Uric Acid as a potential cue to screen for iron overload.
Mainous AG 3rd, Knoll ME, Everett CJ, Matheson EM, Hulihan MM, Grant
AM.
SourceDepartment of Family Medicine, Medical University of South
Carolina, Charleston.
J Am Board Fam Med. 2011 Jul-Aug;24(4):415-21.

Abstract
BACKGROUND: It is suggested that targeted screening for
hemochromatosis and iron overload may be worthwhile. The aim of this
study was to examine uric acid as a potential indicator of the
presence of iron overload.

METHODS: We analyzed adults aged 20 and older in the National Health
and Nutrition Examination Survey 1999 to 2002. We computed logistic
regressions controlling for age, sex, race/ethnicity, liver or kidney
condition, and alcohol use to see the relationship between
combinations of uric acid and ferritin with the outcomes of elevated
liver enzymes and proteinuria.

RESULTS: In unadjusted analyses, 20.7% of individuals with high uric
acid had high ferritin levels versus 8.8% of individuals with low uric
acid levels (P < .001). Individuals with both elevated uric acid and
elevated ferritin levels had significantly higher liver enzymes than
individuals with either elevated uric acid or ferritin. With low uric
acid and low ferritin as the reference category, individuals with high
uric acid and high ferritin were significantly more likely to also
have proteinuria (odds ratio, 2.66; 95% CI, 1.82-3.91).

CONCLUSIONS: Elevated levels of uric acid is associated with elevated
ferritin levels and may serve as a risk stratification variable for
presence of iron overload and hemochromatosis.

PMID:21737766

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

Coincidentally gout which has high uric acid / is treated with
bloodletting /
iron depletion.

Effect of gradual accumulation of iron, molybdenum and sulfur, slow
depletion of zinc and copper, ethanol or fructose ingestion and
phlebotomy in gout.
Med Hypotheses 1999 Nov;53(5):407-12
Johnson S

Gout affects mostly males over 40 years old and, occasionally,
postmenopausal women. This pattern coincides with the pattern of
iron accumulation. On the other hand, menstruating women are seldom
afflicted by gout, because the monthly blood loss causes them to
accumulate iron to a much lesser degree. Gout involves seven
aspects:
(1) uric acid overproduction from increased purines in the diet;
(2) uric acid overproduction from ATP degradation;
(3) uric acid overproduction from increased de novo synthesis of
purines;
(4) uric acid overproduction from increased DNA breakdown from cell
damage;
(5) decreased uric acid elimination, caused by molybdenum and sulfur
binding to copper in the kidneys;
(6) precipitation of sodium urate-iron crystals in the joints due to
high
ferritin and saturated transferrin and low CuZn-SOD and Cu-thionein
in
the joint;
(7) development of inflammation, triggered by tyrosine bonding to the
sodium-urate-iron crystals and being transformed by tyrosine
kinase. Alcohol and iron greatly affect most of these aspects.
Therefore,
phlebotomy is suggested as therapy for gout patients, in order to
eliminate the accumulated Fe. Furthermore, yearly blood donation
is recommended for males with a family history of gout, so as to
prevent Fe accumulation and avoid gout.

PMID: 10616042, UI: 20081788


__________________________________________________ _______________

The NIH is now recruiting for a clinical trial of
iron depletion for diabetes and NAFLD and it TOO has a high uric acid
level.
--------------------------------------------------------

Risk of Developing Diabetes Increases With Rising Serum Uric Acid
Levels


NEW YORK (Reuters Health) Feb 26 - Serum uric acid is a strong and
independent risk factor for diabetes, according to findings published
in the February issue of Diabetes Care.


"Serum uric acid is positively associated with serum glucose in
healthy subjects," Dr. Jacqueline C. M. Witteman and colleagues from
Erasmus Medical Center, Rotterdam, the Netherlands, write. "However,
this association is not consistent between healthy and diabetic
individuals, as a low serum level of uric acid is reported in the
hyperglycemic state," they note. "Since most individuals experience a
phase of impaired glucose tolerance before progression to diabetes,
it
is not clear whether raised serum uric acid predicts the risk of type
2 diabetes."


