THE Fatigue
AIHA
of CFIDS is proof EGBE is the root cause
CFIDS
Fatigue
Hemolytic Anemias
Rarely (if AIHA of CFIDS
... more often than found by doctors),
anemia is due to problems that cause the red blood
cells to break down prematurely. Normally, red cells
live in the blood for about 4 months. In hemolytic
anemia, this time is shortened, sometimes to only a
few days.
Sickle cell anemia
is a
hereditary problem that can cause minor difficulties
as the “trait” (when you carry one mutated
gene
from one of your parents) but severe clinical
problems as the “disease” (when you carry two
mutated genes, one from each of your parents). The
red blood cells are misshapen and clog the blood
vessels, causing pain and anemia.
Screening
is
usually done on newborns – particularly those of
African descent. Treatment is usually based on the
symptoms.
Thalassemia
is a hereditary abnormality of hemoglobin production
and causes small red blood cells that resemble those
seen in iron deficiency. In its most severe form,
the red cells have a shortened life span. In milder
forms, anemia is usually mild or absent, and the
disease may be detected by finding small blood cells
on a routine
CBC.
This genetic disease is found frequently in people
of Mediterranean, African, and Asian heritage. The
defect in production may involve any of the two
major components of hemoglobin, and the disease is
defined as betal thalassemia or alpha thalassemia
accordingly. The "beta minor" form (sometimes called
beta thal trait, as with sickle cell) occurs when a
person inherits half normal genes and half beta
thalassemia genes. It causes a mild anemia and no
symptoms. The "beta major" form (due to inheriting
two beta thalassemia genes and also called Cooley’s
anemia) is more severe and may result in growth
problems,
jaundice
(yellowing of the skin and whites of the eyes), and
severe anemia. The hemoglobin electrophoresis shows
an increase in hemoglobin A2 and/or hemoglobin F in
beta thalassemia form, but may be relatively normal
in the other form.
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