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Anemia of chronic disease (ACD) is also referred to as anemia of inflammatory

response. Although ACD can accompany life-threatening illness, anemia of
inflammatory response is in fact a protective and natural mechanism that the
human body uses to limit the amount of iron available when potentially harmful
things get into our body. All living things, including bacteria and cancer cells,
which are living things, depend upon iron to sustain life just like humans and
plants do. This system was described by Eugene Weinberg, Ph.D., Indiana
University in the early 1980s.

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When the body senses a potential threat, iron gets shuttled to ferritin to be
contained so that the harmful invader cannot get to the iron. Just enough iron is
made available to make red blood cells but no surplus is left to nourish harmful
pathogens. Depending on the underlying cause of disease, a person with ACD
will experience a modest decline in hemoglobin. This will take place over time
following the onset of inflammation due to the presence of the infection or

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disease. Hemoglobin values will generally reach a low normal range of 9.510.5
g/dL and remain there within this moderately low range until the underlying
condition is cured. If disease that results in blood loss is present, the person will
develop iron deficiency anemia (IDA). ACD and IDA can be distinguished with a
serum ferritin test.
Taking iron pills for anemia of chronic disease could be harmful, even fatal.

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The exact mechanism of ACD is not fully understood. Dr. Eugene Weinberg,

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http://www.irondisorders.org/anemia-of-chronic-disease

Professor of Microbiology Indiana University and Iron Disorders Institute Medical

& Scientific Advisory Board Member, is an expert in anemia of chronic disease.
Since the mid 1950s Weinberg has been aware of the bodys alteration of iron
metabolism during disease. He first defined the Iron Withholding Defense
System in the early 1980s where he described how the human body recognizes
iron as a potential hazard to health. Iron is one metal that cannot be excreted by
the body effeciently; so, extra precautions are taken by humans to avoid
absorbing too much iron. When a harmful germ invades the body, the immune
system team of white blood cells charge to the site to destroy the pathogen
before it has time to multiply. Inflammation results as a part of this natural
immune response. Inflammation triggers the release of chemicals that signal the
iron regulation mechanism to adopt a defense mode.
What physicians see when the iron withholding defense system is activated is a
mild drop in hemoglobin. However, what many physicians miss is that less iron is
being absorbed and extra free iron is being collected by macrophages and
stored in liver cells (hepatocytes). As a result serum ferritin rises. Anemia of
chronic disease is not progressive. Hemoglobin values may remain in a slightly
low range, but the levels can drop to as low as 7.0 g/dL depending on the
severity of the inflammation and the length of time present. Other tests such as
serum ferritin or C-reactive protein (CRP) can be performed to help differentiate
between iron-deficiency anemia, where oral iron can be beneficial and anemia of
chronic disease, where oral iron should not be given.
In a U.S. Department of Agriculture study, investigators illustrate the Iron
Withholding Defense System at work. Drs. Fariba Roughead and Janet Hunt of
the USDA Grand Forks Human Nutrition Research Center conducted a study of
the effects of iron supplements on the bodys control of iron absorption. In a
randomized, placebo-controlled trial, heme and nonheme iron absorption by
healthy men and women were measured from a test meal containing a
hamburger, potatoes, and milkshake. These absorption measurements were
made before and after a period of twelve weeks when the 57 participants were
given 50 milligrams of supplemental iron or placebo daily while they consumed
their usual diets.
Serum ferritin and fecal ferritin were measured during supplementation and for a
period of 6 months after supplementation was discontinued. Volunteers who took
iron supplements, even those with initial ferritin less than 21 ng/mL, adapted to
absorb less nonheme iron, but not less heme iron from meat.
Daily iron supplements caused these volunteers to absorb 36 percent less
nonheme iron and 25 percent less total iron from food, and to have higher iron
stores than those in the placebo group. The higher ferritin persisted for 6 months

