Talk:Gilbert's syndrome

Gilbert's syndrome is much more than hyperbilirubinemia. UGT1A1, UGT1A6, and UGT1A7 (enzymes deficient in most people with Gilbert's syndrome) deal with much more than just bilirubin. This wiki page is outdated and inaccurate because it fails to mention what other substances the enzymes process and the effects of their deficiency in people with Gilbert's syndrome, theoretically speaking. It needs to explain the work of the enzymes and offer a reasonable hypothesis on the effects of the enzyme deficiencies, with references to related research as proof. This outdated wiki page needs to be updated with complete information.

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)Reply

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)Reply

It's just hearsay, but there seems to be a huge overlap in symptoms between Celiac disease and the "elevated frequency of symptoms" in Gilbert's. A bit of googling shows me that many people with Gilbert's have had success with going on a Celiac diet. It worked for my mum (and technically my grandmother as well, though she was undiagnosed her entire life), and it seems to be working for me. Totally unscientific, though. Someone with a bio degree should do a study. :D68.148.104.28 (talk) 15:21, 26 November 2009 (UTC)BlairReply

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)Reply

Stem cell treatment is said to work well for this syndrome. — Preceding unsigned comment added by 2602:306:CE4E:E310:F190:5B8D:817D:F456 (talk) 20:41, 23 April 2013 (UTC)Reply

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)Reply

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)Reply

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)Reply

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)Reply

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)Reply

Gilbert's does not cause haemolysis. It is a disorder of glucuronidation. JFW | T@lk 02:20, 19 August 2005 (UTC)Reply

This whole thing puzzles me. Elp gr 15:26, 19 August 2005 (UTC)Reply

I guess it is clear that a better and more thorough synopsis of the research in this area is needed as outlined below: --Ben Houston 16:26, 25 September 2005 (UTC)Reply

I've added a section on problematic foods and drugs/substances as well as on recommended foods. Right now it is in a list format but I don't find it to be as concise as it should be. Many of the foods are listed for different reasons and the current format doesn't allow easy denotation of that. I am thinking that maybe a few table based format would work with columns that give reasons for each food would work better.

A column in the table could also point to the references (in numeric citation form or something similarly compact) that support the classification of the food. Currently, I have combined a couple of web pages together to make the list and thus it is not fully sourced on any one page. In all honesty, I feel that the list is fairly decent, and provides people with something to go on but I do not think it is 100% accurate. Personally, I need to learn more about the various liver pathways and then reference specifically that each food or substance taxes the relevant pathways. Also the good foods may not be specifically good for Gilbert's syndrome but rather just good for those with decreased liver function.

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)Reply

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)Reply

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)Reply

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)i have Gilbert's syndrome and from my understanding of the condition and my experience it is most likely picked up during a routine liver function blood test and it is most likely that the condition will not be picked up or recognised at all by a doctor if the individual tested is prepubescent! as the sex hormones at puberty are substrates of the deficient enzymes which then impair the function of those enzymes, which in turn raises the levels of bilirubin (which is also a substrate of the same already deficient enzyme) in the blood to a point where it shows on the blood test as a concern. i can confirm i had full blood works carried out as a child and at age 11 with no abnormality's detected and later at age 14-15 with very high levels of bilirubin which indicated i had the condition. be aware that high bilirubin is actually a diagnostic indicator of the condition! and the actual condition is deficient enzyme activity or production which impairs metabolism of that specific but not exclusive substrate and having said that i would say there are possibly variations of the condition within the general population who have deficiency's of the other enzyme deficiency's as well as unrelated ones not involved in the condition which have not been detected because they do not involve metabolism of bilirubin!!! scientists should look in to this!!!!. (nemo.shark)Reply

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)Reply

[[Image:''''''':Actually, GS can be extremely disruptive. There are many symptoms commonly reported by those with GS, including myself. I've taken down a list of the symptoms listed by 286 people on the main bulletin board for GS, and they are all remarkably similar. Not only this, but there have been studies showing that there are a wide range of effects caused by GS - gastroparesis, immune suppression, swollen liver, essential tremor, increased likelihood of chronic fatigue syndrome and schizophrenia, and more. My site GilbertsSyndrome.com has links to these studies. Shambala 22:42, 13 July 2006''''''']]