To investigate, the researchers used data from the Rotterdam Study, a
large population-based, prospective cohort study among subjects aged
55 years and older. Included in the study were 4536 subjects free
from
diabetes at baseline.


The mean serum uric acid level measured at baseline was 323.7
micromol/
L (range, 107 to 756 micromol/L). Among the participants, 462
developed diabetes during a mean follow-up of 10.1 years.


The age- and sex-adjusted hazard ratios for diabetes were 1.30, 1.63,
and 2.83 for the second, third, and fourth quartiles of serum uric
acid, in comparison with the first quartile. On multivariate
analysis,
the corresponding hazard ratios dropped to 1.08, 1.12, and 1.68, the
researchers report.


"Our findings, together with those from previous literature, indicate
that lowering uric acid may be a novel treatment target for
preventing
diabetes and justify a prospective clinical trial on the possible
benefits of the measurement and lowering of serum uric acid on
multiple chronic disease end points," Dr. Witteman and colleagues
conclude.


Diabetes Care 2008;31:361-362.


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

Diabetes has a 'secondary marker' of increased red blood cell
production
which again coincidentally CAUSES high uric acid.

Original Investigations: Pathogenesis and Treatment of Kidney Disease
and Hypertension Hyperuricemia, hypertension, and proteinuria
associated
with high-altitude polycythemia*1
J. Ashley Jefferson MD, Elizabeth Escudero MD, Maria-Elena Hurtado
MD,
Jackeline Pando Kelly MD, Erik R. Swenson MD, PhD, Mark H. Wener MD,
Michel Burnier MD, Marc Maillard PhD, George F. Schreiner MD, PhD,
Robert B. Schoene MD, Abdias Hurtado MD and Richard J. Johnson MD
From the Department of Medicine and Laboratory Medicine, University
of
Washington Medical Center, Seattle, WA; The Carlos Monge Cassinelli
Nephrology Center, Hospital Loayza, Division of Nephrology,
University
Cayetano Heredia, Lima, Peru; Division of Hypertension and Vascular
Medicine, Centre Hospitalier Universitaire Vaudois, Lausanne,
Switzerland; Scios Inc, Sunnyvale, CA; and the Department of
Medicine,
Baylor College of Medicine, Houston, TX.
Received 12 October 2001. Available online 11 June 2002.


Abstract
Chronic exposure to high altitude is associated with the development
of erythrocytosis, proteinuria, and, in some cases, hyperuricemia. We
examined the relationship between high-altitude polycythemia and
proteinuria and hyperuricemia in Cerro de Pasco, Peru (altitude,
4,300
m). We studied 25 adult men with hematocrits less than 65% and 27
subjects with excessive erythrocytosis (EE; hematocrit > 65%) living
in Cerro de Pasco, Peru and compared them with 28 control subjects
living in Lima, Peru (at sea level) and after 48 hours of exposure to
high altitude. Serum urate levels were significantly elevated in
patients with EE at altitude, and gout occurred in 4 of 27 of these
subjects. Urate level strongly correlated with hematocrit (r = 0.71;
P
< 0.0001). Urate production (24-hour urine urate excretion and urine
urate-creatinine ratio) was increased in this group compared with
those at sea level. Fractional urate excretion was not increased, and
fractional lithium excretion was reduced, in keeping with increased
proximal reabsorption of filtrate. Significantly higher blood
pressures and decreased renin levels in the EE group were in keeping
with increased proximal sodium reabsorption. Serum urate levels
correlated with mean blood pressure (r = 0.50; P < 0.0001).
Significant proteinuria was more prevalent in the EE group despite
normal renal function. Hyperuricemia is common in subjects living at
high altitude and associated with EE, hypertension, and proteinuria.
The increase in uric acid levels appears to be caused by increased
urate generation secondary to systemic hypoxia, although a relative
impairment in renal excretion also may contribute.


*1 Supported in part by an extramural grant from Baxter.


American Journal of Kidney Diseases
Volume 39, Issue 6, June 2002, Pages 1135-1142

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


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