Bilirubin acts as a multipotent guardian of cardiovascular integrity: more than just a radical idea.
Bulmer AC , et al.
«Bilirubin, a potentially toxic catabolite of heme and indicator of hepatobiliary insufficiency, exhibits potent cardiac and vascular protective properties. Individuals with Gilbert's syndrome (GS) may experience hyperbilirubinemia in response to stressors including reduced hepatic bilirubin excretion/increased red blood cell breakdown, with individuals usually informed by their clinician that their condition is of little consequence. However, GS appears to protect from all-cause mortality, with progressively elevated total bilirubin associated with protection from ischemic heart and chronic obstructive pulmonary diseases. Bilirubin may protect against these diseases and associated mortality by reducing circulating cholesterol, oxidative lipid/protein modifications, and blood pressure. In addition, bilirubin inhibits platelet activation and protects the heart from ischemia-reperfusion injury. These effects attenuate multiple stages of the atherosclerotic process in addition to protecting the heart during resultant ischemic stress, likely underpinning the profound reduction in cardiovascular mortality in hyperbilirubinemic GS. This review outlines our current knowledge of and uses for bilirubin in clinical medicine and summarizes recent progress in revealing the physiological importance of this poorly understood molecule. We believe that this review will be of significant interest to clinicians, medical researchers, and individuals who have GS.»
atherosclerosis, heart, heme oxygenase, hepatic, lipid
Endothelial dysfunction contributes to the early stages of atherosclerosis
, whereby 97 expression of adhesion molecules and oxidant generating NADPH
oxidase (NOX) draws 98 leukocytes to sites of injury/lipid accumulation, propagating vascular injury and encouraging 99 vascular smooth muscle proliferation and neointima formation. Increased
NOX driven 100 reactive oxygen species
) production and intimal thickening contribute to hypertension
101 and impaired vasodilatation, involving sequestration of released nitric oxide
. Based upon its 102 ROS
properties, it is hypothesized that bilirubin
has the potential to 103 reduce
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The effects of Gilbert's syndrome on the mean platelet volume and other hematological parameters.
Cure MC , et al.
«The protective effect of increased levels of indirect bilirubin on atherosclerotic heart disease in patients of Gilbert's syndrome is well known. The aim of the study was to investigate the effects of increased levels of bilirubin on the mean platelet volume (MPV) and other hematological parameters. Thirty-two men and 36 women (a total of 68 Gilbert's syndrome patients) and a similar age group of 68 healthy individuals (32 men and 36 women) were included in the study. Hematologic tests, C-reactive protein (CRP) and biochemical values of the two groups were checked. MPV level of Gilbert's syndrome group was 7.8±1.0fl and CRP 0.2±0.27mg/dl. In the control group MPV was 8.6±1.0fl and CRP 0.3±0.38mg/dl. MPV of patients group (P<0.001) and CRP (P=0.037) were significantly lower than the control group. When dividing Gilbert's syndrome and control groups according to sex into subgroups the level of indirect bilirubin in men with Gilbert's syndrome (1.8±0.8mg/dl) was found to be higher than other groups. Healthy men had higher levels of MPV (8.8±0.9fl) whereas Gilbert's syndrome male patients had lower levels (7.7±1.1fl), (P<0.001). The elevated levels of bilirubin and decreasing levels of MPV and CRP in Gilbert's syndrome patients may have an effect on the slowing down of the atherosclerotic process.»
Adolescent, Adult, Bilirubin, Blood Platelets, C-Reactive Protein, Female, Gilbert Disease, Hemoglobins, Humans, Male, Middle Aged, Sex Factors
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on May 1, 2019
5 months ago
on Apr 10, 2019.