Seems .. hyperferritinemia .. does NOT .. "evidence inflammation" ..

Increased ferritin / hyperferritinemia has been used and IS used to
assess .. "infammatory states" .. and this marker has been used to
avoid .. iron depletion therapy .. BUT .. now .. it seems it has very
little .. use .. AS .. an inflammatory .. marker ..

Thereby effectively allowing the assessment of INCREASED iron to be
assessed BY .. iron / ferritin .. ALONE ..

Therefore .. since Still's disease USES .. hyperferritinemia TO ..
diagnose .. disease states .. it has NOW been rendered veritably
USELESS .. and thusly ruling IN .. iron OVERLOAD .. in .. Juvenile
Rheumatoid Arthritis ..

Whoda .. thunk ..

<<snip>>
effect of the inflammatory status factor on ferritin level was very
weak.
<<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]


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Sooo .. this study makes sense .. NOW .. since hyperferritinemia
EXISTS .. in juvenile rheumatoid arthritis .. and hyperferritinemia
has ALWAYS been used .. to say .. "there is no iron in these kids" ..
when in fact .. PAIN .. was **never used** AS a .. marker ..
obviously.

Sort of how they fail to use .. DB's .. as a .. marker ..

EXPERIMENTAL BIOLOGY UPDATE: Arthritic kids' iron supplements may
hasten joint
deterioration


By Diana Swift


WWASHINGTON, D.C. - The iron supplements that many arthritic children
take to
combat concomitant anemia may be hastening the deterioration of their
joints,
Houston researchers say.


Led by biologist Roman Shypailo of the Children's Nutrition Research
Centre at
Baylor College of Medicine, a Texas team looked at eight children
being treated
for juvenile rheumatoid arthritis. The patients, aged five to 15
years,
received an intravenous radioactive tracer dose of iron (0.03
microsievert).
Iron activity in affected joints was monitored on a position/energy-
sensitive
gamma counter, while a second machine monitored whole-body iron
retention. Iron
deposition was measured two hours post-infusion and again at days
seven, 14, 28
and 56.


Anemic
"We found that iron excessively accumulates in arthritic joints and
probably
contributes to the chronic damage," said Shypailo. "That puts you
between a
rock and a hard place because many of these arthritic kids are anemic
and need
iron supplements, which may worsen the disease."


The study found a high level of agreement between the joint data and
the
whole-body data, with a greater than 90% retention rate of the infused
iron
both in joints and systemically. Furthermore, six of eight patients
showed
increased uptake at the affected joints: 165% over the first 30 days
compared
with initial uptake at two hours.


The next step, he says, is to see if there is excessive deposition of
dietary
iron in arthritic joints.


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


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Tom


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http://jesuswasavegetarian.7h.com


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


DEAD PEOPLE WALKING
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On 14 Apr 2007 11:21:47 -0700, "ironjustice" 
wrote:

>Seems .. hyperferritinemia .. does NOT .. "evidence inflammation" ..

charter abuse reports to abuse@telus.com

hemoglobin [hemo + L. globus, globe]

 The iron-containing pigment of red blood cells that carries oxygen from
 the lungs to the tissues.  The amount of hemoglobin in the blood
 averages 16 g/100 ml in women, 14 to 18 g/100 ml in men.  Hemoglobin
 is a crystallizable, conjugated protein consisting of heme, an iron-
 containing pigment, and globin, a simple protein.  In the lungs, 1 g of
  hemoglobin combines readily with 1.36 cc of oxygen, by a process
 called oxygenation, to form oxyhemoglobin, an unstable compound.
 In the tissues where oxygen concentration is low and carbon dioxide
 concentration is high [low pH], hemoglobin releases its oxygen.
 Hemoglobin also acts as a buffer for the hydrogen ions produced in red
 blood cells when carbon dioxide is converted to bicarbonate ions for
 transport in the plasma.

 When old RBCs are phagocytized by macrophages in the liver, spleen,
 and red bone marrow, the iron of hemoglobin is resused immediately to
 produce new RBCs or is stored in the liver until needed.  The globin is
 converted to animo acids for the synthesis of other proteins.  The heme
 portion is of no further use and is converted to bilirubin, a bile
 pigment excreted by the liver in bile.

 Hemoglobin combines with carbon monoxide to form the stable compound
 carboxyhemoglobin, which renders hemoglobin unable to bond with oxygen
 and results in hypoxia of tissues.  Oxidation of the ferrous iron or
 hemoglobin to the ferric state produces methemoglobin.

