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Neonatal jaundice
Published in Alison Edwards, Postnatal and Neonatal Midwifery Skills, 2020
Neonatal jaundice develops as a result of the breakdown of the excess fetal red blood cells, no longer required after birth, into haem and globin. There is also a simultaneous change of cell haemoglobin from fetal to adult haemoglobin. The haem component is reduced into unconjugated bilirubin, which is fat soluble and requires proteins to transport it to the liver for disposal. If this protein is absent there is a risk that unconjugated bilirubin can remain in the circulation and cross into the brain.
DRCOG OSCE for Circuit C Answers
Published in Una F. Coales, DRCOG: Practice MCQs and OSCEs: How to Pass First Time three Complete MCQ Practice Exams (180 MCQs) Three Complete OSCE Practice Papers (60 Questions) Detailed Answers and Tips, 2020
Initial tests used to investigate prolonged neonatal jaundice (jaundice lasting > 14 days) include serum total and direct bilirubin levels, serum liver function tests, full blood count and film, full infection screen, and thyroid function tests. An abdominal ultrasound scan, colloid liver scanning and biopsy are second-line investigations.
Haematology and oncology
Published in Jagdish M. Gupta, John Beveridge, MCQs in Paediatrics, 2020
Jagdish M. Gupta, John Beveridge
9.12. Which of the following statements is/are true of hereditary spherocytosis (HS)?About 50% of affected infants have moderately severe neonatal jaundice.The presence of spherocytes on examination of a blood film in the newborn confirms the diagnosis.Aplastic crises occur due to parvovirus infection.Intravascular haemolysis is a common feature.Red blood cell osmotic fragility is increased.
Inhibitory Effects of Bilirubin on Colonization and Migration of A431 and SK-MEL-3 Skin Cancer Cells Compared with Human Dermal Fibroblasts (HDF)
Published in Cancer Investigation, 2021
Javad Saffari-Chaleshtori, Ali Shojaeian, Esfandiar Heidarian, Sayed Mohammad Shafiee
Bilirubin is a tetrapyrrole and an endogenous catabolic product that is formed during heme catabolism. After lysis of the erythrocytes in the spleen and liver, macrophages remove the hemoglobin and separate the heme group. Subsequently, heme oxygenase converts heme to biliverdin that in turn is converted to unconjugated bilirubin by biliverdin reductase. Unconjugated bilirubin combines with glucuronic acid to form conjugated bilirubin in the liver and is then excreted in bile (11). The normal level of (unconjugated) bilirubin under physiological conditions is around 0.2 mg/dl (3.42 µM) (12). Bilirubin is a lipophilic compound and tends to cross the blood-brain barrier (13). This compound, at high concentrations, can exert neurotoxic effects and therefore induce severe complications in neurons (14). Neonatal jaundice is the most common cause of bilirubinemia. The genetic causes of this condition include Gilbert-Meulengracht, Crigler-Najjar, and Rotor syndrome (12). Serum bilirubin concentrations lower than 12–14 mg/dl are tolerable while higher levels lead to mental retardation especially in neonates (15). However, the mutation in the UDP-glycuronyltransferase gene causes a natural increase in bilirubin up to 1–3 mg/dl (17–51 µM) in Gilbert-Meulengracht syndrome (16).
Tet1-mediated DNA demethylation involves in neuron damage induced by bilirubin in vitro
Published in Toxicology Mechanisms and Methods, 2018
Panhong Gou, Xiaoling Qi, Rui Yuan, Haojie Li, Xiaoling Gao, Junling Wang, Benzhong Zhang
Neonatal jaundice is the result of an increase in serum-free bilirubin and is present in two thirds of all newborns during the first week of life (Gartner 1994; Hanko et al. 2005). Clinical evidence suggested that the duration of UCB-mediated stress is an important factor in the pathogenesis of bilirubin-induced brain damage (de Vries et al. 1985). The concentration of glutamate increased when neuron cells were exposed to UCB in vitro and in vivo, which is associated with the role of excitotoxin as an initiator of apoptosis (Mattson 2003). Although oxidative stress as a result of compromised free radical scavenging activity or increased production of ROS has been proposed as one mechanism for bilirubin-induced neurotoxicity (Brito et al. 2008; Lange et al. 2008; Silva et al. 2012; Qaisiya et al. 2014), so far, the underlying mechanisms of the neurotoxicity of bilirubin in the hyperbilirubinemia remain unclear. In this study, primary neuron culture was used as a model for investigating the neurotoxicity of bilirubin. Our work presented evidence to support the notion that bilirubin-mediated neurotoxicity is related to oxidative stress, and an increase in neuronal cell apoptosis.
Neonatal outcomes and congenital anomalies in pregnancies affected by hypothyroidism
Published in Annals of Medicine, 2021
Zareen Kiran, Aisha Sheikh, Khadija Nuzhat Humayun, Najmul Islam
We divided the gestational age at birth into “extremely preterm (<28)”, “very preterm (28–31)”, “late preterm (32–36)”, “term (37–42)” and “post-term (>42)”. Birth Weight: Defined as “Low (<2500 g)”, “Appropriate (2500–4000 g)” and “Large (>4000 g)”. Low APGAR score at 5 min: Assessment of physical health is noted in the one-minute APGAR score (scored from 0 to 10) and then again at five minutes to assess how the baby has responded to any resuscitation attempts. A score below 7 is considered low at 5 min. Respiratory complications (including respiratory distress syndrome, neonatal sepsis, and need for phototherapy): As indicated by the physician’s notes. Neonatal jaundice: Total bilirubin levels above 17 µmol/L checked within 48–72 h of birth. Hypocalcaemia: Serum calcium levels below the reference range defined for neonates in our hospital, that is, 146.2–173.4 µmol/L checked at any time after birth till hospital discharge. NICU (neonatal intensive care unit) admission: Neonates requiring ICU admission for 24 h or more. Neonatal death: Classified further as early; if occurs in less than 7 days or late; if occurs between 7 and 28 days of life. Congenital anomalies are defined using International Classification of Diseases (ICD-10) codes Q00-Q99 but excludes “inborn errors of metabolism” (codes E70-E90). Conditions of clinical importance like cardiovascular defects, nervous system defects and urogenital anomalies were grouped separately. Rest of the conditions of less clinical importance were also noted and detailed in the results.