Talk:Gilbert's syndrome

message: My mum believes she has this condition, and suspects that I also might. This would be interesting, as I have been diagnosed with another condition mentioned on this page. However, she tells me that it is particularly common in people of Irish ancestry, and that it is advisable for those with the condition to avoid alcohol and wheat/gluten - none of which are even remotely mentioned in this article. Is there anything to back these theories up?--MartinUK (talk) 22:28, 3 December 2010 (UTC)
thread_title: Two questions about this condition

message: With the large number people dealing with this condition everyday, and a portion of them reading this must be wanting to know what treatment is advised, as I do. I've seen numerous articles on the internet making advice which didnt seem to be based on the facts.  I can see plenty of facts here on the wiki, but not being a doctor myself, could someone please write about treatment of Gilbert's syndrome purley based on the facts we know.  —Preceding unsigned comment added by 86.148.139.121 (talk) 23:24, 21 March 2008 (UTC)
replies: text: Wish I'd noticed this before I made my post above. Would an absolute strict Coeliac diet be needed, or would simply avoiding large amounts of gluten (ow merely wheat?) be important?--MartinUK (talk) 22:41, 3 December 2010 (UTC)
thread_title: Treatment

message: Bold text
GS interferes with more than just the conjugation of Bilirubin.  For example, UGT1A1 also degrades C18 steroids.  So why not picture one of them instead of the most visibly affected compound?
I think it would make much more sense to picture either UGT1A1 in the infobox, or have an infobox about a disease, or have an infobox about the TA7 mutation.  But bilirubin is kind of on-topic but not as relevant as the infobox display would imply. Heathhunnicutt 19:18, 13 June 2006 (UTC)
replies: text: I was the person who added the bilirubin image earlier today, and I removed it per this objection. I have no objection to Heathhunnicutt's proposal. --Arcadian 03:19, 14 June 2006 (UTC)
replies: text: Thanks, Arcadian.  I was thinking, how cool would it be if we had a photo of Bilirubin before and after, with the UGT1A1 enzyme shown as the intermediary.  How does art get done for the Wikipedia?  Do I just advertise for an artist on craigslist, or what? Heathhunnicutt 16:59, 14 June 2006 (UTC)
thread_title: Disagreement with picture of Bilirubin molecule

message: It would be good to add information regarding what causes high bilirubin episodes. Also, there is another similar deficiency, which can lead to death: the G6PD deficiency. Elp_gr
:In what sense do you consider G6PD and Gilbert's similar? JFW | T@lk 10:11, 18 August 2005 (UTC)
replies: text: In that they both cause haemolysis - triggered by different causes, of course, but you still get it. I happen to have both Gilbert's and G6PD deficiency. Elp gr 15:59, 18 August 2005 (UTC)

text: Gilbert's does not cause haemolysis. It is a disorder of glucuronidation. JFW | T@lk 02:20, 19 August 2005 (UTC)
replies: text: This whole thing puzzles me. Elp gr 15:26, 19 August 2005 (UTC)
thread_title: Previously

message: The (conventional) clinical definition is of mild elevation in bilirubin, with only symptom being of occassional mild jaundice. Leaving aside more severe disorders of bilirubin metabolism, most people with GS do not report symptoms, indeed most cases are found by chance on routine blood tests. To use the term 'many' to describe those who report symptoms is POV, as it is only a minority who so report. 'Some' is therefore NPOV (my own preference of 'rarely' I suspect might be seen by others as POV in the other direction).
Many doctors prefer the term Gilbert's condition as syndrome suggests a collection of disease symptoms, where as this 'thing' is present in upto 10% of the normal population and most doctors would therefore view it almost as a normal varient. The 'risk' is that unrecognised, it might be wrongly inferred that a patient is developing a liver disorder such as acute viral hepatitis, whereas in reality the patient is well and will remain so; the patient is therefore at risk from their doctors of undergoing lengthly series of further blood tests & investigations for what will turn out to be a benign, non-infectious condition. The true cause of a patient's new onset of illness therefore may go unrecognised whilst GS is identified.
The dietary changes suggested are not accepted by conventional medicine, and are therefore 'alternative' in nature. Given that conventional medicine therefore disputes these suggestions, they are de facto 'controversial' (again I would suggest this is a NPOV term, whereas my own thoughts might be of 'alternative', 'pseudoscience', etc etc).
There were some useful additions to the list of claimed symptoms that I have left in (to claim something is NPOV) and I agree better to describe "people with GS" rather than "GS sufferers".
If people dispute my revisions and wish to edit, please can you ensure WP:Verify and WP:Cite to help in any further discussions.  David Ruben  Talk  04:41, 15 February 2006 (UTC)
replies: text: Support the revert. The pathophysiology is well understood. At the levels of bilirubin normally experienced in GS, no symptoms apart from mild itch are usually present. JFW | T@lk 00:31, 16 February 2006 (UTC)

