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unconjugated hyperbilirubinemia

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https://www.readbyqxmd.com/read/28321066/gilbert-syndrome-with-concomitant-hereditary-spherocytosis-presenting-with-moderate-unconjugated-hyperbilirubinemia
#1
Mitsuhiko Aiso, Minami Yagi, Atsushi Tanaka, Kotaro Miura, Ryo Miura, Toshihiko Arizumi, Yoriyuki Takamori, Sayuri Nakahara, Yoshihiro Maruo, Hajime Takikawa
We experienced a case of a 19-year-old man with Gilbert syndrome with concomitant hereditary spherocytosis. The patient presented with moderate unconjugated hyperbilirubinemia, and inherited etiology was strongly suspected. The diagnosis of Gilbert syndrome was confirmed by the genetic analysis of the UGT1A1 gene, demonstrating UGT1A1*28 and compound heterozygote UGT1A1*6. In addition, since the laboratory findings and imaging studies revealed lysemia as well as gallstone and splenomegaly, a diagnosis of hereditary spherocytosis was made as a comorbidity...
2017: Internal Medicine
https://www.readbyqxmd.com/read/28300459/mildly-elevated-unconjugated-bilirubin-is-associated-with-reduced-platelet-activation-related-thrombogenesis-and-inflammation-in-gilbert-s-syndrome
#2
Avinash R Kundur, Abishek B Santhakumar, Andrew C Bulmer, Indu Singh
Gilbert's syndrome (GS) is associated with a mild unconjugated hyperbilirubinemia, increased circulating antioxidant capacity, and reduced cardiovascular disease (CVD) risk. The current study investigated whether mildly elevated circulating unconjugated bilirubin (UCB) is negatively associated with multiple thrombotic risk factors including platelet activity, hemostatic function, and inflammation in individuals with GS. Blood samples were collected from matched GS and control subjects (14 per group). Activation-dependent platelet surface marker expression of PAC-1 (binds to GPIIb/IIIa surface receptors on activated platelets) and CD62P (marker for P-selectin released from activated degranulated platelets) was assessed in adenosine diphosphate (ADP)-stimulated platelets using flow cytometry...
March 16, 2017: Platelets
https://www.readbyqxmd.com/read/28296739/ugt1a1-28-relationship-with-abnormal-total-bilirubin-levels-in-chronic-hepatitis-c-patients-outcomes-from-a-case-control-study
#3
Marcelo Moreira Tavares de Souza, Victor Van Vaisberg, Rodrigo Martins Abreu, Aline Siqueira Ferreira, Camila daSilvaFerreira, Paulo Dominguez Nasser, Helena Scavone Paschoale, Flair José Carrilho, Suzane Kioko Ono
Gilbert syndrome (GS) is a frequent benign clinical condition, marked by intermittent unconjugated hyperbilirubinemia, mostly due to the polymorphism uridine diphosphate-glucuronosyltransferase 1A1*28 (UGT1A1*28). Hyperbilirubinemia has been reported in a GS patient undergoing hepatitis C treatment, and other UGT isoforms polymorphisms have been linked to worse outcomes in viral hepatitis. Yet, little is known to GS contributions' to the liver disease scenario. Our aim was to assess UGT1A1 genotypes' frequency in chronic hepatitis C (CHC) patients and correlate with total bilirubin (TB)...
March 2017: Medicine (Baltimore)
https://www.readbyqxmd.com/read/28296151/bilirubin-protects-the-aging-heart
#4
EDITORIAL
Samuel O Adeosun, David E Stec
In this issue of Acta Physiologica, Bakrania, et al., examined the effects of hyperbilirubinemia on the aging male heart under basal conditions and after ischemic injury (1) . Heart disease is a significant problem for the aging population in general and males in particular. Ischemic heart disease is a leading cause of global mortality for males and is responsible for one out of four deaths in males in the United States. Therefore, developing novel strategies to combat the development and progression of heart disease has the potential to save millions of lives a year...
March 10, 2017: Acta Physiologica
https://www.readbyqxmd.com/read/28283555/developmental-genetic-dietary-and-xenobiotic-influences-on-neonatal-hyperbilirubinemia
#5
Mei-Fei Yueh, Shujuan Chen, Nghia Nguyen, Robert H Tukey
Hyperbilirubinemia, caused by the accumulation of unconjugated bilirubin, is one of the most common clinical diagnoses in both premature and term newborns. Owing to the fact that bilirubin is metabolized solely through glucuronidation by UDP-glucuronosyltransferase (UGT) 1A1, it is now known that immaturity of UGT1A1 in combination with overproduction of bilirubin during the developmental stage acts as a bottleneck to bilirubin elimination and predisposes the infant to high TBS levels. While neonatal jaundice is mostly benign, excessively high levels of serum bilirubin in a small percentage of newborns can cause bilirubin-induced neurologic dysfunction (BIND), potentially leading to permanent brain damage, a condition known as kernicterus...
