the results. After her symptoms continued to worsen, she underwent similar blood work in July. This time, the results caught the attention of her primary care provider.
Her ferritin level was 227, compared with a normal range of 15-150 ng / mL. She also had low TIBC( total iron-binding capacity) and UIBC( unsaturated ironbinding capacity), along with elevated circulating iron and iron saturation. Her provider referred her to the hospital’ s Hematology department for additional testing.
With the results pointing toward an issue involving iron, Nantz began researching possible explanations herself.
That was when she encountered hereditary hemochromatosis.
“ Please advocate for yourself. If you know your body or mind do not feel right for you, keep asserting that, even if your labs supposedly appear acceptable. You know yourself and your‘ normal’ better than anyone.”
“ The symptoms matched, but I didn’ t fully trust that that’ s what it was because of how much later in life women are typically diagnosed,” she said.“ It was in the back of my mind though.”
Additional laboratory testing in August confirmed that Nantz was homozygous for the C282Y mutation associated with hereditary hemochromatosis.
Rather than being frightened by the diagnosis, she felt relieved to finally have an explanation.
“ This might sound odd, but when I saw that I was homozygous for the C282Y mutation, I was so relieved,” Nantz said.“ I was just happy to finally have an explanation at all and hopefully get on the best path to feeling like myself again.”
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Hereditary hemochromatosis causes the body to absorb and store too much iron. Nantz describes it as essentially the opposite of anemia: instead of having too little iron, her body stores too much. If left untreated, excessive iron can cause serious organ damage and other long-term issues down the road.
Nantz currently has active iron overload, although she said she is unsure how much impact it has had on her organs.
She also learned that being homozygous for the C282Y mutation means she has two copies of the mutated gene, one inherited from each parent. The mutation is associated with a higher risk of iron overload and organ damage.
While the diagnosis brought
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