Ferritin for the Clinician
Ferritin isn't the same thing as iron. Ferritin is a protein that stores iron, releasing it when your body needs it. If you have too little or too much ferritin in your blood. relationship makes the serum or plasma assay for ferritin an ideal non invasive test of iron status. if the direct relationship between plasma [ferritin] and the iron storage pool is not disturbed by ferritin .. balamut.info A ferritin blood test shows how much iron is stored in your body. Find out why you might need this test and how it's done.
I now realize I have to demand followup treatment and testing and perhaps go to a hematologist. Any other ideas are welcomed. Sun, September 11, 6: I need to correct myself in my last post. My serum iron was only 40 and should be about My iron binding factor was also low. Mon, September 12, 5: Have just found this website.
Could someone advise me if I have anemia. I am on ferrous sulphate mg twice daily prescribed by my consultant who has said that my serum ferritin is low. Have been to see another consultant and was asked as to why I was taking iron supplements as my iron level was normal. I had been told by the consultant who prescribed the iron that it would take 6 to 12 months to restore my iron levels and to feel better. But now I am totally confused as to whether I should actually be taking iron supplement or not.
Could someone please advise. Thu, September 15, 6: I have been under the care of a gastroenterologist since for Crohn's disease. I also have iron deficiency anemia. I had a bone marrow biopsy done and the biopsy showed "0" iron in the bone marrow. My hgb is slightly low, I get iron infusions occasionally but only when my hgb. My doctor states he doesn't want to give me iron infusions very often "because it could have serious side effects" I can't believe any side effects could be worse than the symptoms I'm having now.
I can truthfully say the iron infusions make me feel like a different person. I get 3 doses in 3 days. After the 2nd infusion, I can tell a huge difference in my energy level.
I told the doctor I'm going to start bootlegging the iron if he won't give it to me when I feel I need it. I highly recommend iron infusions! Mon, September 19, 3: I am a 64 yr old diagnosed with primary genetic hemochromatosis. Prior to that I also had been diagnosed with chronic Depression, Chronic Fatigue Syndrome and have had weight loss surgery.
Fatigue has been a constant and it gets harder to manage My ferritin stays low and has gotten down to to 2 at one point. I have had iron infusions several times, but they don't make me feel much better. Has anyone else had similar problems? Thu, September 29, I have had low ferritin for years.
Ferritin for the Clinician
Levels of about I have tried every supplement on the market, and my levels are not increasing I can imaging what they would be like if I had not taken any supplements. I feel like life is going by, and I can not catch it. I feel like I am going crazy. I am so tired. I am working out, but have gained no muscle in a year. My cardio is horrible. I even feel that certain fabrics on my skin are intolerable. The always wanting to move my legs is so frustrating as well.
I am set to have four Venofer infusions, one every two weeks. Does anyone know how long it takes to work? I have two young children, and a husband who need me. Wed, October 12, 4: I don't see on here where people are being checked for Celiac Disease. This can be done with a simple blood test for transglutaninase Antibodies tTGA. This is the most common cause if you can't get your iron levels to increase with supplementation and there is no obvious cause found, i.
Quite possible to be an asymtomatic celiac. My husband has it and only had neurological symptoms, no gut symptoms at all! The villi in the small intestine are damaged and therefore cannot absorb the iron.
- Ferritin Level Blood Test
- Iron-Deficiency Anemia
Must be on a gluten free diet in order for the villi to grow back and takes strict adherence to the diet. It takes a few months for the villi to fully recover so be patient. Googleq celiac disease and anemia. Not many docs are very good at looking for this. Wed, October 26, 4: Hello, New to the site and very frustrated and looking for anwsers, which I guesseveryone is. Dx with Iron def March '10 but decided to try to boost myself with diet.
Saw my doc who decided on maintenance therapy. I felt better as well and my blood actually was getting red instead of black. Prior to starting maintenance which is every other week Iron infusion for 10 wks I became symptomatic extreme, very emotional, palpitations, very short of breath, etc. My concern is whether they are missing something and maybe I have something else going on. Being worked up for heavy menstrual period for cause but nothing unusual.
I am perimenopausal and bleeding slightly more but never really had any issues with my reproductive. Always heavy periods but not convinced that is the culprit.
