14
Table 5. Clinical Features of Adrenal Insufficiency,
Glucocorticoid Withdrawal Syndrome and Common
Underlying Conditions
General remarks: Patients with glucocorticoid-induced adrenal insufficiency
may be asymptomatic at baseline conditions but can develop symptoms
— from mild to life-threatening adrenal crisis — when exposed to potential
triggers (see Table 9). When present, symptoms of adrenal insufficiency
are often non-specific and can overlap with those of the disease for which
glucocorticoids are prescribed. Recurrence of underlying autoimmune
diseases can occur during tapering of exogenous glucocorticoids. Signs and
symptoms of adrenal insufficiency can overlap with those of glucocorticoid
withdrawal syndrome, which arises from the discontinuation of rapid
tapering of glucocorticoid therapy in patients who developed a tolerance to
supraphysiologic glucocorticoid levels. In patients on glucocorticoids close to
the physiological range, adrenal insufficiency and glucocorticoid withdrawal
syndrome cannot be distinguished with complete accuracy.
Glucocorticoid
withdrawal
syndrome
Adrenal
insufficiency
Underlying
condition for which
glucocorticoids
were initially
prescribed
Symptoms General malaise,
fatigue, nausea, muscle
and joint pain, sleep
disturbances, mood
change
General malaise,
fatigue, nausea,
muscle and joint
pain
Depending on
condition (e.g., joint
pain in rheumatoid
arthritis). Common
overlapping symptoms
(general malaise,
fatigue)
Signs Cushingoid features
common, especially
earlier in the
glucocorticoid taper
Weight loss (*),
hypotension,
orthostasis
Disease-specific signs
reappear
Timing of
symptoms
and signs
occurrence
At any point during
glucocorticoid
taper, usually when
prednisone is decreased
<15 mg/day.
Higher risk with long-
term supraphysiologic
glucocorticoid therapy
Only when
not treated
with optimal
glucocorticoid
therapy
(subphysiologic
glucocorticoid
dose, increased
glucocorticoid
requirements due
to sickness)
At any point during
glucocorticoid taper
if the underlying
condition is sub-
optimally controlled
with a non-
glucocorticoid agent
Tables
