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Li-Ping
PECULIAR
OBESITY-
THE CUSHING'S
SYNDROME
From an analysis of the clinical
and pathologic
lindings
in
a series of
1
2 patients,
Harvey
Cushin
g,
in 1922,
established a syndrome characterized
by truncal obesity,
hypertension,
fatigability
and
weakness,
amenorrea,
hirsutism, purplish abdominal striae,
edema, glucosuria, and
osteoporosis.'
As
knowledge
ol
this
syndrome
in-
creased and
as
clinical
tests
of
adrenocortical function became stand-
ardized
and
readily
available,
it
has
been
apparently shown that, regardless
ol
its etiology, all cases of Cushing's
syndrome
are due
to increased produc-
tion of
cortisol
by
the adrenal
gland.
The
majority of cases are due to bilateral
adrenal
of
ACTH (adrenocorticotropin
hormone)-producing tumors like
pitui-
tary adenomas. Other cases are occa-
sionally
responsible
for
Cushing's
syndrome secondary
to
other
causes including prolonged use of
glucocorticoids or ACTH.
When an adenoma or carcinoma
is
suspected, adrenal exploration
is
per-
formed, with excision ol the tumor. The
principal antitumor drug
used
to chemi-
cally inhibit
adrenal cortical function due
to
carcinoma is O,P'-DDD(2,2-bis(-
chlorophenyl,
4-chorophenyl)-1,1
-
dichloroethane), an isomer
of
the insec-
ticide
DDT.
These forms
of
therapy
hold
great
promise, and
the majority
of
the
cases
will
recover from the syndrome.
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