Editing Hereditary haemochromatosis (section)

== Treatment ==

===Phlebotomy===
Early diagnosis is vital, as the late effects of iron accumulation can be wholly prevented by periodic [[Venipuncture|phlebotomies]] (by venesection) comparable in volume to [[blood donation]]s.<ref>{{cite web |url=http://www.mayoclinic.com/health/hemochromatosis/DS00455/DSECTION=7 |title=Hemochromatosis: Treatments and drugs |work=Mayo Foundation for Medical Education and Research (MFMER) |access-date=17 March 2007 |archive-date=7 March 2008 |archive-url=https://web.archive.org/web/20080307063713/http://www.mayoclinic.com/health/hemochromatosis/DS00455/DSECTION=7 |url-status=live }}</ref><ref>{{cite journal|title=EASL clinical practice guidelines for HFE hemochromatosis|doi=10.1016/j.jhep.2010.03.001|pmid=20471131|url=http://www.journal-of-hepatology.eu/article/S0168-8278%2810%2900197-2/abstract?cc=y=|volume=53|issue=1|journal=Journal of Hepatology|pages=3–22|year=2010|author1=European Association For The Study Of The Liver.|access-date=25 May 2015|archive-date=28 August 2021|archive-url=https://web.archive.org/web/20210828105049/https://www.journal-of-hepatology.eu/article/S0168-8278%2810%2900197-2/fulltext|url-status=live}}</ref>

Phlebotomy (or [[bloodletting]]) is usually done at a weekly or each two weeks interval until ferritin levels are 50 μg/L or less. To prevent iron reaccumulation, subsequent phlebotomies are normally carried out about once every three to four months for males, and twice a year for females to keep the serum ferritin between 50 and 100&nbsp;ug/L<ref>{{cite book|last1=Kowdley|first1=KV|last2=Bennett|first2=RL|last3=Motulsky|first3=AG|last4=Pagon|first4=RA|last5=Adam|first5=MP|last6=Ardinger|first6=HH|last7=Wallace|first7=SE|last8=Amemiya|first8=A|last9=Bean|first9=LJH|last10=Bird|first10=TD|last11=Dolan|first11=CR|last12=Fong|first12=CT|last13=Smith|first13=RJH|last14=Stephens|first14=K|title=''HFE''-Associated Hereditary Hemochromatosis|chapter=HFE Hemochromatosis|date=1993|publisher=University of Washington, Seattle|pmid=20301613|chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK1440/|access-date=25 May 2015|archive-date=18 January 2017|archive-url=https://web.archive.org/web/20170118124842/https://www.ncbi.nlm.nih.gov/books/NBK1440/|url-status=live}}</ref>

===Iron chelation therapy===
Where venesection is not possible, long-term administration of an iron [[chelation|chelator]] as [[Deferoxamine]] (or Desferrioxamine), [[Deferasirox]] and [[Deferiprone]] is useful. Deferoxamine is an iron-chelating compound, and excretion induced by deferoxamine is enhanced by administration of vitamin C. It cannot be used during pregnancy or breast-feeding due to risk of defects in the child.{{citation needed|date=May 2015}}

===Organ damage===
* Treatment of organ damage (heart failure with [[diuretic]]s and [[ACE inhibitor]] therapy){{citation needed|date=May 2015}}. [[Hepatic transplantation]] in patients with liver failure.

