Novel Biomarkers in Autoimmune Diseases

Novel Biomarkers in Autoimmune Diseases

"Hyperferritinemia was detected in 23% of SLE patients, 15% of DM
patients, 8% of MS patients, and 4% of RA patients."

WHEN 'they' actually SEE / recognise this iron / ferritin it is
rather .. high / hyperferritinemia .
Seeing that they HAVE seen it now at such a HIGH rate makes one wonder
how many DO have .. high ferritin / hyperferritinemia / high iron.
Everyone has ALSO low levels of vitamin D which is ..
coincidentally .. destroyed / depleted by iron.
They say this high ferritin / hyperferritinemia / high iron may be
used as an "acute-phase reactant marker" but fail to say it also
PREVENTS someone from being diagnosed with iron overload.

In Stills' disease it has ALWAYS been used to disregard the
POSSIBILITY of iron and recently has been found to be USELESS in
Stills' and when the second marker is used .. ?
They have iron overload.

Are they killing .. you .. too .. ?
------------------------------------------------------
"Hyperferritinemia was detected in 23% of SLE patients, 15% of DM
patients, 8% of MS patients, and 4% of RA patients."

Novel Biomarkers in Autoimmune Diseases
Authors: ORBACH, HEDI1; ZANDMAN-GODDARD, GISELE; AMITAL, HOWARD;
BARAK, VIVIAN2; SZEKANECZ, ZOLTAN3; SZUCS, GABRIELLA3; DANKO,
KATALIN3; NAGY, ENDRE4; CSEPANY, TUNDE5; CARVALHO, JOZELIO F.6; DORIA,
ANDREA7; SHOENFELD, YEHUDA

Source: Annals of the New York Academy of Sciences, Volume 1109,
Number 1, August 2007 , pp. 385-400(16)

Abstract:

The development of autoimmune diseases may be influenced by hormonal,
immunomodulatory, and metabolic pathways. Prolactin (PRL), ferritin,
vitamin D, and the tumor marker tissue polypeptide antigen (TPA) were
measured in autoimmune diseases: systemic lupus erythematosus (SLE),
systemic sclerosis (SSc), rheumatoid arthritis (RA), polymyositis
(PM), dermatomyositis (DM), multiple sclerosis (MS), autoimmune
thyroid diseases, and antiphospholipid syndrome. Hyperprolactinemia
(HPRL) was detected in 24% of PM patients, in 21% of SLE patients, in
6.7% of MS patients, 6% of RA patients, and in 3% of SSc patients.
Hyperferritinemia was detected in 23% of SLE patients, 15% of DM
patients, 8% of MS patients, and 4% of RA patients. The patients had
relatively low levels of 25 OH Vitamin D: the average results (mean ±
SD) were between 9.3 ± 4.4 to 13.7 ± 7.1 ng/mL in the different
diseases, while the 25 OH Vitamin D concentrations less than 20 ng/mL
are regarded as deficient. TPA levels were in the same range of the
controls, elevated only in SLE. HPRL, hyperferritinemia,
hypovitaminosis D, and TPA levels did not correlate with SLE activity
elevated levels of rheumatoid factor or anti-CCP antibodies in RA.
HPRL, hyperferritinemia, and hypovitaminosis D have different
immunological implications in the pathogenesis of the autoimmune
diseases. Preventive treatment with vitamin D or therapy for HPRL with
dopamine agonists, may be considered in certain cases.
Hyperferritinemia may be used as an acute-phase reactant marker in
autoimmune diseases mainly SLE. TPA may be used to indicate the
tendency for malignancies.
Keywords: prolactin; ferritin; vitamin D; tissue polypeptide antigen;
TPA; SLE; rheumatoid arthritis; multiple sclerosis; polymyositis;
dermatomyositis

Document Type: Research article

DOI: 10.1196/annals.1398.044

Affiliations: 1: Department of Medicine B, Wolfson Medical Center,
Holon, Israel 2: Immunology Lab for Tumor Diagnosis, Hadassah-Hebrew
University Medical Center, Jerusalem, Israel 3: Third Department of
Medicine, University of Debrecen Medical and Health Science Center,
Debrecen, Hungary 4: First Department of Medicine, University of
Debrecen Medical and Health Science Center, Debrecen, Hungary 5:
Neurology Department, University of Debrecen Medical and Health
Science Center, Debrecen, Hungary 6: Rheumatology Division, Sao Paulo
University Medical School Hospital, Sao Paulo, SP, Brazil 7: Division
of Rheumatology and Department of Clinical and Experimental Medicine,
University of Padova, Padova, Italy
--------------------------------

These guys seem to think the hyperferritinemia is NOT governed by
inflammation THAT much and thusly it is to BE used as a marker of iron
OVERLOAD.

<<snip>>
effect of the inflammatory status factor on ferritin level was very
weak.
<<snip>>
<<snip>>
Serum iron (SI) had the strongest effect on serum ferritin elevation
<<snip>>

Clin Biochem. 2007 Mar;40(5-6):359-64. Epub 2007 Jan 5. Links
Evaluation of a model of latent pathologic factors in relation to
serum ferritin elevation.
Yamanishi H, Kimura S, Hata N, Iyama S, Kanakura Y, Iwatani Y.
Laboratory for Clinical Investigation, Osaka University Hospital,
2-15
Yamadaoka, Suita, Osaka 565-0871, Japan. yam...@hp-lab.med.osaka-
u.ac.jp