Should we reconsider iron administration based on prevailing ferritin and hepcidin concentrations?
The GI workup is - so what else could it be and how do I get it worked up to know for sure. Any ideas or suggestions? Seeing a hematologist but thinking I should see someone else different speciality any ideas on that as well. Best to you all n your own challenges with this iron dilemmia. I've been experiencing symptoms of anemia but can't seem to get my doc to take me seriously. He says my numbers aren't low enough for me to be symptomatic. Fatigue, excess shedding of my hair, any basic exertion makes my heart race My FE is 29, and percentage of saturation is 8.
But my Ferritin is 51 which is in the normal range.
Does anyone have any suggestions? Do these numbers indicate iron deficiency? My menstrual cycle is very regular, but extremely heavy. Any advice would be appreciated. Wed, November 9, 7: Hi Buffy - my story is very similar to yours except my ferritin is 40 still in the normal range.
I'm in the process of eating more iron-rich foods along with vitamin C - I'm desperate to feel better. I'll even eat liver if it makes things better!
I am also going to ask my doctor about supplements. Thu, November 10, Mary, thanks for the info. I didn't know that about the ferritin level. I also make a point to eat iron rich foods, cook on cast iron I read that trace minerals can be absorbedand I also juice kale and spinach and drink wheat grass daily.
I'll draw the line at liver though! I remember having to eat it as a child. Good luck to you. Thu, November 10, 4: I Have IDA as well as most of you and have recently been refereed to a hemotalagist. My blood work is way out of whack Serum Iron was 2 Ferritin 2.
They told me to change my supplement to Ferrus Gluconate and take it twice a day with vitamin c. I was curious if anyone knew what I should expect at the hemotologist visit as they assess me for Iron infusions and how that process would work.
Also they told me I may need my bone marrow tested has anyone had that done? Fri, December 30, 6: My anemia adventure started back in August I was feeling really crappy and was having real bad back pain.
Went to the emergency room and found out during a bunch of blood work that I was mildly anemic.Iron Physiology
Followed up with my GP and after a barrage of more blood test was told it was chronic disease anemia. At this time my iron was normal everything out of wak was around my red blood counts and my protein was low.
Its been down hill since, because of getting no true cause answers and getting more frustrated and worse by the day started seeing a hematologist by this time I had paid another visit to the ER this time for low potassium and magnesium and hemo was getting lower.
I didn't have the energy to do anything started missing a lot of work I was tested for bleeding from my gastro specialist and I found out my beta carotenes were low. Kept getting worse started seeing the hema in November had an Iron infusion first week of December my ferritin serum jumped up to so now its high but my saturation is still low and my hema came up to almost normal Specialist retested my beta and now liver counts and my beta is down to 5 so my immunity is compromised right now.
I was told 3 weeks from the infusion I would feel like a new woman. Still waiting for that new woman because she never showed up. My husband and I are very frustrated and need answers but so far nothing on what is causing this. As far as my blood work its always been pretty normal accept for by type II diabetes which its the one thing that is under control now. My mom had mylodisplasia syndrome and I am concerned this is the onslot of it but they have yet to do a bone marrow test and I am not quite sure why not.
Should we reconsider iron administration based on prevailing ferritin and hepcidin concentrations?
Never feel like I am asking the right questions. Wed, January 4, 9: I am a 65 year old women who has been in petty good health until some blood tests revealed I was borderline iron deficient.
After repeating the RBC a few months later, it was found I had a very low ferritin levelbut was not yet anemic. My doctor said this was a precursore to anemia and I should get it checked out with a hematologist.
It occurs because of blood loss into dialysis lines and filters, frequent laboratory testing, and gastrointestinal bleeding, to name but a few causes. Many patients who have borderline low iron stores at the start of ESA therapy develop absolute iron deficiency as these stores become depleted during the production of new red blood cells.
Others with adequate or even excessive iron stores may develop FID. The latter occurs when sufficient amounts of iron cannot be released from its reserves, mostly the reticuloendothelial system RES to satisfy the increased demand of the bone marrow during ESA-induced erythropoiesis, as is often the case in ACD [ 2021 ].
