Confused

How confusing for you when they are giving you such differing responses. Have you had genetic test? My daughter was told that if her ferritin goes above 200 she will have venesection. Her tsat was 42%. Won't actually be diagnosed as haemochromatosis unless treatment needed. Someone here should be able to answer your query.

A fatty liver can cause high ferritin.  It is not classic hereditary haemochromatosis when your TS% is <45 for females and <50 for males.  Eliminate sugars and starches from your diet - these are now known to cause a fatty liver.  As your fatty liver is being reduced so will your ferritin levels.

It is not likely to hurt you to have blood taken now and then but it won't be a cure for your fatty liver.  As you don't have haemochromatosis, you will not be able to sustain frequent venesections.  About every 3 months for those who do not have haemochromatosis.

Fatty liver would not mask liver iron on an MRI scan. 

Inflammation can put up ferritin.  If your C-reactive protein or sed rate is high, that means you have inflammation.  However, I've been told that inflammation all by itself would not explain a ferritin over 1000 ug/L. 

Still, there is no rule that says you can’t have both inflammation and hemochromatosis.  If you do have both, and the inflammation is going up and down, the part of your high ferritin that is caused by the inflammation would go up and down along with the inflammation, whereas the part of your high ferritin that is caused by hemochromatosis wouldn’t.

There are different types of hemochromatosis, and not all of them put up your saturation.  For example, one type of hemochromatosis, called ferroportin-loss-of-function disease, involves your ferroportin not working properly.  Ferroportin is the protein responsible for pumping iron out of cells.  If your ferroportin is not working properly, you don't absorb iron into your body very well, and you don't recycle iron inside your body very well.  The result is iron building up mostly in macrophages, the cells that recycle the iron-containing red blood cells.  People who have this kind of hemochromatosis show some iron buildup in the liver, but more iron buildup in the spine and the spleen. Because iron isn’t absorbed or recycled very well when ferroportin isn’t working properly, it takes longer after each phlebotomy for the disabled ferroportin to slowly get more iron out of the overloaded macrophages into the bloodstream where it can be picked up by the bone marrow to make enough new red blood cells to be ready for another phlebotomy. This is quite different from the usual HFE-related type of hemochromatosis (C282Y gene mutation) where both ferritin and saturation go up, where the liver ends up with heavy iron deposits, and where iron is recycled to make new red blood cells just fine, so phlebotomies can be done once a week – or even twice a week, at least at the beginning.

In addition to figuring out what's going on with your iron metabolism and getting rid of any extra iron, I think you also want to figure out what's making your liver fatty and fixing that.  The most common culprits causing fatty liver are high triglycerides (which can happen with above-normal blood sugars) or drinking too much alcohol - so it might be worth asking your doctor about cutting down refined carbs (sugar, flour, starch) and alcohol and also asking if you might be starting to get diabetes.

(In case it’s of interest, here’s what happened to me:  at the end of December 2009, my ferritin was 895 ug/L.  Three years later, in December 2012, my ferritin had gone up to 1438 ug/L (its highest), with an iron saturation of 38%.  In January 2010, I weighed 192 lb, 87.1 kg, BMI 33 – so I was overweight.  I lost weight until in December 2012, I weighed 129 lb, 58.3 kg, BMI 22.1 – so back down to normal weight.  During this time, my C-reactive protein, a measure of inflammation, went from a high of 4.7 mg/L (normal less than 1 mg/L) at the end of December 2009 back down to a normal 0.7 mg/L in December 2012.  In my case, losing weight worked to cut down inflammation as measured by my C-reactive protein going back to normal, but my ferritin just kept right on going up until I started having de-ironing phlebotomies.  Unfortunately, I couldn’t persuade any of my doctors to order an MRI for iron until after I had been de-ironed so I don’t know whether my extra iron was more in my liver or more in my spine and spleen.  The good news is that the MRI did show that the de-ironing had worked – my tissue iron levels were all normal by the time I got an MRI.) 

I hope some of this will be helpful for you -