March 10, 2017: Molecular Pharmacology
https://www.readbyqxmd.com/read/28263463/drug-and-drug-abuse-associated-hyperbilirubinemia-experience-with-atazanavir
#6
Jayanta Roy-Chowdhury, Namita Roy-Chowdhury, Irving Listowsky, Allan W Wolkoff
Hyperbilirubinemia is a common finding in individuals with a history of substance abuse. Although this may indicate a serious disorder of liver function, this is not always the case. An understanding of bilirubin formation, metabolism, and transport can provide a helpful approach to dealing with these patients. This is typified by studies of patients treated with the antiretroviral drug atazanavir. Atazanavir has been associated with hyperbilirubinemia in as many as one-third of individuals for whom it has been prescribed, evoking concerns of hepatotoxicity...
March 2017: Clinical Pharmacology in Drug Development
https://www.readbyqxmd.com/read/28243614/curated-human-hyperbilirubinemia-data-and-the-respective-oatp1b1-and-1b3-inhibition-predictions
#7
Eleni Kotsampasakou, Sylvia E Escher, Gerhard F Ecker
Hyperbilirubinemia is a pathological condition, very often indicative of underlying liver condition that is characterized by excessive accumulation of conjugated or unconjugated bilirubin in sinusoidal blood. In literature there are several indications associating the inhibition of the basolateral hepatic transporters Organic anion transporting polypeptide 1B1 and 1B3 (OATP1B1 and 1B3) with hyperbilirubinemia. In this article, we present a curated human hyperbilirubinemia dataset and the respective OATP1B1 and 1B3 inhibition predictions obtained from an effort to generate a classification model for hyperbilirubinemia...
April 2017: Data in Brief
https://www.readbyqxmd.com/read/28206723/clinical-study-on-amplitude-integrated-electroencephalogram-in-cerebral-injury-caused-by-severe-neonatal-hyperbilirubinemia
#8
Hongwei Wu, Zhenguang Li, Jinfeng Liu, Gang Liu, Xia Yang
BACKGROUND: This study was designed in order to assess the validity of the use of amplitude-integrated electroencephalogram (aEEG) in cerebral injury caused by severe neonatal hyperbilirubinemia. METHODS: A total of 56 full-term neonates diagnosed with severe neonatal hyperbilirubinemia and admitted to the NICU of our hospital from July 2013 to December 2014 were continuously selected for the study. The total serum bilirubin (TSB) was higher than 342 μmo/l, and was dominated by a higher amount of unconjugated bilirubin...
February 15, 2017: Minerva Pediatrica
https://www.readbyqxmd.com/read/28183002/unconjugated-free-bilirubin-in-preterm-infants
#9
Lori W E van der Schoor, Peter H Dijk, Henkjan J Verkade, Anna C J Kamsma, Andrea B Schreuder, Henk Groen, Christian V Hulzebos
BACKGROUND: Hyperbilirubinemia guidelines are based on total serum bilirubin (TSB), in combination with either gestational age (GA) or birth weight (BW), postnatal age and specific risk factors. However, TSB is a poor predictor of bilirubin-induced neurotoxicity (BIND). Free unconjugated bilirubin (UCBfree) and the UCBfree/TSB ratio are more directly related to BIND, but data on their postnatal courses are unknown. AIMS: To characterize the postnatal courses of UCBfree and UCBfree/TSB ratio, and assess their relationships with clinical characteristics...
February 6, 2017: Early Human Development
https://www.readbyqxmd.com/read/28145671/evaluation-of-jaundice-in-adults
#10
Matthew V Fargo, Scott P Grogan, Aaron Saguil
Jaundice in adults can be an indicator of significant underlying disease. It is caused by elevated serum bilirubin levels in the unconjugated or conjugated form. The evaluation of jaundice relies on the history and physical examination. The initial laboratory evaluation should include fractionated bilirubin, a complete blood count, alanine transaminase, aspartate transaminase, alkaline phosphatase, ?-glutamyltransferase, prothrombin time and/or international normalized ratio, albumin, and protein. Imaging with ultrasonography or computed tomography can differentiate between extrahepatic obstructive and intrahepatic parenchymal disorders...
