Hep C Discussion Forum

SF,

More on our discussions about iron. Regarding your iron overload (hemochromatosis), and mine, we cannot really compare to each other to completely figure this condition out. Nor have our doctors really provided us with a full explanation for it. I think, at the moment, we may never get a satisfactory explanation for why, except for the general reason that "it IS seen" in people with HCV. Both of us had "hereditary" reasons for our iron accumulation ruled out (HH - hereditary hemochromatosis). We learned non-hereditary caused iron overload, is much less commonly found in young women, occurs more so in adult males and also in post-menopausal women like myself. The silent elephant in the room seems to be people with HCV and high iron loads.

Your iron load was higher than mine, and was treated with phlebotomy to decrease it prior to HCV treatment. I have no idea how long I may have had a higher iron load over my 40+years of HCV. (HCV, let alone ferritin levels, were never looked for, in me). I was very lucky that my ferritin levels were ever tested for (I think they were only reluctantly looking to rule out an unlikely possible anemia reason to silence my health woe whining), and, because my ferritin was found to be elevated, only that led me to further blood work, enzyme testing and eventually to HCV testing. I could still be sitting here with undiagnosed HCV had it not been for that one high ferritin test and a good young newly trained student GP doing her due diligence to hear my complaints of unwellness, who wanted to know why my ferritin was elevated. I was lucky for that, for her and her stumbling over my high ferritin by near accident.

I did much reading while waiting for HCV treatment, that my treatment outcome "might" be hindered by high iron overload, so it concerned me, to suddenly discover only about 8 months prior to my HCV treatment that I had some iron overload. I was wishing I had more factors "on my side" before commencing treatment to ensure the best possible outcome. I already had some factors against me, long standing HCV, history of HBV, older age, having GT3, known fatty liver, most likely a high F score, and somewhat less importantly a high VL.

My highest HCV pre-treatment testings were: iron 42 (normal 9-32), ferritin 563 (normal 15-300), saturation .81 (normal .15-0.45). I asked about phlebotomy for myself too, but unless they found my ferritin over 1000, they were not so inclined.

Your delay to SOT for HCV due to phlebotomies was stress invoking. I was stressed too, in my trepidation in approaching treatment with a perceived belief that my somewhat higher iron load was another possible hindrance to best outcome. You and I exchanged pm's on the subjects of iron and HBV, but I thought maybe I would just share this now, for the odd hi-iron person out there. As it turned out, my somewhat high ferritin level, seemingly, was no impediment at all when it came to the effectiveness of the powerful new triple sof/vel/vox I got in my 8 week trial!

In preparation for treatment, on my own (I did tell my docs about it) I immediately set about reducing high quality sources of "heme" iron (meat based) and "non-heme" iron (plant based) in my diet (decreasing red meats, plant based foods high in iron or plant based foods that they "fortify" with iron). I stopped taking vit C supplements. I never did take multi-vits that contained iron with any great regularity anyway. But I had, as I aged, tried to make sure ate enough vit C for it"s antioxidant qualities and other benefits. Because C and iron together enhance iron absorption, I immediately made a concerted effort not to consume vit C foods with any meal that had high iron content.To get my C, I mostly had to take vit C fruits, etc., quite separately from meals containing iron. Little can be done to impede absorption of "heme" iron (meat based), but measures can be tried to impede of absorption "non-heme" iron (plant based). 

I continued to maintain a lower dietary iron intake (both heme and non-heme). I also made sure to take some calcium, magnesium with the highest iron content meal of the day, as these somewhat "compete" with iron for absorption. I also increased phytates in my diet via various plant foods which are said to help impede iron absorption. I stopped cooking in my cast iron pans. (Miss those!)

After my HCV cure, my iron, ferritin and iron saturation have, so far, returned to be within normal limits (22, 191, 0.39 respectively). Why? I may never know. Were my pre-treatment elevated iron labs really just innocuous, inconsequential "blip" oddities due to "impairments" while I carried HCV? I had read that the body has few means to rid itself of excessive accumulated iron stores, thus the reason for reductions via treatment by phlebotomy (life long repeated phlebotomies can be necessary for those with established hereditary type hemochromatosis). Was I simply causing iron accumulation by my vit C intake enhancing the absorption of my iron rich diet? Did any of my iron absorption impeding measures have any effect? At best, if any of my dietary interventions had a mitigating effect, I would have expected no more than to simply prevent my iron load from increasing, not for my iron to decrease from what I had already accumulated. Now cured of HCV, perhaps if I resumed consuming a high iron/vit C diet again, and I do not ever show high ferritin levels again in the future, I may have a better guess. In retrospect, were my high iron readings (while having HCV) really a potential problem for me even to consider? I am just glad, post-treatment, that I have now had one set of normal iron, ferritin and saturation readings again.

Below, focuses more on ruling out "hereditary" reasons for iron accumulation, but is still an interesting read, especially the bit in red (considering all).

Iron Tests

Excess iron may accumulate in the liver and other organs for a variety of reasons. Some individuals have a genetic disorder while others may accumulate too much iron for other reasons. Among the genetic iron-overload conditions, the most common in individuals of Northern European ancestry is related to an autosomal recessive disorder, hereditary hemochromatosis. Before ordering tests it is important to be clear about what question is being asked. Most of the time the question is: Does my patient have iron overload?

This question should be entertained in the following situations:

• Any adult with liver disease, especially men and post-menopausal women
• Patients with symptoms suggestive of or having a family history of HH

The initial evaluation for iron overload includes measurement of serum ferritin, iron, iron-binding capacity, and transferrin saturation levels. Transferrin saturation less than 45%, in addition to normal serum ferritin level usually rules out iron overload (negative predictive value of 97%), and no further testing is necessary. Transferrin saturation greater than 45% and/or a serum ferritin above normal level warrants further investigation. ⁹ However, these thresholds are low, and most patients who exceed these limits will not prove to have iron overload as explained below.

Limitations of Serum-Based Tests of Iron Overload

Because both iron and ferritin are stored in liver cells, any condition that results in hepatocyte injury and release of intracellular contents into the blood will falsely raise iron, transferrin saturation, and ferritin levels. Therefore, in acute hepatic injury these tests will falsely suggest iron overload. Acute inflammation outside the liver may also falsely elevate the results of serum-based iron tests. Tests of serum ferritin levels, iron, iron-binding capacity, and percentage saturation determined in the setting of markedly elevated aminotransferase levels (AST and ALT), such as those seen in acute viral hepatitis or massive hepatic necrosis, will be identical to those seen in hemochromatosis. Iron studies cannot be interpreted in the face of major elevations of transaminase levels.

 Another learning thing I read, interesting (to me anyway):  http://www.pathologystudent.com/?p=2124