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Cancer Increase In Juvenile Arthritis

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  1. #1
    ironjustice Guest

    Default Cancer Increase In Juvenile Arthritis

    Cancer Rate 4 Times Higher in Children With Juvenile Arthritis

    HOBOKEN, NJ -- February 13, 2012 -- Findings published in the journal
    Arthritis & Rheumatism shows that incident malignancy among children
    with juvenile idiopathic arthritis (JIA) is 4 times higher than in
    those without the disease.

    Results of the study suggest that JIA treatment, such as tumour
    necrosis factor (TNF) inhibitors, does not necessarily explain the
    development of cancer in this paediatric population.

    Possible cancer risk has been associated with TNF treatment, prompting
    the US Food and Drug Administration (FDA) to place black box warnings
    of the potential malignancy risk on TNF inhibitors labels.

    In the present study, Timothy Beukelman, MD, University of Alabama at
    Birmingham, Birmingham, Alabama, and colleagues conducted one of the
    largest investigations into the rates of incident malignancy among
    patients with JIA relative to their treatment.

    Using data from the US Medicaid records from 2000 through 2005,
    researchers identified 7,812 children with JIA and 2 comparator groups
    without JIA; 1 group with asthma (652,234 children) and the second
    with attention-deficit/hyperactivity disorder (ADHD; 321,821

    The team categorised patients' treatment with methotrexate and TNF
    inhibitors as "ever" or "never" used, though many children with JIA
    did not receive either of these treatments during the study. The
    research team did not have access to detailed medical records, and
    therefore categorised the identified incident malignancies as
    "possible," "probable," or "highly probable."

    Children diagnosed with JIA had a total follow-up time of 12,614
    person-years with 1,484 children in this group contributing 2,922
    person-years of anti-TNF exposure.

    The team determined that among all children with JIA, compared with
    those without JIA, the incidence rate was 4.4 times higher for
    probable and highly probable malignancies. Paediatric patients with
    JIA treated with methotrexate without TNF inhibitors had a similarly
    increased incidence of cancer, which was 3.9 times higher than
    children without JIA. No probable or highly probable malignancies were
    identified in patients following any use of anti-TNF during the study

    In an accompanying editorial, Karen B. Onel, MD, and Kenan Onel, MD,
    University of Chicago, Chicago, Illinois, said that the results of the
    study indicate that children with JIA may be at increased cancer risk
    from the disease, but suggests that anti-TNF therapy may not be
    associated with a further increased cancer risk. "Larger studies in
    different populations and with longer follow up are required to
    confirm Dr. Beukelman's findings," they wrote. They also pointed out
    that most patients in the study were treated with etanercept, a
    soluble TNF receptor blocker, and the investigation of other anti-TNF
    agents working by different mechanisms may yield different results.
    Nonetheless, "by focusing on the possible cancer risk associated with
    the use of TNF inhibitors, the underlying cancer risk associated with
    JIA may have been understated, and it is important to make patients,
    families, and physicians aware of the possible late consequences of
    this disease," they wrote.

    SOURCE: Wiley-Blackwell


    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
    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
    aged five to 15 years, received an intravenous radioactive tracer
    of iron (0.03 microsievert). Iron activity in affected joints was
    monitored on a position/energy-sensitive gamma counter, while a
    machine monitored whole-body iron retention. Iron deposition was
    measured two hours post-infusion and again at days seven, 14, 28 and
    "We found that iron excessively accumulates in arthritic joints and
    probably contributes to the chronic damage," said Shypailo. "That
    you between a rock and a hard place because many of these arthritic
    kids are anemic and need iron supplements, which may worsen the
    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
    patients showed increased uptake at the affected joints: 165% over
    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.




    Interpretive Summary:
    We wanted to develop an accurate and noninvasive way of
    determining the amount of iron deposited in the joints of
    patients with juvenile rheumatoid arthritis. Children with JRA
    often develop excess iron in their joints, so doctors need a
    way of monitoring the iron level, particularly when prescribing
    iron supplements for the common problem of anemia. However, the
    only method currently available is to take a biopsy. We adapted
    a machine called a gamma counter to measure the iron in eight
    patients' joints after giving them an iron isotope by vein.
    Then we compared the results with the total amount of iron in
    their bodies, measured by a whole-body counter. We found that
    we had developed an accurate new way of measuring iron in these
    patients' joints. We also found that six of the eight subjects
    had excess uptake of the iron isotope in their joints. That
    provided a signal that a preponderance of JRA patients are
    prone to have this problem, and clinicians should take special
    care to monitor them for it. Moreover, this is the first time a
    noninvasive way of performing this measurement has been

    energy reproduction growth body composition women infants
    children water potassium bioelectrical impedance conductance
    bromide space lactating iron adipose tissue lipid motabolism
    beta-adrenergic receptor cell culture neutron activation
    nitrogen carbon calcium sodium chlorine phosphorus hormonal
    changes differentiation adipocyte hnrim021125

    1100 BATES ST.
    TX 77030
    FAX: (713)798-7130

    Approved Date: 1999-01-07

    United States Department of Agriculture
    Agricultural Research Service

    Updated: 1999-01-16


    "iron induced increase in synovitis "

    Effect of iron complexes on adjuvant arthritis in rats.
    Ann Rheum Dis. 1992 Apr;51(4):516-21
    Dabbagh AJ, Blake DR, Morris CJ.
    Inflammation Group, London Hospital Medical College, United Kingdom.

