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  #1  
Old 04-26-2008, 07:42 PM
ironjustice
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Posts: n/a
Default Complete Cure Of Aplastic Anemia

"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]
---------------------------------------------------------------------------*-----

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


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

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  #2  
Old 05-02-2008, 09:15 AM
wrthomps@ix.netcom.com
Guest
 
Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia

The Pherrous Phuckwit <halfbaked@my.bbq.com> trolled:

> "Complete recovery after iron chelation in aplastic anemia"


http://www.youtube.com/watch?v=S524O_XNoLM

--Bill Thompson
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  #3  
Old 05-03-2008, 03:14 AM
ironjustice
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Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia

On May 1, 11:55*pm, "wrtho...@ix.netcom.com" <wrthomp...@gmail.com>
wrote:
http://www.youtube.com/watch?v=S524O_XNoLM <<

"Complete recovery after iron chelation in aplastic anemia"

Now I don't suppose .. complete recovery after iron chelation in
aplastic anemia .. actually MEANS anything to .. you .. but it does to
some .. sooo .. just in case .. let me cut and paste it .. again ..
below .. ok willie .. ?

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]
---------------------------------------------------------------------------**-----


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk




Reply With Quote
  #4  
Old 05-03-2008, 06:20 AM
wrthomps@ix.netcom.com
Guest
 
Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia

The Pherrous Phuckwit <nobrains@all> danced to my tune wih:

> "wrtho...@ix.netcom.com" <wrthomp...@gmail.com>
> brilliantly commented upon Rusty with:


> *http://www.youtube.com/watch?v=S524O_XNoLM


> "Complete recovery after iron chelation in aplastic anemia"


> Now I don't suppose .. complete recovery after iron chelation in
> aplastic anemia .. actually MEANS anything


What's this, Rusty? You posted it and you didn't think it meant
anything? Honesty in you is such a surprise! But I knew I could
make you dance if I played a little--Heavy Metal!

Give us another little dance, Rusty. Do the "TeamTanner
Two-Step." Stamp your widdle feet and get red in the face to
this song:

http://www.youtube.com/watch?v=7E1zE6uH-ng

--Bill Thompson
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  #5  
Old 05-03-2008, 12:31 PM
ironjustice
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Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia

On May 2, 10:12*pm, "wrtho...@ix.netcom.com" <wrthomp...@gmail.com>
wrote:Stamp your widdle feet and get red in the face to
this song: <<

Let me cut and paste it .. again .. below .. ok willie .. ?

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]
---------------------------------------------------------------------------***-----


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk


> The Pherrous Phuckwit <nobrains@all> danced to my tune wih:
>
> > "wrtho...@ix.netcom.com" <wrthomp...@gmail.com>
> > brilliantly commented upon Rusty with:
> > *http://www.youtube.com/watch?v=S524O_XNoLM
> > "Complete recovery after iron chelation in aplastic anemia"
> > Now I don't suppose .. complete recovery after iron chelation in
> > aplastic anemia .. actually MEANS anything

>
> What's this, Rusty? *You posted it and you didn't think it meant
> anything? *Honesty in you is such a surprise! *But I knew I could
> make you dance if I played a little--Heavy Metal!
>
> Give us another little dance, Rusty. *Do the "TeamTanner
> Two-Step." *Stamp your widdle feet and get red in the face to
> this song:
>
> http://www.youtube.com/watch?v=7E1zE6uH-ng
>
> --Bill Thompson


Reply With Quote
  #6  
Old 05-03-2008, 03:38 PM
Mair
Guest
 
Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia


"wrthomps@ix.netcom.com" <wrthomps06@gmail.com> wrote in message
news:c7bb20a1-1c2a-41ac-aa18-ad6026c84d81@y38g2000hsy.googlegroups.com...
The Pherrous Phuckwit <nobrains@all> danced to my tune wih:

> "wrtho...@ix.netcom.com" <wrthomp...@gmail.com>
> brilliantly commented upon Rusty with:


> http://www.youtube.com/watch?v=S524O_XNoLM


> "Complete recovery after iron chelation in aplastic anemia"


> Now I don't suppose .. complete recovery after iron chelation in
> aplastic anemia .. actually MEANS anything


What's this, Rusty? You posted it and you didn't think it meant
anything? Honesty in you is such a surprise! But I knew I could
make you dance if I played a little--Heavy Metal!

Give us another little dance, Rusty. Do the "TeamTanner
Two-Step." Stamp your widdle feet and get red in the face to
this song:

http://www.youtube.com/watch?v=7E1zE6uH-ng

Marilyn Manson--very entertaining! I've not seen/heard him before, so I
guess I should crawl out from under my rock more often...hopefully at the
same time when this character is out from under his.

Mair


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  #7  
Old 05-04-2008, 03:56 AM
wrthomps@ix.netcom.com
Guest
 
Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia

Le Phuquewitte de Pherrousse <no.brains@all> danced to my tune with:

> "wrtho...@ix.netcom.com" <wrthomp...@gmail.com> wrote:


>Stamp your widdle feet and get red in the face to this song:


> Let me cut and paste it .. again ..


Again, eh? I've noticed somethng about you, Rusty. You claim
you're only interested in iron, but somehow you always turn the
subject to--blood! And when I post a link to Marlyn Manson, you
lose what little self-control you had. It's obvious where you're
coming from! Yes, you are--Nosferrousatu! So here's a song
going out to you and all the bats in your belfry:

http://www.youtube.com/watch?v=ZY-QjUl6Swo

--Bill Thompson
Reply With Quote
  #8  
Old 05-04-2008, 08:48 AM
William R. Thompson
Guest
 
Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia

"Mair" wrote:

> wrthomps06@gmail.com wrote


>> Give us another little dance, Rusty. Do the "TeamTanner
>> Two-Step." Stamp your widdle feet and get red in the face to
>> this song:


>> http://www.youtube.com/watch?v=7E1zE6uH-ng


> Marilyn Manson--very entertaining! I've not seen/heard him before, so I
> guess I should crawl out from under my rock more often...hopefully at the
> same time when this character is out from under his.


Funny, I found Marilyn Manson by crawling under rocks. These days you
have to go out of your way to find good music, and he fills the void left
by Alice Cooper.

What impresses me is the way Rusty enjoys him. Who'd have thought?

--Bill Thompson


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  #9  
Old 05-04-2008, 02:51 PM
ironjustice
Guest
 
Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia

"Complete recovery after iron chelation in aplastic anemia"

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]
---------------------------------------------------------------------------****-----


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk


> Le Phuquewitte de Pherrousse <no.brains@all> danced to my tune with:
>
> > "wrtho...@ix.netcom.com" <wrthomp...@gmail.com> wrote:
> >Stamp your widdle feet and get red in the face to this song:
> > Let me cut and paste it .. again ..