 Hundreds of different types of hemoglobin have been discovered.  Some
 of these, such as hemoglobin S, are described in subentries that
 follow.

 h.Atc...Hemoblogin A that contains a glucose group linked to the
 terminal animo acid of the beta chains of the molecule.

 h.C disease...A genetic variant of the hemoglobin molecule that causes
 a chronic hemolytic anemia.

 h.E disease...A genetic variant of hemoglobin that produces a mild form
 of hemolytic anemia.  It is primarily in persons of SE Asian origin, in
 whom it may provide protection against falciparum malaria.

 h.H disease...A genetic variant of hemoglobin that causes a chronic
 hemolytic anemia.

 h.M disorder...A genetic variant of hemoglobin that causes cyanosis and
 methemoglobinemia.

 h.S disease...A genetic variant of hemoglobin that causes sickle cell
 trait in heterozygotes, and sickle cell disease in hemozygotes.  It is
 common, especially in persons of African ancestry in whom sickle cell
 trait is found in 8%-10% of the population.

 h.SC disease...A disease of persons who have inherited two abnormal
 forms of hemoglobin, S and C.  Affected person my have vaso-occlusive
 crises similar to those seen in sickle cell anemia, with bony and
 viaceral infarcts.

"california_chief"  wrote in message
news:9rCTh.44499$EJ6.8897@newsfe24.lga...
> hemoglobin [hemo + L. globus, globe]
>
>  The iron-containing pigment of red blood cells that carries oxygen from
>  the lungs to the tissues.  The amount of hemoglobin in the blood
>  averages 16 g/100 ml in women, 14 to 18 g/100 ml in men.  Hemoglobin
>  is a crystallizable, conjugated protein consisting of heme, an iron-
>  containing pigment, and globin, a simple protein.  In the lungs, 1 g of
>   hemoglobin combines readily with 1.36 cc of oxygen, by a process
>  called oxygenation, to form oxyhemoglobin, an unstable compound.
>  In the tissues where oxygen concentration is low and carbon dioxide
>  concentration is high [low pH], hemoglobin releases its oxygen.
>  Hemoglobin also acts as a buffer for the hydrogen ions produced in red
>  blood cells when carbon dioxide is converted to bicarbonate ions for
>  transport in the plasma.
>
>  When old RBCs are phagocytized by macrophages in the liver, spleen,
>  and red bone marrow, the iron of hemoglobin is resused immediately to
>  produce new RBCs or is stored in the liver until needed.  The globin is
>  converted to animo acids for the synthesis of other proteins.  The heme
>  portion is of no further use and is converted to bilirubin, a bile
>  pigment excreted by the liver in bile.
>
>  Hemoglobin combines with carbon monoxide to form the stable compound
>  carboxyhemoglobin, which renders hemoglobin unable to bond with oxygen
>  and results in hypoxia of tissues.  Oxidation of the ferrous iron or
>  hemoglobin to the ferric state produces methemoglobin.
>
>  Hundreds of different types of hemoglobin have been discovered.  Some
>  of these, such as hemoglobin S, are described in subentries that
>  follow.
>
>  h.Atc...Hemoblogin A that contains a glucose group linked to the
>  terminal animo acid of the beta chains of the molecule.
>
>  h.C disease...A genetic variant of the hemoglobin molecule that causes
>  a chronic hemolytic anemia.
>
>  h.E disease...A genetic variant of hemoglobin that produces a mild form
>  of hemolytic anemia.  It is primarily in persons of SE Asian origin, in
>  whom it may provide protection against falciparum malaria.
>
>  h.H disease...A genetic variant of hemoglobin that causes a chronic
>  hemolytic anemia.
>
>  h.M disorder...A genetic variant of hemoglobin that causes cyanosis and
>  methemoglobinemia.
>
>  h.S disease...A genetic variant of hemoglobin that causes sickle cell
>  trait in heterozygotes, and sickle cell disease in hemozygotes.  It is
>  common, especially in persons of African ancestry in whom sickle cell
>  trait is found in 8%-10% of the population.
>
>  h.SC disease...A disease of persons who have inherited two abnormal
>  forms of hemoglobin, S and C.  Affected person my have vaso-occlusive
>  crises similar to those seen in sickle cell anemia, with bony and
>  viaceral infarcts.
>
>
>
>
>
very nice;)))
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<<<<
at first I was surprised, honestly