PH1.38 Describe the mechanism of action, types, doses, side effects, indications and contraindications of corticosteroids

1. PH1.38 Describe the mechanism of action, types,
doses, side effects, indications and
contraindications of corticosteroids
Dr Pankaj Kumar Gupta, MD
Assistant Professor,
Department of Pharmacology,
ESIC Medical College & Hospital,
Faridabad (HARYANA) INDIA

2. Specific Learning Objectives
• What are the corticosteroids
• History and Biosynthesis
• Mechanism of action
• Physiological and Pharmacological actions
• Pharmacokinetics and preparations
• Distinctive Features of different corticosteroids
• Uses – therapeutic and diagnostic
• Adverse reactions
• Contraindications

3. What are the Corticosteroids

4. What are the Corticosteroids
• Corticosteroids are a class of chemicals
encompassing both laboratory-synthesized and
naturally produced hormones.
• ‘Corticosteroid’ or ‘corticoid’ includes natural
gluco- and mineralo-corticoids and their synthetic
analogues.
• Steroid hormones help control metabolism,
inflammation, immune functions, salt and water
balance, development of sexual characteristics,
and the ability to withstand illness and injury.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4052587/
https://www.mdpi.com/journal/nutrients/special_issues/steroid_hormones

5. History
• 1855 – Addison`s disease (adrenal insufficiency)
• 1856 – Adrenal glands essential for life
• 1930 – Cortex > medulla
• 1932 – Cushing’s syndrome (a disorder caused by
excessive production or administration of glucocorticoid hormones)
• 1952 – Aldosterone

6. Biosynthesis
• The corticoids (both gluco and mineralo) are 21 carbon
compounds having a cyclopentanoperhydro-
phenanthrene (steroid) nucleus.
• They are synthesized in the adrenal cortical cells from
cholesterol.
• Adrenal steroidogenesis takes place under the influence
of ACTH which makes more cholesterol available for
conversion to pregnenolone and induces steroidogenic
enzymes.

7. Corticosteroid biosynthesis
Δ4-Androstendione
Testosterone

9. • Adrenal cortical cells store only minute
quantities of the hormones, rate of release is
governed by the rate of biosynthesis.
• The normal rate of secretion of the two
principal corticoids in man is—
– Hydrocortisone — 10–20 mg daily (nearly half of
this in the few morning hours).
– Aldosterone — 0.125 mg daily.

10. Feed-back regulation of HPA Axis
• The circulating
corticosteroids inhibit
ACTH release from
pituitary as well as CRH
production from
hypothalamus and thus
provide negative feed
back regulation of the
hypothalamo-pituitary-
adrenal (HPA) axis.

12. Mechanism of action
• Corticosteroids penetrate cells and bind to a high affinity
cytoplasmic receptor protein, due to which a structural
change occurs in the steroid receptor complex that allows its
migration into the nucleus and binding to glucocorticoid
response elements (GRE) on the chromatin promoting
transcription of specific m-RNA → regulation of protein
synthesis.
• This process takes at least 30–60 min, effects of corticosteroid
are not immediate, and once the appropriate proteins are
synthesized—effects persist much longer than the steroid
itself.

13. Mechanism of action

14. Rang et al. Pharmacology – 5st Ed. (2003)

15. Physiological and
Pharmacological actions

16. Mineralo-corticoid Action
• The most important physiological mineralocorticoid is
aldosterone.
• It acts on a specific mineralocorticoid receptor (MR) in DCT.
• Producing sodium and fluid retention and potassium
excretion.
• Aldosterone exerts the 90% of the mineralocorticoid activity.
Cortisol also have mineralocorticoid activity, but only 1/400th
that of aldosterone.
• Excess aldosterone causes hypokalemia & muscle weakness.
• Excess aldosterone increases tubular (intercalated cells)
hydrogen ion secretion, with resultant mild alkalosis.
• Too little aldosterone causes hyperkalemia & cardiac toxicity.