OBJECTIVES:
Serum ferritin increases in various disorders and clinical
conditions. However, causal associations between the serum ferritin
level and clinical factors that influence serum ferritin level are
not well characterized. We report a model that quantitatively
analyzes
the causal relations between the serum ferritin level and clinical
factors.
DESIGN AND METHODS:
We analyzed the ferritin level and other
laboratory data in the sera of 274 patients. Structural equation
modeling was used to verify causal relations and the adequacy of
latent factors.
RESULTS:
Three factors representing clinical status
were identified: cell damage, hepatic function, and inflammation.
Serum iron (SI) had the strongest effect on serum ferritin elevation.
The effect of the cell damage factor on serum ferritin indicated cell
destruction, and that of the hepatic function factor represented
decreased serum ferritin clearance. The cell damage factor also
indirectly increased the ferritin level via SI or the hepatic
function factor.
The total effect of the inflammatory status factor on
ferritin level was very weak.
CONCLUSIONS:
These causal relations may explain
the mechanism of serum ferritin level elevation in various clinical
conditions.


PMID: 17292875 [PubMed - in process]

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

Now WHY .. in these three DIFFERENT diseases .. does the drop of iron
.. PARALLEL .. the drop in alanine aminotransferase (ALT) .. but in
the
disease of .. juvenile rheumatoid arthritis / Still's .. do they
NOT ..
use this marker .. WHEN .. iron HAS been shown to BE a ..
problem .. ?

Especially .. when they have such high liver injury rates. Two
thirds.

Stupidity .. ?

<<snip>>
There was a positive correlation between transaminases and serum
ferritin
<<snip>>


J Nephrol. 2003 Sep-Oct; 16(5): 703-9. Related Articles, Links


Comparative study of intravenous ascorbic acid versus low-dose
desferroxamine
in patients on hemodialysis with hyperferritinemia.


Deira J, Diego J, Martinez R, Oyarbide A, Gonzalez A, Diaz H, Grande
J.


Department of Internal Medicine, Division of Nephrology, Hospital
Virgen de la
Concha, Zamora, Spain. jde...@saludalia . com


BACKGROUND:
In patients on hemodialysis (HD), parenteral iron improves the
response to recombinant human erythropoietin (rhuEPO) therapy, but in
some subjects it produces an iron overload, increasing their morbidity
and
mortality rates. In these cases, iron administration must be
discontinued.
This study aimed to investigate the efficiency of treatment with
ascorbic
acid (AA) or desferroxamine (DFO) to mobilize and reduce iron stores,
and to
determine the effect of these compounds on erythropoiesis.
METHODS:
We performed a prospective and randomized trial over 6 months, which
included 27 patients with serum ferritin levels >800 ng/mL, TSAT >30%
and stabilized hemoglobin (Hb) and rhuEPO doses.
All patients had previously received parenteral iron (Ferlecit).
Nine patients received 200 mg of intravenous (i.v.) AA 3 times/week
and
nine patients received 1 mg/Kg/week of DFO; the remaining nine
patients
were the control group.
RESULTS:
There were no significant differences in iron
loss or mobilization due to dialysis. When Ferlecit was discontinued,
functional iron did not vary and the epoetin resistance index
(rhuEPO dose/Hb) was reduced by 21% in the i.v. AA group.
In the DFO and control groups, functional iron levels fell.
In the DFO group the epoetin resistance index increased by 20%,
with no modifications in the control group.
There was a positive correlation between transaminases and serum
ferritin.
CONCLUSIONS:
In HD patients with an iron overload, neither i.v. AA administration
or low-dose
DFO increased iron mobilization or iron loss due to dialysis. I.v. AA
administration
allows elimination of iron from stores without any drop in the
functional iron
produced by discontinuing parenteral maintenance iron; it also
improves
the response to rhuEPO. DFO did not elicit any positive effects on
erythropoiesis.


PMID: 14733417 [PubMed - in process]
------

<<snip>>
The treatment reduced mean serum alanine aminotransferase (ALT)
activity
<<snip>>


Effect of iron reduction by phlebotomy in Japanese patients with
nonalcoholic steatohepatitis: A pilot study.
Sumida Y, Kanemasa K, Fukumoto K, Yoshida N, Sakai K, Nakashima T,
Okanoue T
Hepatol Res. 2006 Sep 11;


Increased hepatic iron deposition may play a role in the pathogenesis
of nonalcoholic steatohepatitis (NASH). This study aimed to test
whether iron removal by phlebotomy improves serum transaminase
activities in patients with NASH. Eleven patients (six males and five
females) with biopsy-proven NASH underwent phlebotomy biweekly until
they reached near-iron deficiency (NID) (serum ferritin concentration
lower than or equal to 30ng/ml). Nine patients completed this study.
Serum ferritin levels in these patients fell from 563+/-322 to
18+/-9ng/ml (p=0.001). The treatment reduced mean serum alanine
aminotransferase (ALT) activity from 126+/-47 to 56+/-17IU/l
(p=0.002).

Their weight did not change significantly throughout the study
period.
Although two patients withdrew from the study, none was affected by
any
side effects of repeated phlebotomy that required discontinuing the
treatment. In conclusion, this pilot study suggests that iron
reduction
therapy by phlebotomy will be one of the promising therapies for
NASH.


---------------------------------------------------------------------------
<<snip>>
Serum alanine aminotransferase levels were significantly improved
<<snip>>


Hepatogastroenterology. 2005 Mar-Apr;52(62):563-6. Related Articles,
Links


Additional effect of low iron diet on iron reduction therapy by
phlebotomy for chronic hepatitis C.


Kimura F, Hayashi H, Yano M, Yoshioka K, Matsumura T, Fukuda T,
Shigeto


N, Yamahara S, Koushi F, Mishima Y, Yoshino T, Tanimoto M, Kimura I.


