GRAEFE’ S SIGN
GOUT
Gout is a common joint disease, affecting
1 0
times more men than women. In men
it may occur at any time after puberty; in women it usually occurs only after the
menopause. There is often a family history of the disorder. Hyperuricaemia (excess
uric acid in the blood) leads to the formation of uric acid crystals inside joints.
Crystals may also be deposited in the soft tissues in the ears and around tendons.
P a t e ll a
C r y s t a ls in
j o i n t s p a c e
Crystal precipitation
Crystals of uric acid precipitate (solidify) into
the joint space and surrounding tissues ofthe
knee, causing intense inflammation and
extreme pain.
Appearance of gout
Deposition of uric acid crystals in the joint
space has caused inflammation and swelling of
the patient’s affected left knee.
DIAGNOSIS
Gout is suspected if an attack
ofarthritis affects a single joint.
A blood test is usually performed;
a high level of uric acid will suggest
gout. Examination of fluid from the
joint may confirm the diagnosis.
Aspiration
Fluid is aspirated (removed through a
needle into a syringe) from the swollen
joint and examined under a microscope to
detect any uric acid crystals.
Microscopic evidence
The presence of uric acid crystals in the
fluid confirms the diagnosis of gout.
F e m u r
T ib ia
attacks, more joints may be involved, and
there may be constant pain due to joint
damage from chronic inflammation. In
addition, gout may be associated with
kidney stones (see
calculus, urinary tract)
or, rarely, with kidney damage due to the
deposition of crystals in the kidney tissue.
The diagnosis is confirmed by tests
on blood or fluid from the affected
joint to measure uric acid levels.
The pain and inflammation of acute
(of sudden onset) attacks can be con-
trolled by
nonsteroidal anti-inflammatory
drugs
(NSAIDs) or by
colchicine.
If these
drugs are ineffective, a
corticosteroid drug
may be injected into the joint. Many
people require no further treatment.
Long-term treatment w ith drugs that
help to lower urate levels, such as
allo-
purinol
or
sulfinpyrazone,
can stop or
reduce
the
frequency
of
recurrent
attacks. These drugs, however, may trig-
ger an attack at the start of treatment, so
are initially prescribed with NSAIDs.
Graefe’s sign
Lagging of the upper eyelid (see
lid lag)
as it follows the downward rotation of
the eyeball in
Graves’ disease.
grafting
The process of transplanting healthy tis-
sue from
one part
of the body to
another
(autografting)
or
from
one
person to another (allografting). Tissue
transplantation from an animal to a per-
son (xenografting) is also carried out.
Grafting is used to repair or replace
diseased, damaged, or defective tissues
or organs. Common operations of this
type are
skin graft, bone graft, bone marrow
transplant, corneal graft, kidney transplant,
heart transplant, liver transplant, heart-lung
transplant
,
heart-valve surgery,
and
micro-
surgery
on blood vessels and nerves.
COMPLICATIONS
W ith autografting, the grafted tissue is
usually assimilated well into the sur-
rounding tissue at the new site.
There is a risk of tissue rejection fol-
lowing other forms of grafting. The only
exceptions are grafts between identical
twins,
because
their
tissue
matches
exactly, and corneal grafting, because
the cornea has no blood supply and
therefore no white blood cells and anti-
bodies to act as a defence system against
the foreign cells.
To overcome rejection, as close a
match as possible between the tissues of
recipient and the tissues of donor is
sought (see
tissue-typing
). The recipient is
given
immunosuppressant drugs
to sup-
press the body’s natural defences. (See
also
transplant surgery.)
graft-versus-host disease
A complication of a
bone marrow trans-
plant
in w hich certain
immune system
cells, called killer
7-lymphocytes,
in the
transplanted marrow attack the tissues
of the recipient.
Graft-versus-host (GVH) disease may
occur soon after transplantation or may
take some months to appear. The first
sign is usually a skin rash. This may be
followed by diarrhoea, abdominal pain,
jaundice, inflammation
of the eyes and
mouth, and breathlessness. Most people
with GVH recover w ithin a year, but
about one in five may eventually devel-
op fatal complications.
GVH disease can usually be prevented
by giving
immunosuppressant drugs
to all
transplant patients. If, despite prophy-
lactic treatment, the disease develops, it
can be treated with
corticosteroid drugs
and immunosuppressant drugs such as
ciclosporin.
In some cases, however, it
can be difficult to control.
348
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