    When a total dose infusion of iron dextran is given to anaemic
    rheumatoid patients an exacerbation of inflammatory synovitis in
    previously affected joints is observed. The adjuvant arthritis model
    inflammation in rats has been used to investigate the mechanism of
    promoted synovitis. Either iron dextran (5 mg injected intravenously)
    with a dextran C control, or iron sorbitol (7.5 mg injected
    intramuscularly) with a sorbitol citrate complex control was given at
    the onset of clinical joint inflammation. Iron dextran significantly
    increased joint inflammation (assessed by joint scoring) at days 12,
    13, 14, and 16 after injection. Similarly, iron sorbitol produced a
    significant increase in the joint score at days 17, 18, 19, and 21.
    addition, extensive osteoporosis was observed in the rats treated
    iron sorbitol. These pro-inflammatory effects of iron coincide with
    presence of positive results for synovial iron (III) using Perl's
    and neutrophil infiltration. The results of this study suggest that
    iron induced increase in synovitis in adjuvant arthritis is a result
    iron promoted oxidative damage and is not likely to be due to the
    dextran C or the sorbitol citric acid components. It is suggested
    a similar mechanism may occur in rheumatoid patients given iron

    PMID: 1586252


    A Role For Iron In Oesophageal Adenocarcinoma
    A thesis submitted to The University of Birmingham For the degree of
    DOCTOR OF PHILOSOPHY School of Cancer Sciences
    The University of Birmingham October 2010
    Increasing evidence associates iron excess with the development of
    oesophageal adenocarcinoma.
    This study hypothesises that expression of iron and haem transport
    proteins becomes modulated in the progression to oesophageal
    Furthermore it is postulated that exposing oesophageal adenocarcinoma
    cells to iron or haem affect proliferation and a malignant phenotype.
    Finally chelating iron with alginates may provide a simple and non
    way of inhibiting iron mediated effects.
    In Western populations the incidence of oesophageal adenocarcinoma
    (OAC) is increasing greater than any other malignant disease.
    Increasing epidemiological and experimental evidence associates iron
    with OAC.
    Our understanding of iron physiology has increased enormously in
    years due to the elucidation of transport proteins and regulatory
    Haem scavenging and metabolism remains to be clearly characterised
    although candidate import proteins have been identified.
    This project aimed to characterise the iron transport machinery in
    progression of OAC and the effects of iron exposure in-vitro.
    Overexpression of iron and haem import proteins, with a repression of
    iron export, was identified in the progression of Barrett’s metaplasia
    OAC suggesting a role for iron in disease progression.
    Interestingly expression of hepcidin, the hepatic peptide responsible
    systemic control of iron, was identified in samples of OAC.
    Culturing OAC cells with iron or haem increased cell proliferation,
    and anchorage independent growth.

    Iron Excess and Cancer. Charronne F. Davis and M. Tevfik Dorak
    Environmental Factors, Genes, and the Development of Human Cancers
    2010, Part 3, 445-475.
    In the last two decades, strong observational and experimental
    evidence has
    been presented for the role of iron excess in cancer development.
    The hereditary hemochromatosis gene HFE variants that increase body
    levels are associated with increased cancer risk.
    The first such association was reported by us in childhood acute
    With the identification of molecular mechanisms of potentiation of
    by iron, epidemiologic associations have been gaining more weight.
    Experimental data also increase the credibility of suggestions that
    iron excess can
    both initiate (genotoxic effect) and promote (via its effect on immune
    function) cancer
    Both environmental and genetic factors may lead to iron excess but the
    effect is
    strongest in combination.
    Iron excess may contribute to cancer development in many different
    ways, most of which
    yet unappreciated and most relevant of those possible connections are
    discussed in this
    Since reduction in smoking, alcohol and red meat consumption
    eliminates excessive
    exposure to iron, eating fruits and vegetables does not expose the
    body to too much
    bioavailable iron and perhaps replaces other iron-rich food stuff and
    avoidance of
    excess iron levels reduces infections, iron is indirectly involved in
    the success of these
    preventive measures.
    Perhaps it is time to emphasize lower exposure to environmental iron
    directly as an
    important factor to reduce the cancer burden in the industrialized

    Who loves ya.

    Jesus Was A Vegetarian!

    Man Is A Herbivore!


  2. #2
    [email protected] Guest

    Default Re: Cancer Increase In Juvenile Arthritis

    On Tue, 14 Feb 2012 07:34:24 -0800 (PST), ironjustice
    <[email protected]> wrote:

    Even after all these years you are still full of **** that NO one
    takes any notice of Tom.

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