February 1, 2017: American Family Physician
https://www.readbyqxmd.com/read/28100328/-repeated-yellowing-of-the-skin-and-sclera-for-2-years
#11
Xiao-Ye Yuan, Xiang-Ling He, Hui Zou, Run-Ying Zou
A two-year-old girl was admitted due to repeated yellowing of the skin and sclera for 2 years and had no other specific symptoms or signs. The use of phenobarbital could relieve the symptoms of jaundice. Multiple examinations showed increased indirect bilirubin levels, and the results of aminotransferases and liver imaging were normal. There was no evidence of hemolysis. The analysis of UGT1A1 gene in her family found that this child had double homozygous mutation of c.211G>A(G71R) and c.1456T>G(Y486D), which had been reported as the pathogenic mutation for Gilbert syndrome...
January 2017: Zhongguo Dang Dai Er Ke za Zhi, Chinese Journal of Contemporary Pediatrics
https://www.readbyqxmd.com/read/28096081/mice-with-hyperbilirubinemia-due-to-gilbert-s-syndrome-polymorphism-are-resistant-to-hepatic-steatosis-by-decreased-serine-73-phosphorylation-of-ppar%C3%AE
#12
Terry D Hinds, Peter A Hosick, Michael W Hankins, Andrea Nestor-Kalinoski, David E Stec
Gilbert's syndrome is derived from a polymorphism (TA repeat) in the hepatic UGT1A1 gene which results in decreased conjugation and increased levels of unconjugated bilirubin. Recently, we have shown that bilirubin binds directly to the fat burning nuclear peroxisome proliferator-activated receptor α (PPARα). Additionally, we have shown that serine 73 phosphorylation (Ser(P)(73)) of PPARα decreases activity by reducing its protein levels and transcriptional activity. The aim of this study was to determine if humanized mice with the Gilbert's polymorphism (HuUGT*28) have increased PPARα activation and reduced hepatic fat accumulation...
January 17, 2017: American Journal of Physiology. Endocrinology and Metabolism
https://www.readbyqxmd.com/read/28094087/-management-of-jaundice-in-the-newborn%C3%A2-35%C3%A2-gw-from-screening-to-follow-up-after-discharge-guidelines-for-clinical-practice
#13
A Cortey, L Renesme, J Raignoux, A Bedu, C Casper, P Tourneux, P Truffert
Jaundice due to unconjugated bilirubin is an everyday condition in the neonatal period because it results from the adaptation of bilirubin metabolism at this time of life. Hyperbilirubinemia has a potential neurotoxicity and although it most often resolves spontaneously, it can lead to acute and sometimes chronic encephalopathy. The latter condition is called kernicterus and induces severe and irreversible neurological sequelae. This rare complication is still reported in all countries throughout the world even if severe hyperbilirubinemia can be prevented and critical points points of failure in jaundice management are identified...
February 2017: Archives de Pédiatrie: Organe Officiel de la Sociéte Française de Pédiatrie
https://www.readbyqxmd.com/read/28093842/gilbert-syndrome-in-patients-with-type-1-diabetes-prevalence-glycemic-control-and-microalbuminuria
#14
Sigal Singer, Nurit Pilpel, Orit Pinhas-Hamiel
BACKGROUND: Gilbert syndrome (GS) is a common hereditary condition, characterized by intermittent unconjugated hyperbilirubinemia. In adults with type 2 diabetes and GS, a markedly lower prevalence of nephropathy was documented, suggesting a beneficial effect of hyperbilirubinemia. We investigated the prevalence of GS among individuals with type 1 diabetes mellitus (T1DM), and the prevalence of microalbuminuria. METHODS: The prevalence of GS was assessed in 401 (204 female) patients with T1DM, median age 21...
January 17, 2017: Pediatric Diabetes
https://www.readbyqxmd.com/read/28063966/linking-organic-anion-transporting-polypeptide-1b1-and-1b3-oatp1b1-and-oatp1b3-interaction-profiles-to-hepatotoxicity-the-hyperbilirubinemia-use-case
#15
Eleni Kotsampasakou, Sylvia E Escher, Gerhard F Ecker
Hyperbilirubinemia is a pathological condition of excessive accumulation of conjugated or unconjugated bilirubin in blood. It has been associated with neurotoxicity and non-neural organ dysfunctions, while it can also be a warning of liver side effects. Hyperbilirubinemia can either be a result of overproduction of bilirubin due to hemolysis or dyserythropoiesis, or the outcome of impaired bilirubin elimination due to liver transporter malfunction or inhibition. There are several reports in literature that inhibition of organic anion transporting polypeptides 1B1 and 1B3 (OATP1B1 and OATP1B3) might lead to hyperbilirubinemia...