===Diet===
Diet can be a powerful but understudied and utilized tool in prevention of iron overload. It can strongly affect the incidence of disease and treatment. Especially in the Western world where many foods are fortified and animal protein (heme iron) is relatively convenient and inexpensive, it is very common for people to eat more than the [https://ods.od.nih.gov/factsheets/Iron-HealthProfessional/ Recommended Dietary Allowance of iron] even in a single meal. For example, one serving of several popular cereals, such as Cheerios or Grape Nuts, has about two times the RDA of iron for a man or non menstruating woman. Menstruating women have roughly twice the iron requirements of a man or non menstruating woman. For this reason, it can very helpful for those recently diagnosed to track their iron and vitamin C consumption for a time and comparing it to the RDA. 
* Limiting intake of [[alcoholic beverage]]s, high iron fortified foods such as certain cereals and supplements, [[vitamin C]] (increases iron absorption in the gut), heme iron [[animal products]] (high in [[iron]]), and potential causes of [[food poisoning]] ([[shellfish]], raw [[seafood]])<ref>{{cite journal|last1=Plaut|first1=David|last2=McLellan|first2=William|title=Hereditary hemochromatosis|journal=Journal of Continuing Education Topics & Issues|date=2009|volume=11|issue=1|url=http://www.freepatentsonline.com/article/Journal-Continuing-Education-Topics-Issues/193344102.html|access-date=11 October 2016|archive-url=https://web.archive.org/web/20161011225535/http://www.freepatentsonline.com/article/Journal-Continuing-Education-Topics-Issues/193344102.html|archive-date=11 October 2016}}</ref>
* Increasing intake of substances that inhibit iron absorption, such as high-[[tannin]] [[tea]], [[Calcium in biology|calcium]], black or green teas, and foods containing [[Oxalic acid|oxalic]] and [[phytic acid]]s (such as [[collard greens]], which must be consumed at the same time as the iron-containing foods to be effective){{citation needed|date=April 2021}}

===Chelating polymers===
A novel experimental approach to the hereditary haemochromatosis treatment is the maintenance therapy with polymeric chelators.<ref name="Polomoscanik2005">{{cite journal |last1=Polomoscanik |first1=Steven C. |last2=Cannon |first2=C. Pat |last3=Neenan |first3=Thomas X. |last4=Holmes-Farley |first4=S. Randall |last5=Mandeville |first5=W. Harry |last6=Dhal |first6=Pradeep K. |title=Hydroxamic Acid-Containing Hydrogels for Nonabsorbed Iron Chelation Therapy: Synthesis, Characterization, and Biological Evaluation |journal=Biomacromolecules |date=November 2005 |volume=6 |issue=6 |pages=2946–2953 |doi=10.1021/bm050036p |pmid=16283713 }}</ref><ref name="QianSullivan2017">{{cite journal |last1=Qian |first1=Jian |last2=Sullivan |first2=Bradley P. |last3=Peterson |first3=Samuel J. |last4=Berkland |first4=Cory |title=Nonabsorbable Iron Binding Polymers Prevent Dietary Iron Absorption for the Treatment of Iron Overload |journal=ACS Macro Letters |date=18 April 2017 |volume=6 |issue=4 |pages=350–353 |doi=10.1021/acsmacrolett.6b00945 |pmid=35610854 }}</ref><ref name="Groborz2020">{{cite journal |last1=Groborz |first1=Ondřej |last2=Poláková |first2=Lenka |last3=Kolouchová |first3=Kristýna |last4=Švec |first4=Pavel |last5=Loukotová |first5=Lenka |last6=Miriyala |first6=Vijay Madhav |last7=Francová |first7=Pavla |last8=Kučka |first8=Jan |last9=Krijt |first9=Jan |last10=Páral |first10=Petr |last11=Báječný |first11=Martin |last12=Heizer |first12=Tomáš |last13=Pohl |first13=Radek |last14=Dunlop |first14=David |last15=Czernek |first15=Jiří |last16=Šefc |first16=Luděk |last17=Beneš |first17=Jiří |last18=Štěpánek |first18=Petr |last19=Hobza |first19=Pavel |last20=Hrubý |first20=Martin |title=Chelating Polymers for Hereditary Hemochromatosis Treatment |journal=Macromolecular Bioscience |date=December 2020 |volume=20 |issue=12 |page=2000254 |doi=10.1002/mabi.202000254 |pmid=32954629 |s2cid=221827050 }}</ref> These polymers or particles have a negligible or null systemic [[bioavailability|biological availability]] and they are designed to form stable complexes with Fe<sup>2+</sup> and Fe<sup>3+</sup> in the [[gastrointestinal tract|GIT]] and thus limiting the uptake of these ions and their long-term accumulation. Although this method has only a limited efficacy, unlike [[chelation therapy|small-molecular chelators]], such an approach has virtually no [[side effects]] in [[chronic toxicity|sub-chronic studies]].<ref name="Groborz2020" /> Interestingly, the simultaneous chelation of Fe<sup>2+</sup> and Fe<sup>3+</sup> increases the treatment efficacy.<ref name="Groborz2020" />