18. Action of Glucocorticoids
• Metabolic
• Anti-inflammatory
• Immunosuppressive
• Others
1. Carbohydrate
2. Protein
3. Lipid
4. Calcium metabolism
5. Electrolyte and H2O
6. CVS
7. Skeletal Muscle
8. CNS
9. Stomach
10. Growth and Cell Division
11. Blood
12. Anti-inflammatory
13. Immunosuppressant

19. Action of Glucocorticoids
SN Action Glucocorticoids are Catabolic
Hormone
Clinical Picture
1 Carbohydrate
metabolism
•↑ Glycogenesis (↑ Glycogen deposition
in liver by activation of hepatic glycogen
synthase)
•↑ Gluconeogenesis (↓Glucose utilization
by peripheral tissues, ↑ Glucose release
from liver)
•Hyperglycaemia
•Resistance to insulin
•A diabetes-like state
2 Protein
metabolism
•↑ Protein breakdown
•↑ Amino acid mobilization from
peripheral tissues
•Production of excess urea
•Negative nitrogen balance
•↑Uric acid excretion
•Muscle wasting
•Lympholysis
•Loss of osteoid from bone
•Thinning of skin
3 Fat metabolism •Permissive action
•Promote lipolysis due to glucagon,
growth hormone, Adr and thyroxine
•↑cAMP induced breakdown of
triglycerides
•Redistribution of body fat
(Subcutaneous tissue over extremities
loses fat which is deposited over face,
neck and shoulder)
•‘Moon face’, ‘fish mouth’ and ‘buffalo
hump’
Peripheral adipocytes are less sensitive to insulin and more sensitive to corticosteroid-facilitated lipolytic action of
GH and Adr, break down of fat predominates, whereas truncal adipocytes respond mainly to raised insulin levels
caused by glucocorticoid induced hyperglycaemia.

20. Moon Face

21. Redistribution of Fat

22. Buffalo Hump

23. Action of Glucocorticoids
SN Action Clinical Picture
4 Calcium
metabolism
•↓ Intestinal absorption
•↑ Renal excretion of Ca2+
•Loss of osteoid (decreased formation
and increased resorption) indirectly
results in loss of Ca2+ from bone
•Negative calcium balance
•Spongy bones (vertebrae, ribs, pelvis, etc.)
are more sensitive (Osteoporosis)
5 Water
excretion
•The effect on water excretion is
independent of action on Na+
transport;
•Hydrocortisone, but not aldosterone,
maintain normal g.f.r.
6 CVS •Permissive role for the pressor action
of Adr and angiotensin, as well as a
permissive role in the development of
hypertension.
•Adrenal insufficiency is attended by low
cardiac output, arteriolar dilatation, poor
vasoconstrictor response to Adr. These
changes along with hypovolemia (due to lack
of mineralocorticoid) are responsible for
cardiovascular collapse.
7 Stomach •↑Secretion of gastric acid and
Pepsin
May aggravate peptic ulcer

24. Action of Glucocorticoids
SN Action Clinical Picture
8 Skeletal
muscles
•Needed for maintaining the normal function
of Skeletal muscle
•Weakness occurs in both hypo- and
hypercorticism
•Hypocorticism: diminished work
capacity and weakness- due to
hypodynamic circulation.
•Hypercorticism:
•excess mineralocorticoid action
produces hypokalaemia → weakness;
•Excess glucocorticoid action causes
muscle wasting and myopathy →
weakness.
•Prolonged use: steroid myopathy
9 CNS •Mild euphoria due to direct effect on brain.
•Independent of relief of disease symptoms,
and sometimes progresses to cause
increased motor activity, insomnia,
hypomania or depression.
•Maintain the level of sensory perception
and normal level of excitability of neurones.
High doses lower seizure threshold.
Addison’s disease pts suffer from
apathy, depression and occasionally
psychosis.
10 Foetal
lungs
•Stimulate production of pulmonary
surfactants which are essential for inflation
of foetal lungs at birth and air breathing.
•Glucocorticoids promote structural and
functional maturation of foetal lungs
near term

25. Action of Glucocorticoids
SN Action Clinical Picture
11 Lymphoid tissue
and blood cells
↑ the rate of destruction of lymphoid cells (T
cells are more sensitive than B cells)
↑ the no. of RBCs, platelets and neutrophils
in circulation.
Lymphocytes, eosinophils and basophils-
count is ↓ due to their sequestration in
tissues. Blood counts come back to normal
after 24 hours.
A marked lytic response is
shown by malignant
lymphatic cells- basis of their
use in lymphomas.
12 Inflammatory
responses
•Interfere at several steps in the
inflammatory response, especially by
limitation of recruitment of inflammatory cells
at the local site and production of pro-
inflammatory mediators like PGs, LTs, PAF
through indirect inhibition of phospholipase
A2.
•Only palliative; do not
remove the cause of
inflammation
13 Immunological
and allergic
responses
Suppress all types of hypersensitization and
allergic phenomena.
Factors involved may be inhibition of IL-1
release from macrophages; inhibition of IL-2
formation and action → T cell proliferation is
not stimulated; suppression of natural killer
cells, etc.
Basis is the suppression of
CMI in which T cells are
primarily involved, e.g.
delayed hypersensitivity and
graft rejection. Suppression
of CMI is the basis of their
use in autoimmune diseases
and organ transplantation.

