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Blood With Too Much Iron In It

The good news about hemochromatosis is that it has the potential to save the lives of others. The bad news is that the genetic blood disorder in which the body absorbs too much iron leads to a host of potential health problems ranging from impotence to diabetes mellitus to cirrhosis of the liver. Fortunately, if the patient’s hemochromatosis is caught early enough it’s quite simple to treat the disorder a blood draw is usually all it takes to get a patient’s iron level down to an acceptable level. But sadly, this iron-rich bloodletting routine usually has to be kept up periodically for the rest of a patient’s life. In the rare cases where readings show that an unsafe amount of blood would need to be drawn to get iron levels down, docs must turn to deferoxamine injections which bind to iron in patients’ blood next stop the kidneys then finally the iron-laced deferoxamine gets tinkled out.

Hemochromatosis is sometimes called “The Bronze Disease” due to the permanent tan that develops in untreated cases. One of the first detectable signs of the disorder is joint pain or arthritis in the knuckles of the index and middle fingers.

Unfortunately there’s still no simple inexpensive screening test for the disorder. An accurate but costly genetic test does exist and it’s a good idea to run it on folks with a family history or if you suspect it in a patient with one or more of the following symptoms: high liver enzymes, joint disease, severe fatigue, heart disease, sexual dysfunction or diabetes.

WHAT CAUSES IT?

Until quite recently, hemochromatosis was thought to be very rare, but now it’s believed that about one in every 250 Caucasians has the disorder and that between 10-15% of the population carries the gene responsible. It is much less common among non-Caucasians. A groundbreaking paper on the cause of hemochromatosis was published in March in the journal Cell Metabolism. The investigators, based at the Children’s Hospital Boston and Harvard Medical School, were the first to find solid evidence that the protein ferroportin is the culprit behind the disorder. Future treatments will likely use drugs that inhibit ferroportin but what of the here and now?

http://www.nationalreviewofmedicine.com/issue/2005/09_30/2_patients_practice06_16.html

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