On Jul 19, 10:20 am, "ironjust...@aol.com" <ironjust...@aol.com>
wrote: hemolytic anemia <<

I guess it is well KNOWN .. hemolysis DOES .. happen in Lupus JUST
like sickle cell.

http://www.itzarion.com/lupusanemia.html

If this were a .. drug.

"Striking decrease of hospitalization days"
"Viscosity"

Arch Pediatr
2000 Mar;7(3):249-55
[Prevention of sickle cell crises with multiple phlebotomies].

Bouchair N, Manigne P, Kanfer A, Raphalen P, de Montalembert M,
Hagege
I, Verschuur A, Maier-Redelsperger M, Girot R
Service de pediatrie, CHU,
Constantine, Algerie.

OBJECTIVES:
Sickle cell disease patients suffering from frequent painful crises
were submitted to phlebotomies in order to reduce hospitalization
days
due to pain, through hemoglobin (Hb) level reduction and iron
deficiency in patients with an hemoglobin level equal to or above 9.5
g/dL.

PATIENTS:
Seven sickle cell disease patients (four SC, three SS), aged four to
24
years, were submitted to sequential phlebotomies during periods from
18
months to four years.

METHODS:
The number of hospitalization days for crises was considered.
The volumes and frequencies of phlebotomies were adjusted according
to
the patients ages, the hemoglobin concentrations and the serum
ferritin
levels.

RESULTS:
One hundred and forty-four hospitalization days were recorded in the
seven patients in the year preceding the treatment.
During the study period, the annual numbers of hospitalization days
were respectively 20, five, six and one.
Mean hemoglobin concentration was 10.7 g/dL before phlebotomies and
8.8
to 9.2 g/dL during the four years of treatment.
Mean corpuscular volume, mean corpuscular hemoglobin concentration
and
serum ferritin were also reduced.
The volume of phlebotomies was 116 to 39 mL/kg/year according to the
patients.
COMMENTS AND CONCLUSION:
The striking decrease of the number of hospitalization days for all
the
patients suggests a closed relationship between therapy and clinical
improvement.
The mechanism of this effect is probably multifactorial:
a) the concentration of Hb level is known to influence the blood
viscosity and its decrease always improved rheology in sickle cell
disease patients;
b) the mean corpuscular hemoglobin concentration is a critical factor
concerning the HbS molecule polymerization in sickle cell disease,
and
its slight reduction may have an important biological effect.
We observed these two biological modifications in our patients and
suggest that they mediate the clinical effects.
The iron deficiency induced by phlebotomies has no evident
deleterious
consequence either on height and weight in the children or on
intellectual performance in any patients.

PMID: 10761600, UI: 20224666
----------------------

"Hb of 5.5 g/dl be used as an indication for transfusion"

Annals of Clinical and Laboratory Science, Vol 24, Issue 5, 396-400
Copyright © 1994 by Association of Clinical Scientists

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

Articles

When to transfuse blood in sickle cell disease? Lessons from
Jehovah's
Witnesses
ES Pearlman and SK Ballas

Hemoglobin concentration of 7 to 8 g/dl has been considered an
indication for transfusion in the general adult population and has
also been frequently applied to patients with sickle cell disease
(SCD). Through a review of the case histories of two patients with
SCD
who were also Jehovah's Witnesses and developed severe anemia, and
considering as well the clinical characteristics of this population
and the basic physiology of oxygen transport, the appropriateness is
questioned of this transfusion "trigger" in patients with SCD. It is
suggested for the latter that a Hb of 5.5 g/dl be used as an
indication for transfusion except in very specific clinical
circumstances.

Copyright © 1994 by the Association of Clinical Scientists.

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

Who loves ya.
Tom

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

Man Is A Herbivore!
http://tinyurl.com/4rq595

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

"Thalassemia and Sickle Cell anemia.
Sickle Cell anemia and Thalassemia are iron LOADING diseases."

