theres so much iron in the blood that it has to go somewhere. it goes into the cells in the body (increased ferritin) and it binds to the carrier transport protein transferrin. because it binds to all the transferrin you have low free transferrin. but your body senses the low free transferrin and goes "ok all my transferrin are full of iron I guess im ok i dont need anymore iron" so it stops making transferrin. so low transferrin or total iron binding capacity (remember this is just a fancy way of saying it doesnt want transferrin).... now %transferrin sat is just math (i hate math) its like this: iron/TIBC, we already got high iron so numerator is high, and low denominator bc like i said TIBC is low so overall your %transferrin saturation is very high. this is the best indicator for hemochromatosis
hereditary hemochromatosis.
HFE is mutated => the intestines perpetually interpret a strong transferrin signal as if the body were deficient in iron. This leads to maximal iron absorption from ingested foods and iron overload in the tissues.
https://en.wikipedia.org/wiki/HFE_hereditary_haemochromatosis#Pathophysiology
submitted by chillqd(9), 2019-06-08T02:52:24Z
The Stem is describing hemochromatosis, characterized by abnormal iron sensing and increased intestinal absorption. This increases Iron, increasing ferritin. In response, TIBC is decreased, which increases transferrin saturation as there is less circulating carrier molecules.
With excess iron in the blood, it will accumulate in tissues including the liver, skin, pancreas. Sequelae include dilated cardiomyopathy, hypogonadism, diabetes, arthropathy 2/2 calcium pyrophosphate deposition, nd Hepatocellular Carcinoma