text: It's hardly a normal variant, as several enzymes necessary for glucuronidation, one of the body's main detoxification systems, are reduced to a small fraction of their normal levels. Shambala 22:53, 27 July 2006 (UTC)
thread_title: Revert to 27 Jan

message: I once heard that it is usually discovered in puberty and that girls hence usually show symptoms sooner than boys.
Is that correct and should it be included?
If it is of any relevance, I know someone with this syndrome personally.
Nemo.shark (talk) 01:58, 24 March 2011 (UTC)
replies: text: NO - it normally is not identified at all - most people with the condition are without any symptoms. Its commonest identification is as part of normal liver fuction blood tests undertaken for other medical reasons. At 5% of the western-world population, many doctors prefer to call this 'Gilbert's condition' (rather than something that suggests a disease) and view it as a normal varient. There are of course other more severe disruptions to metabolism of bilirubin than Gilbert's and there shoud be relevant articles about these conditions. David Ruben  Talk  03:05, 25 February 2006 (UTC)
replies: text: So some fraction of people with GS have symptoms, and the rest are forced along with the ride?  I have GS also, and I have no symptoms at all.  I found out about it during a routine blood test, and they were all "OMG, the Bilirubin level is way too high, this isn't good."  After a number of tests from a liver specialist, he concluded that it must be GS, as there were no further indicators.  I hardly bother mentioning it to doctors anymore, because I've never even had mild jaundice from GS.  It really didn't come up until I was speaking with my gynecologist regarding hormones, and we ran a liver panel, and I was astute enough to tell him that I had Gilbert's Syndrome, so fortunately, when the tests came back, and I had some 4.9 mg/dl, the doctor didn't freak out.  I agree that I have a fairly low level of Billirubin from what is typical for most people with GS, but I still have elevated Billirubin levels, and I still have GS, and I've never had any symptoms. If you run a site about GS, then you're going to get people who have symptomatic GS, and not asymptomatic GC (Gilbert's Condition), because the people with GC just don't care, because it doesn't affect their life. --Puellanivis 21:42, 2 October 2006 (UTC)
replies: text: Pellanaivis -- I see from your user page that you are a biological man who is undergoing transgendering via hormone therapy involving estrogen.  I see from your above comments that you have GS.  Are you aware that GS also slows the metabolism of estrogen and other C18 steroids?  How has this impacted your transgendering plan, from start to finish? Heathhunnicutt 00:27, 23 October 2006 (UTC)
replies: text: I'm putting the response to this in my talk page, as I feel it likely has a greater relevance there than in this article.  As a short answer, I was unaware of this, and I appreciate the feedback. --Puellanivis 18:41, 23 October 2006 (UTC)
thread_title:  discovery age 

message: Frome this artile
 "More controversially, some patients report experiencing unpleasant physical symptoms during episodes of high bilirubin levels. These may include persistent or meal-related fatigue, dizziness, tremors, nausea, abdominal pain, and "brain fog", with or without jaundice[citation needed]. There is some evidence that Gilbert's syndrome also reduces the liver's ability to detoxify certain chemicals; it may be wise to avoid drugs that tax liver function, such as paracetamol."
:Is Action on Gilbert's Syndrome a decent source.  if it is it mentons this on What is Gilbert's Syndrome?.  Is it a source or is it some randome person on the web.  I had a tough time a few years ago when all of thoes side effects listed hapened to me and i had alot of Blood test to find out what wrong.  Afterwords i found the sight but my parece told me the sight wasn't true. (please not Testimonials are by nature misleading becoe they represent a disproporinate amout of people so don't take what i said as a testimonial.  I have sevral rare explanation for my condition, each being rare enoguh not really qualifying as any explanation)--E-Bod 23:26, 26 March 2006 (UTC)
replies: text: Sorry the quote is breaking the page--E-Bod 23:26, 26 March 2006 (UTC)
replies: text:  Another metnion of just "Symptoms of this defect in liver detoxification are anorexia (loss of appetite), malaise (weakness), fatigue, a chronically elevated serum bilirubin level and a slight yellowing of the white of the eye in the absence of hepatitis." and this page is already citted in the artile.  actually same as Action on Gilbert's Syndrome is already under links it could be copied to refrences.  If the sorce is reputable.--E-Bod 23:35, 26 March 2006 (UTC)