March 30, 2017: European Journal of Pharmaceutical Sciences
https://www.readbyqxmd.com/read/28036021/monitoring-the-response-of-hyperbilirubinemia-in-the-mouse-brain-by-in-vivo-bioluminescence-imaging
#16
Isabella Manni, Giuliana Di Rocco, Salvatore Fusco, Lucia Leone, Saviana Antonella Barbati, Carmine Maria Carapella, Claudio Grassi, Giulia Piaggio, Gabriele Toietta
Increased levels of unconjugated bilirubin are neurotoxic, but the mechanism leading to neurological damage has not been completely elucidated. Innovative strategies of investigation are needed to more precisely define this pathological process. By longitudinal in vivo bioluminescence imaging, we noninvasively visualized the brain response to hyperbilirubinemia in the MITO-Luc mouse, in which light emission is restricted to the regions of active cell proliferation. We assessed that acute hyperbilirubinemia promotes bioluminescence in the brain region, indicating an increment in the cell proliferation rate...
December 28, 2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28025333/modulation-of-bilirubin-neurotoxicity-by-the-abcb1-transporter-in-the-ugt1-lethal-mouse-model-of-neonatal-hyperbilirubinemia
#17
Luka Bočkor, Giulia Bortolussi, Simone Vodret, Alessandra Iaconcig, Jana Jašprová, Jaroslav Zelenka, Libor Vitek, Claudio Tiribelli, Andrés F Muro
Moderate neonatal jaundice is the most common clinical condition during newborn life. However, a combination of factors may result in acute hyperbilirubinemia, placing infants at risk of developing bilirubin encephalopathy and death by kernicterus. While most risk factors are known, the mechanisms acting to reduce susceptibility to bilirubin neurotoxicity remain unclear. The presence of modifier genes modulating the risk of developing bilirubin-induced brain damage is increasingly being recognised. The Abcb1 and Abcc1 members of the ABC family of transporters have been suggested to have an active role in exporting unconjugated bilirubin from the central nervous system into plasma...
December 25, 2016: Human Molecular Genetics
https://www.readbyqxmd.com/read/27995496/neuroprotective-effect-of-erythropoietin-on-phenylhydrazine-induced-hemolytic-hyperbilirubinemia-in-neonatal-rats
#18
Asli Memisoglu, Meltem Kolgazi, Akan Yaman, Elif Bahadir, Serap Sirvanci, Berrak Ç Yeğen, Eren Ozek
Neonatal unconjugated hyperbilirubinemia might cause severe bilirubin neurotoxicity in especially hemolytic conditions. The study aimed to elucidate the potential neuroprotective effects of erythropoietin (EPO) in hemolysis-induced hyperbilirubinemia. In newborn rats, hyperbilirubinemia secondary to hemolysis was induced by injecting with phenylhydrazine hydrochloride (PHZ) and rats were injected with either vehicle or EPO. At 54th hour of the PHZ injection, rats were decapitated. Serum levels of TNF-α, IL-1β, IL-10, brain-derived neurotrophic factor (BDNF) and S100-B and brain malondialdehyde, glutathione levels and myeloperoxidase activities were measured...
December 19, 2016: Neurochemical Research
https://www.readbyqxmd.com/read/27980881/obstetric-obesity-is-associated-with-neonatal-hyperbilirubinemia-with-high-prevalence-in-native-hawaiians-and-pacific-island-women
#19
Luc Ra Rougée, Shogo J Miyagi, Abby C Collier
Obesity and pregnancy both place the liver under metabolic stress, but interactions between obstetric obesity and bilirubin metabolism have not been studied. We determined associations between obesity, maternal/neonatal bilirubin levels, and uridine 5'diphosphate-glucuronosyltransferase 1A1 (UGT1A1) enzyme that eliminates bilirubin. Adult livers were analyzed for UGT1A1 expression, activity, and bilirubin clearance by pharmacokinetic modeling. Then, matched maternal and neonatal sera (N = 450) were assayed for total and unconjugated bilirubin...
December 2016: Hawai'i Journal of Medicine & Public Health: a Journal of Asia Pacific Medicine & Public Health
https://www.readbyqxmd.com/read/27978934/-the-analysis-of-ugt1a1-gene-mutations-in-hereditary-unconjugated-hyperbilirubinemia
#20
L Sun, L Zhang, M Li, X Y Teng, L M Qi, X G Zhou, Z W Lang, P Wang
No abstract text is available yet for this article.
November 20, 2016: Zhonghua Gan Zang Bing za Zhi, Zhonghua Ganzangbing Zazhi, Chinese Journal of Hepatology
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