26. Anti-inflammatory actions of corticosteroids
Corticosteroid inhibitory effect

27. • Inhibit cell division
or synthesis of DNA
• Delay the process of
healing
• Retard the growth of
children
Growth and Cell division

28. Pharmacokinetics and
Preparations

29. Glucocorticoids
Kinetics:
• Well absorbed orally
• Bound to corticosteroid-binding globulin and albumin
• Distributed all over the body & passes the BBB
• In the liver, cortisol is reversibly converted to cortisone
& conjugated with glucuronic & sulfuric acid
• Excreted in urine as 17-hydroxy corticosteroids

30. Circadian Rhythm
• Corticosteroid production follow a circadian rhythm.

31. Classification

32. Relative activity of systemic
corticosteroids

33. Endogenous Glucocorticoids
Hydrocortisone
Corticosterone

34. Distinctive Features of different
corticosteroids
SN Steroid Distinctive properties Dose & brand
1 Hydrocortisone
(cortisol)
•Acts rapidly but has short duration of action
•Both glucocorticoid & mineralocorticoid
activity significantly
•Uses:
•Replacement therapy
•Shock, status asthmaticus, acute
adrenal insufficiency
•Topically
•As suspension for enema in ulcerative
colitis
•LYCORTIN-S 100 mg/3 ml,
200 mg/5 ml inj;
•20 mg morning + 10 mg
afternoon orally
•100 mg i.v. bolus + 100 mg 8
hourly IV infusion
2 Prednisolone •4 times more potent than hydrocortisone
•More selective glucocorticoid
•Fluid retention with high doses.
•Intermediate duration of action: causes less
pituitary-adrenal suppression when a single
morning dose or alternate day treatment is
given.
•Uses
•for allergic, inflammatory, autoimmune
diseases and in malignancies:
•OMNACORTIL 2.5 mg, 5 mg,
10 mg, 20 mg, 30 mg, 40 mg
tab, 5 mg/ml
•Oral susp, 5 mg/ml oral drops
•5–60 mg/day oral,
•10–40 mg IM., Intraarticular

35. Distinctive Features of different
corticosteroids
SN Steroid Distinctive properties Dose & brand
3 Methylprednisolone •Slightly more potent and more
selective than prednisolone: 4–32
mg/day oral.
•Methylprednisolone acetate has
been used as a retention enema in
ulcerative colitis.
•Pulse therapy with high dose
methylprednisolone (1 g infused IV
every 6–8 weeks) in in
nonresponsive active rheumatoid
arthritis, renal transplant,
pemphigus.
•Minimal suppression of pituitary-
adrenal axis.
•SOLU-MEDROL
Methylprednisolone (as sod.
succinate) 4 mg tab; 40 mg, 125
mg, 0.5 g (8 ml) and 1.0 g (16
ml) inj, for IM or slow IV inj,
•DEESOLONE 4, 16 mg tabs,
0.5 g and 1.0 g. inj.
•DEPOT MEDROL
Methylprednisolone acetate 40
mg/ml and 80 mg/ml susp. for IM
or intraarticular injection.
4 Triamcinolone •Slightly more potent than
prednisolone but highly selective
glucocorticoid
•Dose: 4–32 mg/day oral, 5–40
mg IM intraarticular
•KENACORT, TRICORT 1, 4, 8
mg tab., 10 mg/ml, 40 mg/ml (as
•acetonide) for i.m., intraarticular
inj.