text: Is the sorce Reputabe? (sorry if i'm having a conversation with myslef)--E-Bod 23:35, 26 March 2006 (UTC)
thread_title:  citation needed/found 

message: The information on acetaminophen (Tylenol) has gone back and forth a bit, but it's settled on an answer. Here's what happened:
There was an original study that showed that people with GS had 31% slower processing of acetaminophen, so it was thought to be processed by UGT1A1, the enzyme deficient in GS. The advice given was for people with GS to avoid acetaminophen. Later experiments showed that acetaminophen was actually processed by UGT1A7, and so acetaminophin was given the green light for people with GS. Later still, it was shown that most people with the UGT1A1 mutation also had an even worse mutation in UGT1A7. This explained the results of both the previous studies, and justified the results of the original experiment - that people with GS should avoid acetaminophen (Tylenol).
I've updated the article with references to each of these three studies. Shambala 12:34, 16 July 2006 (UTC)
replies: text: It would be worthwile, then, to update the page on acetaminophen/paracetamol as well, as it still lists UGT1A1 as one of the enzymes that metabolizes it. The quote from the paracetamol page states: "Glucuronidation by UGT1A1 and UGT1A6 accounts for 50–70% of the drug metabolism." The reference cited at the end of the sentence after that links to a PubMed article published in 2013 that lists these two enzymes as acting upon acetaminophen, and it does not list UGT1A7 at all. There does not appear to be any errata published for that article so either the study cited in the paracetamol article is wrong, or the articles you found are wrong, and I am nowhere near scholarly enough to figure out which one is correct. Lumberjane Lilly (talk) 18:09, 27 January 2023 (UTC)
thread_title:  Acetaminophen Metabolism 

message: I apologize if my posts/edits are inexpert. I've been reading Wikipedia a long time and have just started editing. I take issue with the "More controversially" part, as I have been diagnosed with Gilbert's Syndrome and have had these symptoms for a long time. From every source I have found on the web from those who actually have it, I have seen these symptoms described. How is it that doctors can invalidate this widespread report of similar symptoms? In truth, there hasnt been many studies on Gilbert's Syndrome, and lack of knowledge is no reason to invalidate the reported symptoms of a population. Shambala 02:58, 23 April 2006 (UTC)
replies: text: I started to suffer from "brain fog", fatigue and nerves during my early 20s, about 6 years ago.  My GP diagnosed me with Gilbert's Syndrome, via a blood test.  I later moved interstate and my new GP argues against my first doctor's assertion that GS would be the cause of my symptoms.  I have no medical knowledge and I am wary of trusting any website but I have seen those pages that correlate my symptoms with Gilbert's Syndrome.   Anyway, in recent times, I have found that a Vitamin B supplement (including B12) over the counter from the chemist has helped me enormously.  Within 4-5 days, my nerves were much more settled, the brain fog had disappeared and I am nowhere near as tired.  As I say, I have no medical background at all but this may help some people.  I still have no idea if my symptoms were related to GS or not but the Vitamin B helped.  Fairly sure it wasn't just a placebo effect for me.  Hope this knowledge can help someone else.  Perhaps a real medical student or researcher out there can do a study to determine if there is a link between the two?  202.138.16.49 (talk) 10:11, 8 March 2009 (UTC)
thread_title:  regarding symptoms 

message: What is the highest billirubin ever recorded for someone with gilberts, mine has been up to 179 mmol/dl --Dr. B
Mine reached 7 mg/dl  — Preceding unsigned comment added by 2600:4040:2BCD:0:F02A:EC83:6DD6:90FD (talk) 22:16, 17 February 2023 (UTC)
thread_title:  Highest bilirubin 