>
> Again, eh? *I've noticed somethng about you, Rusty. *You claim
> you're only interested in iron, but somehow you always turn the
> subject to--blood! *And when I post a link to Marlyn Manson, you
> lose what little self-control you had. It's obvious where you're
> coming from! *Yes, you are--Nosferrousatu! *So here's a song
> going out to you and all the bats in your belfry:
>
> http://www.youtube.com/watch?v=ZY-QjUl6Swo
>
> --Bill Thompson


Reply With Quote
  #10  
Old 05-04-2008, 05:23 PM
ironjustice
Guest
 
Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia

On May 4, 7:37*am, ironjustice <teamtan...@hotmail.com>
wrote:"Complete recovery after iron chelation in aplastic anemia" <<

http://tinyurl.com/2nn4q8

Recently, researchers have discovered that most cases of severe
aplastic anemia are autoimmune disorders in which the body’s own
immune system attacks tissues and organs.
-------------------

"The infant died."

Aplastic anemia in neonatal lupus erythematosus
B. Wolach, L. Choc, A. Pomeranz, Y. Ben Ari, D. Douer and A. Metzker
Department of Pediatrics, Meir General Hospital, Sapir Medical Center,
Kfar Saba, Israel.

OBJECTIVE--
To describe an infant with neonatal lupus erythematosus associated
with aplastic anemia.
SETTING--
The pediatric department in a tertiary-care hospital.
INTERVENTIONS--
Packed red blood cell transfusions and a 3-week course of high-dose
steroid therapy.
MEASUREMENTS/MAIN RESULTS--
The patient presented with severe anemia and a circumscribed,
reticular, macular rash on the face and neck at 5 months of age. Skin
lesion biopsy revealed epidermic hyperkeratosis, hydropic degeneration
of the basal layer, and deposition of immunoglobulins and granular C1q
at the dermoepidermal junction. Ro/SS-A antibodies were present in the
infant. BFU-E (erythroid progenitor burst-forming unit) colonies in
bone marrow increased by about tenfold when suppressor CD8+ T
lymphocytes were removed, indicating immune suppression of
hematopoiesis. High-dose steroid therapy failed. The infant
subsequently developed gram-negative sepsis, severe metabolic
acidosis, and consumptive coagulopathy and died.
CONCLUSIONS--
Neonatal lupus erythematosus may present as part of a spectrum. The
disease may range from mild and transient to a severe, life-
threatening condition requiring immediate intervention, as in the case
reported here. This is the first report of neonatal lupus associated
with aplastic anemia due to immune-mediated suppression of
hematopoiesis.
Infants Born to Mothers With Anti-SSA/Ro Autoantibodies: Neonatal
Outcome and Follow-up
Zuppa et al.
CLIN PEDIATR 2008;47:231-236.

http://www.aamds.org/aplastic/

MedlinePlus Aplastic anemia is a life-threatening condition. http//
http://www.nlm.nih.gov/medlineplus/e...cle/000554.htm

http://www.nhlbi.nih.gov/health/dci/...ic_whatis.html


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

> "Complete recovery after iron chelation in aplastic anemia"
>
> 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]
> ---------------------------------------------------------------------------*****-----
>
> Who loves ya.
> Tom
>
> Jesus Was A Vegetarian!http://tinyurl.com/2r2nkh
>
> Man Is A Herbivore!http://tinyurl.com/a3cc3
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
>
>
>
> > Le Phuquewitte de Pherrousse <no.brains@all> danced to my tune with:

>
> > > "wrtho...@ix.netcom.com" <wrthomp...@gmail.com> wrote:
> > >Stamp your widdle feet and get red in the face to this song:
> > > Let me cut and paste it .. again ..

>
> > Again, eh? *I've noticed somethng about you, Rusty. *You claim
> > you're only interested in iron, but somehow you always turn the
> > subject to--blood! *And when I post a link to Marlyn Manson, you
> > lose what little self-control you had. It's obvious where you're
> > coming from! *Yes, you are--Nosferrousatu! *So here's a song
> > going out to you and all the bats in your belfry:

>
> >http://www.youtube.com/watch?v=ZY-QjUl6Swo

>
> > --Bill Thompson- Hide quoted text -

>
> - Show quoted text -


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  #11  
Old 05-05-2008, 04:26 AM
wrthomps@ix.netcom.com
Guest
 
Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia

Rusty the Nosferroustu <no.brains@all> danced this little dance for
me:

> Complete recovery after iron chelation in aplastic anemia"


> Recently, researchers have discovered that most cases of severe
> aplastic anemia are autoimmune disorders in which the body’s own
> immune system attacks tissues and organs.


In other words, iron has nothing to do with the problem.
It's a good thing you read my posts, Rusty. My common
sense is beginning to rub off on you.

> Jesus Was A Vegetarian!


Not at all! Don't you remember how he went to Hell after he
died? He went there because his uncle, Satan, loves to
throw a good barbeque! And after the day he'd had, Jesus
really needed to unwind. Thus vented the Lord, "Uncle S.,
why did I let my old man talk me into going into the family
business? Here it is a Friday and I had to work late, when
even those Roman soldiers got to sit around and shoot craps
like they were at Vegas. And you should hear my mom kvetch!
'My son, he could have been a rabbi! Instead he went and
became a Christian!' And what about my mates? Twelve
blokes and only Judas hung around!"

At this point Satan passed Jesus a plate of spare ribs, and yea
verily did the Lord eat heartily of them, annointing them with
A-1 Steak Sauce. Thus did he fortify himself against the sad
knowledge that he had to get up at dawn on Easter Sunday.

http://www.youtube.com/watch?v=8iJDtAqHO-s

--Bill Thompson

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  #12  
Old 05-05-2008, 12:17 PM
ironjustice
Guest
 
Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia

On May 4, 8:38*pm, "wrtho...@ix.netcom.com" <wrthomp...@gmail.com>
wrote: snip <<

:"Complete recovery after iron chelation in aplastic anemia" <<

http://tinyurl.com/2nn4q8


Recently, researchers have discovered that most cases of severe
aplastic anemia are autoimmune disorders in which the body’s own
immune system attacks tissues and organs.
-------------------


"The infant died."


Aplastic anemia in neonatal lupus erythematosus
B. Wolach, L. Choc, A. Pomeranz, Y. Ben Ari, D. Douer and A. Metzker
Department of Pediatrics, Meir General Hospital, Sapir Medical
Center,
Kfar Saba, Israel.