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)Reply

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)Reply

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)Reply

I discovered my GS by accident, during a check-up at the doctors. I have read the symptoms, and I found that I don't remember getting any of them. So, what Puellanivis says is good. Hmm...After re-reading my comment, I have discovered there is no point in saying this. Hooray! YazzaMatazza 10:37, 17 March 2007 (UTC)Reply

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)Reply

Sorry the quote is breaking the page--E-Bod 23:26, 26 March 2006 (UTC)Reply

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)Reply

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

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)Reply

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)Reply

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)Reply

• The web, I'm afraid is not generally a good primary source for establishing accepted/consensus medical opinion on specific diseases. Published peer-reviewed research and subsequent peer-reviewed journals' scientific debate are not reviewed, but rather often one website replicates information found on other sites. The information may or may not be correct, but the number of sites stating an idea is poorly correlated to veracity of checking from primary sources. As an example, the London Lock Hospital is often mistaken for the Albert Dock Seamen's Hospital, the first being world's first venereal disease hospital, the other would become the first tropical disease centre - look here for how same phrasing wrongly duplicated in multiple sites on performing Google "Dock Hospital" - page 2 onwards).
• That aside, Gilbert's is medically considered a benign asymptomatic/usually non-apparent condition (i.e. only occasionally causing symptom of mild jaundice, but being more issue of a laboratory result's significance being wrongly pursued for a possible active hepatitis). So if there are chronic symptoms arising from this condition, then that is controversial in as much as it is in conflict with the current definition of the condition. Is the medical formal description of the condition wrong ? It is possible, there certainly seems to be a lack of evidence to either support or refute the claim. However a possibility, until there is evidence, remains a conjecture and in the absence of citable primary evidence would fail under WP:NOR criteria for inclusion in wikipedia.
• One person's symptoms can not of course infer much, and may be due to some other unrecognised condition. Might not such a collection of people with GS be suffering from one of a number of similar poorly-recognised conditions, e.g. mild lactose intolerance or a mild variety of chronic fatigue syndrome (I’m not saying they are, but one could speculate) ?
• The presence of the websites with claims of more than one patient may of course suggest a real link to GS. Care naturally has to be taken, one could find thousands of people with GS who have heart disease, but as 1 in 3 of the general population die from heart disease anyway, this is not of any special significance. However, if studies were ever to show rates of heart disease in GS being different from that of the general population, then the effect would be proven.
• So, collective claims of illness as a consequence of GS needs to be supported by epidemiological evidence - have such studies been performed ? If so, then they need to be cited and the symptoms linked to GS would not be "controversial" (depending upon the findings of such studies we would then no doubt be discussing terms such as "sometimes", "rarely", "occasionally", "typically", "often") David Ruben ^Talk 04:36, 23 April 2006 (UTC)Reply

-No one is going to study a condition that is considered benign. The disease has been diagnosed in me and one other person in my family. I'm relatively certain others in my family are undiagnosed and mainly asymptomatic except for visible jaundice. GS is far from asymptomatic in my case or in my cousin's, otherwise neither of us would have ever been diagnosed, although our symptoms differ. He complained of chronic stomach aches and my symptoms would be best described as a fatigued/impaired state when in any of the situations leading to jaundice. While this disease won't kill me, it does greatly affect my quality of life. Why I suffer more than others who undoubtedly share the syndrome, I'm not sure, but I have no doubt these and other symptoms come out of some general problem in my liver. Various of these symptoms and conditions are well established in my family tree and are all linked to liver function. It could be GS is just part of a grouping of problems or deviations associated with this organ. It is however offensive to say it's mainly something noticed in a lab by doctors and otherwise "harmless." Although I understand an encyclopedia wants to have mainly only widely accepted statements. I think a lot of people who've been diagnosed with GS might disagree with the known medical description though. 15:16 September 25, 2007 (UTC) —Preceding unsigned comment added by 216.197.244.23 (talk)