message: In this article it is stated that by conjugating bilirubin it becomes water soluble and is excreted by the kidneys. Bilirubin is excreted into the bile ducts and enters the stools, it is not excreted through the kidneys with the urine.
: This was my understanding also.  If I get time I'll research this and do a correction if this indeed the case. Robert Brockway 04:49, 21 August 2007 (UTC)
thread_title:  Bilirubin excretion 

message: Ok, so here's my story again, but this time with more details.
I was taking an anti-depressant (Tofranil) at the time we did a routine liver health panel, and discovered the abnormal billirubin level.  I went to a liver specialist, and he looked through various things and tried various tests, and eventually came to the conclusion that it must be Gilbert's Syndrome, which he indicated to me was "ideopathic jaundice".
Now, what I'm really wondering here, is that my billirubin levels are fairly low for a person with GS, and that Tofranil has "jaudice" listed as a possible side-effect.  I'm thinking that it's possible that the Tofranil caused a change in my liver functions, which resulted in ideopathic jaundice, which would be a bit different in etiology than GS.  I'm just wondering if anyone has any clues to how I could determine the actual cause of GS, rather than simply "unexplained ideopathic asymptomless jaundice" and grouped in with GS.
Also of note, I've had no problems with the metabolization of Estradiol that I have been taking orally for over a year now.  This is also one of the reasons for my interest in determining if I have the specific action of GS, or do I simply have GS-like symptoms. --Puellanivis 19:09, 17 October 2007 (UTC)
thread_title:  GS vs. Medication-induced ideopathic jaundice 

message: i just wanted to add this in here, i have gilberts syndrome and have researched it for a while.
recently i have come across the fact that gilberts syndrome gives men a greater chance of getting gynecomastia, but i can find no explanations for the mechanisms involved for this increased susceptibility, i think this is interesting and could lead to more of an understanding into some of the proclaimed anecdotal symptoms of gilberts syndrome. (nemo)  —Preceding unsigned comment added by Nemo.shark (talk • contribs) 04:19, 4 January 2008 (UTC)
thread_title:  gynecomastia 

message: ive read on the net that gilberts syndrome actually has a positive effect on (ldl) Low-density lipoprotein. (bad cholesterol)
im unsure what effects if any this may have on synthesis of hormones cortisol, aldosterone, and the sex hormones progesterone, the various estrogen's, testosterone and derivatives. (which are all synthesised from cholesterol)Nemo.shark (talk) 03:39, 5 January 2008 (UTC)
thread_title:  cholesterol 

message: Regarding the need to exclude haemolysis as a cause of hyperbilirubinaemia when making a diagnosis of GS:  I added that one would note a reticulocytosis in the presence of haemolysis; indeed this is an important investigation in confirming/diagnosing haemolytic anaemia and it seems relevant to add it.  —Preceding unsigned comment added by Trefusismadding (talk • contribs) 19:17, 18 February 2008 (UTC)
thread_title:  Exclusion of haemolysis 

message: after doing much reading about gilberts syndrome over the past few months its become apparent that the condition could be classified into different variants. 
could it be that the Polysymptomatic nature of gilberts syndrome is the fact that there are different variants of the disorder? and catogorising it with the emergence of genetic tests in to type 1, type 2, (ect) variants could be indicative of similarity's between the variants? (nemo)  —Preceding unsigned comment added by Nemo.shark (talk • contribs) 07:35, 4 March 2008 (UTC)
thread_title:  classification for different variants of gilberts syndrome 

message: I updated the main GS page with a reference to the 'British Liver Trust' (an august and reputable research charity) listing commonly reported symptoms - having written and asked them for their permission to use their information. Somebody (it looks like a user called Anome) decided to remove this information. Why? Is it not important to recognise that if more and more people who are diagnosed with GS have identical symptoms, then there is a good possibility that they are significant and more research is needed? I did actually refer to them as "commonly reported symptoms" as distinct from "diagnosed symtpoms" and, I repeat, I did get written permission from a charitable research organisation (who would know that a lot of people do, in fact, report these symptoms). So, unless somebody can tell me why this information should not be part of the GS-page (?), I shall be re-entering it.  —Preceding unsigned comment added by Philipm12 (talk • contribs) 11:48, 14 March 2008 (UTC)
thread_title:  Why has somebody removed my reference to reported symptoms? 