Nope, they are genetic disorders which are mutations to a specific
disease.  What is that disease?  How can it provide relief from that
disease?  How do they relate geographically to that disease?  Them thar
questions ain't gonna go away.

"All the markers the medical profession use to assess the overall
picture of a person with lupus points to the fact they HAVE iron
**overload**.

That is using .. science .. reason .. logic."

Nope, here is the definitions of various forms oflupis:

    * Systemic lupus erythematosus (SLE), commonly known as "Lupus".
      When the term 'lupus' is used without modification, it usually
      means SLE, especially in a medical context.
         + Drug-induced lupus erythematosus, a drug-induced form of SLE
         + Lupus nephritis, an inflammation of the kidneys caused by
           SLE, when anti-DNA antibodies, which the body makes,
           precipitate in the kidneys.
    * Lupus pernio, a feature of sarcoidosis.
    * Lupus vulgaris, a feature of cutaneous tuberculosis
    * Lupus anticoagulant, an antibody causing a delay in coagulation

Jesus ate a mediterranean diet.

On Jul 19, 10:20 am, "ironjust...@aol.com" <ironjust...@aol.com>
wrote: Urate dehydrogenase "sign of red blood cell hemolysis raised "
<<

Whoops ..

Lactic acid dehydrogenase .. NOT urate dehydrogenase ..

"Serum LDH is a criterion for hemolysis. LDH is not specific because
it is ubiquitous and can be released from the neoplastic cells of the
liver or other damaged organs.
Although an increase in LDH isozyme 1 and 2 is more specific for RBC
destruction, these enzymes are also increased in patients with
myocardial infarction."

Who loves ya.
Tom

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

Man Is A Herbivore!
http://tinyurl.com/4rq595

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

On Jul 19, 10:20 am, "ironjust...@aol.com" <ironjust...@aol.com>
wrote:"ironbinding sunscreen targeting lupus patients".. <<

"UVA-induced necrotic cell death reflects the intracellular level of
LIP (iron) "

J Invest Dermatol. 2004 Oct;123(4):771-80.  Related Articles, Links

Susceptibility of Skin Cells to UVA-induced Necrotic Cell Death
Reflects the
Intracellular Level of Labile Iron.

Zhong JL, Yiakouvaki A, Holley P, Tyrrell RM, Pourzand C.

Department of Pharmacy and Pharmacology, University of Bath, Bath,
UK.

The mechanism of resistance of keratinocytes to ultraviolet A (UVA)
(320-400
nm)-induced oxidative damage has not yet been elucidated. Here, we
examined the
possible link between the intracellular level of the labile iron pool
(LIP) and
the susceptibility to UVA-induced cell death using a series of human
skin
fibroblast and keratinocyte cell lines as a model. Resistance of
keratinocytes
to UVA-induced cell death was confirmed by flow cytometry and in
fibroblasts
necrosis was found to be the primary mode of cell death induced by
UVA. The
percentage of necrosis in fibroblasts also correlated with the extent
of
intracellular ATP depletion, a hallmark of necrotic cell death. The
evaluation
of the intracellular level of LIP by calcein assay revealed that both
"basal"
and "UVA-induced" levels of LIP in keratinocytes were several fold
lower than
in fibroblasts. Accordingly the dose to give an equivalent level of
necrosis
was several fold lower in fibroblasts than in keratinocytes.
Furthermore, the
modulation of "basal" or "UVA-induced" level of LIP by either Desferal
and/or
hemin treatment significantly affected the extent of UVA-induced
necrotic cell
death and ATP depletion in all the cell lines. Cellular susceptibility
to
UVA-induced necrotic cell death appears to reflect the intracellular
level of
LIP.