Department of Internal Medicine, Tamano-Municipal Hospital, Tamano
City, Okayama, Japan. f-kim...@po1.oninet.ne.jp


BACKGROUND/AIMS:
Iron-induced oxidative stress plays an important role
in the pathogenesis of chronic hepatitis C. Both phlebotomy for
removing body iron stores and low iron diet for minimizing portal
iron
supply to the liver have been shown to improve serum transaminase
levels in patients with the disease. However, the cooperative effects
of phlebotomy and low iron diet have not yet been elucidated in
detail.


METHODOLOGY:
A pilot study was undertaken to investigate whether a low
iron diet could improve the efficacy of phlebotomy in iron reduction
therapy. Of 21 patients diagnosed with chronic hepatitis C, 10
patients
were treated with phlebotomy alone (group A) while 11 patients were
treated with a low iron plus phlebotomy (group B). Phlebotomy was
repeated biweekly until serum ferritin levels reached 10 ng/mL in
both
A and B groups. In addition, a low iron diet (iron intake of 8 mg/day
or less) was recommended for group B, followed by estimation of iron
intake from daily diet records.


RESULTS:
Serum alanine aminotransferase
levels were significantly improved from 106+/-30 to 68+/-22 IU/L
(p<0.005, paired t-test) in group A and from 100+/-33 to 46+/-10 IU/L
(p<0.002, paired t-test) in group B. The enzyme levels after
treatment
were significantly higher in group A (p<0.02, non-paired t-test),
which
showed a higher upward distribution of the enzyme activity. The
estimated dietary iron intake in group B was reduced from 17.6+/-6.1
to
8.2+/-3.7 mg/day.

CONCLUSIONS:
These findings suggest that phlebotomy
alone does not completely remove iron-induced oxidative stress and a
low iron diet induces an additional effect in iron reduction therapy
for chronic hepatitis C.


PMID: 15816478 [PubMed - in process]


---------------------------------------------------------------------------=
-----




