Role of bilirubin overproduction in revealing Gilbert's syndrome: is dyserythropoiesis an important factor?

Métreau, J M; Yvart, J; Dhumeaux, Daniel; Berthelot, Pièrre

doi:10.1136/gut.19.9.838

Cited by 11 publications

(8 citation statements)

References 21 publications

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“…All of these parameters were found to be relatively elevated in GS versus C individuals. These findings are confirmed by earlier reports 12 , 36 . There were no differences in hematocrit and reticulocytes between the groups, confirming the absence of immoderate hemolysis, defects in erythropoiesis and anemia.…”

Section: Discussionsupporting

confidence: 93%

“…An illustration of this can be found in Supplementary Figure S1 . In confirmation of a postulated theory of mild UCB-mediated hemolysis in GS 12 , 36 , 37 UCB has as well been found negatively correlated to Hpx and Hpt. Furthermore, a connection between Hpx and the HMOX genotype was found in female GS, where short GT-repeats were non-significantly more frequent than in C subjects.…”

Section: Resultssupporting

confidence: 66%

“…The association with UCB is specifically meaningful as a decrease in Hpt is sensitively connected to hemolysis. This pursues the suggested theory of mild hemolysis in GS 12 , 36 , 37 , resulting from a mildly increased UCB-driven breakdown of erythrocytes 12 . Reversely, this mild form hemolysis, however, is said to be insufficient to produce hyperbilirubinemia per se 37 , 55 , 56 .…”

Section: Discussionsupporting

confidence: 58%

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Characteristics of the heme catabolic pathway in mild unconjugated hyperbilirubinemia and their associations with inflammation and disease prevention

Mölzer

Wallner

Kern

et al. 2017

Sci Rep

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Heme catabolism exerts physiological functions that impact health through depressing inflammation. Upon reactive pathway progression, as in Gilbert’s Syndrome (GS; UGT1A1*28 polymorphism), aggravated health effects have been determined. Based on lower inflammation and improved metabolic health reported for GS, inter-group differences in heme catabolism were explored. Therefore, a case-control study including 120 fasted, healthy, age- and gender matched subjects with/without GS, was conducted. Genetic expressions of HMOX-1 and BLVRA were measured. Additionally participants were genotyped for those polymorphisms that are known (UGT1A1*28) or likely (HMOX-1 microsatellites) to impact bilirubinemia. Intracellular interleukins (IL-6, IL-1β, TNFα), circulatory C-reactive protein (CRP), serum amyloid A (SAA) and haptoglobin (Hpt) were analysed as inflammatory markers. To assess intracellular heme oxygenase 1 (HO-1) isolated PBMCs were used. In GS vs. C, inflammation markers were significantly decreased. This was supported by an altered heme catabolism, indirectly reflecting in elevated unconjugated bilirubin (UCB; main phenotypic feature of GS) and iron, decreased hemopexin (Hpx) and Hpt and in up-regulated biliverdin reductase (BLVRA) gene expressions. Moreover, HMOX (GT)n short alleles were non-significantly more prominent in female GS individuals. Herewith, we propose a concept to elucidate why GS individuals encounter lower inflammation, and are thus less prone to oxidative-stress mediated diseases.

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Section: Discussionsupporting

confidence: 93%

Section: Resultssupporting

confidence: 66%

Section: Discussionsupporting

confidence: 58%

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Characteristics of the heme catabolic pathway in mild unconjugated hyperbilirubinemia and their associations with inflammation and disease prevention

Mölzer

Wallner

Kern

et al. 2017

Sci Rep

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“…The average age of diagnosis in studies from over 20 years ago is generally reported as the mid-thirties [12,13,34]. The relatively late age of diagnosis in this study suggests Gilbert's syndrome is largely an incidental finding during routine lab tests in the modern clinical setting.…”

Section: Discussionmentioning

confidence: 56%

“…Gilbert's syndrome is historically regarded as a benign trait, and clinical recognition is often incidental to routine laboratory investigations . However, there has been renewed interest in the condition following the results from more recent genetic association studies.…”

Section: Introductionmentioning

confidence: 99%

Gilbert's syndrome and the risk of death: A population‐based cohort study

Horsfall

Nazareth

Pereira

et al. 2013

J of Gastro and Hepatol

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Background and Aims Gilbert's syndrome is a common familial hyperbilirubinemia that may reduce the risk of various age‐related diseases because of the antioxidant properties of bilirubin. We conducted a large cohort study using The Health Improvement Network primary care database and compared all‐cause mortality rates in those with and without Gilbert's syndrome. Methods Mortality rates in patients with a diagnosis of Gilbert's syndrome and raised bilirubin level (n = 4266) were compared with those of patients with similar characteristics but with normal bilirubin levels (n = 21 968). Multivariate Poisson regression was also used to estimate adjusted mortality rate ratios. Results During the 350 000 PYs of follow up across the Gilbert's and comparison cohorts, there were 1174 deaths. Mortality rates were 24/10 000 PYs in the Gilbert's cohort versus 50/10 000 PYs in the comparison cohort. Mortality rates were around half in patients with Gilbert's syndrome after accounting for sociodemographics and general health indicators (adjusted mortality rate ratio: 0.5 [95% confidence interval; 0.4–0.7; P < 0.001]). Conclusions Mortality rates observed for people with Gilbert's syndrome in the general population are almost half those of people without evidence of Gilbert's syndrome.

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Gilbert syndrome as differential diagnosis of hyperbilirubinemia in acquired aplastic anemia

Svahn

Lanciotti

Dufour

et al. 2005

Pediatr. Blood Cancer

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Role of bilirubin overproduction in revealing Gilbert's syndrome: is dyserythropoiesis an important factor?

Cited by 11 publications

References 21 publications

Characteristics of the heme catabolic pathway in mild unconjugated hyperbilirubinemia and their associations with inflammation and disease prevention

Characteristics of the heme catabolic pathway in mild unconjugated hyperbilirubinemia and their associations with inflammation and disease prevention

Gilbert's syndrome and the risk of death: A population‐based cohort study

Gilbert syndrome as differential diagnosis of hyperbilirubinemia in acquired aplastic anemia

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