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- 1 No bilirubin should be in urine normally
- 2 Trivia Section
- 3 Bilirubin metabolism content
- 4 Where Science meets Art
- 5 More on metabolism
- 6 Formula
- 7 Bilirubin
- 8 Factor V Leiden
- 9 Link to protein isoform page
- 10 Bruises
- 11 yellow urine
- 12 Not instructive illustration
- 13 Recycling
- 14 Toxicity & the blood-brain barrier
- 15 Interpretation of high bilirubin
- 16 External links modified
No bilirubin should be in urine normally
Under Metabolism it says that "Normally, a tiny amount of bilirubin is excreted in the urine, accounting for the light yellow color". But my understanding is that normally, you DON'T have any bilirubin in urine. If you look at the urinalysis article you'll see that the upper limit on bilirubin is 0, so bilirubin in urine would indicate some sort of pathology. As for the yellow color of urine I think it's mostly due to urobilin.
If you're going to include the Silence of the Lambs reference then it's only fair that Juan Luis Guerra's song, 'Me sube la bilirubina' (My bilirubin is increasing), should be included as well. It was very popular, deplored hospital conditions in the Dominican Republic and is very catchy and easy to dance to.
Bilirubin metabolism content
Christianpunk has added content to bilirubin metabolism, which was previously a redirect pointing at this article. I think it would be best to have that material merged into bilirubin and restore the title to its former status as a redirect. Comments? --User:Ceyockey (talk to me) 15:28, 28 December 2006 (UTC)
Where Science meets Art
More on metabolism
- Diagram shows each N with 3 bonds now (inc one to the adjacent H). Rod57 (talk) 00:19, 19 November 2008 (UTC)
"Heme is formed from hemoglobin, a principle component of red blood cells." I'm pretty sure this is not quite right, since heme is a part of hemoglobin, it doesn't make sense that it would be formed from hemoglobin. If anyone with more knowledge than I can comment, that would be great, otherwise I'll try to look it up and change it soon. Acbranch (talk) 19:11, 21 May 2008 (UTC)
Factor V Leiden
I just found that my mother has Factor V Leiden and me and my son need to be tested. I'm hesitant to stress him out about the issue as he is a policeman and under a lot of stress. My question is this......his Bilirubin level is sligthly raised. Would the Factor V Leiden interfer with his Bilirubin? Anyone with information on this could email me at email@example.com. thank you, Jo Simpson —Preceding unsigned comment added by 184.108.40.206 (talk) 03:48, 21 September 2008 (UTC)
Link to protein isoform page
The link from the term isoform to the page on protein isoforms is incorrect. Bilirubin is not a protein but a haem metabolite. Thanks. —Preceding unsigned comment added by 220.127.116.11 (talk) 16:22, 13 February 2009 (UTC)
The biliverdin page says that biliverdin is responsible for yellow bruises. This page says it's bilirubin. Which is correct?
Yellow urine cannot be solely described by excretion of urobilin but can also be the result of excreted riboflavin and [riboflavin-catabolism] — Preceding unsigned comment added by Pr0f3550r (talk • contribs) 17:01, 4 February 2011 (UTC)
Not instructive illustration
The illustration does not mention the liver, in particular conjugation of bilirubin to make it water-soluble. A better illustration could be something based on the illustration used in the following external wiki medrevise.co.uk (Bilirubin). — Preceding unsigned comment added by 18.104.22.168 (talk) 12:54, 17 July 2012 (UTC)
The present article states under "Metabolism : Conjugated ("Direct")":
- "In the liver bilirubin is conjugated with glucuronic acid by the enzyme glucuronyltransferase, making it soluble in water. Much of it goes into the bile and thus out into the small intestine. However, 95% of the secreted bilirubin is reabsorbed by the intestines(Terminal Ileum) and reaches the liver by portal circulation and then resecreted by the liver into the small intestine. This process is known as enterohepatic circulation. "
I would like to see the reference supporting the statement I italicised above. I have a suspicion that bilirubin has been confused with bile salts here. According to a review article on the subject of enterohepatic circulation of bilirubin, this is a minor phenomenon, absolutely restricted to unconjugated bilirubin and significant only in pathological conditions:
- "In contrast to bile salts, which undergo a highly efficient enterohepatic circulation with multiple regulatory and physiologic functions, glucuronic acid conjugates of bilirubin are biliary excretory molecules that in health do not have a continuing biologic life. Intestinal absorptive cells are devoid of recapture transporters for bilirubin conjugates, and their large size and polarity prevent absorption by passive diffusion. However, unconjugated bilirubin, the beta-glucuronidase hydrolysis product of bilirubin glucuronides can be absorbed passively from any part of the small and large intestines. This can occur only if unconjugated bilirubin is kept in solution and does not undergo rapid bacterial reduction to form urobilinoids. Here we collect, and in some cases reinterpret, experimental and clinical evidence to show that in addition to the well-known occurrence in newborns, enterohepatic cycling of unconjugated bilirubin can reappear in adult life. This happens as a result of several common conditions, particularly associated with bile salt leakage from the small intestine, the most notable ileal dysfunction resulting from any medical or surgical cause. We propose that when present in excess, colonic bile salts solubilize unconjugated bilirubin, delay urobilinoid formation, prevent calcium complexing of unconjugated bilirubin and promote passive absorption of unconjugated bilirubin from the large intestine. Following uptake, reconjugation, and resecretion into bile, this source of 'hyperbilirubinbilia' may be the important pathophysiological risk factor for 'black' pigment gallstone formation in predisposed adult humans."
- (L. Vítek, M. C. Carey, Enterohepatic cycling of bilirubin as a cause of ‘black’ pigment gallstones in adult life. European Journal of Clinical Investigation, Volume 33, Issue 9, pages 799–810, September 2003)
I would be happy to see a comment on this discrepancy please. If there is no reply, I will venture to change this section of the article as it seems misleading.
I think I have found the source of this confusion. Urobilin, the result of deconjugation and further metabolism of bilirubin diglucuronate by intestinal microbes, is subject to enterohepatic recirculation, although the majority of it is excreted with feces, according to the textbook on clinical chemistry I consulted. Wdanbae (talk) 11:21, 12 December 2013 (UTC)
I was also suspicious, and looked at the actual Kuntz source that this article cited for the bilirubin recycling---it indicates quite the opposite of what was written, literally stating "Bilirubin diglucuronide is discharged into the intestine together with the bile. Absorption is neither possible from the gall bladder nor from the intestine; in general, no enterohepatic reabsorption of bilirubin takes place." I can only imagine that the "95% reabsorption" figure was lifted from the Wiki bile salts page, and this source was only used to verify the urobilin/stercobilin conversion. I've rewritten both paragraphs; hopefully they are now both more concise and more correct!
Toxicity & the blood-brain barrier
As I write this, the 'Toxicity' section contains this sentence: "The neurotoxicity of neonatal hyperbilirubinemia manifests because the blood–brain barrier has yet to develop fully, ..." But at the same time, the 'Development' section of the Blood-brain barrier page begins "Originally, experiments in the 1920s showed that the blood–brain barrier (BBB) was still immature in newborns. The reason for this mistake was an error in methodology ..." Obviously, one of these sentences is wrong. Which one? I'm inclined to believe the BBB page is correct. 22.214.171.124 (talk) 04:32, 3 September 2014 (UTC)
Interpretation of high bilirubin
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