Who loves ya.
Tom


Jesus Was A Vegetarian!
* jesuswasavegetarian.7h . com


Man Is A Herbivore!
* tinyurl . com /a3cc3


DEAD PEOPLE WALKING
* tinyurl . com /zk9fk

Re: Novel Biomarkers in Autoimmune Diseases

On Nov 12, 6:15 pm, ironjustice <teamtan...@hotmail . com > wrote:
> "Hyperferritinemia was detected in 23% of SLE patients, 15% of DM
> patients, 8% of MS patients, and 4% of RA patients."
>
> WHEN 'they' actually SEE / recognise this iron / ferritin it is
> rather .. high / hyperferritinemia .
> Seeing that they HAVE seen it now at such a HIGH rate makes one wonder
> how many DO have .. high ferritin / hyperferritinemia / high iron.
> Everyone has ALSO low levels of vitamin D which is ..
> coincidentally .. destroyed / depleted by iron.
> They say this high ferritin / hyperferritinemia / high iron may be
> used as an "acute-phase reactant marker" but fail to say it also
> PREVENTS someone from being diagnosed with iron overload.
>
> In Stills' disease it has ALWAYS been used to disregard the
> POSSIBILITY of iron and recently has been found to be USELESS in
> Stills' and when the second marker is used .. ?
> They have iron overload.
>
> Are they killing .. you .. too .. ?
> ------------------------------------------------------
> "Hyperferritinemia was detected in 23% of SLE patients, 15% of DM
> patients, 8% of MS patients, and 4% of RA patients."
>
> Novel Biomarkers in Autoimmune Diseases
> Authors: ORBACH, HEDI1; ZANDMAN-GODDARD, GISELE; AMITAL, HOWARD;
> BARAK, VIVIAN2; SZEKANECZ, ZOLTAN3; SZUCS, GABRIELLA3; DANKO,
> KATALIN3; NAGY, ENDRE4; CSEPANY, TUNDE5; CARVALHO, JOZELIO F.6; DORIA,
> ANDREA7; SHOENFELD, YEHUDA
>
> Source: Annals of the New York Academy of Sciences, Volume 1109,
> Number 1, August 2007 , pp. 385-400(16)
>
> Abstract:
>
> The development of autoimmune diseases may be influenced by hormonal,
> immunomodulatory, and metabolic pathways. Prolactin (PRL), ferritin,
> vitamin D, and the tumor marker tissue polypeptide antigen (TPA) were
> measured in autoimmune diseases: systemic lupus erythematosus (SLE),
> systemic sclerosis (SSc), rheumatoid arthritis (RA), polymyositis
> (PM), dermatomyositis (DM), multiple sclerosis (MS), autoimmune
> thyroid diseases, and antiphospholipid syndrome. Hyperprolactinemia
> (HPRL) was detected in 24% of PM patients, in 21% of SLE patients, in
> 6.7% of MS patients, 6% of RA patients, and in 3% of SSc patients.
> Hyperferritinemia was detected in 23% of SLE patients, 15% of DM
> patients, 8% of MS patients, and 4% of RA patients. The patients had
> relatively low levels of 25 OH Vitamin D: the average results (mean ±
> SD) were between 9.3 ± 4.4 to 13.7 ± 7.1 ng/mL in the different
> diseases, while the 25 OH Vitamin D concentrations less than 20 ng/mL
> are regarded as deficient. TPA levels were in the same range of the
> controls, elevated only in SLE. HPRL, hyperferritinemia,
> hypovitaminosis D, and TPA levels did not correlate with SLE activity
> elevated levels of rheumatoid factor or anti-CCP antibodies in RA.
> HPRL, hyperferritinemia, and hypovitaminosis D have different
> immunological implications in the pathogenesis of the autoimmune
> diseases. Preventive treatment with vitamin D or therapy for HPRL with
> dopamine agonists, may be considered in certain cases.
> Hyperferritinemia may be used as an acute-phase reactant marker in
> autoimmune diseases mainly SLE. TPA may be used to indicate the
> tendency for malignancies.
> Keywords: prolactin; ferritin; vitamin D; tissue polypeptide antigen;
> TPA; SLE; rheumatoid arthritis; multiple sclerosis; polymyositis;
> dermatomyositis
>
> Document Type: Research article
>
> DOI: 10.1196/annals.1398.044
>
> Affiliations: 1: Department of Medicine B, Wolfson Medical Center,
> Holon, Israel 2: Immunology Lab for Tumor Diagnosis, Hadassah-Hebrew
> University Medical Center, Jerusalem, Israel 3: Third Department of
> Medicine, University of Debrecen Medical and Health Science Center,
> Debrecen, Hungary 4: First Department of Medicine, University of
> Debrecen Medical and Health Science Center, Debrecen, Hungary 5:
> Neurology Department, University of Debrecen Medical and Health
> Science Center, Debrecen, Hungary 6: Rheumatology Division, Sao Paulo
> University Medical School Hospital, Sao Paulo, SP, Brazil 7: Division
> of Rheumatology and Department of Clinical and Experimental Medicine,
> University of Padova, Padova, Italy
> --------------------------------
>
> These guys seem to think the hyperferritinemia is NOT governed by
> inflammation THAT much and thusly it is to BE used as a marker of iron
> OVERLOAD.
>
> <<snip>>
> effect of the inflammatory status factor on ferritin level was very
> weak.
> <<snip>>
> <<snip>>
> Serum iron (SI) had the strongest effect on serum ferritin elevation
> <<snip>>
>
> Clin Biochem. 2007 Mar;40(5-6):359-64. Epub 2007 Jan 5. Links
> Evaluation of a model of latent pathologic factors in relation to
> serum ferritin elevation.
> Yamanishi H, Kimura S, Hata N, Iyama S, Kanakura Y, Iwatani Y.
> Laboratory for Clinical Investigation, Osaka University Hospital,
> 2-15
> Yamadaoka, Suita, Osaka 565-0871, Japan. yam...@hp-lab.med.osaka-
> u.ac.jp
>
> OBJECTIVES:
> Serum ferritin increases in various disorders and clinical
> conditions. However, causal associations between the serum ferritin
> level and clinical factors that influence serum ferritin level are
> not well characterized. We report a model that quantitatively
> analyzes
> the causal relations between the serum ferritin level and clinical
> factors.
> DESIGN AND METHODS:
> We analyzed the ferritin level and other
> laboratory data in the sera of 274 patients. Structural equation
> modeling was used to verify causal relations and the adequacy of
> latent factors.
> RESULTS:
> Three factors representing clinical status
> were identified: cell damage, hepatic function, and inflammation.
> Serum iron (SI) had the strongest effect on serum ferritin elevation.
> The effect of the cell damage factor on serum ferritin indicated cell
> destruction, and that of the hepatic function factor represented
> decreased serum ferritin clearance. The cell damage factor also
> indirectly increased the ferritin level via SI or the hepatic
> function factor.
> The total effect of the inflammatory status factor on
> ferritin level was very weak.
> CONCLUSIONS:
> These causal relations may explain
> the mechanism of serum ferritin level elevation in various clinical
> conditions.
>
> PMID: 17292875 [PubMed - in process]
>
> -------------------------------
>
> Now WHY .. in these three DIFFERENT diseases .. does the drop of iron
> .. PARALLEL .. the drop in alanine aminotransferase (ALT) .. but in
> the
> disease of .. juvenile rheumatoid arthritis / Still's .. do they
