HOME
TEKTRAN
_________________________________________________________________
IRON DEPOSITION IN THE JOINTS OF CHILDREN WITH JUVENILE RHEUMATOID ARTHRITIS
Author(s):
SHYPAILO ROMAN J
ELLIS KENNETH J
PEREZ MARIA
ABRAMS STEVEN A
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
available.
Keywords:
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
Contact:
USDA/ARS CHILDREN'S NUTR
1100 BATES ST.
HOUSTON
TX 77030
FAX: (713)798-7130
Email: kellis@bcm.tmc.edu
Approved Date: 1999-01-07
______________________________________________________________________
TEKTRAN
United States Department of Agriculture
Agricultural Research Service
Updated: 1999-01-16
Arthritis Rheum 1999 Apr;42(4):799-806
Elevated parathyroid hormone 44-68 and osteoarticular changes in patients with
genetic hemochromatosis.
Pawlotsky Y, Le Dantec P, Moirand R, Guggenbuhl P, Jouanolle AM, Catheline
M, Meadeb J, Brissot P, Deugnier Y, Chales G
Centre Hospitalier et Universitaire, Rennes, France.
OBJECTIVE: To determine whether the osteoarticular changes associated
with genetic hemochromatosis could be explained by metabolic
parathyroid hormone (PTH) disorders. METHODS: The study involved 210
patients with liver iron overload syndromes. Osteoarticular changes
were numerically scored as the number of damaged joints. PTH 1-84 and
44-68 were assayed. RESULTS: An increase in serum PTH 44-68 levels was
found in one-third of untreated patients who had no calcium or PTH
1-84 abnormalities. Serum PTH 44-68 levels correlated positively with
serum ferritin levels. In multivariate analyses, the number of
affected joints correlated positively with age, serum PTH 44-68
levels, and serum ferritin levels. CONCLUSION: Liver iron overload
syndromes, especially genetic hemochromatosis, are associated with
elevated circulating levels of PTH fragments containing the 44-68
region, which appears to play a role in osteoarticular changes. This
increase seems to be a consequence of iron overload.
PMID: 10211896, UI: 99226878
_________________________________________________________________
_________________________________________________________________
Free Radic Res 1999 May;30(5):395-405
Aggrecan degradation in chondrocytes is mediated by reactive oxygen species and
protected by antioxidants.
Tiku ML, Gupta S, Deshmukh DR
Department of Medicine, UMDNJ-Robert Wood Johnson Medical School, New
Brunswick, NJ 08903-0019, USA.
Reactive oxygen species (ROS) are implicated in aging of cartilage and
in the pathogenesis of osteoarthritis. However, the biological role of
chondrocytes-derived ROS has not been elucidated. An in-vitro model
was developed to study the role of chondrocyte-derived ROS in
cartilage matrix degradation. The primary articular chondrocytes were
cultured and the aggrecan matrix was radiolabeled with 35-sulfate. The
labeled aggrecan matrix was washed to remove unincorporated label and
chondrocytes were returned to serum free balanced salt solution. The
cell-monolayer-matrix sensitivity to oxidative damage due to either
hydrogen peroxide or glucose oxidase was established by monitoring the
release of labeled aggrecan into the medium. Lipopolysaccharide (LPS)
treatment of chondrocyte-monolayer enhanced the release of labeled
aggrecan. Catalase significantly prevented the release of labeled
aggrecan in LPS-chondrocyte cultures, suggesting a role for
chondrocyte-derived hydrogen peroxide in aggrecan degradation.
Superoxide dismutase or boiled catalase had no such inhibitory effect.
The effect of several antioxidants on LPS-chondrocyte-dependent
aggrecan degradation was examined. Hydroxyl radical scavengers
(mannitol and thiourea) significantly decreased aggrecan degradation.
A spin trapping agent N-tert-butyl-phenylnitrone (but not its inactive
analog tert-butyl-phenylcarbonate) significantly decreased aggrecan
degradation. Butylated hydroxytoluene also inhibited aggrecan
degradation, whereas the other lipophilic antioxidant tested, propyl
gallate, had a marked dose-dependent inhibitory effect. These data
indicate that general antioxidants, hydroxyl radical scavengers,
antioxidant vitamins, iron chelating agents, lipophilic antioxidants,
and spin trapping agents can influence chondrocyte-dependent aggrecan
degradation. These studies support the role of a chondrocyte-dependent
oxidative mechanism in aggrecan degradation and indicate that
antioxidants can prevent matrix degradation and therefore may have a
preventive or therapeutic value in arthritis. The enhancement of
oxidative activity in chondrocytes and its damaging effect on matrix
may be an important mechanism of matrix degradation in osteoarthritis.
PMID: 10342332, UI: 99271760
_________________________________________________________________
HOME
Clin Orthop 1998 Apr;(349):108-15
Hemochromatosis of the foot and ankle. Report of three cases and review of the
literature.
