Iron / hepatitis C

The more interesting question is why hep c cause more iron
to be stored in the liver. Iron doesn't cause hep c, but if
you have hep c the more advanced the disease the more iron
is caused to be stored.

Quoted message said:

Am J Gastroenterol. 2004 Feb;99(2):286-91. Links

Clinical significance of hepatic iron deposition and serum
iron values in patients with chronic hepatitis C infection.

Metwally MA, Zein CO, Zein NN.

Division of Gastroenterology and Hepatology and Internal
Medicine, Mayo Clinic, Rochester, Minnesota, USA.

OBJECTIVES: To assess the potential association between
hepatic iron deposition or serum iron values and hepatic
fibrosis and inflammatory activity in patients with chronic
hepatitis C virus infection. METHODS: In 100 consecutive
patients with hepatitis C virus infection, tissue iron
deposition was assessed by quantifying iron stain on liver
biopsy specimens. Serum iron, ferritin, and transferrin
saturation were determined by standard laboratory
procedures. Statistical analyses incorporated potential
confounders associated with hepatic fibrosis. RESULTS: Twenty-
one patients had no fibrosis (stage 0), 13 had portal
fibrosis (stage 1), 31 had periportal fibrosis (stage II),
10 had bridging fibrosis (stage III), and 25 had cirrhosis
(stage IV). Positive iron stain found in liver biopsy
specimens of 19 patients was associated with stage III or
IV fibrosis (p = 0.004). No significant difference was
found between the iron concentration or the hepatic iron
index in patients with stage III or IV fibrosis compared
with patients with stage I or II fibrosis. At least 1 of 3
serum iron values assessed was abnormal in 55 patients. In
univariate analysis, elevated serum iron (p = 0.01), serum
ferritin (p < 0.001), and transferrin saturation (p =
0.002) were associated with stage III or IV fibrosis. In
multivariate analysis, the only independent predictive
factor of severe hepatic fibrosis was serum ferritin (p <
0.02; odds ratio = 11.35). The serum ferritin value and
tissue iron stain had a significant positive correlation (p
< 0.001). CONCLUSIONS: Increased hepatic iron deposition
may be associated with more advanced hepatic fibrosis in
patients with chronic hepatitis C virus infection. The
serum ferritin value, an independent predictor of severe
hepatic fibrosis in patients with chronic hepatitis C virus
infection, may predict hepatic iron deposition and severity
of fibrosis.

PMID: 15046219 [PubMed - in process]

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Quoted message said:

Subject: Re: Iron / hepatitis C
From: [email hidden]
Date: 3/30/2004 9:19 AM Mountain Standard Time
Message-id: <[email hidden]>

The more interesting question is why hep c cause more iron
to be stored in the liver. Iron doesn't cause hep c, but if
you have hep c the more advanced the disease the more iron
is caused to be stored.

Actually no 'question' .. NEEDS to be addressed ..

Iron deposition .. NEEDS to be addressed ..

Simple .. as .. that ..

Quoted message said:

Quoted message said:

Am J Gastroenterol. 2004 Feb;99(2):286-91. Links

Clinical significance of hepatic iron deposition and serum
iron values in patients with chronic hepatitis C
infection.

Metwally MA, Zein CO, Zein NN.

Division of Gastroenterology and Hepatology and Internal
Medicine, Mayo

Clinic,

Quoted message said:

Rochester, Minnesota, USA.

OBJECTIVES: To assess the potential association between
hepatic iron

deposition

Quoted message said:

or serum iron values and hepatic fibrosis and inflammatory
activity in

patients

Quoted message said:

with chronic hepatitis C virus infection. METHODS: In 100
consecutive

patients

Quoted message said:

with hepatitis C virus infection, tissue iron deposition
was assessed by quantifying iron stain on liver biopsy
specimens. Serum iron, ferritin, and transferrin
saturation were determined by standard laboratory
procedures. Statistical analyses incorporated potential
confounders associated with

hepatic

Quoted message said:

fibrosis. RESULTS: Twenty-one patients had no fibrosis
(stage 0), 13 had

portal

Quoted message said:

fibrosis (stage 1), 31 had periportal fibrosis (stage II),
10 had bridging fibrosis (stage III), and 25 had cirrhosis
(stage IV). Positive iron stain found in liver biopsy
specimens of 19 patients was associated with stage III

or

Quoted message said:

IV fibrosis (p = 0.004). No significant difference was
found between the

iron

Quoted message said:

concentration or the hepatic iron index in patients with
stage III or IV fibrosis compared with patients with stage
I or II fibrosis. At least 1 of 3 serum iron values
assessed was abnormal in 55 patients. In univariate

analysis,

Quoted message said:

elevated serum iron (p = 0.01), serum ferritin (p <
0.001), and transferrin saturation (p = 0.002) were
associated with stage III or IV fibrosis. In multivariate
analysis, the only independent predictive factor of severe

hepatic

Quoted message said:

fibrosis was serum ferritin (p < 0.02; odds ratio =
11.35). The serum

ferritin

Quoted message said:

value and tissue iron stain had a significant positive
correlation (p <

.001).