> NOT ..
> use this marker .. WHEN .. iron HAS been shown to BE a ..
> problem .. ?
>
> Especially .. when they have such high liver injury rates. Two
> thirds.
>
> Stupidity .. ?
>
> <<snip>>
> There was a positive correlation between transaminases and serum
> ferritin
> <<snip>>
>
> J Nephrol. 2003 Sep-Oct; 16(5): 703-9. Related Articles, Links
>
> Comparative study of intravenous ascorbic acid versus low-dose
> desferroxamine
> in patients on hemodialysis with hyperferritinemia.
>
> Deira J, Diego J, Martinez R, Oyarbide A, Gonzalez A, Diaz H, Grande
> J.
>
> Department of Internal Medicine, Division of Nephrology, Hospital
> Virgen de la
> Concha, Zamora, Spain. jde...@saludalia . com
>
> BACKGROUND:
> In patients on hemodialysis (HD), parenteral iron improves the
> response to recombinant human erythropoietin (rhuEPO) therapy, but in
> some subjects it produces an iron overload, increasing their morbidity
> and
> mortality rates. In these cases, iron administration must be
> discontinued.
> This study aimed to investigate the efficiency of treatment with
> ascorbic
> acid (AA) or desferroxamine (DFO) to mobilize and reduce iron stores,
> and to
> determine the effect of these compounds on erythropoiesis.
> METHODS:
> We performed a prospective and randomized trial over 6 months, which
> included 27 patients with serum ferritin levels >800 ng/mL, TSAT >30%
> and stabilized hemoglobin (Hb) and rhuEPO doses.
> All patients had previously received parenteral iron (Ferlecit).
> Nine patients received 200 mg of intravenous (i.v.) AA 3 times/week
> and
> nine patients received 1 mg/Kg/week of DFO; the remaining nine
> patients
> were the control group.
> RESULTS:
> There were no significant differences in iron
> loss or mobilization due to dialysis. When Ferlecit was discontinued,
> functional iron did not vary and the epoetin resistance index
> (rhuEPO dose/Hb) was reduced by 21% in the i.v. AA group.
> In the DFO and control groups, functional iron levels fell.
> In the DFO group the epoetin resistance index increased by 20%,
> with no modifications in the control group.
> There was a positive correlation between transaminases and serum
> ferritin.
> CONCLUSIONS:
> In HD patients with an iron overload, neither i.v. AA administration
> or low-dose
> DFO increased iron mobilization or iron loss due to dialysis. I.v. AA
> administration
> allows elimination of iron from stores without any drop in the
> functional iron
> produced by discontinuing parenteral maintenance iron; it also
> improves
> the response to rhuEPO. DFO did not elicit any positive effects on
> erythropoiesis.
>
> PMID: 14733417 [PubMed - in process]
> ------
>
> <<snip>>
> The treatment reduced mean serum alanine aminotransferase (ALT)
> activity
> <<snip>>
>
> Effect of iron reduction by phlebotomy in Japanese patients with
> nonalcoholic steatohepatitis: A pilot study.
> Sumida Y, Kanemasa K, Fukumoto K, Yoshida N, Sakai K, Nakashima T,
> Okanoue T
> Hepatol Res. 2006 Sep 11;
>
> Increased hepatic iron deposition may play a role in the pathogenesis
> of nonalcoholic steatohepatitis (NASH). This study aimed to test
> whether iron removal by phlebotomy improves serum transaminase
> activities in patients with NASH. Eleven patients (six males and five
> females) with biopsy-proven NASH underwent phlebotomy biweekly until
> they reached near-iron deficiency (NID) (serum ferritin concentration
> lower than or equal to 30ng/ml). Nine patients completed this study.
> Serum ferritin levels in these patients fell from 563+/-322 to
> 18+/-9ng/ml (p=0.001). The treatment reduced mean serum alanine
> aminotransferase (ALT) activity from 126+/-47 to 56+/-17IU/l
> (p=0.002).
>
> Their weight did not change significantly throughout the study
> period.
> Although two patients withdrew from the study, none was affected by
> any
> side effects of repeated phlebotomy that required discontinuing the
> treatment. In conclusion, this pilot study suggests that iron
> reduction
> therapy by phlebotomy will be one of the promising therapies for
> NASH.
>
> -------------------------------------------------------------------------=
--
> <<snip>>
> Serum alanine aminotransferase levels were significantly improved
> <<snip>>
>
> Hepatogastroenterology. 2005 Mar-Apr;52(62):563-6. Related Articles,
> Links
>
> Additional effect of low iron diet on iron reduction therapy by
> phlebotomy for chronic hepatitis C.
>
> Kimura F, Hayashi H, Yano M, Yoshioka K, Matsumura T, Fukuda T,
> Shigeto
>
> N, Yamahara S, Koushi F, Mishima Y, Yoshino T, Tanimoto M, Kimura I.
>
> Department of Internal Medicine, Tamano-Municipal Hospital, Tamano
> City, Okayama, Japan. f-kim...@po1.oninet.ne.jp
>
> BACKGROUND/AIMS:
> Iron-induced oxidative stress plays an important role
> in the pathogenesis of chronic hepatitis C. Both phlebotomy for
> removing body iron stores and low iron diet for minimizing portal
> iron
> supply to the liver have been shown to improve serum transaminase
> levels in patients with the disease. However, the cooperative effects
> of phlebotomy and low iron diet have not yet been elucidated in
> detail.
>
> METHODOLOGY:
> A pilot study was undertaken to investigate whether a low
> iron diet could improve the efficacy of phlebotomy in iron reduction
> therapy. Of 21 patients diagnosed with chronic hepatitis C, 10
> patients
> were treated with phlebotomy alone (group A) while 11 patients were
> treated with a low iron plus phlebotomy (group B). Phlebotomy was
> repeated biweekly until serum ferritin levels reached 10 ng/mL in
> both
> A and B groups. In addition, a low iron diet (iron intake of 8 mg/day
> or less) was recommended for group B, followed by estimation of iron
> intake from daily diet records.
>
> RESULTS:
> Serum alanine aminotransferase
> levels were significantly improved from 106+/-30 to 68+/-22 IU/L
> (p<0.005, paired t-test) in group A and from 100+/-33 to 46+/-10 IU/L
> (p<0.002, paired t-test) in group B. The enzyme levels after
> treatment
> were significantly higher in group A (p<0.02, non-paired t-test),
> which
> showed a higher upward distribution of the enzyme activity. The
> estimated dietary iron intake in group B was reduced from 17.6+/-6.1
> to
> 8.2+/-3.7 mg/day.
>
> CONCLUSIONS:
> These findings suggest that phlebotomy
> alone does not completely remove iron-induced oxidative stress and a
> low iron diet induces an additional effect in iron reduction therapy
> for chronic hepatitis C.
>
> PMID: 15816478 [PubMed - in process]
>
> -------------------------------------------------------------------------=
-------
>
> Who loves ya.
> Tom
>
> Jesus Was A Vegetarian! * jesuswasavegetarian.7h . com
>
> Man Is A Herbivore! * tinyurl . com /a3cc3
>
> DEAD PEOPLE WALKING * tinyurl . com /zk9fk

