Joan R, 71, was coping pretty well with her dialysis routine,
until she started experiencing arthritis-like attacks
caused by gout. The added complication has cut down on
her mobility and her autonomy, but there's a bright spot
on the horizon for Joan — a new drug called sevelamer
may help reduce the risk of gout in dialysis patients.
A recent study shows that it outperforms the current treatment
— calcium-based phosphate binders — when it
comes to reducing serum uric acid.
OUT
WITH GOUT
Gout is a common complication that plagues dialysis
patients, as failing kidneys leave excess uric acid
in the bloodstream that crystallizes and builds up in
the joints. Hyperurecemia not only leads to gout but
can come with a host of other problems such as inflammatory
arthritis and cutaneous tophi — white chalky deposits
on the skin. In addition, it can also exacerbate insulin
resistance, dylipidemia, hypertension and cardiac disease.
Dialysis patients suffering from
gout are usually given calcium-based phosphate binders
to reduce the amount of uric acid in the blood. One
drawback of this treatment is a risk of developing hypercalcemia.
Fortunately, a new study shows that the drug sevelamer
— a hydrogel that can be taken as a tablet with
meals — can more effectively eliminate excess uric
acid from the serum of dialysis patients and
cut down on the risk of hypercalcemia, according to
a study published in the January issue of Arthritis
& Rheumatism.
"Given the limitations of existing
therapies," said study author Dr Jay Garg, "it would
be beneficial to find alternative agents that could
decrease serum uric acid concentrations without a significant
risk of adverse events."
DOWN
WITH URIC ACID
The year-long, randomized, multi-centred trial included
169 participants — 81 received sevelamer while
the other 88 were treated with either calcium acetate
or calcium carbonate tablets. After a year of treatment,
the sevelamer group had an average of 0.64mg/dl less
uric acid in their blood serum than before. The group
taking calcium-based supplements experienced a meager
0.26mg/dl decline.
"The change in uric acid level
was proportional to the severity of hyperuricemia at
baseline," observed the authors. Participants with the
most uric acid in their blood streams at the beginning
of the study showed the greatest improvement after taking
sevelamer. Nearly one in four patients taking sevelamer
experienced a decline of 1.5mg/dl or more during the
trial. Only 10% of those taking calcium-based phosphate
binders showed a comparable reduction in uric acid concentrations.
Further study is needed to measure
whether sevelamer treatment reduces the incidence of
mortality, hospitalization or 'hard' outcomes of excess
uric acid accumulation including flares of gout. The
researchers are also unsure of how sevelamer actually
works. Although they believe that sevelamer directly
absorbs excess uric acid in the gut, it may also inhibit
uric acid production by interacting with a precursor
in its metabolic pathway.
Arthritis Rheum Jan, 2005;52(1):290-5
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