OBJECTIVE--
To describe an infant with neonatal lupus erythematosus associated
with aplastic anemia.
SETTING--
The pediatric department in a tertiary-care hospital.
INTERVENTIONS--
Packed red blood cell transfusions and a 3-week course of high-dose
steroid therapy.
MEASUREMENTS/MAIN RESULTS--
The patient presented with severe anemia and a circumscribed,
reticular, macular rash on the face and neck at 5 months of age. Skin
lesion biopsy revealed epidermic hyperkeratosis, hydropic
degeneration
of the basal layer, and deposition of immunoglobulins and granular
C1q
at the dermoepidermal junction. Ro/SS-A antibodies were present in
the
infant. BFU-E (erythroid progenitor burst-forming unit) colonies in
bone marrow increased by about tenfold when suppressor CD8+ T
lymphocytes were removed, indicating immune suppression of
hematopoiesis. High-dose steroid therapy failed. The infant
subsequently developed gram-negative sepsis, severe metabolic
acidosis, and consumptive coagulopathy and died.
CONCLUSIONS--
Neonatal lupus erythematosus may present as part of a spectrum. The
disease may range from mild and transient to a severe, life-
threatening condition requiring immediate intervention, as in the
case
reported here. This is the first report of neonatal lupus associated
with aplastic anemia due to immune-mediated suppression of
hematopoiesis.
Infants Born to Mothers With Anti-SSA/Ro Autoantibodies: Neonatal
Outcome and Follow-up
Zuppa et al.
CLIN PEDIATR 2008;47:231-236.


http://www.aamds.org/aplastic/


MedlinePlus Aplastic anemia is a life-threatening condition. http//
http://www.nlm.nih.gov/medlineplus/e...cle/000554.htm


http://www.nhlbi.nih.gov/health/dci/...plastic_whatis...


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk


Reply With Quote
  #13  
Old 05-08-2008, 03:04 AM
ironjustice
Guest
 
Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia

On May 5, 2:26Â*am, ironjustice <teamtan...@hotmail.com> wrote:
"Complete recovery after iron chelation in aplastic anemia" <<

Well it seems in dogs .. females are "overrepresented" and in dogs
they 'coincidentally' have a high **iron** .. load.

Might explain why iron chelation works ..

"Hyperferremia and high percentage saturation of transferrin"

--------------------------------------------------
Pure erythrocyte aplasia is a recognised feature of systemic lupus
erythematosus (SLE)
http://lup.sagepub.com/cgi/content/refs/4/5/407

--------------------------------------------------
Abstract
Journal of the American Veterinary Medical Association
May 1, 2000, Vol. 216, No. 9, Pages 1429-1436

Idiopathic pure red cell aplasia and nonregenerative immune-mediated
anemia in dogs: 43 cases (1988–1999)

Tracy Stokol , BVSc, PhD, DACVP Julia T. Blue , DVM, PhD, DACVP Tracy
W. French , DVM, DACVP
Department of Biomedical Sciences, College of Veterinary Medicine,
Cornell University, Ithaca, NY 14853-6401. (Stokol, Blue, French)
Objective—To examine clinical features, laboratory test results,
treatment, and outcome of dogs with pure red cell aplasia (PRCA) and
idiopathic nonregenerative immune-mediated anemia (NRIMA).

Design—Retrospective study.

Animals—43 dogs with severe nonregenerative anemia.

Procedure—Medical records of dogs determined to have PRCA, NRIMA, or
ineffective erythropoiesis on the basis of bone marrow analysis
between 1988 and 1999 were reviewed. Criteria for inclusion were ≥ 5-
day history of severe nonregenerative anemia (Hct < 20%; < 60.0 X 103
reticulocytes/µl) with no underlying diseases. Information was
retrieved on signalment, clinical signs, laboratory test results,
treatment, and outcome.

Results—Median age of the dogs was 6.5 years. Spayed females and
Labrador Retrievers were significantly overrepresented. Median Hct was
11% with no evidence of regeneration (median, 1.5 X 103 reticulocytes/
µl). Direct Coombs' test results were positive in 57% of dogs.
Biochemical abnormalities included hyperferremia and high percentage
saturation of transferrin. Bone marrow findings ranged from PRCA (5%)
to erythroid hyperplasia (55%). Myelofibrosis was common. Dogs were
treated with immunosuppressive drugs and the response was complete,
partial, and poor in 55, 18, and 27% of the dogs, respectively.
Mortality rate was 28%.

Conclusion and Clinical Relevance—An immunemediated pathogenesis
should be considered in dogs with severe, nonregenerative anemia,
normal WBC and platelet counts, hyperferremia, mild clinical signs,
and no evidence of underlying disease. Bone marrow findings range from
the rare PRCA to erythroid hyperplasia. Myelofibrosis is often
detected in affected dogs and may prevent bone marrow aspiration. (J
Am Vet Med Assoc 2000;216:1429–1436)
doi: 10.2460/javma.2000.216.1429
-----------------------------------

In Europe, the focus is on stem cell transplant
http://www.hopkins-arthritis.org/arthritis-info/lupus/