message: I downgraded this to start class for now due to the large lack of citations in the diagnosis section, which could also use a decent amount of work. The pathogenesis also seems to be lacking other than a very general "enzyme problem". Feel free to bump back to B-class if you think it was ok at that level. Schu1321 (talk) 20:51, 2 June 2008 (UTC)
thread_title:  MedGen Class 

message: It's French.  —Preceding unsigned comment added by 66.167.95.160 (talk) 03:20, 20 October 2008 (UTC)
thread_title:  "Gilbert's" is pronounced "Joe-BEAR's"   

message: im adding a link here because its quite a recent discovery and feel it should be added to the main gs page, can someone look in to this and if they feel it should be added to the main page as people should be aware of it???
http://www.news-medical.net/news/20100607/Study-identifies-potential-link-between-Gilberts-Syndrome-childhood-acute-lymphoblastic-leukemia.aspx (nemo.shark)Nemo.shark (talk) 02:19, 24 March 2011 (UTC)
thread_title:  increased susceptibility to childhood leukemia associated with gilbert's syndrome. 

message: Under 'Differential diagnosis' it states that, "Cholestasis can be excluded by the absence of lactate dehydrogenase"... I don't think that is correct, unless LDH has been found to be useful in diagnosing obstructive jaundice, which seems unlikely as its elevation is related to "significant impairment of hepatocytes".
I think the writer meant alkaline phosphatase, and this should read something like, "Cholestasis can be excluded by the absence of elevated levels of alkaline phosphatase"...
Krebiozen (talk) 11:07, 16 September 2012 (UTC)
thread_title:  Absence of lactate dehydrogenase excludes cholestasis? 

message: I feel that it would be a good idea to add a "not to be confused with" label at the top of the page to distinguish between Gilbert's and Guillain–Barré syndromes. The latter is often pronounced like "gillie-bear" while Gilbert's is sometimes pronounced "jill-bear" (apologies for the bad formatting), opening up the possibility of people looking at the incorrect article, so I'm going to add a  tag to both articles. I leave this section open to discussion of the topic as both can be confusing to spell given their non-English etymologies.
Zedtwitz (talk) 02:19, 18 February 2014 (UTC)
thread_title:  Distinguishing between Gilbert and Guillain–Barré Syndromes 

message: Here is a reputable source which could explain gastrointestinal symptoms such as nausea and stomach cramps:
"Delayed gastric emptying in subjects with Gilbert's syndrome."
I have Gilberts syndrome and have always had (even before diagnosis) fatigue, low tolerance to alcohol, and stomach problems/gastroperasis symptoms which don't seem to be getting any better on a low FODMAP diet (despite a gluten-free diet helping for the past 4 years). So i am interested in learning why GS sufferers have digestive issues, in particular with grains. I thought it may be because we dont produce enough bile? Maybe that is the reason for delayed gastric emptying?
I was also diagnosed with dust mite allergy and Gilberts syndrome within the space of a fortnight and wonder if one caused the other as it seems like a big coincidence!
— Preceding unsigned comment added by 62.200.73.162 (talk) 11:49, 30 July 2014 (UTC)
thread_title:  Gastroperasis and Gliberts syndrome 

message: While I do understand and thank the cleaning of this page since it lacked reliable sources, the connection to limonene and Gilbert's should be looked after. It really increases UDPGT activity... but on mice. That's what the two PubMed articles say. So I'm leaving this reminder in case an article on humans gets published. --Bowtartar (talk) 02:16, 3 July 2017 (UTC)
replies: text: We tend to stick with review articles per WP:MEDRS rather than use primary sources. Doc James (talk · contribs · email) 04:34, 3 July 2017 (UTC)
thread_title:  Limonene 

message: The antiinflammatory effects and protective effects of Gilbert's show up in chromosome telemeres.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4772088/ Senior.sport (talk) 17:49, 21 May 2023 (UTC)
thread_title:  Gilbert's and telemeres 

message: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9237193/
 Senior.sport (talk) 18:04, 21 May 2023 (UTC)
thread_title:  Elevated bilirubin and increased athletic ability. 

message: Is it proper that this disease's name is randomly spelled two different ways ("Gilbert's syndrome" and "Gilbert syndrome") in the current version of this article? 98.123.38.211 (talk) 02:06, 18 April 2024 (UTC)
thread_title:  Name spelled randomly two different ways in current version of this article