Look GS sufferers (myself included) I want the straight answer, are the symptoms some have requiring a source so we blame GS or is there an actual connection to GS. I'm looking for somebody that was diagnosed 40 years ago and can tell how his/her health has been for their entire life? I mean are the GS patients "with" symptoms suffering from some other disorder? I've also wondered WHY all the websites out there (about four main ones) are British based. Going off the high estimate there are 30 million people in the USA with GS(670 million for the world population). That is a staggering number to only have 4 UK websites and some appear to be for financial scams! One appeared to be profiting by selling a e-book on what foods to eat and the like. Could there be levels of GS disorders or what. Add your two cents please. —Preceding unsigned comment added by Pavelow235 (talk • contribs) 03:39, 2 March 2008 (UTC)Reply

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)Reply

i have gs and have been diagnosed with b12 deficiency, pernicious anemia has been totally ruled out and im not or ever have been a86.185.120.18 (talk) 15:10, 29 March 2011 (UTC) vegan. (nemo)Reply

Whilst there are people who have Gilberts syndrome without any symptoms not everyone is so fortunate. Working shifts tempts me to put any fatigue down to just that but I can't blame my jaundiced eyes on them. From pale yellow to the yellow of a New York taxi cab when I had to take some antibiotics (!!!) I have struggled with trying to look professional at work and to not dislike what I see in the mirror at home. There is no information on what sort of make up could be worn to disguise the tinges of yellow and I can't seem to find any colours that improve it...the only thing perhaps would be for me to start wearing bright lipstick to divert peoples focus to them. With regards to supplements: There is some suggestions on using milk thistle (can be taken in a capsule or drank as a tea) to detoxify the liver. Whether taking a vitamin B supplement makes you feel better or is the placebo effect if it works for you then you could see if you can stay focused when you stop taking it. I have had quite bad concentration levels/ brain fog which has improved with me taking gingko biloba. I also try to look after myself: force myself to try to sleep more when on nights, balanced diet, making time to relax. I try to minimise how much paracetamol I take if I need it although not all research supports that GS causes increased chance of paracetamol toxicity. Although I'd rather not take that risk - paracetamol toxicity is rather nasty. (Mindymoo1 (talk) 03:36, 17 January 2010 (UTC))Reply

I'm not familiar with a specific recommendation targeted at patients with Gilbert's syndrome for hep A and hep B vaccinations. Anyone else out there more knowledgeable about this? Andrew73 11:42, 26 May 2006 (UTC)Reply

I've never heard of this. In fact, I know of a few people with GS (including myself) whose symptoms became permanently worse shortly after hepatitis vaccinations. I've commented this out as it could be dangerous, and I see no reason why it would be helpful. Shambala 22:36, 13 July 2006 (UTC)Reply

I have GS, and I have received exactly this recommendation from my GP. I got the vaccination series and experienced no GS symptoms. I have experienced terrible GS symptoms in the past, for example when I had mononucleosis and became very jaundiced for many weeks. The Hep B vaccine is a protein, not even a killed virus. All it will do is generate an immune response, and nothing it does will be liver-specific.

On the other hand, a Hep B infection will be very, very, bad for someone with GS. This was my GP's advice, and I followed it. That makes my statement not citable, but WP:OR. However, I think you are very wrong.

For those of you physicians who doubt that GS patients notice GS, please stop doubting. I went to physicians many, many times and asked them why I was so ill. I would be tired, nearly exhausted, and become somewhat jaundiced. I came to believe that my mononucleosis infection might actually have been chronic hepatitis or something. I would go to doctors with slight jaundice, a headache, exhaustion, and a cold. They made marks in my chart about how they knew I had GS but was a bit of a hypochondriac and should not be told.

Finally, I gained access to a detailed liver panel test taken from my own blood. My ratio of unconjugated:conjugated bilirubin was 5-times higher than expected! So I went to a new GP with my 'proof' and he finally was the doctor who told me that I have GS. Now, I'm completely not worried about it.

