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WHEN IMPLANTS BECOME CLOUDY...
By
Richard A. Lewis, M.D.
In modern cataract
surgery, most patients elect to have an artificial lens
implant placed in the operate eye. These plastic
implants, or artificial lenses, permit rapid
rehabilitation of vision and avoid the frustrations of
contract lenses and the cosmetic and functional
disabilities of the old-fashioned aphakic spectacles,
with strong magnification properties.
When the human
lens is removed, the surgeon makes a small incision in
the front wall or capsule of the lens and removes the
internal contents of the lens. However, the back wall or
capsule of the lens is left intact, and the plastic
artificial lens is placed inside the capsule, sometimes
termed by the operating surgeon "in the bag."
No matter how carefully a surgeon attempts to remove all
the cells from the inside of the capsule of the cataract,
a few cells remain. Over the next few months or year or
two, a cloudy film or membrane may form, much like a
sheet of wax paper, across the capsule behind the
artificial lens implant. This cloudy film is termed a
"secondary membrane" or a "secondary
cataract." Even the best of situations, at least
80-85% of people having cataract surgery with artificial
lens implants will develop a secondary membrane within
two years of their surgery.
In past years,
such membranes needed to be cut or incised with a
surgical incision with a very tiny knife. The procedure
usually required another trip to the operating room, to
be certain that the entire procedure could be conducted
safely and under sterile conditions. Not all patients who
have had cataracts removed by this technique will require
an opening in this secondary membrane. The opening is
necessary only if the membrane becomes sufficiently
cloudy to impair a clear optical image reaching the
retina and optic nerve.
In
recent years, however, a newer technique has been used to
cut open this secondary membrane. The opening is made
with a special type of laser, commonly nicknamed a
"Nd:YAG laser". Its real name is
"Neodymium-YttriumAluminum-Garnet laser".
The Nd :YAG laser can cut or open the grey or opaque
membranes by creating a series of tiny explosions in a
line or cross pattern which literally shear apart the
tissues in this opacified posterior capsule. Thus, if you
have already had cataract surgery and you should
experience decreased vision because of this secondary
membrane, the ND:YAG laser can promptly restore your
vision with a simple outpatient procedure which does not
require an incision into the eye and, therefore, no risk
of bleeding or infection inside the eye.
Please remember,
however, that the laser is not used for cataract surgery.
Many patients ask to "have their cataracts
removed" with laser surgery. Cataract surgery cannot
be done with a laser by any surgeon at this time.
Cataracts are removed surgically by conventional methods
usually by removing all the cataract except the outer
membrane or capsule. Thus the ND:YAG laser is not useful
for the removal of ordinary (primary) cataracts. The
ND:YAG laser, however, is used to treat, that is, to cut
open, "secondary cataracts" or secondary
membranes. *
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MACULAR DEGENERATION
By
Richard A. Lewis, M.D.
Macular
degeneration is a complex group of disorders which affect
approximately 1.7 million individuals in the United
States and is the most common cause of the acquired
visual impairment in those over the age of 65. Although
age-related macular degeneration is not considered a
disease, people with age-related macular degeneration
often have a family history of other individuals with
macular degeneration, especially among
European-Americans.
The most common
hereditary cause for central visual loss, that is, a
hereditary macular dystrophy, is called Stargardt's
disease. Stargardt's disease is characterized by onset in
the juvenile to young adult age, loss of central vision
and reading vision, color vision and recognizing faces
vision and a characteristic appearance to the retina and
retinal pigment epithelium. A similar retinal disorder,
sometimes alternately called Fundus Flavimaculatus,
allegedly begins at a later age and has a slower
progression. The gene for Stargardt's disease and for
Fundus Flavimaculatus of a classical recessive type which
requires that each parent be a carrier for one copy of
the mutant gene, was assigned to the short arm of human
Chromosome 1 several years ago by a French group. About
two years ago, we refined the localization of the
Stargardt's gene to a region about 4 million base pairs
of DNA in this region.
Recently, in
collaboration with Dr. Michael Dean at the National
Cancer Institute, Dr. Jeremy Nathans at the Howard Hughes
Medical Institute at Johns Hopkins University, and our
continuing collaboration with Dr. Mark Leppert and his
team of research scientists at the University of Utah,
Dr. James Lupski and I at Baylor have demonstrated that a
gene, called ABCR, not only maps in the region where the
Stargardt's gene exists, but shows mutations which occur
in single copy in each parent of this disease and in two
copies in affected individuals. Therefore, ABCR appears
to be the gene responsible for Stargardt's disease.
What does the
identification and discovery of this gene mean, as it was
published in the March 1997 issue of Nature Genetics?
It allows us a
brand new gene, never before known to exist in the
retina, to study. In effect, we now have a new mystery:
what does this normal gene produce? What is the product
and where does it go in the normal retina? If this gene
is expressed as a protein predominantly in rod cells of
the retina, why does the disease appear to affect the
retinal pigment epithelium and the cones, rather than the
rods? If ABCR appears to be a "transporter"
whose function is to carry materials from inside of cells
to the outside, or possibly from the outside through the
wall of the cell to the inside, is there any way of
altering its behavior with drugs and medicine? In other
words, now that we have the instruction manual for this
piece of machinery, is there a possibility that we can
alter the natural course of the disease, repair the
machinery, or slow down the degeneration or deterioration
of the machinery in a way to prolong visual function or
to prevent loss of visual function in younger brothers or
sisters who might also have two copies of the gene?
All these
questions will await further research. The first families
were enrolled in this program in 1987 and more than 200
families have participated to date. There is a great deal
of work left to be done. We will also wish to look at the
genes' instruction for individuals with age-related
macular degeneration, particularly those who have other
members of the family with macular degeneration, to see
if they also have altered ABCR genes, even though that is
quite unlikely at the moment. Nonetheless, ABCR becomes a
useful model for studying other types of macular
degeneration and other types of retinal disorders, just
as the genes for rhodopsin and peripherin, originally
assigned as causes for dominantly inherited retinitis
pigmentosa, have become models and markers for other
types of retinal diseases as well.
Again, as we have
said in this column previously, there is no substitute
for participation in research programs. There is no
substitute for human white blood cells and DNA and
reproductive material is contained in them. Volunteers
are needed by researchers all over the world who have
reputable, scrupulous programs for research in these
areas, whether it is Usher syndrome, retinitis
pigmentosa, Stargardt's disease, and other known genetic
disorders.
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