In 1932 American neurosurgeon Harvey Cushing described the clinical findings that provided

the link between specific physical characteristics (e.g., abnormal obesity of the face and trunk)
and a specific type of pituitary tumour. This pituitary disorder which he initially termed
"polyglandular syndrome" became known as Cushing syndrome.

CUSHING’S SYNDROME or hypercortisolism

Is a constellation of clinical features that result from chronic exposure to abnormally high levels
of cortisol or other glucocorticoids in the blood.

The most common cause of hypercortisolism is exogenous administration of

steroids.

Endogenous hypercortisolism most often is secondary to an ACTH-producing

pituitary microadenoma (Cushing disease), followed by primary adrenal
neoplasms (ACTH- independent hypercortisolism) and paraneoplastic ACTH
production by tumors (e.g., small cell lung cancer).

Cushing syndrome develops slowly and can be quite subtle in its early
manifestations. Early stages of the disorder may present with hypertension and
weight gain. With time the more characteristic central pattern of adipose tissue
deposition becomes apparent in the form of truncal obesity, moon facies, and
accumulation of fat in the posterior neck and back (buffalo hump).
Hypercortisolism causes selective atrophy of fast-twitch (type 2) myofibers,
resulting in decreased muscle mass and proximal limb weakness.
Glucocorticoids induce gluco- neogenesis and inhibit the uptake of glucose by
cells, with resultant hyperglycemia, glucosuria and polydipsia (secondary diabetes).
The catabolic effects cause loss of collagen and resorption of bones. Consequently
the skin is thin, fragile, and easily bruised; wound healing is poor; and cutaneous
striae are particularly common in the abdominal area (Fig. 24-44). Bone
resorption results in the development of osteoporosis, with consequent backache
and increased sus- ceptibility to fractures. Persons with Cushing syndrome are at
increased risk for a variety of infections, because glucocorticoids suppress the
immune response. Additional manifestations include several mental disturbances,
includ- ing mood swings, depression, and frank psychosis, as well as hirsutism
and menstrual abnormalities.

How to distinguish normal obesity from Cushing’s? By the presence of supraclavicular fat pad
and temporal fat pad, which are more common in Cushing’s.

Overnight 1mg Dexamethasone Suppression Test

CommonlyusedinthePhilippines,becauseitistheonlyone available in most
institutions
 Dexamethasone 1mg given at 11PM; cortisol checked at 8am.

Plasma cortisol > 50 nmol/L: Cushing’s syndrome

< 50 nmol/L: normal response
 Exogenous steroid will suppress ACTH production leading
to decrease in cortisol production: negative feedback
 Useful in renal failure and adrenal
incidentalomas