13-Oct-15 1 Interpreting iron studies iron overload & deficiency tips & traps Dr David Iser 10 TH October 2015 Gastroenterologist & Hepatologist St. Vincent’s & The Alfred Hospitals Outline Interpreting iron studies Low iron Iron deficiency How to replace How to investigate High ferritin Hereditary haemochromatosis Fatty liver disease Other causes Aims To understand the basics of iron metabolism To be able to interpret iron studies To have a greater understanding of how to investigate abnormal iron studies To know when to refer to a gastroenterologist or haematologist Disclosures I am a gastroenterologist, not a haematologist or pathologist I have no disclosures relevant to this presentation Interpreting iron studies What do we get? Iron μmol/L Transferrin g/L Ferritin μg/L Transferrin saturation % What did we previously receive? TIBC (Total iron binding capacity) μ mol/L = another way of expressing transferrin Basics of iron metabolism 65% of the body’s iron is stored in haemoglobin 15% is stored in muscle some in cellular enzymes The remainder (excess): ferritin in the liver haemosiderin in macrophages
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TH · Liver disease (without true iron overload) Viral hepatitis Alcoholic liver disease Fatty liver disease Case 3: iron overload 50 yo man with chronic hepatitis B, controlled on
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13-Oct-15
1
Interpreting iron studiesiron overload & deficiency
tips & traps
Dr David Iser10TH October 2015
Gastroenterologist & Hepatologist
St. Vincent’s & The Alfred Hospitals
Outline
Interpreting iron studies
Low iron
Iron deficiency
How to replace
How to investigate
High ferritin
Hereditary haemochromatosis
Fatty liver disease
Other causes
Aims
To understand the basics of iron metabolism
To be able to interpret iron studies
To have a greater understanding of how to
investigate abnormal iron studies
To know when to refer to a gastroenterologist or
haematologist
Disclosures
I am a gastroenterologist, not a haematologist
or pathologist
I have no disclosures relevant to this presentation
Interpreting iron studies
What do we get?
Iron µmol/L
Transferrin g/L
Ferritin µg/L
Transferrin saturation %
What did we previously receive?
TIBC (Total iron binding capacity) µmol/L
= another way of expressing transferrin
Basics of iron metabolism
65% of the body’s iron is stored in
haemoglobin
15% is stored in muscle
some in cellular enzymes
The remainder (excess):
ferritin in the liver
haemosiderin in macrophages
13-Oct-15
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Iron
Absorption
Mainly in duodenum
Some from distal small bowel
Ferroportin (protein channel on cell membrane)
Controls export of iron from cells (RBCs,
enterocytes, macrophages)
Increases free iron
Important because free iron causes tissue
damage via reactive oxygen species
Free iron favours bacteria
Hepcidin
Main hormone controlling iron metabolism
Produced in the liver
Reduces free iron
Binds ferroportin and degrades it
Reduces iron absorption from gut
Reduces iron release from macrophages
Reduces free iron available to bacteria
More on hepcidin
More hepcidin when less iron is required
Infection
Inflammation
Anaemia of chronic disease
Less hepcidin when more iron is required
Iron deficiency
Hypoxia
Anaemia due to haemorrhage or haemolysis
Hepcidin Ferroportin Iron
Normal absorption
Ferroportin
Hepcidin
Enterocyte
Iron deficiency
Less hepcidin
HFE haemochromatosis
Inactive
hepcidin
Back to iron studies: Ferritin
Intracellular storage protein in most cells and most organisms, also in serum
Binds up to 4000 iron atoms
Serum ferritin reflects intracellular ferritin
Also acute-phase reactant, increased in hypoxia, inflammation, infection, malignancy, liver disease, renal disease, anorexia, malnutrition, haemophagocytic syndrome
Low = iron deficiency
Transferrin (& transferrin saturation)
Transferrin = apotransferrin + 1 or 2 iron atoms
apotransferrin = iron transporting protein
Produced in the liver
High levels in iron deficiency or high oestrogen
Low levels in liver disease, high iron or as acute