Whether people should or should not get the hepatitis vaccination to go with GS is not something I am an expert on. I can definitely say that I got it and suffered no GS-related symptoms. However, since GS-related disorders are a spectrum, it is possible that some who have been diagnosed with "GS" actually have a more severe disorder of bilirubin conjugation. Perhaps the vaccination could harm such people, but I can't imagine how. Namaste, Heathhunnicutt 22:40, 14 July 2006 (UTC)Reply

Caveat: I already had Hep A antibodies, so there was no need for me to get the Hep A vaccine. The Hep A vaccine is "attenuated" by passage through cell types that aren't its normal habitat. Perhaps vaccination with attenuated Hep A virus really could cause symptoms in a GS patient. It is hard for me to see how such symptoms could be permanent, though. I really can't see how it is in any way possible that Hep B would cause a problem, and I would be sort of surprised if Hep A did, even though the Hep A vaccines are live virus. Heathhunnicutt 23:03, 14 July 2006 (UTC)Reply

For myself, the vaccination was one of several events during the onset of my symptoms which could have brought them on (the others being severe food poisoning and simply getting older), but I've talked to others who have had symptoms intensify soon after the vaccination. Thinking that hepatitis would be worse for someone with GS seems to make sense, but I havent heard evidence of this. There's also talk that the mercury (previously? still?) used in the vaccinations can cause long-term problems. At any rate, you're right, it's WP:OR. It shouldnt be in the article. And I'm glad you found a doctor who would talk to you about it. Keeping GS secret seems to be a not uncommon practice. Shambala 12:16, 16 July 2006 (UTC)Reply

No, Shambala, I'm right that my experience was WP:OR, but the question of whether that is common practice remains open, and you haven't produced any evidence other than your gut feel. Also, no there is no longer mercury (thimerosal) in very many vaccines, and there is ample evidence that thimerosal was harmless to begin with. (See Talk:MMR_Vaccine). Heathhunnicutt 00:19, 17 July 2006 (UTC)Reply

The burden of proof rests on the one making the claim. Shambala 22:50, 27 July 2006 (UTC)Reply

That is laughable, considering the level of 'proof' you have brought in comparison. Heathhunnicutt 16:03, 29 July 2006 (UTC)Reply

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)Reply

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)Reply

conjugated bilirubin is excreted in bile, not via the kidneys. excretion via the kidneys (bilirubinuria] occurs in hyperbilirubinaemia which is high levels of conjugated bilirubin - a condition that will not occur in Gilbert's syndrome since conjugation is deficient. - 89.100.205.6 (talk) 21:44, 28 November 2007 (UTC)brenReply

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)Reply

I suppose the only reasonable way to rule out your medication as a cause would be to stop taking it (under the strict supervision of your doctor, and only after consultation with him/her and their agreement) to see if your bilirubin returns to normal levels. Your medication is Imipramine, and as far as I recall, jaundice would be quite a rare side-effect. Given that some 5% of the population have Gilbert's, it is probably a more likely cause on balance. Out of interest, have your LFTs shown changes in liver enzymes, particularly ALT/AST? Putting all this aside, neither cause of your increased bilirubin/jaundice would be reflective of underlying liver disease (assuming all other lab studies are normal) and so it would only really be of academic interest in your personal case. —Preceding unsigned comment added by Trefusismadding (talk • contribs) 02:15, 19 February 2008 (UTC)Reply

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)Reply

The likely explanation here probably involves the role of UGT1A1 in the processing of C18 steroids ("oestrogen"). Since this enzyme (UGT1A1) is hypoeffective in Gilbert's, it would follow that oestrogen would be allowed to rise to levels in the male which could induce gynaecomastia. I shall review the literature tomorrow and look for studies which confirm this.

i think your right its got something to do with estradiol, i think its a substrate of one of the deficient enzymes. ive recently been reading about the effects of dht on the prostate and found out that although dht does make the prostate enlarge its recently been discovered that estradiol also has the same effect. bacically its dht that initially enlarges the prostate during puberty so inhibiting 5ar will reduce its size. but its estradiol that increases in the male body with age that initiates a second phase of growth (bph). if people with gilberts syndrome have higher than normal ranges of estradiol that cause gynecomastia, it could be that people with gilberts also have a higher chance of this kind of prostate enlargement? however ive read a studdy about using dht as a treatment to reduce bph in men and it was successful, due to dht's inhibitory automatise effects. i think people with gilberts syndrome also have higher than normal levels of dht as it is also a substrate of one of the deficient enzymes? so maybe its this effect that prevents people with gilberts syndrome having an increased risk of bph? although the increased risk of gynecomastia however small that may be, may also transfer to a slightly higher risk of bph? i have gilberts and ive had my hormones tested my dht is high and my testosterone to estradiol ratio is more close to 2-100 in favor of testosterone than 1-200 in favor of testosterone like it should more respectably be. (nemo) —Preceding unsigned comment added by Nemo.shark (talk • contribs) 07:28, 2 March 2008 (UTC)Reply

