Cirrhosis Support Group

Cirrhosis is a consequence of chronic liver disease, most commonly caused by alcoholism and hepatitis C. Ascites is the most common complication of cirrhosis and is associated with a poor quality of life, increased risk of infections, and a poor long term outcome. Liver damage from cirrhosis cannot be reversed, but treatment can stop or delay further progression and reduce complications.

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what exactly is this ALT and AST.. and what effects they have on the liver? my last labs the doc said they were up slightly up from prior values.. to me they looked wayyyyyyyyyyyyyyyyyyyy up since the last ones! what makes them go up and what can i do?
my bilirubin totals are down from 2.4 to 1.8 that sounds good and i hope it is!
i still have swelling in my legs if i'm standing too long. i also have varicose veins and as long as i wear support stockings there's no swelling! anyone else experienced this?
thanks much,



I recommending joining this site to learn more, it is a terrific resource for anything to do with the Liver and or living with liver disease. I learned that stop drinking meant NOT EVEN 1, of course that is your call and you have your own set of circumstances and/or diagnosis.

Here is the link for the site and some prelim info on the AST/ALT etc. Good luck to you.

Markers of Hepatocellular Injury
The most commonly used markers of hepatocyte injury are aspartate aminotransferase (AST, formerly serum glutamic-oxaloacetic transaminase [SGOT]) and alanine aminotransferase (ALT, formerly serum glutamate-pyruvate transaminase [SGPT]). While ALT is cytosolic, AST has both cytosolic and mitochondrial forms.

Hepatocyte necrosis in acute hepatitis, toxic injury or ischemic injury results in the leakage of enzymes into the circulation. However, in chronic liver diseases such as hepatitis C and cirrhosis, the serum ALT level correlates only moderately well with liver inflammation. In hepatitis C, liver cell death occurs by apoptosis (programmed cell death) as well as by necrosis. Hepatocytes dying by apoptosis presumably synthesize less AST and ALT as they wither away. This probably explains why at least one third of patients infected with hepatitis C virus have persistently normal serum ALT levels despite the presence of inflammation on liver biopsy.6,7 Patients with cirrhosis often have normal or only slightly elevated serum AST and ALT levels. Thus, AST and ALT lack some sensitivity in detecting chronic liver injury. Of course, AST and ALT levels tend to be higher in cirrhotic patients with continuing inflammation or necrosis than in those without continuing liver injury.

As markers of hepatocellular injury, AST and ALT also lack some specificity because they are found in skeletal muscle. Levels of these aminotransferases can rise to several times normal after severe muscular exertion or other muscle injury, as in polymyositis,8 or in the presence of hypothyroidism, which can cause mild muscle injury and the release of aminotransferases. In fact, AST and ALT were once used in the diagnosis of myocardial infarction.

Slight AST or ALT elevations (within 1.5 times the upper limits of normal) do not necessarily indicate liver disease. Part of this ambiguity has to do with the fact that unlike the values in many other biochemical tests, serum AST and ALT levels do not follow a normal bell-shaped distribution in the population.9 Instead, AST and ALT values have a skewed distribution characterized by a long tail at the high end of the scale (Figure 1).5 For example, the mean values for ALT are very similar from one population to another, but the degree to which the distribution is skewed varies by gender and ethnicity. The ALT distributions in males and nonwhites (i.e., blacks and Hispanics) tend to have a larger tail at the high end, so that more values fall above the upper limits of normal set for the average population.10,11

thank you!

If you do continue/start to drink. these numbers will change, and you will be so busted by your doctor.

If you end up on the transplant list, these numbers mean a lot, as in you're not following the rules and will probably be dropped from the list until alcohol free for at least six months.

I don't remember my original numbers, will check at my next appointment, but I wasn't expected to live. I flipped a switch and stopped alcohol immediately, three months later my numbers were fairly normal.

I'm still a medical maintenance nightmare. See my GI at least four times a year, twice a year MRIs and Upper Endoscopies. I gave up keeping track of blood tests, but they average about every six weeks.

Think my bilirubin was 3.0 originally, but has finally settled down to about 1.8 like yours. Not great, but it has been stable for about three years now.

I would ask your doctor for furosimide, it's a diuretic and can really help with the excess fluid an swelling. I'm off it for the most part, but still take a pill two or three times a month.

Things are very manageable, but just have to be careful. Watch your weight, blood pressure and check into the furosimide, it can be really helpful.

i DO NOT drink any alcohol.. haven't since the day i was told of the cirrohsis! didn't have to tell me but one time!

Good for you srd1967, stop the alcohol and stop immediately.

I stopped nearly five years ago, no withdrawls, DTs or any other symptoms. Were you the same way?

People always question me about it, but I just flat out stopped, no gradual stopping or any kind or any tapering process, I was done. I can't explain it, nothing happened, I simply stopped drinking alcohol.

Just curious how your stopping went.

Had a question from someone else a few days ago related to this. Looked at my latest labs and forgot that many labs no longer use AST or ALT in their results.

SGOT is what used to be AST
SGPT is what used to be ALT

Both numbers should be below 50 to be considered normal. Haven't done much research into why they changed the names, but will post if I come across why.
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