Serum bilirubin fractions in healthy subjects and patients with unconjugated hyperbilirubinemia

Adachi, Yukihiko; Katoh, Hiroko; Fuchi, Isao; Yamamoto, Tetsuro

doi:10.1016/0009-9120(90)90705-y

Cited by 7 publications

(3 citation statements)

References 30 publications

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“…It has been proposed as autosomal dominant with variable expression [5]. Black and Billings [a] found hepatic bilirubinglucuronyl transferase activity to be consistently decreased, averaging 25% of normal, though Zeneroli and associates [7] found evidence that GS is an heterogeneous condition with respect to bilirubin turnover rate, suggesting a complex biochemical etiology, and Adachi and associates [8] detected delta-bilirubin in one of 15 patients with GS. Delta-bilirubin, according to these authors, is reported to be produced from covalent binding of albumin exclusively to conjugated bilirubin.…”

Section: Discussionmentioning

confidence: 98%

Gilbert's Disease: Symptomatic Response to Nutritional Supplementation in Ten Patients

Lonsdale¹

1992

Journal of Nutritional Medicine

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This paper reports on 10 patients who were found from routine laboratory studies to have Gilbert 3 syndrome (CS). also known as benign hyperbilinibinemia. Each patient came to our clinic with multiple symptoms which appear to have become increasingly common in the population of the USA as a whole. Each received only nutrient therapy and symptomatic improvement was generally experienced by all of them. Although we observed a gradual decrease of serum bilirubin to normal in three of the patients, it is known that patients with this syndrome experience fluctuations in concentration of serum bilirubin which can be in the normal or abnormal range at difSerent times. The many symptoms reported in GS are not specific to the syndrome and are experienced by individuals with normal serum bilirubin concentrations. Keywords: Gilbert's syndrome, serum bilirubin.patients, with fatigue as the next commonest in six. Chest pain, of a non specific nature, was the complaint of five. Our experience is that this symptom is extremely common. It is usually intermittent and either centrally located or occumng under the 319 J Nutr Environ Med Downloaded from informahealthcare.com by McMaster University on 11/03/14 For personal use only. J Nutr Environ Med Downloaded from informahealthcare.com by McMaster University on 11/03/14 For personal use only.

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Section: Discussionmentioning

confidence: 98%

Gilbert's Disease: Symptomatic Response to Nutritional Supplementation in Ten Patients

Lonsdale¹

1992

Journal of Nutritional Medicine

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“…99,107 Another example is that BMG is the predominant conjugated bilirubin in neonatal bile, whereas BDG is the predominant conjugated bilirubin in adult bile (80%). 11,102 Thus, these studies should not be interpreted as evidence against the decreased role of GST-hep level in G6PD deficiency-associated hyperbilirubinemia.…”

Section: Decreased Glutathione S-transferase-hep Levels and The Magnimentioning

confidence: 98%

“…102 For this reason, HPLC data have to be interpreted with caution in neonates. 102 At the very least, the DL should be 0.03 µmol/L for BMG and 0.06 µmol/L for BDG by using 0.2 mL serum.…”

Section: Decreased Glutathione S-transferase-hep Levels and The Magnimentioning

confidence: 99%

Decreased Glutathione S-transferase Level and Neonatal Hyperbilirubinemia Associated with Glucose-6-phosphate Dehydrogenase Deficiency: A Perspective Review

Al-Abdi

2016

Amer J Perinatol

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Classically, genetically decreased bilirubin conjugation and/or hemolysis account for the mechanisms contributing to neonatal hyperbilirubinemia associated with glucose-6-phosphate dehydrogenase (G6PD) deficiency. However, these mechanisms are not involved in most cases of this hyperbilirubinemia. Additional plausible mechanisms for G6PD deficiency-associated hyperbilirubinemia need to be considered. Glutathione S-transferases (GST) activity depends on a steady quantity of reduced form of glutathione (GSH). If GSH is oxidized, it is reduced back by glutathione reductase, which requires the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH). The main source of NADPH is the pentose phosphate pathway, in which G6PD is the first enzyme. Rat kidney GSH, rat liver GST, and human red blood cell GST levels have been found to positively correlate with G6PD levels in their respective tissues. As G6PD is expressed in hepatocytes, it is expected that GST levels would be significantly decreased in hepatocytes of G6PD-deficient neonates. As hepatic GST binds bilirubin and prevents their reflux into circulation, hypothesis that decreased GST levels in hepatocytes is an additional mechanism contributing to G6PD deficiency-associated hyperbilirubinemia seems plausible. Evidence for and against this hypothesis are discussed in this article hoping to stimulate further research on the role of GST in G6PD deficiency-associated hyperbilirubinemia.

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A new enzymatic assay for selectively measuring conjugated bilirubin concentration in serum with use of bilirubin oxidase

Kurosaka

Senba

Tsubota³

et al. 1998

Clinica Chimica Acta

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Serum bilirubin fractions in healthy subjects and patients with unconjugated hyperbilirubinemia

Cited by 7 publications

References 30 publications

Gilbert's Disease: Symptomatic Response to Nutritional Supplementation in Ten Patients

Gilbert's Disease: Symptomatic Response to Nutritional Supplementation in Ten Patients

Decreased Glutathione S-transferase Level and Neonatal Hyperbilirubinemia Associated with Glucose-6-phosphate Dehydrogenase Deficiency: A Perspective Review

A new enzymatic assay for selectively measuring conjugated bilirubin concentration in serum with use of bilirubin oxidase

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