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk




> On May 4, 8:38Â*pm, "wrtho...@ix.netcom.com" <wrthomp...@gmail.com>
> wrote: snip <<
>
> :"Complete recovery after iron chelation in aplastic anemia" <<
>
> http://tinyurl.com/2nn4q8
>
> Recently, researchers have discovered that most cases of severe
> aplastic anemia are autoimmune disorders in which the body’s own
> immune system attacks tissues and organs.
> -------------------
>
> "The infant died."
>
> Aplastic anemia in neonatal lupus erythematosus
> B. Wolach, L. Choc, A. Pomeranz, Y. Ben Ari, D. Douer and A. Metzker
> Department of Pediatrics, Meir General Hospital, Sapir Medical
> Center,
> Kfar Saba, Israel.
>
> OBJECTIVE--
> To describe an infant with neonatal lupus erythematosus associated
> with aplastic anemia.
> SETTING--
> The pediatric department in a tertiary-care hospital.
> INTERVENTIONS--
> Packed red blood cell transfusions and a 3-week course of high-dose
> steroid therapy.
> MEASUREMENTS/MAIN RESULTS--
> The patient presented with severe anemia and a circumscribed,
> reticular, macular rash on the face and neck at 5 months of age. Skin
> lesion biopsy revealed epidermic hyperkeratosis, hydropic
> degeneration
> of the basal layer, and deposition of immunoglobulins and granular
> C1q
> at the dermoepidermal junction. Ro/SS-A antibodies were present in
> the
> infant. BFU-E (erythroid progenitor burst-forming unit) colonies in
> bone marrow increased by about tenfold when suppressor CD8+ T
> lymphocytes were removed, indicating immune suppression of
> hematopoiesis. High-dose steroid therapy failed. The infant
> subsequently developed gram-negative sepsis, severe metabolic
> acidosis, and consumptive coagulopathy and died.
> CONCLUSIONS--
> Neonatal lupus erythematosus may present as part of a spectrum. The
> disease may range from mild and transient to a severe, life-
> threatening condition requiring immediate intervention, as in the
> case
> reported here. This is the first report of neonatal lupus associated
> with aplastic anemia due to immune-mediated suppression of
> hematopoiesis.
> Infants Born to Mothers With Anti-SSA/Ro Autoantibodies: Neonatal
> Outcome and Follow-up
> Zuppa et al.
> CLIN PEDIATR 2008;47:231-236.
>
> http://www.aamds.org/aplastic/
>
> MedlinePlus Aplastic anemia is a life-threatening condition. http//www.nlm..nih.gov/medlineplus/ency/article/000554.htm
>
> http://www.nhlbi.nih.gov/health/dci/...plastic_whatis...
>
> Who loves ya.
> Tom
>
> Jesus Was A Vegetarian!http://tinyurl.com/2r2nkh
>
> Man Is A Herbivore!http://tinyurl.com/a3cc3
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk


Reply With Quote
  #14  
Old 05-08-2008, 03:04 AM
wrthomps@ix.netcom.com
Guest
 
Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia

The Ferrous Fuckwit <ironjust...@bullshitte.com> netkooked:

> Well it seems in dogs .. females are "overrepresented" and in dogs
> they 'coincidentally' have a high **iron** .. load.


Do you have any idea what you're saying, or are you in
fact a bit of software that strings together words at random?

> Might explain why iron chelation works ..


You're stll talking off-topic nonsense, Rusty. Try to
explain why anyone with lupus, fibro, cancer or chronic
pain would want to undergo a treatment for an utterly
irrelevant condition. But you can't do that, so you'll just
repost the exact same twaddle, which is fine. Your bizarre
spews do nothing but show newbies that you're nuts.

Meanwhile, the voices in your head are getting bored with
your inane drivel, so they phoned in this request:

http://www.youtube.com/watch?v=i4qrBtavjEQ

--Bill Thompson
Reply With Quote
  #15  
Old 05-08-2008, 07:30 AM
ironjustice
Guest
 
Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia

On May 7, 8:49*pm, "wrtho...@ix.netcom.com" <wrthomp...@gmail.com>
wrote: utterly irrelevant condition<<

Try to read to comprehend.

Pure erythrocyte aplasia is a recognised feature of systemic lupus
erythematosus (SLE)
http://lup.sagepub.com/cgi/content/refs/4/5/407


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk



> The Ferrous Fuckwit <ironjust...@bullshitte.com> netkooked:
>
> > Well it seems in dogs .. females are "overrepresented" and in dogs
> > they 'coincidentally' have a high **iron** .. load.

>
> Do you have any idea what you're saying, or are you in
> fact a bit of software that strings together words at random?
>
> > Might explain why iron chelation works ..

>
> You're stll talking off-topic nonsense, Rusty. *Try to
> explain why anyone with lupus, fibro, cancer or chronic
> pain would want to undergo a treatment for an utterly
> irrelevant condition. But you can't do that, so you'll just
> repost the exact same twaddle, which is fine. *Your bizarre
> spews do nothing but show newbies that you're nuts.
>
> Meanwhile, the voices in your head are getting bored with
> your inane drivel, so they phoned in this request:
>
> http://www.youtube.com/watch?v=i4qrBtavjEQ
>
> --Bill Thompson


Reply With Quote
  #16  
Old 05-09-2008, 03:57 AM
wrthomps@ix.netcom.com
Guest
 
Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia

The Ferrous Fuckwit <injust...@horseshitte.com> put this twist on
reality:

> Try to read to comprehend.


Yes, Rusty, why don't you try that? You might enjoy the change of
pace.

> Pure erythrocyte aplasia is a recognised feature of systemic lupus
> erythematosus (SLE)http://lup.sagepub.com/cgi/content/refs/4/5/407


No, I'm not going to waste my time reading something that amounts
to "We don't really understand this problem, but if we've guessed
right, iron might be involved somewhere in the process and maybe
you could, uh, chelate it or something and that might not kill the
patient, but don't blame us if we're mistaken." Stick it back up
your
ass, if your head doesn't block the entry.

You keep offering medical advice. I say you are not qualified to
do that. Everyone agrees with me on that. Let's see you post
your qualifications to give medical advice, Fuckwit.

> Who loves ya.
> Tom the Telly Savalas Worshipper


> Jesus Was A Vegetarian!


No, he wasn't.

> Man Is A Herbivore!


No, he isn't. Neither is Woman. You are a herbivore, Fuckwit,
but that's because you're not a man. You're a mouse.

Hey, Rusty, Joni Mitchell is playing your song!
Dance Fuckwit dance!

http://www.youtube.com/watch?v=IKIQSo7JbKQ

--Bill Thompson
Reply With Quote
  #17  
Old 05-09-2008, 02:45 PM
ironjustice
Guest
 
Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia

On May 8, 8:45*pm, "wrtho...@ix.netcom.com" <wrthomp...@gmail.com>
wrote:
Fuckwit Stick it back up your ass, Fuckwit. Fuckwit, Fuckwit
No, I'm not going to waste my time reading something <<

"Erythrocyte aplasia is a feature of lupus"


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk


Reply With Quote
  #18  
Old 05-09-2008, 04:32 PM
ironjustice
Guest
 
Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia

On May 9, 7:29Â*am, ironjustice <ironjust...@cashette.com>
wrote:"Erythrocyte aplasia is a feature of lupus" <<

PEDIATRICS Vol. 22 No. 5 November 1958, pp. 910-922 This Article

STUDIES OF CONGENITAL HEMOLYTIC SYNDROMES
I. Rates of Destruction and Production of Erythrocytes in Thalassemia
Marion E. Erlandson M.D.1, Irving Schulman M.D.1, Gertrude Stern M.D.
1, and Carl H. Smith M.D.1

1 Department of Pediatrics, the New York Hospital-Cornell Medical
Center

Rates of destruction of erythrocytes and of effective production of
erythrocytes and hemoglobin have been determined in 10 patients with
homozygous Cooley's anemia. The method employed was based upon
survival of Cr51-labeled cells in patients in whom a state of
equilibrium of erythrocytes was present.