Bailey EJ, Gardner AB
Emory University School of Medicine, Atlanta, GA 30322, USA.
Genetic hemochromatosis is a disorder of iron metabolism that results
in deposition of massive amounts of iron in the tissues. Arthropathy
is one of numerous clinical manifestations associated with this
disease. Characteristic radiographic features have been reported in
the hand and wrist, and the hip; however, there is no mention in the
literature of joint manifestations in the foot and ankle. In this
report, the authors present three patients with hemochromatosis
arthropathy of the foot and ankle. Two patients presented primarily
with foot pain and were treated initially with orthoses. One of these
patients went on to have to midfoot arthrodesis performed. The third
patient presented with ankle joint symptoms, and was treated
successfully with an ankle foot orthosis. The arthritis of
hemochromatosis has classic radiographic findings. However, the
arthritis of hemochromatosis may be difficult to differentiate from
several other joint diseases. Characteristic features of this disease
in the foot and ankle are discussed.
Publication Types:
* Review
* Review literature
PMID: 9584373, UI: 98245352
HOME
_________________________________________________________________
Title: Mechanism of exacerbation of rheumatoid synovitis by total-dose
iron-dextran infusion: in-vivo demonstration of iron-promoted oxidant
stress.
Author(s): Winyard PG; Blake DR; Chirico S; Gutteridge JM; Lunec J
Source: Lancet 1987 Jan 10;1(8524):69-72
Abstract: The mechanism by which a synovial flare occurred in a
patient with rheumatoid arthritis after intravenous infusion of
iron-dextran was investigated. After the infusion, serum and
synovial-fluid iron-binding capacity became saturated, giving rise to
low-molecular-mass iron chelates with the capacity to cause oxidative
damage ("bleomycin-iron"). At the same time lipid peroxidation and the
concentration of oxidised ascorbic acid (dehydroascorbate) increased
in both serum and synovial fluid, and red-cell glutathione fell. These
changes corresponded closely to an exacerbation of rheumatoid
synovitis. Hepatic function was transiently disturbed 7 days after the
infusion, reflecting hepatic oxidant stress within the iron-loaded
liver. Such changes provide clear evidence that iron-catalysed
oxidative reactions influence the inflammatory process in human beings
Major Indexes:
* Arthritis, Rheumatoid [metabolism]
* Iron-Dextran Complex [adverse effects]
* Iron [metabolism]
* Synovitis [metabolism]
Minor Indexes:
* Bleomycins [diagnostic use]
* Glutathione [blood]
* Infusions, Intravenous
* Iron-Dextran Complex [administration & dosage]
* Knee Joint [physiopathology]
* Lipid Peroxides [metabolism]
* Liver [metabolism]
* Middle Age
Reagent Names:
* 0 (Bleomycins)
* 0 (Lipid Peroxides)
* 70-18-8 (Glutathione)
* 7439-89-6 (Iron)
* 9004-66-4 (Iron-Dextran Complex)
Subject: Arthritis
Since there are over a hundred forms of arthritis caused by many factors,
some of which remain unknown, we have no cure for this painful and
crippling disease.
Free radicals contribute to the pain, swelling and joint injury of
arthritis. Serum iron accumulates in the membranes and fluids
surrounding affected joints and interacts with oxygen to form
free-radicals called superoxide anion radicals. These, in turn, damage
red blood cells, causing them to leak their contents into the inflamed
area, which then produces the most damaging of all the free-radicals
known-- hydroxyl radicals - that destroy DNA and break down the
protective fluid that normally lubricates joints. The less fluid, the
more stiffness and pain. The free-radicals also interact with unsaturated
fats in the body, producing even more free-radicals and more injury.
During this process , lysozomes (little sacs that contain powerful
protein-disolving enxymes) are destroyed, leaking their enzymes into the
damaged area, which further increases the damage to joint membranes.
Most physicians who specialize in the study and treatment of arthritis
and related diseases will tell you that diet has little to do with
causing arthritis or relieving its pain and stiffness.
High fat, high cholesterol diets that are low in natural antioxidants
such as vitamin E, beta carotene, vitamin C, and antioxidant metals such
as selenium and zinc contribute to the damage done by oxygen and other
unavoidable free radical stimulants.
Rely on antioxidants to prevent excessive production of harmful free
radicals. Antioxidants can reduce the damage from most traumatic injuries
and minimize free radical destruction of joint tissues.
DG DISPATCH - INFLAMMATION: Oxidised LDL Linked To Disease
Activity In Rheumatoid Arthritis
http://www.pslgroup.com/dg/10de6e.htm
Oxidised low density lipoprotein may be involved in the pathogenesis of
rheumatoid arthritis and may serve as an additional marker of disease activity,
researchers report.
(HOME)