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)Reply

I've read that too, but like with the symptoms some people describe to have with GS I take them with a grain of salt. —Preceding unsigned comment added by Pavelow235 (talk • contribs) 03:48, 2 March 2008 (UTC)Reply

i think i may have an answer to this question, theres a recent study thats been published about the menopause and its effects on bad cholesterol, apparently its the reduction of estrogen's at the menopause that causes the rise in bad cholesterol. so it could be that gilberts syndrome has a positive effect on bad cholesterol because of the increased levels of estrogen's.

if i remeber right estrogen's are made from cholesterol, so could it be the reduction in conversion of cholesterol to estrogen's that is making the bad cholesterol rise, i think so. (nemo) —Preceding unsigned comment added by 86.157.127.174 (talk) 12:52, 6 March 2008 (UTC)Reply

i think this may explain why gilberts has a positive effect on cholesterol, this link explains why niacin effects cholesterol, its because of its effects on the liver.

http://www.ncbi.nlm.nih.gov/pubmed/18316796

i know that niacin makes gilberts worce so i think it must be a substrate of one of the deficient enzymes. —Preceding unsigned comment added by Nemo.shark (talk • contribs) 13:51, 10 June 2008 (UTC)Reply

When I got my blood tests back with extremely high Bilirubin, my cholestrol was extremely low, even lower than the healthy range. Just figured I would put in my little bit of evidence. — Preceding unsigned comment added by 220.233.6.31 (talk) 04:08, 10 August 2012 (UTC)Reply

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)Reply

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)Reply

i find it strange that the clinical perception of gs is practically the same as what it was when the syndrome was discovered over 100 years ago! a lot more is known now but its just disregarded, probably because the drugs company's aren't going to publish data thats indicative of why up to 10% of the population aren't good candidates for there psychiatric medication. the 10% of the population with gilberts are the most likely to go to there doctors to complain about something that is wrong with them, the doctor then does a blood test and tells you that your fine nothing to worry about you just have gs its a benign condition and it doesn't explain your other symptom's. which will then lead your doctor into thinking that whats wrong with you is psychological.

i think theres more going on with gs than meets the eye, i dont believe that so many people that have the same condition can all be hypochondriac's!

people with gs have higher levels of estrogen's, this signals the pituitary into thinking enough testosterone is being produced and it effects the ammount of testosterone that is produced. so if its a fact that people with gs have higher levels of estrogen's they will in turn have low to moderate levels of testosterone.

its already thought that depression is more likely in people with low testosterone, there was a study released about it this week.

http://news.bbc.co.uk/1/hi/health/7274481.stm

wouldn't lower levels of testosterone explain fatigue?

im sure this isnt the full explanation, but i am sure its a contributing factor.

im also sure that a lot more is known about gs by the drugs company's and the information is suppressed as its not in there financial interests to releace it. (nemo) —Preceding unsigned comment added by 86.157.127.174 (talk) 13:32, 6 March 2008 (UTC)Reply

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)Reply

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)Reply

It's French. —Preceding unsigned comment added by 66.167.95.160 (talk) 03:20, 20 October 2008 (UTC)Reply

No itsnot. —Preceding unsigned comment added by Dro162 (talk • contribs) 23:11, 6 July 2009 (UTC)Reply

If it were pronounced "Joe-Bear" it would be spelled Jaubert. —Preceding unsigned comment added by 207.59.112.114 (talk) 20:23, 1 April 2010 (UTC)Reply

Actually its pronounced "zheel-bears" as it is french. — Preceding unsigned comment added by 90.192.134.85 (talk) 15:47, 9 July 2012 (UTC)Reply

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)Reply

If you can find the journal source for that information, feel free to add it -- but a news.net site isn't very reputable. Zedtwitz (talk) 02:21, 18 February 2014 (UTC)Reply

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)Reply

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)Reply

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)Reply

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)Reply

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)Reply

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)Reply

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9237193/

Senior.sport (talk) 18:04, 21 May 2023 (UTC)Reply

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)Reply