While a marked hemohytic defect is present, this defect does not, by
itself, determine the degree of anemia present.

Rates of effective production of erythrocytes are increased above
normal but are not increased to the same degree found in patients with
other hemolytic diseases.

Rates of effective synthesis of hemoglobin were found to be less than
those obtained for production of erythrocytes.

The rates of production of fetal hemoglobin in these patients are
remarkably elevated but cannot be directly correlated with the rate of
destruction of erythrocytes, rate of production of erythrocytes, or
the degree of anemia present.

The hemolytic defect in patients with intermediate Cooley's anemia was
comparable to that in the majority of the patients with the severe
form of disease. However, the most marked hemolytic defects were among
patients with the severe and not with the intermediate form of
disease. Production of erythrocytes and hemoglobin did not differ
significantly in the two forms of this disease.

Results in two splenectomized patients did not differ significantly
from results in the non-splenectomized group of patients. However,
since pre-splenectomy data were not available, no statement may be
made as to possible individual benefit derived from the operation.

The final status of each patient is determined by the particular
balance obtained between rates of destruction and production. Neither
production nor destruction alone determines the degree of anemia.

The compensation index, as a measure of final status in each patient,
was lowest in the severe form of Cooley's anemia. It is presumed to be
lower still in many patients who could not be studied because
transfusion therapy was in progress. The compensation index is
somewhat higher in patients with intermediate Cooley's anemia and in
two splenectomized individuals not requiring frequent transfusions.
Values in these patients approach the higher levels found in patients
with sickle cell anemia and congenital spherocytosis.

Submitted on April 7, 1958
Accepted on May 15, 1958
--------------------

Association of systemic lupus erythematosus and hemolytic uremic
syndrome in a child
Journal Pediatric Nephrology
SpringerLink Date Monday, January 03, 2000

Brief Report
Association of systemic lupus erythematosus and hemolytic uremic
syndrome in a child
T. Ogawa1, H. Arai1, K. Maruyama1, T. Watanabe1, Y. Kobayashi1, O.
Kikuchi1 and A. Morikawa1

(1) Department of Pediatrics, Gunma University School of Medicine,
3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan Tel.:
+81-27-220-8205, Fax: +81-27-220-8215, JP

Abstract  We describe a 10-year-old girl with systemic lupus
erythematosus (SLE) who first presented with hemolytic uremic syndrome
(HUS). Diagnoses were based on the classic HUS triad, including the
observation of fragmented red blood cells, and on the American College
of Rheumatology criteria for SLE. Plasma exchange may have been
effective against both HUS and SLE in this patient, as it was
associated with improvement of platelet counts, renal function, and
serological findings.
Key words Systemic lupus erythematosus - Hemolytic uremic syndrome -
Plasma exchange

Received: 24 September 1998 / Revised: 4 January 1999 / Accepted: 4
January 1999

---------------
Blood, 1952, Vol. 7, No. 3, pp. 350-357.
© 1952 American Society of Hematology, Inc.
Publisher Springer Berlin / Heidelberg
ISSN 0931-041X (Print) 1432-198X (Online)
Issue Volume 14, Number 1 / January, 2000
Category Brief Report
DOI 10.1007/s004670050016
Pages 62-64

--------------------------------------------------------------------------------

Chronic Hemolytic Anemia Associated with Thalassemia and Sickling
Traits
PHILLIP STURGEON M.D.1, HARVEY A. ITANO M.D., PH.D.1, and WILLIAM N.
VALENTINE M.D.1
1 Department of Research, Los Angeles Childrens’s Hospital, and the
Department of Pediatrics, University of Southern California School of
Medicine, Los Angeles; the Gates and Crellin Laboratories of Chemistry
(Contribution No. 1602), California Institute of Technology, Pasadena;
and the Department of Medicine, School of Medicine, University of
California Medical Center, Los Angeles.

The family history, case history and genealogy of a 6 year old girl
suffering from a chronic hemolytic anemia is presented. The disease,
resulting from her inheritance of both the gene for sickle trait and
that for thalassemia trait, is compared to a similar case in a 38 year
old male reported by Powell, et al.

To date the child has had no clinical evidence of an hemolytic anemia,
except for an enlarged spleen. Hematologically, however, all findings
indicate the presence of a brisk hemolytic process.

Electrophoretic analysis of the patient’s hemoglobin reveals a unique
pattern intermediate between the usual sickle cell trait and sickle
anemia patterns.

Submitted on August 20, 1951
Accepted on November 7, 1951
------------------------

Hematology 2005
© 2005 The American Society of Hematology

Cardiopulmonary Complications of Sickle Cell Disease: Role of Nitric
Oxide and Hemolytic Anemia
Mark T. Gladwin and Gregory J. Kato
Correspondence: Dr. Mark T. Gladwin, Head, Vascular Therapeutics
Section, Cardiovascular Branch, NHLBI, Critical Care Medicine
Department, Clinical Center, National Institutes of Health, Building
10-CRC, Room 5-5140, 10 Center Drive, MSC 1476, Bethesda MD
20892-1476; Phone (301) 435-2310; Fax (301) 451-7091; mgladwin@nih.gov


Abstract

Medical advances in the management of patients with sickle cell
disease, thalassemia, and other hemolytic anemias have led to
significant increases in life expectancy. Improved public health,
neonatal screening, parental and patient education, advances in red
cell transfusion medicine, iron chelation therapy, penicillin
prophylaxis for children, pneumococcal immunization, and hydroxyurea
therapy have all likely contributed to this effect on longevity.1,2
Importantly, as a generation of patients with sickle cell disease and
thalassemia ages, new chronic complications of these
hemoglobinopathies develop. In this context, pulmonary hypertension is
emerging as one of the leading causes of morbidity and mortality in
adult sickle cell and thalassemia patients, and likely in patients
with other hemolytic anemias. A common feature of both sickle cell
disease and thalassemia is intravascular hemolysis and chronic anemia.
Recent data suggest that chronic intravascular hemolysis is associated
with a state of endothelial dysfunction characterized by reduced
nitric oxide (NO) bioavailability, pro-oxidant and pro-inflammatory
stress and coagulopathy, leading to vasomotor instability and
ultimately producing a proliferative vasculopathy, a hallmark of which
is the development of pulmonary hypertension in adulthood.3–5 In
conclusion, pulmonary hypertension is common in patients with
hereditary hemolytic anemias and is associated with a high risk of
death in patients with sickle cell disease. New therapies targeting
this vasculopathy and aimed at normalizing the
vasodilator:vasoconstrictor balance are discussed.


