Elevated LFTs

[whereisthenearestbathroom]

Hello all, just wanted to update you after my previous posts introducing myself and asking for some chicken soup recipes to help with three weeks of no appetite and mucusy diarrhea.

Spoke to my doc this morning who said all my inflammatory markers were fine (although he did admit sometimes they don't always show inflammation) but my LfTs were high. They had been increasing slowly since the beginning of the year by apparently they have increased quite dramatically. He is referring me for a liver scan. He did think it could be my gall bladder until I pointed out I had that removed in 2008!

The doc is being very thorough and keeping an open mind, and told me off for not coming to him sooner, which I think I needed to hear.

Anyone here have any probs with their liver or LFTs? Just seems to be one thing after another at the moment!

 

[nogutsnoglory]

What meds are you taking? Anything new or new dose? Certain meds can raise LFT very quickly.

 

[whereisthenearestbathroom]

One of the ibd nurses upped my pentasa from 2gms a day to 4gms last week, the doc seem concerned my diarrhea and mucus had got worse since then, and my weight is now starting to drop. Thankfully I have some to spare ;-)

Is pentasa likely to affect the liver?

 

[nogutsnoglory]

Any drug can affect the liver but I'm assuming your blood test was done before since you are only upping it for 1 week.

Sometimes the LFT can rise temporarily and the liver is incredibly resilient. If you don't find it goes back down in the next 2 weeks it may be wise to look at the meds as an issue.

 

[whereisthenearestbathroom]

Thank you nogutsnoglory. The bloods were taken on weds after he told me off for not coming to chat with him when I put in a repeat prescription for pentasa. He did mention that it may be due to my meds, I've been on paracetamol/codeine for 10 years, only 2 per day before bed but I know paracetamol is one, if not the, most common cause of liver disease.

I have to ring him and my nurse next week if things are still continuing. At least I have him in my corner, which is luckier than some people on here!

My mum passed away from liver failure (self induced as she was an alcoholic) so I know a little about the liver but not in relation to Crohns, I appreciate you taking the time to reply

 

[nikimazur]

I have Autoimmune Hepatitis, along with Crohn's disease. Elevated LFTs are to be of concern in those of us with IBD, for there are three autoimmune liver diseases that are more commonly seen in IBD patients. Primary Billiary Cirrhosis, Primary Sclerosing Cholangitis and Autoimmune Hepatitis. Though your elevated LFTs are most likely benign, it's wise to follow up on them, on the small chance you have an associated liver disease. It could also be medication related.

 

[baistuff]

There are 3 "systems" within liver function that manifest in what we know as LFT's.

1) hepatocellular function- or the workhorse cells of the liver. They breakdown meds, drugs, alcohol, toxins, clean the blood that comes directly from the gut. in LFTs, hepatocellular function is seen in the ALT and AST, especially the ALT ( AST is also found in muscle.) Elevations in these result from injury or "insult" directly to liver cells- from medications- very commonly statins, tylenol but also IBD drugs-, viruses, autoimmume hepatitis, alcohol, lack of blood flow.

2) Drainage of bile- Bile is produced in the liver and strored in the gallbladder (or in the liver if GB is removed) and released after eating. Any blockage of the bile ducts within the liver, outside the liver, or a stone in a duct can block flow. Also tumors (primary or metatstatic) scarring (PSC, cirrhosis) can cause blockage. The LFT's associated with this (called CHOLESTASIS) is seen in the Bilirubin, Alkaline Phosphatase (Alk phos is also found in bone, kidney, gut, so not always specific, but we think liver/GB first.) Bilirubin can further be evaluated as direct or indirect, but that is for another time.

3) Synthetic function- The liver also has the primary function to produce clotting factors and churn out protein. Severe liver damage of any cause (infection, cancer, drug, cirrhosis, etc...) if either severe enough acutely, or chronic and progressive eventually affect synthetic function- most often measured by an albumin and a PT/INR. Keep in mind those can be altered by other things as well- poor nutrition, acute infection, medications.


