were also sent for further follow up to both groups. The results of the study were as follows: Sixty-one of 505 male (12.08%) had RBC G6PD deficiency (Group I). The rest (444 cases) had normal G6PD (Group II). In Group I, 49.15% developed neonatal jaundice, of which 28.82% were physiologic and 20.33% were pathologic jaundice. In group II, 23.68% developed jaundice; 16.51% were physiologic and 7.17% were pathologic jaundice, respectively. Onset of jaundice, date of peak bilirubin and peak bilirubin level in Group I and Group II were not statistically different. ABO incompatibility was associated with Group I in 17.24% and with Group II in 9.09%. Hospitalization day in Groups I and II were not statistically different. Other associated diseases were found in both groups, ie infection, congenital malformation, respiratory distress syndrome, but there was no significant difference in terms of jaundice. Phototherapy was required in 18.64% and 10.28% in Group I and II with a duration of 3.91 +/- 1.24 and 3.21 +/- 1.75 days, respectively. One case in Group I who was also premature received one exchange blood transfusion due to severe sepsis but he did not survive. One case in Group II who had polycythemia was successfully treated by partial exchange transfusion with plasma.
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PMID:Glucose-6-phosphate dehydrogenase deficiency in the newborn: its prevalence and relation to neonatal jaundice. 862 93

Technetium Tc-99m disofenin cholescintigraphy (CS) and ultrasonography (US) are two major clinical methods used in differentiating biliary atresia (BA) from neonatal jaundice. To compare the diagnostic utility of these two modalities, 66 patients with neonatal cholestasis (15 BA, 3 choledochal cyst (CC), 32 neonatal hepatitis, 13 prolonged jaundice, 2 total parenteral nutrition, and 1 sepsis) underwent Tc-99m disofenin CS and US. The diagnostic sensitivity, specificity, and accuracy of CS in differentiating BA from other forms of neonatal jaundice was 100%, 87.5%, and 90.5%, respectively, and for US 86.7%, 77.1%, and 79.4%, respectively. Tc-99m disofenin CS after premedication with phenobarbital and cholestyramine is a convenient and reliable method of differentiating BA from neonatal hepatitis, with a diagnostic accuracy superior to that of US. However, US is the initial imaging procedure of choice in patients presenting with jaundice to rule out anatomic anomalies such as CC.
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PMID:Comparison technetium of Tc-99m disofenin cholescintigraphy with ultrasonography in the differentiation of biliary atresia from other forms of neonatal jaundice. 903 6

Sepsis is believed to increase the risk of bilirubin brain toxicity, but the mechanism is not known. Adult male Sprague-Dawley rats were injected intraperitoneally with either 20 mg/kg Escherichia coli lipopolysaccharide, approximately 5 x 10(9)/kg CFU Listeria monocytogenes or vehicle 48 h prior to sacrifice. Rats were killed with an intraperitoneal injection of pentobarbital. Mitochondrial membrane fractions were produced by homogenization of the brains and differential centrifugation in 0.32 M sucrose. The mitochondrial pellet was resuspended in distilled water and sonicated to rupture the mitochondria. The protein concentration of the suspension was standardized to 2.5 mg/ml. Bilirubin oxidation was assayed in a pH 8.2, 0.1 M barbital buffer containing 10 microM bilirubin, 5 mM EDTA, and 500 U/ml catalase. Optical density was measured at 440 nm before and after a 60-min incubation at 37.5 degrees C. There were no differences between the control, endotoxemic, and septic groups as far as the ability of brain mitochondrial membranes to oxidize bilirubin (bilirubin oxidation rate: 289 +/- 11 vs. 295 +/- 9 vs. 296 +/- 12 pmol/min/mg protein, mean +/- SD). We conclude that endotoxemia or sepsis do not change the ability of brain mitochondrial membranes to oxidize bilirubin. If sepsis truly increases the risk of bilirubin encephalopathy in neonatal jaundice, this is likely to involve other mechanisms.
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PMID:Effects of endotoxemia and sepsis on bilirubin oxidation by rat brain mitochondrial membranes. 957 65

Auditory brainstem responses (ABR) were studied in 52 children upto the age of 3 months, suffering from neonatal jaundice, prematurity, pyogenic meningitis and septicemia. Absolute latency of wave I and interpeak latency I-V were found to be significantly delayed in cases of jaundice and absolute latency of wave V and interpeak latency I-V were prolonged in cases with prematurity. In cases following pyogenic meningitis absolute latency of wave V and interpeak latency of I-III, I-V were significantly delayed compared to septicemia where absolute latency I, V and interpeak latency I-V were significantly delayed (P < 0.05). Maximum auditory insult was seen in cases with neonatal jaundice where 30.77% each had severe SN deafness and 30.77% had moderate degree of deafness compared to prematurity, meningitis and septicemia where 14.28, 7.69 and 25% were found to have severe SN deafness and 7.14, 38.46 and 25% had moderate deafness. Overall incidence of deafness of any kind in these factors was 44.23%.
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PMID:Comparative ABR profile in high risk infants. 967 26

