Resin Hemoperfusion for Unconjugated Bilirubin Removal

2015 ◽  
pp. 90-100 ◽  
Author(s):  
S. Sideman ◽  
L. Mor ◽  
M. Mihich ◽  
D. Mordohovich ◽  
S. Lupovich ◽  
...  
Keyword(s):  
Unconjugated Bilirubin

scholarly journals Dynamics of neuron-glia interplay upon exposure to unconjugated bilirubin

2011 ◽  
Vol 117 (3) ◽  
pp. 412-424 ◽  
Author(s):  
Sandra L. Silva ◽  
Catarina Osório ◽  
Ana R. Vaz ◽  
Andreia Barateiro ◽  
Ana S. Falcão ◽  
...  
Keyword(s):  
Unconjugated Bilirubin

scholarly journals Unconjugated bilirubin induces apoptosis in colon cancer cells by triggering mitochondrial depolarization

2004 ◽  
Vol 112 (3) ◽  
pp. 433-445 ◽  
Author(s):  
Pavitra Keshavan ◽  
Sandy J. Schwemberger ◽  
Darcey L.H. Smith ◽  
George F. Babcock ◽  
Stephen D. Zucker
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Unconjugated Bilirubin ◽  
Colon Cancer Cells ◽  
Mitochondrial Depolarization

Hepatic clearance of unconjugated bilirubin in cholestatic liver diseases

1974 ◽  
Vol 19 (1) ◽  
pp. 9-14 ◽  
Author(s):  
Joseph R. Bloomer ◽  
Paul D. Berk ◽  
Robert B. Howe
Keyword(s):  
Liver Diseases ◽  
Hepatic Clearance ◽  
Unconjugated Bilirubin

scholarly journals Impact of voxelotor (GBT440) on unconjugated bilirubin and jaundice in sickle cell disease

2018 ◽  
Vol 10 (2) ◽  
Author(s):  
Paul Telfer ◽  
Irene Agodoa ◽  
Kathleen M. Fox ◽  
Laurie Burke ◽  
Timothy Mant ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Oxygen Affinity ◽  
Well Being ◽  
Unconjugated Bilirubin ◽  
Cell Disease ◽  
Case Patient ◽  
Disease Manifestation ◽  
Patient Reported ◽  
Hemoglobin Oxygen Affinity

For many patients with sickle cell disease (SCD), jaundice is a significant clinical disease manifestation that impacts on patient well-being. We report a case of a patient with SCD and chronic jaundice treated with voxelotor (GBT440), a novel small molecule hemoglobin oxygen affinity modulator and potential disease-modifying therapy for SCD. The case patient is a 27- year-old Black male with a long history of SCD with clinical jaundice and scleral icterus. After starting voxelotor, the patient reported that his jaundice cleared within one week, and that he felt much better with more energy, and was relieved after his eyes cleared. Voxelotor reduced bilirubin and unconjugated bilirubin (by up to 76%), and hemoglobin improved from 9.9 g/dL at baseline to 11.1 g/dL at 90 days. Jaundice impacts many adults with SCD, significantly impacting self-image. Voxelotor treatment reduced bilirubin levels and improved jaundice, resulting in an improved sense of well-being in our case patient.

How dangerous Gilbert's syndrome is

2021 ◽  
pp. 8-12
Author(s):  
Roman Petrovich Stepchenkov
Keyword(s):  
Pathological Condition ◽  
Inhibitory Effect ◽  
Unconjugated Bilirubin ◽  
Breakdown Product ◽  
Gilbert’S Syndrome ◽  
Gilbert's Syndrome ◽  
Bilirubin Metabolism ◽  
Gallbladder Dyskinesia ◽  
Conjugation Process ◽  
Loss Of Appetite

Gilbert's syndrome is a benign (functional) hyperbilirubinemia, which is based on a hereditary disorder of bilirubin metabolism, as a result of which the concentration of unbound bilirubin can increase several times. Bilirubin, being a breakdown product of hemoglobin, circulates through the bloodstream, combining with albumin molecules. Such bilirubin is called indirect. In the endoplasmic reticulum, it is conjugated; the enzyme glucuronyltransferase is responsible for this process. In Gilbert's syndrome, as a result of insufficient production of this enzyme, the conjugation process is disrupted, and, as a result, the concentration of unconjugated bilirubin increases. According to statistics, this pathological condition is observed in about 5 % of Russians. This syndrome was first described in 1901 by the French physician Augustin Nicolas Gilbert, and was subsequently named after him. The literature also contains references to this syndrome, described as «constitutional hepatic dysfunction», «familial non-hemolytic hyperbilirubinemia», «idiopathic non-conjugated hyperbilirubinemia». Gilbert's syndrome is inherited in an autosomal recessive manner; men get ill 3–4 times more often than women. A number of scientists associate this with a possible inhibitory effect of testosterone on the enzyme UDP-GT1, which breaks down bilirubin. Clinically, Gilbert's syndrome is manifested by episodes of jaundice caused by an increase in the level of unconjugated bilirubin in the blood serum. Against the background of icterus of the sclera and skin, there is increased fatigue, the appearance of a feeling of bitterness in the mouth, loss of appetite, nausea, and sometimes vomiting. The association of Gilbert's syndrome with functional disorders of the biliary tract, in particular, with gallbladder dyskinesia, is often noted.