You may be confusing a side effect with the cause.

V

Re: Novel Biomarkers in Autoimmune Diseases

On Nov 14, 4:25 pm, crinoidgirl <virginialsm...@gmail . com > wrote:You
may be confusing a side effect with the cause. <<

That is if you forget science and the overwhelming .. evidence.

Oxidation is the underlying cause of every disease it .. seems /
Harmon / Pauling , etc.

Now how and why would there BE so much oxidation in an animal?

The bodies .. immune system firing off right and left .. ?

That is a possible .. consequence .. as ALL.. **all** .. disease IS.

The immune system begins to fire / oxidation at itself.

The skin begins to turn to elephant hide.

The eyes get so bad they cannot stand the light.

You get cancer and it eats you alive.

You get flesh eating disease and it too eats you alive.

The iron has to be addressed so it can now be removed from the
scenario.

They believe the hyper-ferritinemia to be .. a .. "marker for
inflammation" and to be .. "disregarded" and have NEVER really used it
for .. anything OTHER than a marker of inflammation.

NOW with people WATCHING for whatever reason .. voila .. there is no
iron deficiency in the world.

There is starvation .. there are people / children dying skinny to the
bone .. and they are NOT deficient in iron.

'They' .. will TELL you they are and they will feed them mush with
iron IN it and kill the kids and say .. ""oh oh aren't we all
wonderful" ..

THAT is PRECISELY what they say .. and still say and continue to
say .. look look how active this kid is .. hyperactive.