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post supplementation, except in individuals who had low iron stores at the
beginning of the study. Since iron stores were greater after iron supplementation,
Drs. Roughead and Hunts study demonstrated that adaptation in absorption did
not completely prevent differences in body iron stores.
The adaptation to reduce iron absorption even in volunteers with low iron stores
may indicate a localized control system to prevent excessive iron exposure of
intestinal cells. The study is consistent with two systems at work, one that
regulates how much iron we must absorb for normal function, and the iron
withholding defense system, which protects us from nurturing harmful pathogens
with excesses of iron we dont presently need.
In adults, anemia of chronic disease is likely due to some common ailment such
as urinary tract infection, a head or chest cold, mononucleosis, tonsillitis or strep,
stomach or intestinal flu, and bacterial infections such as H. pylori. ACD can also
occur when an autoimmune disease is present. Most of these conditions are
treatable and when the patient is cured, the anemia will be corrected. If the
anemia persists once an illness is cured, the doctor will want to investigate
further for a secondary underlying cause of anemia that may be more serious
such as kidney disease, tumor, or cancer.
Anemia of chronic disease can be an indicator that a serious life-threatening
condition is in the initial stages of development. However, when disease
advances beyond this mild form of anemia, where treatment of the underlying
condition cannot affect a cure, levels such as serum ferritin and transferrin iron
saturation percentage change. For this reason, persons who have experienced
anemia of chronic disease, where suspected underlying conditions have been
addressed but the anemia persists, further investigation is needed. Blood loss,
kidney function, bone marrow function, cancer, abnormal absorption or chronic
hemolysis could be pursued as causes.
Anemia of chronic disease can also be present even when tissues have
excessive levels of iron. Tissue iron is different from functional iron in
hemoglobin. Persons with hereditary hemochromatosis can have excessively
high tissue iron but develop anemia because of iron damage to the kidney,
anterior pituitary, or bone marrow. The damaged kidney produces less
erythropoietin, a hormone vital to red blood cell production (erythropoiesis). An
inflamed or damaged anterior pituitary can result in hypothyroidism, which
causes diminished erythropoiesis and mild anemia. The bone marrow is the site
of red blood cell formation.
Differentiating between anemia of chronic disease and iron-deficiency anemia
Patients with anemia of chronic disease do not generally have hemoglobin

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values below 9.5 g/dL, although levels can go much lower. Iron-deficiency
anemia is often suspected in patients with anemia of chronic disease because
the two conditions have many similarities. In both conditions, the serum iron level
is low. Small or microcytic cells can be present in either disorder, though this type
of cell is more indicative of true iron deficiency. Transferrin, a protein that
transports iron, is elevated in iron-deficiency anemia, indicating that the body
needs more iron. The total iron-binding capacity (TIBC), an indirect
measurement of transferrin, is low in anemia of chronic disease because there is
ample iron, but it is not easily available. TIBC tends to be increased when iron
stores are diminished and decreased when they are elevated. In iron-deficiency
anemia, the TIBC is higher than 400450 mcg/dL because stores are low. In
anemia of chronic disease, the TIBC is usually below normal because the iron
stores are elevated.
In nearly two-thirds of the patients, the serum ferritin is one test that can be used
to distinguish between anemia of chronic disease and iron-deficiency anemia.
Ferritin is an acute-phase reactant, which means that it can be elevated in the
presence of inflammation and this factor must be taken into consideration when
examining the findings. Serum ferritin can be raised to normal levels even in the
presence of iron deficiency. For this reason, difficulties arise in distinguishing iron
deficiency in a patient with inflammation or infection from the anemia of chronic
disease. Tests for inflammation like CRP are not helpful in this case. For some
cases in which both iron deficiency and anemia of chronic disease are possible,
bone marrow aspiration with iron staining is the traditional means of determining
that a person is iron deficient. However the serum transferrin receptor test can
be used to help differentiate between iron-deficiency anemia and anemia of
chronic disease. The serum transferrin receptor is much less affected by
inflammation than serum ferritin; results will be high in iron-deficiency anemia
and usually low to low-normal in anemia of chronic disease. The ratio of the
serum transferrin receptor to the logarithim of the serum ferritin concentration is
better able to distinguish anemia of chronic disease from iron deficiency than is
either test alone.
The greatest risk for harm is mistaking anemia of chronic disease for
iron-deficiency anemia and allowing the patient to take iron pills. This risk can be
reduced or eliminated by differenetiating between to the two iron disorders with
serum ferrtin test and by informing the patient about the differences in these two
iron disorders.

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Treatment
There is no treatment for anemia of chronic disease except to address the
underlying condition. Iron supplementation is inappropriate in these patients
because the added iron can become free to nourish bacteria and cancer cells.

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