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Hemolytic Disease of the Fetus and Newborn
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Pedro Argoti, Ana M. Angarita, Giancarlo Mari
Anemic neonates are usually treated with transfusions or exchange transfusions as necessary. They often need phototherapy for hyperbilirubinemia. Breastfeeding is not contraindicated. A hearing screening test is indicated during the neonatal period and at 2 years of age given that hyperbilirubinemia can cause sensorineural hearing loss.
Erythroblastosis fetalis
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Avinash Patil, Brian Brocato, Rebecca A. Uhlmann, Giancarlo Mari
Neonatology management of an infant with hemolytic disease of the newborn focuses on monitoring the level of anemia and hyperbilirubinemia. Symptoms of anemia, such as tachycardia, usually warrant RBC transfusions. In severe cases, exchange transfusions may be necessary to remove the maternal antibodies from the circulation of the infant. Hyperbilirubinemia clinically presents as jaundice. Bilirubin levels are monitored and controlled with phototherapy and IV hydration.
Adenosine kinase deficiency
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
First symptoms can be severe or prolonged conjugated hyperbilirubinemia and hypoglycemia. Liver disease is variable with hepatomegaly, increases of liver transaminases and cholestasis, ranging from mild hepatopathy to liver failure. It tends to improve with increasing age. Microvesicular hepatic steatosis is a typical finding. Furthermore, in five patients examined, liver biopsy revealed portal or periportal fibrosis (four patients), cholestasis (two patients), a reduced number of bile ducts (two patients) and mild lobular hepatitis (one patient) [2].
Recognizing skin conditions in patients with cirrhosis: a narrative review
Published in Annals of Medicine, 2022
Ying Liu, Yunyu Zhao, Xu Gao, Jiashu Liu, Fanpu Ji, Yao-Chun Hsu, Zhengxiao Li, Mindie H. Nguyen
Jaundice (Figure 3(c)) describes discolouration of the skin, sclera and mucous membranes that is attributable to the accumulation of bilirubin and its metabolites in the tissues. Jaundice generally begins to become visible when the concentration of serum bilirubin surpasses about 2 mg/dL (34 mmol/L). The colour of the skin varies from lemon yellow to apple green, gradually evolving as the serum bilirubin level becomes elevated. According to the presence of conjugated or unconjugated components of bilirubin, we can classify the three major groups of underlying causes of jaundice: prehepatic, intrahepatic or post-hepatic. Prehepatic jaundice involves haemolytic anemias, which can also be seen in neonatal physiological jaundice and breast milk jaundice. Intrahepatic jaundice involves both conjugated and unconjugated hyperbilirubinemia resulting from liver failure-associated severe acute hepatitis or cirrhosis. Other intrahepatic causes of hyperbilirubinemia include intrahepatic cholestatic diseases, such as PBC and the various congenital genetic disorders involving bilirubin metabolism or transport such as Gilbert, Crigler–Najjar syndrome, or Dubin-Johnson syndrome. Post-hepatic jaundice involves conjugated hyperbilirubinemia arising from extrahepatic issues, such as biliary tract obstruction [1].
Pharmaceutical strategies for preventing toxicity and promoting antioxidant and anti-inflammatory actions of bilirubin
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
Alessio Nocentini, Alessandro Bonardi, Simone Pratesi, Paola Gratteri, Carlo Dani, Claudiu T. Supuran
Disruptions along these metabolic/transport pathways can cause an increase in unconjugated bilirubin (e.g. from increased red blood cell destruction or impaired bilirubin conjugation) or conjugated bilirubin (e.g. from hepatocellular damage or biliary tract obstructions)1,8. Hyperbilirubinemia is traditionally defined as serum BR concentrations above 1 mg/dL, while jaundice (i.e. yellow discoloration of skin and sclera of eyes) usually occurs at serum concentration above 2–3 mg/dL9–12. Depending on the cause, hyperbilirubinaemia may appear at birth or at any time afterwards. Unconjugated hyperbilirubinaemia may cause the lipid-soluble BR to accumulate in brain, potentially causing seizures and irreversible neurological damage, leading to a condition known as acute bilirubin encephalopathy (ABE) and kernicterus spectrum disorders (KSDs), with devastating, permanent neurodevelopmental handicaps or exitus13–19.
Prevalence, risk factors, and audiological characteristics of auditory neuropathy
Published in International Journal of Audiology, 2022
Ali A. Almishaal, Shaza Saleh, Hala Alferaih, Osamah Alhelo
To document risk factors associated with ANSD, medical record review was conducted for 97 patients whom pre-, peri-, and postnatal medical history was available and complete (Supplementary File 1). The most prevalent risk factors for ANSD were consanguinity followed by a positive family history for hearing loss (Table 2). In 48 out of 97 (49.5%) children with ANSD, parents had consanguinity and 40 patients (39.6%) had family history of hearing loss or genetic basis for developing hearing loss. Birth type was reported normal spontaneous vaginal delivery in 81.4% (79/97) and caesarean section in 18.5% (18/97). Admittance to NICU as newborns was reported in 30.9% (30/97) ANSD cases. A history of hyperbilirubinemia was reported in 27 patients (27.8%) and hypoxia was observed in 9 patients (9.3%). Fever at an early age was reported in 12.8% (7/97), the oldest age at which fever had been observed was 9 months. Meningitis and ototoxic medications were reported in one infant (1.03%) and 2 infants (2.06%), respectively. Other pre and postnatal medical conditions were also noted. Among these conditions, vision problems (2.1%), developmental delay (5.15%), cleft lip/palate (2.1%), gestational diabetes (2.1%), and congenital heart problems (3.1%) were reported in children identified with ANSD.