Who loves ya.
Tom


Jesus Was A Vegetarian! * jesuswasavegetarian.7h . com


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> On Nov 12, 6:15 pm, ironjustice <teamtan...@hotmail . com > wrote:
>
> > "Hyperferritinemia was detected in 23% of SLE patients, 15% of DM
> > patients, 8% of MS patients, and 4% of RA patients."
>
> > WHEN 'they' actually SEE / recognise this iron / ferritin it is
> > rather .. high / hyperferritinemia .
> > Seeing that they HAVE seen it now at such a HIGH rate makes one wonder
> > how many DO have .. high ferritin / hyperferritinemia / high iron.
> > Everyone has ALSO low levels of vitamin D which is ..
> > coincidentally .. destroyed / depleted by iron.
> > They say this high ferritin / hyperferritinemia / high iron may be
> > used as an "acute-phase reactant marker" but fail to say it also
> > PREVENTS someone from being diagnosed with iron overload.
>
> > In Stills' disease it has ALWAYS been used to disregard the
> > POSSIBILITY of iron and recently has been found to be USELESS in
> > Stills' and when the second marker is used .. ?
> > They have iron overload.
>
> > Are they killing .. you .. too .. ?
> > ------------------------------------------------------
> > "Hyperferritinemia was detected in 23% of SLE patients, 15% of DM
> > patients, 8% of MS patients, and 4% of RA patients."
>
> > Novel Biomarkers in Autoimmune Diseases
> > Authors: ORBACH, HEDI1; ZANDMAN-GODDARD, GISELE; AMITAL, HOWARD;
> > BARAK, VIVIAN2; SZEKANECZ, ZOLTAN3; SZUCS, GABRIELLA3; DANKO,
> > KATALIN3; NAGY, ENDRE4; CSEPANY, TUNDE5; CARVALHO, JOZELIO F.6; DORIA,
> > ANDREA7; SHOENFELD, YEHUDA
>
> > Source: Annals of the New York Academy of Sciences, Volume 1109,
> > Number 1, August 2007 , pp. 385-400(16)
>
> > Abstract:
>
> > The development of autoimmune diseases may be influenced by hormonal,
> > immunomodulatory, and metabolic pathways. Prolactin (PRL), ferritin,
> > vitamin D, and the tumor marker tissue polypeptide antigen (TPA) were
> > measured in autoimmune diseases: systemic lupus erythematosus (SLE),
> > systemic sclerosis (SSc), rheumatoid arthritis (RA), polymyositis
> > (PM), dermatomyositis (DM), multiple sclerosis (MS), autoimmune
> > thyroid diseases, and antiphospholipid syndrome. Hyperprolactinemia
> > (HPRL) was detected in 24% of PM patients, in 21% of SLE patients, in
> > 6.7% of MS patients, 6% of RA patients, and in 3% of SSc patients.
> > Hyperferritinemia was detected in 23% of SLE patients, 15% of DM
> > patients, 8% of MS patients, and 4% of RA patients. The patients had
> > relatively low levels of 25 OH Vitamin D: the average results (mean ±
> > SD) were between 9.3 ± 4.4 to 13.7 ± 7.1 ng/mL in the different
> > diseases, while the 25 OH Vitamin D concentrations less than 20 ng/mL
> > are regarded as deficient. TPA levels were in the same range of the
> > controls, elevated only in SLE. HPRL, hyperferritinemia,
> > hypovitaminosis D, and TPA levels did not correlate with SLE activity
> > elevated levels of rheumatoid factor or anti-CCP antibodies in RA.
> > HPRL, hyperferritinemia, and hypovitaminosis D have different
> > immunological implications in the pathogenesis of the autoimmune
> > diseases. Preventive treatment with vitamin D or therapy for HPRL with
> > dopamine agonists, may be considered in certain cases.
> > Hyperferritinemia may be used as an acute-phase reactant marker in
> > autoimmune diseases mainly SLE. TPA may be used to indicate the
> > tendency for malignancies.
> > Keywords: prolactin; ferritin; vitamin D; tissue polypeptide antigen;
> > TPA; SLE; rheumatoid arthritis; multiple sclerosis; polymyositis;
> > dermatomyositis
>
> > Document Type: Research article
>
> > DOI: 10.1196/annals.1398.044
>
> > Affiliations: 1: Department of Medicine B, Wolfson Medical Center,
> > Holon, Israel 2: Immunology Lab for Tumor Diagnosis, Hadassah-Hebrew
> > University Medical Center, Jerusalem, Israel 3: Third Department of
> > Medicine, University of Debrecen Medical and Health Science Center,
> > Debrecen, Hungary 4: First Department of Medicine, University of
> > Debrecen Medical and Health Science Center, Debrecen, Hungary 5:
> > Neurology Department, University of Debrecen Medical and Health
> > Science Center, Debrecen, Hungary 6: Rheumatology Division, Sao Paulo
> > University Medical School Hospital, Sao Paulo, SP, Brazil 7: Division
> > of Rheumatology and Department of Clinical and Experimental Medicine,
> > University of Padova, Padova, Italy
> > --------------------------------
>
> > These guys seem to think the hyperferritinemia is NOT governed by
> > inflammation THAT much and thusly it is to BE used as a marker of iron
> > OVERLOAD.
>
> > <<snip>>
> > effect of the inflammatory status factor on ferritin level was very
> > weak.
> > <<snip>>
> > <<snip>>
> > Serum iron (SI) had the strongest effect on serum ferritin elevation
> > <<snip>>
>
> > Clin Biochem. 2007 Mar;40(5-6):359-64. Epub 2007 Jan 5. Links
> > Evaluation of a model of latent pathologic factors in relation to
> > serum ferritin elevation.
> > Yamanishi H, Kimura S, Hata N, Iyama S, Kanakura Y, Iwatani Y.
> > Laboratory for Clinical Investigation, Osaka University Hospital,
> > 2-15
> > Yamadaoka, Suita, Osaka 565-0871, Japan. yam...@hp-lab.med.osaka-
> > u.ac.jp
>
> > OBJECTIVES:
> > Serum ferritin increases in various disorders and clinical
> > conditions. However, causal associations between the serum ferritin
> > level and clinical factors that influence serum ferritin level are
> > not well characterized. We report a model that quantitatively
> > analyzes
> > the causal relations between the serum ferritin level and clinical
> > factors.
> > DESIGN AND METHODS:
> > We analyzed the ferritin level and other
> > laboratory data in the sera of 274 patients. Structural equation
> > modeling was used to verify causal relations and the adequacy of
> > latent factors.
> > RESULTS:
> > Three factors representing clinical status
> > were identified: cell damage, hepatic function, and inflammation.
> > Serum iron (SI) had the strongest effect on serum ferritin elevation.
> > The effect of the cell damage factor on serum ferritin indicated cell
> > destruction, and that of the hepatic function factor represented
> > decreased serum ferritin clearance. The cell damage factor also
> > indirectly increased the ferritin level via SI or the hepatic
> > function factor.
> > The total effect of the inflammatory status factor on
> > ferritin level was very weak.
> > CONCLUSIONS:
> > These causal relations may explain
> > the mechanism of serum ferritin level elevation in various clinical
> > conditions.
>
> > PMID: 17292875 [PubMed - in process]
>
> > -------------------------------
>
> > Now WHY .. in these three DIFFERENT diseases .. does the drop of iron
> > .. PARALLEL .. the drop in alanine aminotransferase (ALT) .. but in
> > the
> > disease of .. juvenile rheumatoid arthritis / Still's .. do they
> > NOT ..
> > use this marker .. WHEN .. iron HAS been shown to BE a ..
> > problem .. ?
>
