On May 7, 4:18 am, "wrtho...@ix.netcom.com" <wrthomp...@gmail.com>
wrote:
I'll cut and paste it here again .. ok .. willie .. ? <<

Aplastic anemia seems to encompass alot of different diseases
including  Fanconi , Sickle , Thalassemia , Leukemia and Lupus.
One might think this treatment would be made available to more people
but it has never even been tested.

This treatment seems to be efficacious in 'turning the tide' / cure
so
to speak in Sickle Cell  and Thalassemia.
One might think testing this treatment would be in order  for
Fanconi , Lupus or Leukemia or other aplastic anemia related disease
process .. ?
------------------
Alternative treatment paradigm for thalassemia using iron chelators.
Szuber N, Buss JL, Soe-Lin S, Felfly H, Trudel M, Ponka P
Exp Hematol 2008 May 2.

OBJECTIVE:
beta-thalassemia major, or Cooley's anemia, is a red blood cell
disorder requiring lifelong blood transfusions for survival.
Erythrocytes accumulate toxic iron at their membranes, triggering an
oxidative cascade that leads to their
premature destruction in high numbers.
We hypothesized that removing this proximate iron compartment
as a primary treatment, using standard and alternative orally active
iron chelators, could prevent hastened red cell removal and,
clinically, perhaps alleviate the need for transfusion.
MATERIALS AND METHODS:
Iron chelators of the pyridoxal isonicotinoyl hydrazone
family (pyridoxal isonicotinoyl hydrazone and its analog pyridoxal
ortho-chlorobenzoyl hydrazone) were evaluated in addition to the
present mainstay, desferrioxamine and deferiprone, in vitro and in
vivo.
RESULTS:
Treatment of human beta-thalassemic erythrocytes with chelators
resulted in significant depletion of membrane-associated iron and
reduction of oxidative stress, as evaluated by methemoglobin levels.
When administered to beta-thalassemic mice, iron chelators mobilized
erythrocyte membrane iron, reduced cellular oxidation, and prolonged
erythrocyte half-life.
The treated thalassemic mice also showed improved hematological
abnormalities.
Remarkably, a beneficial effect as early as the erythroid precursor
stage was manifested by normalized proportions of mature vs immature
reticulocytes.
All four compounds were also found to mitigate iron accumulation in
target organs, a critical determinant for patient survival. In this
respect, pyridoxal ortho-chlorobenzoyl hydrazone displayed higher
activity relative to other chelators tested, further diminishing iron
in liver and spleen by up to approximately fivefold and twofold,
respectively.
CONCLUSION:
Our study demonstrates the ability of iron chelators to improve
several of the fundamental pathological disturbances of thalassemia,
and reveals their potential for clinical use in diminishing
requirement for transfusion when administered early in disease
development.
Experimental hematology [Exp Hematol]
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"Complete recovery after iron chelation in aplastic anemia"

They treated this kid for five years .. aggressively .. and when and
ONLY when the kid was failing DUE TO their interventions / iron
buildup .. did they finally cure the kid.

Removed the iron **totally**  ..
IE: targeted the iron .. and the kid was cured.
---------

Complete hematopoietic recovery after continuous iron chelation
therapy in a patient with severe aplastic anemia with secondary
hemochromatosis.
Park SJ, Han CW

J Korean Med Sci 2008 Apr; 23(2):320-3.

A 16-yr-old male patient with hemochromatosis due to multiple packed
red blood cell transfusions was referred to our emergency center for
the treatment of severe aplastic anemia and dyspnea. He was diagnosed
with aplastic anemia at 11-yr of age.
He had received continuous transfusions because an HLA-matched marrow
donor was unavailable.
Following a continuous, approximately 5-yr transfusion, he was noted
to develop hemochromatosis.
He had a dilated cardiomyopathy and required diuretics and digitalis,
multiple endocrine and liver dysfunction, generalized bleeding, and
skin pigmentation.
A total volume of red blood cell transfusion before deferoxamine
therapy was about 96,000 mL.
He received a regular iron chelation therapy (continuous intravenous
infusion of deferoxamine, 50 mg/kg/day for 5
days q 3-4 weeks) for approximately seven years after the onset of
multiple organ failures.
His cytopenia and organ dysfunctions began to
be gradually recovered since about 2002, following a 4-yr
deferoxamine treatment.
He showed completely normal ranges of peripheral blood cell
counts, heart size, and liver function two years ago.
He has not
received any transfusions for the last four years.
This finding suggests that a continuous deferoxamine infusion may
play
a role in the immune regulation in addition to iron chelation effect.
Journal of Korean medical science
[J Korean Med Sci]
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http://en.wikipedia.org/wiki/Aplastic_anemia

Treating aplastic anemia involves suppression of the immune system,
an
effect achieved by daily medicine intake, or, in more
severe cases, a bone marrow transplant, a potential cure but a risky
procedure.[1]
The transplanted bone marrow replaces the failing bone marrow cells
with new ones from a matching donor. The pluripotent stem cells in
the
bone marrow reconstitute all three blood cell lines, giving the
patient a new immune system, red blood cells, and platelets.
However, besides the risk of graft failure, there is also a risk that
the newly created white blood cells may attack the rest of the body
("graft-versus-host disease").

Medical therapy of aplastic anemia often includes a short course of
anti-thymocyte globulin (ATG) or anti-lymphocyte globulin (ALG) and
several months of treatment with cyclosporin to modulate the immune
system.
Mild chemotherapy with agents such as cyclophosphamide and
vincristine may also be effective.
Antibodies therapy, such as ATG, targets T-cells, which are believed
to attack the bone marrow.
Steroids are generally ineffective.

In the past, before the above treatments became available, patients
with low leukocyte counts were often confined to a sterile room or
bubble (to reduce risk of infections), as in the famed case of Ted
DeVita.[2]

Who loves ya.
Tom

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