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk






> On May 8, 8:45Â*pm, "wrtho...@ix.netcom.com" <wrthomp...@gmail.com>
> wrote:
> Fuckwit Stick it back up your ass, Â*Fuckwit. Fuckwit, Fuckwit
> No, I'm not going to waste my time reading something <<
>
> "Erythrocyte aplasia is a feature of lupus"
>
> Who loves ya.
> Tom
>
> Jesus Was A Vegetarian!http://tinyurl.com/2r2nkh
>
> Man Is A Herbivore!http://tinyurl.com/a3cc3
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk


Reply With Quote
  #19  
Old 05-09-2008, 04:33 PM
ironjustice
Guest
 
Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia

On May 9, 8:22Â*am, ironjustice <ironjust...@cashette.com> wrote:
proliferative vasculopathy is associated with a high risk of death <<

http://rheumatology.oxfordjournals.o.../full/39/1/108

Letters to the Editor

Antiphospholipid syndrome with proliferative vasculopathy and bowel
infarction
Y. I. Patel, A. St John1 and N. J. McHugh2
Department of Medicine, Groote Schuur Hospital, J47 Old Main Building,
Cape Town, South Africa,
1 Directorate of Pathology, Royal United Hospital, Bath BA1 3NG and
2 Royal National Hospital for Rheumatic Diseases, Bath BA1 1RL, UK

Correspondence to: Y. I. Patel.

Sir, Since antiphospholipid syndrome (APS) was first described in 1983
[1], many complications have been reported which result from vascular
occlusion as a result of thrombosis [2]. More recently, a few cases
have been described where a proliferative vasculopathy appears to have
been the major mechanism of vascular occlusion rather than thrombosis
or vasculitis [3–5]. The patient developed pulmonary complications
and died 6 weeks later.

---------------------------------

Widespread vasculopathy with hemolytic uremic syndrome,
perimyocarditis and cystic pancreatitis in a young woman with mixed
connective tissue disease
Journal Rheumatology International
Publisher Springer Berlin / Heidelberg
ISSN 0172-8172 (Print) 1437-160X (Online)
Issue Volume 13, Number 1 / April, 1993
Category Case Report
DOI 10.1007/BF00290331
Pages 31-36
SpringerLink Date Tuesday, November 30, 2004

Case Report
Widespread vasculopathy with hemolytic uremic syndrome,
perimyocarditis and cystic pancreatitis in a young woman with mixed
connective tissue disease
Case report and review of the literature
J. Braun1 , J. Sieper1, A. Schwarz1, F. Hiepe3, T. Lenz1, F.
Keller1, H. Herbst2 and A. Distler1

(1) Abteilung fĂĽr Allgemeine Innere Medizin und Nephrologie, Klinikum
Steglitz FU Berlin, Germany
(2) Abteilung fĂĽr Pathologie, Klinikum Steglitz FU Berlin, Germany
(3) Arbeitsbereich Rheumatologie, Universitätsklinik für Innere
Medizin, Charité HU Berlin, Germany
(4) Med. Klinik und Poliklinik, Abteilung fĂĽr Allgemeine Innere
Medizin und Nephrologie, Univ-Klinikum Steglitz, Hindenburgdamm 30,
1000 Berlin 45

Received: 5 October 1992 Accepted: 14 January 1993

Summary A 15-year-old girl had severe Raynaud's phenomenon and
arthralgias. A high ANA-IF titer was found and undifferentiated
connective tissue disease was diagnosed. After 7 years of moderately
flaring disease the patient deteriorated and presented with congestive
heart failure, pleuropericardial effusion, hemolytic uremic syndrome,
proteinuria and moderate hypertension. Autoantibodies against DNA, Sm-
protein, and very high titers against U1RNP were detected. Therapy
with high steroid doses, a cyclophosphamide pulse and 4 weeks of
plasmapheresis with plasma exchange improved the heart, but not the
renal condition. Symptomatic pancreatitis became the dominant problem
of a progressively consuming process that resulted in the death of the
patient. Postmortem examination revealed widespread vasculopathy with
intima proliferation and only minimal fibrosis involving the kidneys,
heart and other main organs, including the pancreas. Taken together,
the clinical picture was of an overlap between scleroderma and
systemic lupus crythemathosus; the serologic and histopathologic
findings suggest a diagnosis of a severe form of mixed conective
tissue disease (MCTD).
Key words Vasculopathy - Hemolytic uremic syndrome - Mixed connective
tissue disease