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

The aim of this study is to explore the relationship between high cord blood thyroid-stimulating hormone (TSH) level and in-utero stress to the fetus in gestational diabetes mellitus (GDM). Cord blood TSH results were analyzed in 1,578 euthyroid infants from singleton pregnancies with GDM: 103 with elevated TSH (>16 mIU/l) and 1,475 with normal TSH. Maternal characteristics, pregnancy outcome and perinatal complications were compared between the two groups. Multiple logistic regression was used to study the association between high cord blood TSH level and various perinatal complications which reflect in-utero stress in GDM after adjusting for the confounding effects of parity, instrumental delivery, cesarean section and baby gender. High cord blood TSH level was found to be associated with the 1-min Apgar score <7 (OR 3.31, 95% CI 1.78-6.16), birth trauma (OR 3.44, 95% CI 1.11-10.69), neonatal jaundice requiring treatment (OR 2.08, 95% CI 1.30-3.32), neonatal sepsis (OR 2.34, 95% CI 1.24-4.42), respiratory complications (OR 3.45, 95% CI 1.37-8.70), neurological complications (OR 8.01, 95% CI 1.91-33.60) and overall perinatal morbidity (OR 2.41, 95% CI 1.58-3.67). Cord blood TSH level seems to be a better and independent indicator of the in-utero stress to the fetus in GDM when compared to the commonly used sugar profile result and HbA1c level.
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PMID:Neonatal hyperthyrotropinemia in gestational diabetes mellitus and perinatal complications. 1547 63

The records of all low birth weight (LBW) neonates admitted into the Neonatal Unit of the Lagos University Teaching Hospital (LUTH) from January 1997 to December 2001 were retrospectively analysed in order to determine the outcome and risk factors associated with mortality. There were 535 LBW admissions of which 411(76.8%) survived while 124(23.2%) died. The birth weight specific mortality rate for the < 1000g neonates was 818 per 1000, 451 per 1000 for the 1000-1499g, 216 per 1000 for the 1500-1999g, and 67 per 1000 for the 2000-2499g neonates (X2 = 127.70, p = 0.0001). Primary indications for admission were neonatal sepsis (25.2%), perinatal asphyxia (23.0%) and neonatal jaundice (19.6%) with case fatality rates of 20.0%, 34.1% and 10.5% respectively (X2 = 34.24, p = 0.00001). Death occurred within 48 hours of admission in 45.2% of subjects and by the 7th day, 72.6% had died (X2 = 70.07, p = 0.0001). Significant risk factors associated with mortality were birth weight [OR 4.24, 95% CI = 3.14-5.72] and category of LBW [OR 2.79, 95% CI = 1.65-4.69]. Sex, twinning, booking status and mode of delivery had no significant influence on mortality. Since the provision of adequate intensive care for these vulnerable infants remains a major challenge in countries with poor resources, efforts should be intensified to implement effective strategies for the reduction of low birth weight deliveries.
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PMID:Outcome of low birth weight neonates in a tertiary health care centre in Lagos, Nigeria. 1597 35

Unconjugated bilirubin (UCB) encephalopathy is a predominantly early life condition resulting from the impairment of several cellular functions in the brain of severely jaundiced infants. However, only few data exist on the age-dependent effects of UCB and their association with increased vulnerability of premature newborns, particularly in a sepsis condition. We investigated cell death, glutamate efflux, and inflammatory cytokine dynamics after exposure of astrocytes at different stages of differentiation to clinically relevant concentrations of UCB and/or lipopolysaccharide (LPS). Younger astrocytes were more prone to UCB-induced cell death, glutamate efflux, and inflammatory response than older ones. Furthermore, in immature cells, LPS exacerbated UCB effects, such as cell death by necrosis. These findings provide a basis for the increased susceptibility of premature newborns to UCB deleterious effects, namely when associated with sepsis, and underline how crucial the course of cell maturation can be to UCB encephalopathy during moderate to severe neonatal jaundice.
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PMID:Bilirubin-induced inflammatory response, glutamate release, and cell death in rat cortical astrocytes are enhanced in younger cells. 1624 28

Neonatal jaundice (NJ) and sepsis are common causes of neonatal mortality in sub-Saharan Africa, but little is known about the long-term morbidity in this setting. This study aimed to describe the neurological and developmental sequelae of severe neonatal hyperbilirubinaemia and neonatal sepsis (NS) in a district hospital in rural Kenya. Twenty-three term infants with NJ [total serum bilirubin (TSB) >300 mumol/l] and 24 infants with a history of NS were identified from hospital records. These children were compared to 40 children from the community (CC) without neonatal problems. At ages 18-32 months, the children's neurological, motor and developmental status were assessed, and blood groups of the NJ and NS subjects and their mothers were determined. Ten (43%) of the NJ subjects were unable to sit and/or stand independently. The NJ subjects had significantly more neurological, motor and developmental difficulties and caused greater maternal concern than the CCs. Five (21%) of the NJ subjects had possible blood group incompatibility. The NS subjects had significantly more motor and eye-hand difficulties and maternal concerns expressed than the CCs. Severe NJ in term infants (of mainly non-haemolytic origin) was associated with a high prevalence of neurological and developmental sequelae at ages 18-32 months. The NS is also associated with neuro-developmental sequelae, but the pattern is different to those seen in NJ. Since NS is common in resource poor countries, this may be an important cause of neuro-developmental impairment in children living in this setting.
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PMID:Neurological and developmental outcome of neonatal jaundice and sepsis in rural Kenya. 1626 36

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


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