PMID: 15373784 [PubMed - in process]

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

Who loves ya.
Tom

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

Man Is A Herbivore!
http://tinyurl.com/4rq595

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

POPs accumulated in human tissue during the past 1 to 3 decades, will
continue to provide a broad range of effects for decades to come by
triggering AhR-mediated cellular functions.TCDD, a potent dioxin,
triggers iron-requiring, detox enzyme production. Unforetunately, the
dexo enzyme can't detox TCDD. TCDD has a half life of approx 10 years
in the human body.

Effects of contamination level of dioxins and related chemicals on
thyroid hormone and immune response systems in patients with "Yusho".
Effects of polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated
dibenzofurans (PCDFs) and coplanar polychlorinated biphenyls (Co-PCBs)
on thyroid hormone and immune response systems were examined in 16
Yusho patients at about 30 years after the outbreak of the Yusho
accident. Their toxic equivalent (TEQ) levels in the blood were
27.8-1048.5 pg/g fat with the median level of 222.4 pg/g fat, which
was about seven times higher than that of healthy Japanese people.
Even at such high blood TEQ concentrations, they seemed not to affect
the serum levels of thyroid hormones, thyroid stimulating hormone
(TSH), immunoglobulins (A, G and M), autoantibodies (antinuclear
antibody, rheumatoid and lupus erythematosus (LE) factors), and
lymphocyte subsets in the blood. However, positive rates of rheumatoid
factor were considered to increase in higher blood TEQ groups. This
investigation was done using rather small number of Yusho patients, so
further large-scale investigations are needed to get more conclusive
findings concerning their effects on thyroid hormone and immune
response systems. PMID: 11372817

Control of T(reg) and T(H)17 cell differentiation by the aryl
hydrocarbon receptor.
Regulatory T cells (T(reg)) expressing the transcription factor Foxp3
control the autoreactive components of the immune system. The
development of T(reg) cells is reciprocally related to that of pro-
inflammatory T cells producing interleukin-17 (T(H)17). Although
T(reg) cell dysfunction and/or T(H)17 cell dysregulation are thought
to contribute to the development of autoimmune disorders, little is
known about the physiological pathways that control the generation of
these cell lineages. Here we report the identification of the ligand-
activated transcription factor aryl hydrocarbon receptor (AHR) as a
regulator of T(reg) and T(H)17 cell differentiation in mice. AHR
activation by its ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin induced
functional T(reg) cells that suppressed experimental autoimmune
encephalomyelitis. On the other hand, AHR activation by 6-
formylindolo[3,2-b]carbazole interfered with T(reg) cell development,
boosted T(H)17 cell differentiation and increased the severity of
experimental autoimmune encephalomyelitis in mice. Thus, AHR regulates
both T(reg) and T(H)17 cell differentiation in a ligand-specific
fashion, constituting a unique target for therapeutic
immunomodulation. PMID: 18362915

The aryl hydrocarbon receptor links TH17-cell-mediated autoimmunity to
environmental toxins.
The aryl hydrocarbon receptor (AHR) is a ligand-dependent
transcription factor best known for mediating the toxicity of dioxin.
Environmental factors are believed to contribute to the increased
prevalence of autoimmune diseases, many of which are due to the
activity of T(H)17 T cells, a new helper T-cell subset characterized
by the production of the cytokine IL-17. Here we show that in the CD4+
T-cell lineage of mice AHR expression is restricted to the T(H)17 cell
subset and its ligation results in the production of the T(H)17
cytokine interleukin (IL)-22. AHR is also expressed in human T(H)17
cells. Activation of AHR by a high-affinity ligand during T(H)17 cell
development markedly increases the proportion of T(H)17 T cells and
their production of cytokines. CD4+ T cells from AHR-deficient mice
can develop T(H)17 cell responses, but when confronted with AHR ligand
fail to produce IL-22 and do not show enhanced T(H)17 cell
development. AHR activation during induction of experimental
autoimmune encephalomyelitis causes accelerated onset and increased
pathology in wild-type mice, but not AHR-deficient mice. AHR ligands
may therefore represent co-factors in the development of autoimmune
diseases. PMID: 18362914