--------------------------------------------------------------------------------


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk


> On May 9, 7:29Â*am, ironjustice <ironjust...@cashette.com>
> wrote:"Erythrocyte aplasia is a feature of lupus" <<
>
> PEDIATRICS Vol. 22 No. 5 November 1958, pp. 910-922 This Article
>
> STUDIES OF CONGENITAL HEMOLYTIC SYNDROMES
> I. Rates of Destruction and Production of Erythrocytes in Thalassemia
> Marion E. Erlandson M.D.1, Irving Schulman M.D.1, Gertrude Stern M.D.
> 1, and Carl H. Smith M.D.1
>
> 1 Department of Pediatrics, the New York Hospital-Cornell Medical
> Center
>
> Rates of destruction of erythrocytes and of effective production of
> erythrocytes and hemoglobin have been determined in 10 patients with
> homozygous Cooley's anemia. The method employed was based upon
> survival of Cr51-labeled cells in patients in whom a state of
> equilibrium of erythrocytes was present.
>
> While a marked hemohytic defect is present, this defect does not, by
> itself, determine the degree of anemia present.
>
> Rates of effective production of erythrocytes are increased above
> normal but are not increased to the same degree found in patients with
> other hemolytic diseases.
>
> Rates of effective synthesis of hemoglobin were found to be less than
> those obtained for production of erythrocytes.
>
> The rates of production of fetal hemoglobin in these patients are
> remarkably elevated but cannot be directly correlated with the rate of
> destruction of erythrocytes, rate of production of erythrocytes, or
> the degree of anemia present.
>
> The hemolytic defect in patients with intermediate Cooley's anemia was
> comparable to that in the majority of the patients with the severe
> form of disease. However, the most marked hemolytic defects were among
> patients with the severe and not with the intermediate form of
> disease. Production of erythrocytes and hemoglobin did not differ
> significantly in the two forms of this disease.
>
> Results in two splenectomized patients did not differ significantly
> from results in the non-splenectomized group of patients. However,
> since pre-splenectomy data were not available, no statement may be
> made as to possible individual benefit derived from the operation.
>
> The final status of each patient is determined by the particular
> balance obtained between rates of destruction and production. Neither
> production nor destruction alone determines the degree of anemia.
>
> The compensation index, as a measure of final status in each patient,
> was lowest in the severe form of Cooley's anemia. It is presumed to be
> lower still in many patients who could not be studied because
> transfusion therapy was in progress. The compensation index is
> somewhat higher in patients with intermediate Cooley's anemia and in
> two splenectomized individuals not requiring frequent transfusions.
> Values in these patients approach the higher levels found in patients
> with sickle cell anemia and congenital spherocytosis.
>
> Submitted on April 7, 1958
> Accepted on May 15, 1958
> --------------------
>
> Association of systemic lupus erythematosus and hemolytic uremic
> syndrome in a child
> Journal Pediatric Nephrology
> SpringerLink Date Monday, January 03, 2000
>
> Brief Report
> Association of systemic lupus erythematosus and hemolytic uremic
> syndrome in a child
> T. Ogawa1, H. Arai1, K. Maruyama1, T. Watanabe1, Y. Kobayashi1, O.
> Kikuchi1 and A. Morikawa1
>
> (1) Â*Department of Pediatrics, Gunma University School of Medicine,
> 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan Tel.:
> +81-27-220-8205, Fax: +81-27-220-8215, JP
>
> Abstract  Â*We describe a 10-year-old girl with systemic lupus
> erythematosus (SLE) who first presented with hemolytic uremic syndrome
> (HUS). Diagnoses were based on the classic HUS triad, including the
> observation of fragmented red blood cells, and on the American College
> of Rheumatology criteria for SLE. Plasma exchange may have been
> effective against both HUS and SLE in this patient, as it was
> associated with improvement of platelet counts, renal function, and
> serological findings.
> Key words Systemic lupus erythematosus - Hemolytic uremic syndrome-
> Plasma exchange
>
> Received: 24 September 1998 / Revised: 4 January 1999 / Accepted: 4
> January 1999
>
> ---------------
> Blood, 1952, Vol. 7, No. 3, pp. 350-357.
> © 1952 American Society of Hematology, Inc.
> Publisher Springer Berlin / Heidelberg
> ISSN 0931-041X (Print) 1432-198X (Online)
> Issue Volume 14, Number 1 / January, 2000
> Category Brief Report
> DOI 10.1007/s004670050016
> Pages 62-64
>
> ---------------------------------------------------------------------------Â*-----
>
> Chronic Hemolytic Anemia Associated with Thalassemia and Sickling
> Traits
> PHILLIP STURGEON M.D.1, HARVEY A. ITANO M.D., PH.D.1, and WILLIAM N.
> VALENTINE M.D.1
> 1 Department of Research, Los Angeles Childrens’s Hospital, and the
> Department of Pediatrics, University of Southern California School of
> Medicine, Los Angeles; the Gates and Crellin Laboratories of Chemistry
> (Contribution No. 1602), California Institute of Technology, Pasadena;
> and the Department of Medicine, School of Medicine, University of
> California Medical Center, Los Angeles.
>
> The family history, case history and genealogy of a 6 year old girl
> suffering from a chronic hemolytic anemia is presented. The disease,
> resulting from her inheritance of both the gene for sickle trait and
> that for thalassemia trait, is compared to a similar case in a 38 year
> old male reported by Powell, et al.
>
> To date the child has had no clinical evidence of an hemolytic anemia,
> except for an enlarged spleen. Hematologically, however, all findings
> indicate the presence of a brisk hemolytic process.
>
> Electrophoretic analysis of the patient’s hemoglobin reveals a unique
> pattern intermediate between the usual sickle cell trait and sickle
> anemia patterns.
>
> Submitted on August 20, 1951
> Accepted on November 7, 1951
> ------------------------
>
> Hematology 2005
> © 2005 The American Society of Hematology
>
> Cardiopulmonary Complications of Sickle Cell Disease: Role of Nitric
> Oxide and Hemolytic Anemia
> Mark T. Gladwin and Gregory J. Kato
> Correspondence: Dr. Mark T. Gladwin, Head, Vascular Therapeutics
> Section, Cardiovascular Branch, NHLBI, Critical Care Medicine
> Department, Clinical Center, National Institutes of Health, Building
> 10-CRC, Room 5-5140, 10 Center Drive, MSC 1476, Bethesda MD
> 20892-1476; Phone (301) 435-2310; Fax (301) 451-7091; mglad...@nih.gov
>
> Abstract
>
> Medical advances in the management of patients with sickle cell
> disease, thalassemia, and other hemolytic anemias have led to
> significant increases in life expectancy. Improved public health,
> neonatal screening, parental and patient education, advances in red
> cell transfusion medicine, iron chelation therapy, penicillin
> prophylaxis for children, pneumococcal immunization, and hydroxyurea
> therapy have all likely contributed to this effect on longevity.1,2
> Importantly, as a generation of patients with sickle cell disease and
> thalassemia ages, new chronic complications of these
> hemoglobinopathies develop. In this context, pulmonary hypertension is
> emerging as one of the leading causes of morbidity and mortality in
> adult sickle cell and thalassemia patients, and likely in patients
> with other hemolytic anemias. A common feature of both sickle cell
> disease and thalassemia is intravascular hemolysis and chronic anemia.
> Recent data suggest that chronic intravascular hemolysis is associated
> with a state of endothelial dysfunction characterized by reduced
> nitric oxide (NO) bioavailability, pro-oxidant and pro-inflammatory
> stress and coagulopathy, leading to vasomotor instability and
> ultimately producing a proliferative vasculopathy, a hallmark of which
> is the development of pulmonary hypertension in adulthood.3–5 In
> conclusion, pulmonary hypertension is common in patients with
> hereditary hemolytic anemias and is associated with a high risk of
> death in patients with sickle cell disease. New therapies targeting
> this vasculopathy and aimed at normalizing the
> vasodilator:vasoconstrictor balance are discussed.
>
> Who loves ya.
> Tom
>
> Jesus Was A Vegetarian!http://tinyurl.com/2r2nkh
>
> Man Is A Herbivore!http://tinyurl.com/a3cc3
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
>
>
>
> > On May 8, 8:45Â*pm, "wrtho...@ix.netcom.com" <wrthomp...@gmail.com>
> > wrote:
> > Fuckwit Stick it back up your ass, Â*Fuckwit. Fuckwit, Fuckwit
> > No, I'm not going to waste my time reading something <<

