Mis-diagnosis of Gilbert's syndrome vs PSC?

Has anybody heard of misdiagnosis between PSC and Gilbert’s syndrome (GS)?

I have always had normal LFTs except bilirubin has been elevated. One time 5 years ago, based on ERCP and MRI, I got initial diagnosis of PSC (after long debate between two GIs and a radiologist - they were not sure but thought there was some narrowing of bile ducts). Since then nothing has been seen in annual MRI (only vague observation that bile ducts are somewhat narrow in general etc). LFTs and everything is and feels normal, except bilirubin is around 2 (normal range 0.2-1.2).

The ERCP and initial MRI 5 years ago were managed by experienced GIs. Since then I have seen once a year a hepatologist (not PSC specialist, but general hepatologist).
He has ordered annual MRIs but since nothing relevant shows up in tests or symptoms, we typically talk about sports mainly. I haven’t brought up mis-diagnosis yet, and my Internet research implies that there isn’t fully accurate test for GS.
It seems only symptom in GS is elevated bilirubin.

Just curious if anybody has experienced mis-diagnosis, especially if only bilirubin elevated.

Ted,
Thanks for your post. Hopefully someone here on this forum will have some thoughts. I certainly have never heard of this correlation. I will post your question on another liver site and see if we get any responses over there. I’ll post any answers that come in. Someone should have some thoughts that will hopefully give you some directions to pursue.

Mark

1 Like

Hey Ted - what is your typical direct to total bilirubin ratio? Is direct normal? Do you have IBD?

thanks Mark.

jtb:
Yes, I have UC (no symptoms for 3 years).
Direct bilirubin has always been normal e.g. 0.22 or 0.3.
Only “Bilirubin, Total” is mildly elevated (varies between 1.4 and 2.4).
This has been so for years.

MRI has only general statements like this
"Biliary: The intrahepatic ducts are again noted to be generally
diminutive and small in caliber. No intrahepatic or extrahepatic
biliary ductal dilation and no frank masses are seen. "

I read that Gilbert’s Syndrome is a liver disorder that does not register on the Model For End-stage Liver Disease (MELD) and therefore a transplant exception is made for patients with Gilbert’s Syndrome who are in need of a liver transplant.

Both diseases are considered very rare. It is possible for a doctor not acquainted with either disease to make a misdiagnosis. The first of six times I was hospitalized with liver failure, a young resident doctor repeatedly visited during the night to ask questions about PSC. He apologized for disturbing me, but his professor told him he would probably never see a live PSC patient in his career. That’s how uncommon PSC is.

1 Like

Hello!
Wanted to reply to this message because it’s actually quite similar to my situation: I had normal LFTs but elevated bilirubin during a specific blood test. This lead to MRCP which showed somewhat narrow bile ducts according to the first radiologist and he mentioned early stage PSC. However, they referred me to the hospital where specialists re-reviewed my case and they agreed that the size of the bile ducts was well within the margin of error of the MRI/MRCP and therefore not conclusive for PSC. They ordered several other blood tests to be sure, such as ANA/AMA (checking for other conditions most likely) and a new round of LFTs. Those came normal (even the bilirubin was back to low) and they then diagnosed Gilbert’s.
The only thing funky about it is that my direct bilirubin stayed high (and still is a year later, but didnt change) but indirect went back to normal.

For your specific case, the fact that neither GGT nor ALP (or even any of the transaminases) were ever elevated AND that the MRI shows only a small caliber narrowing within the liver (intrahepatic ducts) are quite telling imho.

I’ll quote here the guidelines of the EASL (European Association for the Study of the Liver):

Cholangiography: A detailed cholangiographic assessment of the biliary tree is essential in making a diagnosis of PSC [86]. Efforts should be made to adequately visualize also the intrahepatic ducts to avoid false-negative results by overlooking subtle changes. The characteristic cholangiographic findings of PSC include mural irregularities and diffusely distributed multifocal, short, annular strictures alternating with normal or slightly dilated segments producing a “beaded” pattern [87]. Sometimes outpouchings have a diverticular appearance [87]. With more advanced disease, long, confluent strictures may be seen [87]. In the majority of cases, both the intra- and extrahepatic bile ducts are involved. A variable proportion of patients (<25%) is described to have isolated intrahepatic disease, whereas lesions confined to the extrahepatic ducts are rarely observed (usually <5%) and should only be diagnosed in the presence of adequate filling of the intrahepatic ducts. Since intrahepatic bile duct abnormalities can also be seen in other chronic liver diseases, one must be cautious when diagnosing PSC in the presence of intrahepatic changes only. The gallbladder and cystic duct are involved in some cases, and abnormalities of the pancreatic duct resembling those of chronic pancreatitis have been noted in a variable number of PSC patients [87].