36. Distinctive Features of different
corticosteroids
SN Steroid Distinctive properties Dose & brand
5 Dexamethasone •Very potent and highly selective glucocorticoid.
•Long-acting
•Marked pituitary-adrenal suppression
•Fluid retention and hypertension are not a
problem.
•Uses:
•For inflammatory and allergic conditions
•For shock, cerebral edema
•WYMESONE, DECADRON,
DEXONA 0.5 mg tab, 4 mg/ml
(as sod. phosphate) for IV/IM.
inj., 0.5 mg/ml oral drops;
•0.5–5 mg/day oral
•4–20 mg/day IV infusion or IM
6 Betamethasone •Similar to dexamethasone,
•0.5–5 mg/ day oral,
•4–20 mg IM/IV injection
•Dexamethasone or betamethasone are preferred
in cerebral edema and other states in which fluid
retention must be avoided.
•BETNESOL, BETACORTRIL,
CELESTONE 0.5 mg, 1 mg
tab, 4 mg/ml (as sod.
phosphate) for IV/IM inj., 0.5
mg/ml oral drops
7 Deflazacort •Glucocorticoid potency is less than of
prednisolone, but it lacks mineralocorticoid activity.
•Fewer adverse effects due to its lower potency.
•Lesser growth retardation, particularly
recommended in children
•Uses: for inflammatory and immunological
disorders.
•Dose: 60–120 mg/day initially,
6–18 mg/day for maintenance;
•children 0.25–1.5 mg/kg daily
or on alternate days.
•DEFCORT 1 mg, 6 mg, 12
mg, 18 mg, 24 mg, 30 mg tabs,
6 mg/5 ml syr.

37. Distinctive Features of different
corticosteroids
SN Steroid Distinctive properties Dose & brand
1 Desoxycorticosterone
acetate (DOCA)
•Mineralocorticoid activity only
•Used occasionally for replacement
therapy in Addison’s disease
•2–5 mg sublingual,
•10–20 mg IM once
or twice weekly.
2 Fludrocortisone •Potent mineralocorticoid + some
glucocorticoid activity
•Orally active
•Uses
•Replacement therapy in
Addison’s disease
•Congenital adrenal hyperplasia
in patients with salt wasting
•Idiopathic postural hypotension
FLORICORT 100
μg tab.
50–200 μg daily
50–200 μg/day
100–200 μg/day
3 Aldosterone •Most potent mineralocorticoid.
•Not used clinically because of low
oral bioavailability and difficulties in
regulating doses.

38. Hydrocortisone
Prednisolone
Nonfluorinated
prednisolones
Fluorinated prednisolones
Methylprednisolone
Betamethasone
Dexamethasone
Triamcinolone
The most used glucocorticoids

39. Uses – Therapeutic and Diagnostic

40. Uses
As a replacement Therapy
1 Acute adrenal insufficiency •An emergency.
•Hydrocortisone (100 mg) or dexamethasone (8–16 mg)
are given IV, first as a bolus injection and then as infusion,
along with isotonic saline in glucose solution.
2 Chronic adrenal
insufficiency (Addison’s
disease)
•Hydrocortisone orally along with adequate salt and water
allowance
3 Congenital adrenal
hyperplasia (Adrenogenital
syndrome)
•A familial disorder due to genetic deficiency of
steroidogenic enzymes, mostly 21-hydroxylase.
•Synthesis of hydrocortisone and aldosterone suffers.
•Compensatory increase in ACTH secretion causing
adrenocortical hypertrophy.
•Enzyme deficiency being only partial in most cases,
normal amounts of gluco- and mineralocorticoids are
produced along with excessive amounts of weak
androgens which produce virilization and/or precocious
sexual development.
•Salt wasting in severe deficiency.
•Hydrocortisone 0.6 mg/ kg daily in divided doses round
the clock to maintain feed back suppression of pituitary.
•If salt wasting persists—fludrocortisone 50–200 μg/day

41. Glucocorticoids
Pharmacotherapy
for non endocrine diseases

42. General principles of Glucocorticoids
Pharmacotherapy
for non endocrine diseases
• Steroids are powerful drugs. They may cause dramatic
improvement in many severe diseases as well as produce
equally severe adverse effects if not properly used.
• The use of steroids in non endocrine disease is empirical and
palliative, but may be life-saving.
• The following general principles must be observed.
– Single dose (even excessive) is not harmful.
– Short courses (even high dose) are not likely to be harmful
in the absence of contraindications.
– Long-term use is potentially hazardous.
– No abrupt withdrawal after a corticoid has been given for
more than 2 to 3 weeks: may precipitate adrenal
insufficiency.

43. – Initial dose depends on severity of the disease; start with a
high dose in severe illness, while in mild cases start with
the lowest dose.
– Infection, severe trauma, surgery or any stress during
corticoid therapy—increase the dose.
– Use local therapy (cutaneous, inhaled, intranasal etc.)
wherever possible.