>
> > "Erythrocyte aplasia is a feature of lupus"

>
> > Who loves ya.
> > Tom

>
> > Jesus Was A Vegetarian!http://tinyurl.com/2r2nkh

>
> > Man Is A Herbivore!http://tinyurl.com/a3cc3

>
> > DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk- Hide quoted text -

>
> - Show quoted text -


Reply With Quote
  #20  
Old 05-09-2008, 04:33 PM
ironjustice
Guest
 
Posts: n/a
Default Re: Complete Cure Of Aplastic Anemia

On May 9, 8:42Â*am, ironjustice <ironjust...@cashette.com> wrote:

http://www.nature.com/bmt/journal/v2.../1702992a.html

Case Report
Recovery of erythropoiesis following allogeneic bone marrow
transplantation for chronic lymphocytic leukaemia-associated pure red
cell aplasia

M P de Vetten, M van Gelder and G E de Greef

Department of Hematology, University Hospital Rotterdam/Daniel den
Hoed Cancer Center, Rotterdam, Netherlands


Correspondence to: Dr G E de Greef, Department of Hematology,
University Hospital Rotterdam/Daniel den Hoed Cancer Center, PO Box
5201, 3008 AE Rotterdam, Netherlands


Abstract

Pure red cell aplasia is a rare condition, that can be either
idiopathic or associated with a lymphoproliferative disorder. The
latter is considered to result from T cell-mediated suppression of
haematopoiesis, and usually responds well to treatment with
immunosuppressive medication. We describe a patient with B-CLL-
associated pure red cell aplasia who did not respond to several
courses of immunosuppressive treatment. Erythropoiesis was finally
restored after allogeneic bone marrow transplantation. Bone Marrow
Transplantation (2001) 27, 771-773.


Keywords

pure red cell aplasia; allo-BMT; CLL

--------------------------------

Rheumatology 2000; 39: 1155-1157
© 2000 British Society for Rheumatology

--------------------------------------------------------------------------------

Letters to the Editor


Successful treatment of pure red cell aplasia associated with systemic
lupus erythematosus with cyclosporin A
C. Duarte-Salazar, J. CazarĂ*n-Barrientos, M. V. Goycochea-Robles, J.
Collazo-Jaloma and R. Burgos-Vargas
Rheumatology Service, Haematology Laboratory and Research Division,
Hospital General de México and Faculty of Medicine Universidad
Nacional Autónoma de México

SIR, We report the first case of a patient with pure red cell aplasia
(PRCA) and systemic lupus erythematosus (SLE) failing to respond to
corticosteroids and then being successfully treated with cyclosporin A
(CyA), with no recurrence of the disease in the last 4 yr.

A 21-yr-old female was admitted to our ward with anaemia. Previously,
she had had polyarthritis of the small joints of the hands, knees and
ankles, photosensitivity, and a malar rash that responded well to non-
steroidal anti-inflammatory drugs, which were used from October 1994
to April 1995. She was later seen in the emergency department and
diagnosed with severe anaemia (haemoglobin 3.8 g/dl, haematocrit
11.1%, fatigue, tiredness, cephalalgia and low blood pressure), and
she received two units of red blood cells. After initial improvement,
her clinical condition worsened in the following 2 weeks. Her
haemoglobin level and haematocrit fell to 2.8 g/dl and 8.8%,
respectively. She was transfused again with two units of red blood
cells and transferred to our service. She was dyspnoeic and
semiconscious, with paleness and swelling of the metacarpophalangeal
and hand proximal interphalangeal joints, knees and ankles. Her
laboratory test results were as follows: haemoglobin 6.9 g/dl;
haematocrit 20%; reticulocytes 0.2%; erythrocyte sedimentation rate 75
mm/h. Immunological studies showed a direct Coombs test result of 1:4,
a speckled pattern of antinuclear antibodies at a titre of 1:320, DNA
binding (radioimmunoassay) of 84.3% (normal value <52%), and IgG and
IgM anti-cardiolipin antibodies 2.5 U (normal value <2.0 U) and 5.0 U
(normal value <2.2 U), respectively. The following tests were normal:
bilirubin, total proteins and albumin, prothrombin and partial
thromboplastin; VDRL was negative. An additional search for serum IgG
and IgM anti-B12 parvovirus antibodies was negative. Chest X-rays and
computed tomography were normal.

A bone marrow sample revealed the absence of erythroid precursors
cells, without significant abnormalities of the megakaryocytic,
granulocytic or lymphocytic cell lines. A diagnosis of PRCA associated
with SLE was established, and treatment with 60 mg prednisone (l mg/
kg) daily was started. Ten days later, her haemoglobin level was 5.9 g/
dl, haematocrit 17.6% and reticulocyte count 0.4%; her clinical
symptoms were unchanged. She was transfused for a third time with two
units of red blood cells and treated with 1 g methylprednisolone
intravenously for 3 consecutive days (Fig. 1). Haemoglobin rose to 9.2
g/dl and haematocrit to 27.1%; reticulocyte count remains without
change. She continued with 60 mg of prednisone per day, but 4 weeks
later (5 weeks after starting corticosteroids) symptoms reappeared and
laboratory values dropped again (haemoglobin 6.2 g/dl, haematocrit
17.0%, reticulocyte count 0.4%). She was again transfused and started
on CyA at a dose of 200 mg/day (3.5 mg/kg). Twenty-one days later, her
clinical condition had improved significantly, as had her laboratory
test values, with an increased reticulocyte count (haemoglobin 9.8 g/
dl, haematocrit 31.6%, reticulocyte count 11%). Investigations during
the following 6 months showed continuous improvement in her clinical
condition and laboratory values. CyA was then stopped and azathioprine
was introduced at a dose of 150 mg/day. Since then, the patient was
followed for a mean of 4 yr; there was a favourable clinical outcome
with remission of PRCA but with mild intermittent episodes of
arthralgia and arthritis, which were treated with chloroquine. At the
start of CyA, the patient's serum creatinine value was 0.7 mg/dl and
glomerular filtration rate 101.5 ml/min. Currently, her creatinine
level is 1.0 mg/dl and glomerular filtration rate 112.0 ml/min. During
follow-up, these parameters were monitored closely and remained within
normal limits.


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk






> On May 9, 8:22Â*am, ironjustice <ironjust...@cashette.com> wrote:
> proliferative vasculopathy is associated with a high risk of death Â*<<
>
> http://rheumatology.oxfordjournals.o.../full/39/1/108
>
> Letters to the Editor
>
> Antiphospholipid syndrome with proliferative vasculopathy and bowe