Seasonal Neonatal Hyperbilirubinemia

PEDIATRICS ◽  
1969 ◽  
Vol 43 (4) ◽  
pp. 601-605
Author(s):  
Thomas H. Milby ◽  
James E. Mitchell ◽  
Thomas S. Freeman
Keyword(s):  
Seasonal Variation ◽  
Bilirubin Level ◽  
Tap Water ◽  
Neonatal Hyperbilirubinemia ◽  
Unconjugated Bilirubin ◽  
Hemolytic Disease ◽  
Local Hospital ◽  
Unconjugated Hyperbilirubinemia ◽  
Clear Cut ◽  
Agricultural Community

A seasonal variation in the incidence of neonatal nonhemolytic, unconjugated hyperbilirubinemia has been observed in a small, predominantly agricultural community. A total of 3,096 records, representing all newborns delivered during a 4-year period (1963-1966) in one local hospital and during an overlapping 3-year period (1964-1966) in another, were reviewed. A case was defined as an infant whose highest recorded unconjugated bilirubin level reached 10 mg/100 ml during the first days of life. Infants with clear-cut hemolytic disease of the newborn were excluded from consideration. One hundred seventy cases were identifled. In one hospital, an excess of cases occurred during the fourth quarter of each of the 4 years reviewed. A similar trend was apparent in the second hospital during 2 of the 3 years reviewed. The cause of this systematic fluctuation is unclear. Insofar as possible, factors commonly associated with neonatal hyperbilirubinemia were excluded. During the peak incidence penods, a surplus of cases among infants fed with tap water-containing formula was noted.

Jaundice

2015 ◽  
Author(s):  
Hugo Farne ◽  
Edward Norris-Cervetto ◽  
James Warbrick-Smith
Keyword(s):  
Blood Cells ◽  
Sclerosing Cholangitis ◽  
Bile Ducts ◽  
Water Soluble ◽  
Red Cells ◽  
Unconjugated Bilirubin ◽  
Bile Canaliculi ◽  
Complete Obstruction ◽  
Metabolism Of Bilirubin ◽  
Conjugated Bilirubin

The metabolism of bilirubin in humans is summarized in Figure 14.1 and can be divided into three sequential steps: 1 Production of unconjugated bilirubin. Red blood cells are broken down by macrophages (mainly in the spleen), which degrade haemoglobin into iron and unconjugated (water insoluble) bilirubin. The iron is stored inside transferrin proteins. Unconjugated bilirubin travels to the liver bound to albumin. In disease, unconjugated bilirubin can be produced by haemolysis of red cells intravascularly, rather than in the spleen. 2 Conjugation of bilirubin. Liver hepatocytes uptake unconjugated bilirubin and conjugate it to glucuronate, thus making water soluble, conjugated bilirubin. 3 Excretion of bilirubin. Once conjugated, bilirubin is secreted into the bile canaliculi. Conjugated bilirubin flows with bile down the bile ducts and into the duodenum. Inside the bowel, conjugated bilirubin is metabolized by bacteria into colourless products (urobilinogen, stercobilinogen). Some of these can be reabsorbed by the gut and excreted via the kidneys, but the vast majority are oxidized in the gut into coloured pigments (urobilin, stercobilin) which give faeces their brown colour. Consequently, if there is complete obstruction of the bile ducts there will be no flow of conjugated bilirubin into the gut, no conversion into urobilinogen, and therefore not even a trace of urobilinogen in the urine. The terminology is confusing because different people mean different things. If you are going to use this terminology, make sure that you and your colleagues agree on the definitions. Nonetheless, this is what people usually mean: • Prehepatic jaundice: this refers to jaundice caused by an excessive production of bilirubin. Remember that bilirubin is produced by the breakdown of haemoglobin in the blood vessels or the spleen, hence the term prehepatic. • Hepatic jaundice: for some people, this means any jaundice due to pathology in the liver (anatomically), such as points 3, 4, and 5 in Figure 14.1, and can thus include problems with hepatocytes (e.g. hepatitis) or with the bile canaliculi (e.g. primary sclerosing cholangitis, PSC).

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