Quoted message said:

CONCLUSIONS: Increased hepatic iron deposition may be
associated with more advanced hepatic fibrosis in patients
with chronic hepatitis C virus

infection.

Quoted message said:

The serum ferritin value, an independent predictor of
severe hepatic

fibrosis

Quoted message said:

in patients with chronic hepatitis C virus infection, may
predict hepatic

iron

Quoted message said:

deposition and severity of fibrosis.

PMID: 15046219 [PubMed - in process]

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

Who loves ya. Tom

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Quoted message said:

<[email hidden]> wrote The more interesting question
is why hep c cause more iron to be stored in the liver.
Iron doesn't cause hep c, but if you have hep c the more
advanced the disease the more iron is caused to be stored.

... This is common with any congestive liver disease, no
matter whether the cause is hepatitis, alcohol, or taking
too much Tylenol. In addition to iron, manganese storage
increases as well. When "doe" keeps posting abstracts
linking high iron to diabetes, it is really manganese that
is actively involved in that relationship, not iron.
However, an increase in iron (being associated with
manganese) just happens to be a secondary effect.

Quoted message said:

Subject: Re: Iron / hepatitis C

Quoted message said:

Date: 3/30/2004 6:07 PM Mountain Standard Time Message-id:
<[email hidden]>

Quoted message said:

<[email hidden]> wrote The more interesting question
is why hep c cause more iron to be stored in the liver.
Iron doesn't cause hep c, but if you have hep c the more
advanced the disease the more iron is caused to be
stored.

... This is common with any congestive liver disease, no
matter whether the cause is hepatitis, alcohol, or taking
too much Tylenol. In addition to iron, manganese storage
increases as well. When "doe" keeps posting abstracts
linking high iron to diabetes, it is really manganese that
is actively involved in that relationship, not iron.
However, an increase in iron (being associated with
manganese) just happens to be a secondary effect.

tinyurl.com282rqOpen ↗

Yep .. for .. sure ..

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Tom you missed the ccentral point, iron stores and diabetes
is a 2nd step removed responce to other things. The cross
talk article says nothing to the contrary and it was
specifically delt with here before. This is the main flaw of
your thesis which demands that iron be the clear cause of
human diseases/disorders and abstract after abstract you
post shows it is not. In fact in the very post to which you
respond, it was another substance which caused the iron
storage all of which was first caused by hep c. Your thesis
has completly failed based on the very data you have
presented many times, congratulations.

Quoted message said:

Subject: Re: Iron / hepatitis C
From: [email hidden]
Date: 3/31/2004 8:46 AM Mountain Standard Time
Message-id: <[email hidden]>

Tom you missed the ccentral point, iron stores and diabetes
is a 2nd step removed responce to other things. The cross
talk article says nothing to the contrary and it was
specifically delt with here before. This is the main flaw
of your thesis which demands that iron be the clear cause
of human diseases/disorders and abstract after abstract you
post shows it is not. In fact in the very post to which you
respond, it was another substance which caused the iron
storage all of which was first caused by hep c. Your thesis
has completly failed based on the very data you have
presented many times, congratulations.

I subscribe to evidence based medicine ..

Removal of iron leads to halting of liver cirrhosis ..

Removal of iron leads to normalization of Hepatitis C
liver panels ..

See dictionary for meaning of the above ..

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Ok, let's play, show us the evidence for this:

"Removal of iron leads to normalization of Hepatitis C liver
panels .."

Quoted message said:

Subject: Re: Iron / hepatitis C
From: [email hidden]
Date: 3/31/2004 10:45 AM Mountain Standard Time
Message-id: <[email hidden]>

Ok, let's play, show us the evidence for this:

Play ..?

That IS what it is to you ..

Isn't it .. ya .. creepy .. lttle .. fk ..

Quoted message said:

"Removal of iron leads to normalization of Hepatitis C
liver panels .."

archive.mail-list.commsg03159.htmlOpen ↗

The mean serum levels of ALT, in the phlebotomy group, fell
from 117 to 75 IU/L and remained less than 72 IU/L for the
ensuing 5 yr, during which time additional phlebotomies were
needed every 8 months or so to maintain an iron-depleted
state. There were no adverse effects of chronic iron
reduction.