The conclusion from observations such as this one is that intravenous iron administration can effectively raise Hb even in patients with elevated iron stores. Following the report of the DRIVE study, there has been a tendency towards increasing the upper limit of serum ferritin levels. However, it must be emphasized that there is no proof at present that pushing up Hb levels with excessive iron doses improves the vital prognosis of MHD patients. It could even do the opposite.
Transfer of intravenous iron to erythroid cells We do not completely understand the exact mechanism involved in the improvement of Hb levels or ESA response subsequent to IV iron administration.
Based on previous pharmacokinetic studies, however, one can speculate how parenteral iron may be utilized for erythropoiesis. The pharmacokinetics of parenteral iron sucrose or iron—polysaccharide complexes have been assessed using positron emission tomography [ 2829 ]. These studies demonstrated that non-saturation of the transport system allows iron transfer from the blood to the bone marrow, indicating the presence of a large interstitial transport pool. Similar observations were reported in previous ferrokinetic studies using radiolabeled iron 59Fe where time-dependent accumulation of 59Fe was detected over the sacrum, a site of hematopoietic marrow [ 30 ].
Erythroid precursors have an extremely high iron requirement, especially during Hb synthesis. Although it was believed that the major pathway of iron supplementation for erythropoiesis is the transferrin receptor 1 TfR1 pathway in erythroid cells, another route of iron supplementation to erythroid cells has also been demonstrated [ 3132 ].
Bone marrow macrophages support the development of erythroid progenitors under transferrin Tf -free conditions by delivering essential iron for erythropoiesis in the form of metabolizable ferritin [ 33 ]. Thus, iron can be supplied to erythroid cells for hemoglobin synthesis using transferrin from plasma as well as ferritin from bone marrow macrophages. Recently, Coulon et al. TfR1 engagement by either polymeric immunoglobulin Ig A1 pIgA1 or diferric Tf Fe2-Tf increased cell sensitivity to erythropoietin by inducing activation of mitogen-activated protein kinase and phosphatidylinositol 3-kinase signaling pathways.
Fe2-Tf could act together with pIgA1 on TfR1 to promote robust erythropoiesis in both physiological and pathological situations, which may be relevant to IV iron administration. Further studies are necessary to support and clarify these mechanisms.
Anemia of chronic disease The anemia of CKD shares some of the characteristics of ACD, although decreased erythropoietin production secondary to chronic kidney failure, as well as the anti-proliferative effects of accumulating uremic toxins, significantly contribute to the pathogenesis of the former [ 3536 ].
A hallmark of ACD is disturbed iron homeostasis, with increased import, decreased export and retention of iron within cells of the RES. This leads to a maldistribution of iron from the circulation into storage sites of the RES, subsequent limited iron availability for erythroid progenitor cells, and iron-restricted erythropoiesis.
These proinflammatory stimuli also induce the retention of iron in macrophages by down-regulating the expression of ferroportin FPNthereby blocking the cellular release of iron. Similar findings were made in human umbilical endothelial cells [ 40 ]. The proinflammatory cytokine-related mechanisms, which play a major role in the reduction of iron transfer to the bone marrow, include not only an impairment of iron release and transport from the RES storage tissue but also a decrease in iron absorption from the gut.
One controversial point is that the concentration of proinflammatory cytokines required to affect these iron transport proteins is considerably higher than the serum levels that have are generally observed in patients on MHD.
In contrast to the cytokines, hepcidin appears to affect the expression of iron transport proteins within the range of serum concentrations of healthy subjects and patients with ACD [ 8 ]. Therefore, the discovery of hepcidin and its function had a tremendous impact on our understanding of normal and pathologic iron metabolism and related disorders, including ACD. This small peptide hormone produced by the liver inhibits iron efflux from cells by interacting with the iron export protein, FPN, especially in iron-recycling macrophages, and the iron import protein, DMT1, in duodenal enterocytes.
The binding of hepcidin to FPN results in the internalization and lysosomal degradation of FPN, which inhibits iron release by macrophages [ 43 ].
In addition, hepcidin also degrades DMT1 via the ubiquitin-dependent proteasome pathway, which results in the reduction of intestinal iron absorption [ 44 ].