So whenever someone says they have abnormal LFTs, the question is which ones? is it one "system", multiple? Acute, chronic? how much above normal? Any symptoms (fatigue, jaundice, swelling, nausea, vomiting? )

I would always start with an ultrasound- easy, non invasive, no radiation, cheap, quick and proceed from there- MRCP, CT, depending on what the concern is.

Good luck.

 

[SallyJane]

Hi.

I too have a raised liver profile, which appears to have been rising steadily for months. I don't know the detail, as itbwasn't explained to me, but the level on my blood results said 154, and was highlighted in red as "High".

My consultant is sending me for some kind of specialist MRI liver scan. Having got my Crohns into remission, after taking LDN, I am now worried about my liver - in fact I am more worried about my liver than the Crohns. I do not drink, but I take LDN and raloxifene hydrochloride, along with Calcium D3 Forte, magnesium supplements and a supplement to try and help hair regrowth.

I don't have a gall bladder, but wonder if stones in the ducts could cause this, although I don't have any pain.

Does anyone have any ideas as to what this could be - how did "where is the nearest bathroom" get on? Have you managed to throw any light on your problem yet?

Quite scared about this,

Sally

 

[GHL]

Elevated LFTs---my son was diagnosed with primary sclerosing colangitis (liver) 3 years ago at age 14. Doctors then tested for IBD. 70% of PSC patients have IBD. Indeed he had non-symptomatic Crohns/ulcerative colitis indeterminate. Never knew he had it until scoped after liver diagnosis. Researchers think the IBD might somehow?? transfer to the liver. No cure for PSC, 8 weeks ago my son had a liver transplant. He is doing fine. So immunosuppressed now, that usually the PSC won't come back in the new liver. Have your doctor check the liver number called GGT in your blood test. PSC causes this number to go sky high. Don't want to alarm you as this is SUPER rare. Only 18,000 cases in US under 18 years old. Best regards.

 

[SallyJane]

Hi.

I am so sorry to hear about your son - and at such a young age too. I hope that he continues to do well - such a worry for you.

I have now had an MRI scan on my liver and am waiting for the results. I knew about PSC possibility. Crohns is bad enough, without having to worry about other implications.

Thank you for taking the trouble to reply.

Sally

 

[sue2003]

I had two occasions of increased LFTs, one was explained by CMV virus, other by ( non alcoholic steatohepatitis) which occurs due to steroids or malnutrition.

 

[baistuff]

I had two occasions of increased LFTs, one was explained by CMV virus, other by ( non alcoholic steatohepatitis) which occurs due to steroids or malnutrition.

While CMV certainly can raise LFT's, the most common cause of NASH (it's not really called that anymore) is obesity and metabolic syndome. Malnutrition actually will cause a decrease in many liver function tests, particularly albumin, but can also cause decreases in AST/ALT if bad enough to inhibit hepatocellular function. Steroids usually do not cause significant changes in AST/ALT.

In fact in myositis (muscle inflammation which can elevate AST) one of the clues to determine the cause is to look at AST and CK Autoimmune or inflammatory causes cause increases in these labs, steroids induced myositis typically does not.

 

[2thFairy]

While CMV certainly can raise LFT's, the most common cause of NASH (it's not really called that anymore) is obesity and metabolic syndome.

What is it called now?

 

[baistuff]

What is it called now?

NAFLD

Non-alcoholic fatty liver disease. The reason for the change is to find patients before the liver starts to scar (steatohepatitis) due to the fat. Years ago, we would find folks with some fatty liver changes on ultrasound and when they insisted they don't drink, we sort of blew it off. Now the fatty findings are considered significant in the non drinkers and of course in drinkers, and weight loss, exercise and diet and aggressively pushed in the non drinkers

I realize this seems like splitting hairs, but the distinction is an important one. Fatty changes are reversible. Scarring, if more than mild might not be. So yes, I sort of misspoke, NASH still exists, but the real focus is on NAFLD.

Either way, malnutrition typically would not cause fatty liver disease with or without scarring.