Of greatest importance, the severity of fibrosis (by
the Desmet scoring system) in the iron reduction
group decreased from 2.3 to 1.7 (p < .05), whereas in
controls the mean values were 1.7 at baseline and 2.0
at follow-up (p > 0.05, ns). Furthermore, the
severity of inflammation increased in only one of 13
of the chronic iron reduction group (unchanged in
12/13; mean values = 1.8 and 2.0, p > 0.05), whereas
it increased in
12/13 controls (unchanged in the 13th) (mean values = 2.0
and 2.9, p < .005).

The authors concluded that long term maintenance of
iron depletion by therapeutic phlebotomy prevents
progression of fibrosis in CHC. They suggest that
chronic iron reduction is a good alternative to
interferon in treatment of CHC. To these positive
results may be added recent reports of decreases in
serum -fetoprotein (29) and less frequent development
of hepatocellular carcinoma (HCC) (30) in small groups
of patients with CHC chronically treated with iron
reduction. The notion that iron in the liver is a risk
factor for HCC is supported by the known
cocarcinogenicity of iron (10) and by a recent report
showing a 5.2-fold increased risk of HCC development
in patients with cirrhotic CHC and hepatic iron
deposition relative to those without (31).

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Quoted message said:

Quoted message said:

This is common with any congestive liver disease, no
matter whether the cause is hepatitis, alcohol, or taking
too much Tylenol. In addition to iron, manganese storage
increases as well. When "doe" keeps posting abstracts
linking high iron to diabetes, it is really manganese
that is actively involved in that relationship, not iron.
However, an increase in iron (being associated with
manganese) just happens to be a secondary effect.

"doe" <[email hidden]> wrote
tinyurl.com282rqOpen ↗

Yep .. for .. sure ..

... With phlebotomies or most other iron-lowering
interventions, you automatically also lower manganese, hence
the effect on glucose metabolism. If you were to selectively
lower manganese *without* lowering iron, you would get the
same positive effect.

Impaired liver functions precede excessive iron AND
manganese storage, so unless you know how to manipulate
liver chemistry to lower one without lowering the other, the
approach used in the studies you posted affects both trace
minerals simultaneously.

It's like reducing your daily caloric intake, but
advertising the weight loss as being due to a reduction in
[choose your favorite one] carbs, fat, or protein only.

Intresting, let's continue to play. What does this editoral
by the author, I read it all, suggest about your thesis
about iron being the source of human diseases/disorders and
what do you make of the limitations he notes of the
research to which he referes on your thesis? How do you
account for the majority who responded to meds but didn't
have their iron liver levels lowered, which suggests that
what ever role iron plays in the course of the disease it
is not the cause of it and treatment works in spite of the
iron? What do you make of his observation that the
processes he reviews are found only in a subset of hep b/c
cases and that the reasons they have much higher levels and
some don't isn't known? What do you make of his suggestion
that the best approach might be meds and lowering iron so
all subsets are covered?

I congratulate you for being able to show some support for
your original statement, which was not supported in the
original abstract of this thread.

Quoted message said:

Quoted message said:

"Removal of iron leads to normalization of Hepatitis C
liver panels .."

archive.mail-list.commsg03159.htmlOpen ↗

The mean serum levels of ALT, in the phlebotomy group, fell
from 117 to 75 IU/L and remained less than 72 IU/L for the
ensuing 5 yr, during which time additional phlebotomies
were needed every 8 months or so to maintain an iron-
depleted state. There were no adverse effects of chronic
iron reduction.

Of greatest importance, the severity of fibrosis (by
the Desmet scoring system) in the iron reduction
group decreased from 2.3 to 1.7 (p < .05), whereas in
controls the mean values were 1.7 at baseline and 2.0
at follow-up (p > 0.05, ns). Furthermore, the
severity of inflammation increased in only one of 13
of the chronic iron reduction group (unchanged in
12/13; mean values = 1.8 and 2.0, p > 0.05), whereas
it increased in
12/13 controls (unchanged in the 13th) (mean values = 2.0
and 2.9, p < .005).

The authors concluded that long term maintenance of
iron depletion by therapeutic phlebotomy prevents
progression of fibrosis in CHC. They suggest that
chronic iron reduction is a good alternative to
interferon in treatment of CHC. To these positive
results may be added recent reports of decreases in
serum -fetoprotein (29) and less frequent development
of hepatocellular carcinoma (HCC) (30) in small
groups of patients with CHC chronically treated with
iron reduction. The notion that iron in the liver is
a risk factor for HCC is supported by the known
cocarcinogenicity of iron (10) and by a recent report
showing a 5.2-fold increased risk of HCC development
in patients with cirrhotic CHC and hepatic iron
deposition relative to those without (31).

Quoted message said:

It's like reducing your daily caloric intake, but
advertising the weight loss as being due to a reduction in
[choose your favorite one] carbs, fat, or protein only.

And wassrong wit dat???? 🙂