44. Uses
Pharmacotherapy (for non-endocrine diseases)
1 Arthritides Rheumatoid arthritis: Only in severe cases as adjuvants to NSAIDs
Osteoarthritis: Intra-articular injection of steroid is rare, but may be
used to control an acute exacerbation. Repeated injections may cause
joint destruction.
Rheumatic fever: only in severe cases with myocarditis and CHF.
Gout: Short course in acute gouty arthritis when NSAIDs have failed to
afford relief and colchicine is not tolerated.
2 Collagen
diseases
Steroids are life saving in systemic lupus erythematosus, polyarteritis
nodosa, dermatomyositis, nephrotic syndrome, glomerulonephritis etc.
3 Severe
allergic
reactions
For short periods in anaphylaxis, angioneurotic edema, urticaria and
serum sickness.
In anaphylactic shock and angioedema of larynx Adr (which acts
immediately) is preferred as IV inj of a glucocorticoid takes 1–2 hours to
act.
Topically in allergic conjunctivitis and rhinitis.
4 Autoimmune
diseases
Autoimmune haemolytic anaemia, idiopathic thrombocytopenic
purpura, active chronic hepatitis respond to corticoids.
Prednisolone 1–2 mg/kg/day is given till remission.
As an adjunctive to neostigmine for remission in severe cases of
myasthenia gravis.

45. Uses
Pharmacotherapy (for non-endocrine diseases)
5 Bronchial
asthma
•Chronic Asthma- early institution of inhaled glucocorticoid therapy is now
recommended in most cases needing inhaled β2 agonists almost daily.
•Status asthmaticus- systemic corticosteroids (IV)
•Acute asthma exacerbation- short-course of high dose oral corticoid.
6 Other lung
diseases
•Corticosteroids benefit aspiration pneumonia and pulmonary edema from
drowning.
•Accelerate lung maturation and surfactant production in the foetal lung and
prevent respiratory distress syndrome at birth.
•Two doses of betamethasone or dexamethasone 12 mg IM at 24-hour interval
may be administered to the mother if premature delivery is contemplated.
•Betamethasone or dexamethasone are preferred because of their higher
placental transfer.
7 Infective
diseases
•Indicated only in serious infective diseases to tide over crisis or to prevent
complications administered under effective chemotherapeutic cover.
•E.g. severe forms of tuberculosis (miliary, meningeal, renal, etc.), severe lepra
reaction, certain forms of bacterial meningitis and Pneumocystis carinii
pneumonia with hypoxia in AIDS patients.
8 Eye
diseases
•Used in a large number of inflammatory ocular diseases.
•Topical instillation as eye drops or ointment is effective in diseases of the
anterior chamber, e.g. allergic conjunctivitis, iritis, iridocyclitis, keratitis, etc.
•Should not be used in infective conditions.
•Contraindicated in herpes simplex keratitis and in ocular injuries.

46. Uses
Pharmacotherapy (for non-endocrine diseases)
9 Skin diseases •Topical corticosteroids are highly effective in many eczematous skin
diseases.
•Systemic therapy is needed (may be life-saving) in pemphigus vulgaris,
exfoliative dermatitis, Stevens-Johnson syndrome etc.
10 Intestinal
diseases
•For Ulcerative colitis, Crohn’s disease & coeliac disease.
•Indicated during acute phases—may be used orally or as retention
enema (for colonic involvement). Particularly valuable for patients with
systemic manifestations, and are given in addition to
sulfasalazine/mesalazine + other measures.
•Some specialists advocate small maintenance doses to prevent
relapses.
11 Neurological
conditions
•Cerebral edema due to tumours, tubercular meningitis.
•Dexa- or betamethasone are preferred
•Large doses given i.v. soon after spinal injury may reduce the
resulting neurological sequelae.
•A short course (2–4 weeks) of oral prednisolone can hasten recovery
from Bell’s palsy and acute exacerbation of multiple sclerosis.
•Neurocysticercosis: When albendazole/praziquantel is used to kill
cysticerci lodged in the brain, prednisolone 40 mg/day or equivalent is
given for 2–4 weeks to suppress the reaction to the dying larvae.

47. Uses
Pharmacotherapy (for non-endocrine diseases)
12 Nausea and
vomiting
•Dexamethasone 8–20 mg IV is frequently used to augment
the antiemetic effect of ondansetron or metoclopramide
against highly emetogenic cancer chemotherapy.
•High dose glucocorticoids provide modest protection from
chemotherapy induced & general anaesthesia associated
nausea and vomiting, probably due to their anti-inflammatory
action.
13 Malignancies •In combination with chemotherapy of acute lymphatic
leukaemia, Hodgkin’s and other lymphomas, because of
their marked lympholytic action in these conditions.
•In hormone responsive breast carcinoma —causing HPA
suppression so as to reduce production of adrenal androgens
which are converted to estrogens in the body.
•Corticoids also afford symptomatic relief in other advanced
malignancies by improving appetite and controlling secondary
hypercalcaemia.
14 Organ
transplantation
and skin allograft
•High dose corticoids with other immunosuppressants to
prevent the rejection reaction.
•Low maintenance doses continued over long term +
maintenance doses of companion drugs.

