i saw in the past many articles in witch is said that the levels of AMA are not important after the PBC diagnostic and many Dr s do not perform the test after that.
I think that is wrong!
The levels of Ama are important.
in the stages of Pbc , Ama will change!
When u read about Ama u see that this antibody is related with the mithocondria wich is the energy cell in our body.The grater the Ama is i think that the mithocondria is more affected.
In PBC and other diseases as CFS/chronic fatigue syndrome the mithocondria is drained of its energy.
Many pbc pacients have fatigue and i think that the energy cells are drained of energy.
I also think that Pbc is a very sophisticated disease with many conections in our body.Something is triggering something else!Is like a carousel!
I found some studies about fatigue and i think that with more we understand about the effects we can understand better pbc and maybe in the future to stop the progresion!
Interesting read, thank you for posting. I have a friend diagnosed with CFS and we often compare our symptoms of fatigue. You’d think I had both conditions there so similar. If you like reasearch, you may find the link interesting, it’s a long winded paper, but if you Just read the discussion part you will get the gist, it mentions pbc and it’s relationship to antibodies in last part of the discussion.
Mitochondria are not cells, they are ultra-microscopic 'organelles' and they are found actually 'inside' pretty much all of the many, many, different sorts of cells in our bodies.
There are various different sorts of organelles in our body cells, and they all have different functions. Simply: organelles are somewhat like the organs in our body, but on an ultra-microscopic level, so they act inside the cells of living things.
[EG: chloroplasts are the 'organelles' that are found in plant cells, and they make food for the plant cell (and thus for the plant - and us!) from raw materials and sunlight.].
Mitochondria, in all the human body's cells, release energy from the food chemicals that have been digested, so that humans then have that energy available to them, to live.
AMAs (antimitochondrial antibodies) attack the mitochondria in our cells; and the type of AMA (there are different sorts of AMA, that cause different conditions) that cause PBC, attack the mitochondria in the cells of the liver. Specifically, they attack the cells in the liver that make up the microscopic biliary tubules that throng through every minute part of our liver, and carry away harmful substances.
So , yes, once attacked by the AMAs the mitochondria in the cell of a biliary tubule will die and no longer be releasing energy to give to that cell. But … it isn't really the loss of that energy that affects us in PBC, it is the fact that as the AMAs destroy the mitochondria, that one specific cell will no longer have the energy that was produced - as well as being physically damaged. Plus, as more mitochondria are attacked, that cell will die. Then, as more and more cells die, minute areas of the liver become damaged and scarred: and slowly, gradually … as the area of dead/damaged cells grows and grows, the scarring spreads in the liver, so that there are more and larger damaged areas.
More importantly, the harmful bile that these biliary tubules transport can no longer be removed from the liver, and it is this, that then causes more and more damage to the liver as scarring spreads, and bile builds up.
It is all of this that causes the complex chemical imbalance that is often the first sign of PBC.
Liver scientists at the far reaches of medical research are working, now, trying to find out why these autoimmune antibodies, come into being, and attack our systems, and cause all sorts of different conditions - depending on the different type of antibody.
It's the AMAs (all the different types) that are the problem: they shouldn't be there, and specialists are trying to find out how they come into being, what triggers them to attack their specific targets, and how we can get rid of them.
It is all actually far far. more complicated than I am explaining here, but also - I believe - far more, more complicated than the above suggested explanation that you have given .
However, top research scientists are r working as hard as they can to understand (and thus -hopefully- control all these special, rogue antibodies.
I would have a good read of all the specialist research sections and explanations on the 'PBC Foundations' website, as more is explained there, that can help when tackling research papers. See link at the top of the page.
Your response is spot on...I learned just enough in my college biology/anatomy/exercise physiology to follow what you said! Lol. I’m the one who know just enough to be dangerous.....ha!
When I heard “anti” mitochondrial antibodies from my liver doc it threw me into a higher sense of “scared shi%less” because I knew what the words meant but took me some time to grasp how it all worked...
I’m forever printing studies and going thru them to highlight and look up words or phrases I don’t understand. 🙄. I would have loved to have been smart enough to get into medical research! I’m geeky like that...lol
Great that you made the time and effort to look it all up, and sort it all out in your head once you had the diagnosis. It just helps to understand!
I think the 'PBC Foundation' is great for starting to learn your way around - plus maybe a good Biology book. But later you can graduate to reading the research review articles that are online, but always go back to the 'PBC F' if something doesn't make sense. I was a Biology teacher in a previous existence, but when first told (in 1992) that I was at risk of PBC, because I had AMAs, I became pale and panicky … all because I only really knew enough to think: "'antimitochondrial antibodies' … that sounds mega-serious." Fortunately the consultant was lovely and explained it, a bit. Years later and I joined the 'PBC F' and learned far more.
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Ama question
ama positive, but normal liver enzymes now. 
Fatigue with normal LTF's
Elevated ana, ama and alt
AMAs in blood but nothing esle 