From the description you gave, the MRI doesn’t show any of the characteristic findings for PSC. Also: “Since intrahepatic bile duct abnormalities can also be seen in other chronic liver diseases, one must be cautious when diagnosing PSC in the presence of intrahepatic changes only.” is also quite relevant to your case, though your hepatologist has most likely thought about it and maybe ordered some AMA/ANA tests?

To finish, I’d quote one more thing from the guidelines:

(While speaking about MRCP) The method can also reveal changes within the bile duct walls and pathologies in the liver parenchyma as well as in other organs. However, cases with mild PSC changes without bile duct dilatation may be missed by MRCP and one should therefore be cautious to exclude early PSC on the basis of a normal MRCP.

This is most likely why your doctors went on the side of caution and are looking regularly to see if there is any progression. However since it’s been 5 years, maybe I’d ask them about the GS mis-diagnosis by starting for example with asking whether they would have mentioned PSC if you didn’t have a history of UC. If your hepatologist really wants to stick with PSC, maybe you can ask to have the MRI less frequently since there is no changes at all?

Thanks Ldde.
Do you mean that you do not have a PSC based on your most recent diagnosis (ie GS instead of PSC)?

Yes, in the end they only diagnosed me of GS, but that doesn’t explain why direct bilirubin is elevated. I’ll do yearly blood test to see if everything stay the same

The normal direct bilirubin and very low direct to total ratio points towards Gilbert’s (or something else) rather than PSC. PSC cholestasis would bump up direct. That initial imaging test showing irregularities seems to be the odd man out. Reading those images is a bit of an art and I’ve had two different radiologists find completely different results. I’d rely on what has been the long term trend.

I would bring up Gilbert’s syndrome with your doctor. I think you are on to something here.

Hi Ted,

I have been tracked by Gastroentrology doctors for last 12 years due to my elevated Bilirubin, ALT and AST blood results. First thing they checked was hepatit markers which was OK and they did biopsy to my liver which results that my liver is fatty in 2006. They checked everything and couldn’t diagnose me exactly since then. I was visiting hospital each 6 months. I never have any symtoms which affects my life since then. My blood disorders were found totally incidentally.

In 2015, I experienced obstructive jaundice due to blockage on my gallblader. My liver enzymes elaveted to nearly 10 times of normal range(ALT, AST, GGT, bilirubins, ALP). I became normal in 1 week without a drug income. Since then, they focused on PSC and they did ERCP first, but they failed due to inflamation on my bile ducts, they did colonoscopy with suspect of UC or Crohn disease which I don’t have. They did MRCP with outcome states that I have minimal disorders in my intrahepatic bile ducts.

I started to use URSO which normalize my liver enzymes except bilirubin. I did 2 following MRCP to compare with each other yearly since 2015. All MRCP reports are not clear about PSC diagnosis, at least do not find out any narrowings on bile duct trees.

Therefore, my GI specialist said to to drop URSO 2 months ago since he thinks if I would be PSC, he was expecting to see some progress on MRCP since PSC is a progressive disease. He said to me that maybe I am simply Gilbert, nothing more.

I will go again in 2 weeks, but my blood history tells me that my bilirubins are sligtly elavated (total bil: 2.13), ALT and AST are slight elevated like 2 times, ALP is normal, GGT might be elavated 2-3 times.

Ozgun

1 Like

I have an update on this one.
My hepatologist also thinks now that I have Gilbert’s disease. It is quite harmless condition with elevated bilirubin. No treatment needed.

But he thinks I still have PSC as well (because of some mild irregularities reported via imaging). All lab tests have been great other than bilirubin.

1 Like

Any update since then? They put a possibility of PSC in my notes after diagnosing me with GS. My MRCP isn’t until at least July so I’m nervous on whether I’ve been Mia diagnosed myself.

I had briefly very high LFTs (no symptoms) but after extensive testing (UC,MRI, colonoscopy, lots of blood tests) it was concluded that I have ulcerative colitis flare, causing high LFTs. Now they are returning towards normal level (after colitis flare was taken care of). Going forward, I will take my colitis medication and probiotics dutifully.
This was my first scare since diagnosis 10 years ago.

Otherwise, no changes. MRI still says no changes, bile ducts look somewhat narrow.

1 Like

Got ya. They did an ultrasound on mine and they said the common duct walls were thick, however the lumen was normal. LFTs for me other than bilirubin we’re all perfect too. It’s just been throwing me off what may be causing the thickness of my common duct walls. Thanks for the insight on your condition. Best of luck to ya.