> > Especially .. when they have such high liver injury rates. Two
> > thirds.
>
> > Stupidity .. ?
>
> > <<snip>>
> > There was a positive correlation between transaminases and serum
> > ferritin
> > <<snip>>
>
> > J Nephrol. 2003 Sep-Oct; 16(5): 703-9. Related Articles, Links
>
> > Comparative study of intravenous ascorbic acid versus low-dose
> > desferroxamine
> > in patients on hemodialysis with hyperferritinemia.
>
> > Deira J, Diego J, Martinez R, Oyarbide A, Gonzalez A, Diaz H, Grande
> > J.
>
> > Department of Internal Medicine, Division of Nephrology, Hospital
> > Virgen de la
> > Concha, Zamora, Spain. jde...@saludalia . com
>
> > BACKGROUND:
> > In patients on hemodialysis (HD), parenteral iron improves the
> > response to recombinant human erythropoietin (rhuEPO) therapy, but in
> > some subjects it produces an iron overload, increasing their morbidity
> > and
> > mortality rates. In these cases, iron administration must be
> > discontinued.
> > This study aimed to investigate the efficiency of treatment with
> > ascorbic
> > acid (AA) or desferroxamine (DFO) to mobilize and reduce iron stores,
> > and to
> > determine the effect of these compounds on erythropoiesis.
> > METHODS:
> > We performed a prospective and randomized trial over 6 months, which
> > included 27 patients with serum ferritin levels >800 ng/mL, TSAT >30%
> > and stabilized hemoglobin (Hb) and rhuEPO doses.
> > All patients had previously received parenteral iron (Ferlecit).
> > Nine patients received 200 mg of intravenous (i.v.) AA 3 times/week
> > and
> > nine patients received 1 mg/Kg/week of DFO; the remaining nine
> > patients
> > were the control group.
> > RESULTS:
> > There were no significant differences in iron
> > loss or mobilization due to dialysis. When Ferlecit was discontinued,
> > functional iron did not vary and the epoetin resistance index
> > (rhuEPO dose/Hb) was reduced by 21% in the i.v. AA group.
> > In the DFO and control groups, functional iron levels fell.
> > In the DFO group the epoetin resistance index increased by 20%,
> > with no modifications in the control group.
> > There was a positive correlation between transaminases and serum
> > ferritin.
> > CONCLUSIONS:
> > In HD patients with an iron overload, neither i.v. AA administration
> > or low-dose
> > DFO increased iron mobilization or iron loss due to dialysis. I.v. AA
> > administration
> > allows elimination of iron from stores without any drop in the
> > functional iron
> > produced by discontinuing parenteral maintenance iron; it also
> > improves
> > the response to rhuEPO. DFO did not elicit any positive effects on
> > erythropoiesis.
>
> > PMID: 14733417 [PubMed - in process]
> > ------
>
> > <<snip>>
> > The treatment reduced mean serum alanine aminotransferase (ALT)
> > activity
> > <<snip>>
>
> > Effect of iron reduction by phlebotomy in Japanese patients with
> > nonalcoholic steatohepatitis: A pilot study.
> > Sumida Y, Kanemasa K, Fukumoto K, Yoshida N, Sakai K, Nakashima T,
> > Okanoue T
> > Hepatol Res. 2006 Sep 11;
>
> > Increased hepatic iron deposition may play a role in the pathogenesis
> > of nonalcoholic steatohepatitis (NASH). This study aimed to test
> > whether iron removal by phlebotomy improves serum transaminase
> > activities in patients with NASH. Eleven patients (six males and five
> > females) with biopsy-proven NASH underwent phlebotomy biweekly until
> > they reached near-iron deficiency (NID) (serum ferritin concentration
> > lower than or equal to 30ng/ml). Nine patients completed this study.
> > Serum ferritin levels in these patients fell from 563+/-322 to
> > 18+/-9ng/ml (p=0.001). The treatment reduced mean serum alanine
> > aminotransferase (ALT) activity from 126+/-47 to 56+/-17IU/l
> > (p=0.002).
>
> > Their weight did not change significantly throughout the study
> > period.
> > Although two patients withdrew from the study, none was affected by
> > any
> > side effects of repeated phlebotomy that required discontinuing the
> > treatment. In conclusion, this pilot study suggests that iron
> > reduction
> > therapy by phlebotomy will be one of the promising therapies for
> > NASH.
>
> > ------------------------------------------------------------------------=
---
> > <<snip>>
> > Serum alanine aminotransferase levels were significantly improved
> > <<snip>>
>
> > Hepatogastroenterology. 2005 Mar-Apr;52(62):563-6. Related Articles,
> > Links
>
> > Additional effect of low iron diet on iron reduction therapy by
> > phlebotomy for chronic hepatitis C.
>
> > Kimura F, Hayashi H, Yano M, Yoshioka K, Matsumura T, Fukuda T,
> > Shigeto
>
> > N, Yamahara S, Koushi F, Mishima Y, Yoshino T, Tanimoto M, Kimura I.
>
> > Department of Internal Medicine, Tamano-Municipal Hospital, Tamano
> > City, Okayama, Japan. f-kim...@po1.oninet.ne.jp
>
> > BACKGROUND/AIMS:
> > Iron-induced oxidative stress plays an important role
> > in the pathogenesis of chronic hepatitis C. Both phlebotomy for
> > removing body iron stores and low iron diet for minimizing portal
> > iron
> > supply to the liver have been shown to improve serum transaminase
> > levels in patients with the disease. However, the cooperative effects
> > of phlebotomy and low iron diet have not yet been elucidated in
> > detail.
>
> > METHODOLOGY:
> > A pilot study was undertaken to investigate whether a low
> > iron diet could improve the efficacy of phlebotomy in iron reduction
> > therapy. Of 21 patients diagnosed with chronic hepatitis C, 10
> > patients
> > were treated with phlebotomy alone (group A) while 11 patients were
> > treated with a low iron plus phlebotomy (group B). Phlebotomy was
> > repeated biweekly until serum ferritin levels reached 10 ng/mL in
> > both
> > A and B groups. In addition, a low iron diet (iron intake of 8 mg/day
> > or less) was recommended for group B, followed by estimation of iron
> > intake from daily diet records.
>
> > RESULTS:
> > Serum alanine aminotransferase
> > levels were significantly improved from 106+/-30 to 68+/-22 IU/L
> > (p<0.005, paired t-test) in group A and from 100+/-33 to 46+/-10 IU/L
> > (p<0.002, paired t-test) in group B. The enzyme levels after
> > treatment
> > were significantly higher in group A (p<0.02, non-paired t-test),
> > which
> > showed a higher upward distribution of the enzyme activity. The
> > estimated dietary iron intake in group B was reduced from 17.6+/-6.1
> > to
> > 8.2+/-3.7 mg/day.
>
> > CONCLUSIONS:
> > These findings suggest that phlebotomy
> > alone does not completely remove iron-induced oxidative stress and a
> > low iron diet induces an additional effect in iron reduction therapy
> > for chronic hepatitis C.
>
> > PMID: 15816478 [PubMed - in process]
>
> > ------------------------------------------------------------------------=
------------
>
> > Who loves ya.
> > Tom
>
> > Jesus Was A Vegetarian! * jesuswasavegetarian.7h . com
>
> > Man Is A Herbivore! * tinyurl . com /a3cc3
>
> > DEAD PEOPLE WALKING * tinyurl . com /zk9fk
>
> You may be confusing a side effect with the cause.
>
> V