48. Uses
Pharmacotherapy (for non-endocrine diseases)
15 Septic shock •Low-dose (hydrocortisone 100 mg 8 hourly IV
infusion for 5–7 days) therapy in patients who are
adrenal deficient and who do not respond adequately
to fluid replacement and vasopressors.
16 Thyroid storm •Reduces peripheral T4 to T3 conversion.
Hydrocortisone 100 mg i.v. 8 hourly may improve the
outcome.
17 To test pituitary-
adrenal axis function
•Dexamethasone suppresses pituitary-adrenal axis
at doses which do not contribute to steroid
metabolites in urine.
•Responsiveness of the axis can be tested by
measuring daily urinary steroid metabolite excretion
after dosing with dexamethasone.

49. Adverse reactions and
contraindications

50. • Cushing’s syndrome
• Osteoporosis
• Tendency to hyperglycaemia
• Negative nitrogen balance
• Increased appetite
• Increased susceptibility
to infections
• Obesity, etc.
Cushing’s
syndrome
Adverse effects of Glucocorticoids

51. Contraindications
SN Contraindications Mechanism
1 Peptic ulcer both gastric mucus production and gastric bicarbonate secretion are
impaired by steroid administration, results in a weakening of gastric
mucosal defences, also, can irritate the lining of the stomach by
inhibiting prostaglandins.
2 Diabetes mellitus Steroids induce insulin resistance by directly interfering with signaling
cascades, mainly the GLUT4 transporter, within muscle cells, with the
subsequent 30%-50% reduction in insulin-stimulated glucose uptake
and a 70% reduction in insulin-stimulated glycogen synthesis.
3 Hypertension Cause the body to retain fluid. Extra fluid in the circulation can cause
an increase in blood pressure
4 Pregnancy (risk foetal
defects)
Prolonged corticosteroid therapy during pregnancy increases the risk
of gestational diabetes, pregnancy induced hypertension and
preeclampsia.
5 Tuberculosis, mycoses,
virosis (including Herpes
simplex keratitis), and other
infections
Immune suppression with corticosteroids predisposes to tuberculosis,
mycoses & virosis.

52. Contraindications
SN Contraindications Mechanism
6 Osteoporosis They act to decrease absorption of calcium from the
intestine, and increase urinary calcium loss.
7 Psychosis Abnormalities of the hypothalamo–pituitary–adrenal
(HPA) axis can result in mood disorders
8 Epilepsy Can lower the seizure threshold and can potentially
provoke seizures
9 Chronic heart failure A high dose of corticosteroids may promote sodium
and water retention in patients with HF, potentially
leading to worsening of the disease.
10 Renal failure Due to increase risk of hypertension, diabetes, weight
gain, short stature, fractures, and infections.

53. Dosage withdrawal
• Any patient who has received >20–25 mg/day
hydrocortisone, or ≥5 mg prednisolone/day or
equivalent for longer than 2–3 weeks should be
put on a scheme of gradual withdrawal.
• Administration of ACTH during withdrawal does
not hasten recovery because adrenals recover
earlier than pituitary and hypothalamus.

54. Topical Glucocorticoids
• Glucocorticoids are quite effective when applied topically
and are nontoxic to the skin in the short term.
• The factors that determine local penetration are the
structure of the compound employed, the vehicle, the basic
additives, occlusion versus open use, normal skin versus
diseased skin, and small areas versus large areas of
application.
• Fluorinated steroids (dexamethasone, triamcinolone acetonide,
betamethasone, and beclomethasone) penetrate the skin better
than non-fluorinated steroids, such as hydrocortisone.
However, fluorinated steroids also cause more local
complications and may be associated with systemic
absorption and side effects.
Topical corticosteroids in dermatology. Year: 2016, Volume: 82, Issue: 4, July-August.

56. References
• MLA. Tripathi, K. D. Essentials of Medical Pharmacology. 8th ed., Jaypee
Brothers Medical, 2018.
• Topical corticosteroids in dermatology. Year: 2016, Volume: 82, Issue:
4, July-August.

57. Thanks