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LE Magazine July 2003
A new method
of preventing contrast nephropathy
For years, many patients who elected to undergo coronary
angiography risked prolonged hospitalization and renal
deterioration as a result of the contrast agents used in the
procedure. New research has revealed that the antioxidant
acetylcysteine may help to prevent this potentially
life-threatening toxic damage.
Contrast nephropathy is the deterioration of renal function
following coronary angiography and intervention and has long
been associated with prolonged hospitalization and adverse
clinical outcomes. "Contrast nephropathy is a recognized
complication of coronary angiography," wrote researchers in
the February 5, 2003 issue of JAMA. "It is reported
that 14.5% of patients develop a 25% increase in serum
creatinine levels following cardiac catheterization. This
problem assumes greater and greater importance with increased
use of invasive radiological procedures to diagnose and treat
coronary artery disease."
Although the disease occurs infrequently with normal renal
function, its frequency increases with decreasing renal
function, ranging from 5% in patients with mild renal
insufficiency to as high as 50% in those with severe renal
dysfunction and diabetes [JAMA 2003 Feb 5;289(5):553-8].
Previous studies have attempted to identify methods to
reduce the incidence of contrast nephropathy, particularly in
high-risk groups. Pretreatment with diuretics, such as
furosemide or drugs thought to prevent vasoconstriction, such
as calcium channel blockers have not provided clear benefit
and may even be harmful [JAMA 2003 Feb 5;289(5):553-8].
Because acetylcysteine has well-established antioxidant
properties, researchers speculate that it could in fact
protect against oxidative-mediated contrast nephropathy.
"Several randomized trials have demonstrated a 40% or greater
decrease in the incidence of the disease among patients with
chronic renal insufficiency who received contrast agents while
undergoing computed tomography as well as cardiac
catheterization," wrote Dr. Gary C. Curhan in JAMA.
"However, other studies have found no benefit. These
discrepancies may be due to differences in the timing and dose
of acetylcysteine, total amount of contrast administered,
characteristics of patients and the definition of contrast
nephropathy."
In a recent prospective randomized clinical trial,
researchers in Hong Kong reported on the use of acetylcysteine
in patients undergoing cardiac catheterization. For that
study, 200 Chinese patients with mild to moderate chronic
renal insufficiency were randomly assigned to receive either
placebo or acetylcysteine at 600 mg orally twice daily for a
total of three doses prior to the procedure and one dose after
the procedure. Serum creatinine levels were measured at
admission, at 24 and 48 hours, and at day seven. Contrast
nephropathy was defined as a greater than 25% increase in
serum creatinine concentration within 48 hours after exposure
to the contrast agent.
According to their results, contrast nephropathy developed
significantly more frequently in the control group (12%) than
in the acetylcysteine group (4%). In addition, the average
length of hospitalization was 0.5 days shorter in the
acetylcysteine group. Furthermore, the serum creatinine
concentration decreased significantly after angiography in the
acetylcysteine group, from 1.35 to 1.22 mg/dL at two days
after the administration of the contrast medium. In the
control group, the change in mean serum creatinine
concentration was from 1.36 to 1.38 mg/dL and was considered
"not significant." These results suggests that acetylcysteine
may prevent contrast nephrotoxicity in patients with moderate
chronic renal insufficiency undergoing coronary diagnostic
and/or interventional procedures.
"Oral acetylcysteine is a safe, effective and inexpensive
prophylactic treatment against acute renal dysfunction for
patients with moderate chronic renal insufficiency undergoing
coronary angiographic procedures with minimal adverse effects
and at a low cost," the authors concluded.
Homocysteine
and cancer
Homocysteine is a potentially toxic byproduct of the body's
metabolism of the amino acid, methionine. Methionine is found
in protein, particularly meat protein. Elevated levels of
homocysteine are associated with an increased risk for heart
attack and stroke.
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New research indicates that elevated homocysteine in the
blood is also associated with cancer. Researchers at the
University of Utah and Chang Gung Hospital in Taiwan report
that cancer cells release high amounts of homocysteine. They
also discovered that levels of homocysteine track with cancer
biomarkers. When cancer is treated with drugs that kill it,
homocysteine levels fall. Researchers believe that
homocysteine is indicative of rapidly-dividing cells, i.e.,
cancer cells. If verified by other researchers, homocysteine
could be used in the future as a more sensitive biomarker than
those presently in use since it only indicates the presence of
living cancer cells, whereas traditional biomarkers appear to
indicate both living and dead. For this reason, homocysteine
levels may be a more reliable indicator of whether an
anticancer treatment is working.
Research from the National Cancer Institute supports the
notion that elevated levels of homocysteine may indicate that
cancer is present. In a study on women with invasive cervical
cancer, those with homocysteine levels greater than 6.31
micromoles per liter of blood were two to three times more
likely to have the disease. Interestingly, a lack of folate
did not increase the risk in this study, which may mean that
other homocysteine-lowering vitamins such as B12, B6 or
riboflavin are deficient in women with cervical cancer.
Another possibility is that methylation (which lowers
homocysteine and reduces the risk for cancer) is compromised
in some other way. Similar studies have been done showing that
homocysteine is elevated in colon cancer as well.
The laboratory test for measuring homocysteine levels is
widely available. It is already well-known that lowering
homocysteine can protect against heart attack and stroke.
-Terri Mitchell
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