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Glucocorticoids & Mineralocorticoids

The hormonal steroids may be classified as:

  1. Those having important effects on intermediary metabolism and immune function (glucocorticoids),
  2. Those having principally salt-retaining activity (mineralocorticoids),
  3. Those having androgenic or estrogenic activity.
  4. In humans, the major glucocorticoid is cortisol and the most important mineralocorticoid is aldosterone.


  1. Hormones of adrenal cortex; participate in “fight and flight response” described by Canon.
  2. Corticosteroids are synthesized by CYP mediated reactions from cholesterol.



  1. Glucocorticoids from zona fasciculata
  2. Aldosterone from zona glomerulosa 


Pharmacological actions


Carbohydrate metabolism



Corticosteroids produce hyperglycemia by producing neoglucogensis and reduce glucose utilization. Dexamethasone increases glycogen deposition. This occurs due to increase in glycogeneis from non-hexose substrates such aminoacids. 


Protein metabolism


Corticosteroids are catabolic and produce protein catabolism. This produces muscle weakness.


Lipid metabolism


Redistribute fat due to lipolysis. This leads to ‘buffalo hump’.





Inhibit inflammatory responses by blocking the enzyme phospholipase-A2.

They also inhibit macrophage migration and prevent oxidative burst.

Inhibition of capillary permeability.



Glycocorticoids promote apoptosis of lymphocytes

Inhibit antibody production by B-cells.

This results in suppression of immune responses. These decrease release of interleukin-12 and interferon-gamma from immune cells.   

Topical activity

Cortisone and prednisolone-no topical activity

Betamethasone and dexamethasone have maximum

Mineralocorticoids such as fludrocortisone or desoxycorticosterone acetate-free from topical actions.






  1. Hydrocortisone is the shortest and least potent glucorticoid.
  2. Dexamethasone is the longest and most potent glucocorticoid.
  3. Descorticosterone acetate (DOCA)-pure mineralocorticoid with no glucocorticoid activity.
  4. Prednisone is a prodrug and gets converted into prednisolone.



  1. Predinsolone is the drug of choice for:
    1. Chronic active hepatitis
    2. Primary bilary cirrohosis
    3. Nephrotic syndrome
    4. Temporal arteritis
    5. Methylprednisolone is DOC
    6. Bullous disease
    7. Pemphigous
    8. Pemphigoid
    9. Spinal cord injury (Methylprednisolone is preferred)


  1. Dexmathsone is DOC
    a. Brain edema especially peritumor brain edema.


  1. Fludrocortisone is DOC
    a. Postral hypotension.


  1. Treatment of Disturbed Adrenal Function
  1. Adrenocortical insufficiency: Chronic (Addison’s Disease)- Hydrocortisone and Fludrocortisone Acute: immediate I.v. Hydrocortisone
  2. Congenital adrenal hyperplasia
  3. Chrousos Syndrome: Primary Generalized Glucocorticoid Resistance- Dexamethsone is DOC
  4. After treatment of Cushing syndrome (e.g. adrenelectomy)
  5. Fetal Lung maturation: When delivery is anticipated before 34 weeks of gestation, intramuscular betamethasone, 12 mg, followed by an additional dose of 12 mg 18–24 hours later, is commonly used.
  1. Diagnostic Use:
Dexamethasone Suppression Test:
Low Dose Dst High Dose Dst
  1. For diagnosis of Cushing’s syndrome
  2. As a screening test, 1 mg dexamethasone is given orally at 11 PM, and a plasma sample is obtained the following morning. In normal individuals, the morning cortisol concentration is usually less than 3 mcg/dL, whereas in Cushing’s syndrome the level is usually greater than 5 mcg/dL.
  3. False positive: Psuedo-Cushing Syndrome, (hypercortisolism due to anxiety, depression, and alcoholism)
  4. For Psuedo-Cushing syndrome: A combined test is carried out, consisting of dexamethasone (0.5 mg orally every 6 hours for 2 days) followed by a standard corticotropin-releasing hormone (CRH) test (1 mg/kg given as a bolus intravenous infusion 2 hours after the last dose of dexamethasone).
  1. To distinguish patients with Cushing’s disease from those with steroid-producing tumors of the adrenal cortex or with the ectopic ACTH syndrome
  2. Dexamethasone is given in a dosage of 0.5 mg orally every 6 hours for 2 days, followed by 2 mg orally every 6 hours for 2 days, and the urine is then assayed for cortisol or its metabolites (Liddle’s test); or dexamethasone is given as a single dose of 8 mg at 11 PM, and the plasma cortisol is measured at 8 AM the following day. In patients with Cushing’s disease, the suppressant effect of dexamethasone usually produces a 50% reduction in hormone levels. In patients in whom suppression does not occur, the ACTH level will be low in the presence of a cortisol-producing adrenal tumor and elevated in patients with an ectopic ACTH-producing tumor.
  1. Treatment of Non-Adrenal disorders
Allergic reactions Angioneurotic edema, asthma, bee stings, con- tact dermatitis, drug reactions, allergic rhinitis, serum sickness, urticaria
Collagen-vascular disorders
Giant cell arteritis, lupus erythematosus, mixed connective tissue syndromes, polymyositis, polymyalgia rheumatica, rheumatoid arthritis, temporal arteritis
Eye diseases Acute uveitis, allergic conjunctivitis, choroiditis, optic neuritis
Gastrointestinal diseases Inflammatory bowel disease, nontropical sprue, subacute hepatic necrosis
Hematologic disorders
Acquired hemolytic anemia, acute allergic purpura, leukemia, lymphoma, autoimmune hemolytic anemia, idiopathic thrombocytopenic purpura, multiple myeloma
Systemic inflammation
Acute respiratory distress syndrome (sustained therapy with moderate dosage accelerates recovery and decreases mortality)
Infections Acute respiratory distress syndrome, sepsis
Bones and joints Arthritis, bursitis, tenosynovitis
Neurologic disorders
Cerebral edema (large doses of dexamethasone are given to patients following brain surgery to minimize cerebral edema in the postoperative period), multiple sclerosis
Organ transplants Prevention and treatment of rejection (immunosuppression)
Pulmonary diseases
Aspiration pneumonia, bronchial asthma, prevention of infant respiratory distress syndrome, sarcoidosis
Renal disorders Nephrotic syndrome
Skin diseases
Atopic dermatitis, dermatoses, lichen simplex chronicus (localized neurodermatitis), mycosis fungoides, pemphigus, seborrheic dermatitis, xerosis
Thyroid diseases Malignant exophthalmos, subacute thyroiditis
Miscellaneous Hypercalcemia, mountain sickness


  1. < 2 Weeks: Usually Safe. Insomnia, behavioral changes (primarily hypomania), and acute peptic ulcers are occasionally observed even after only a few days of treatment. Acute pancreatitis is a rare but serious acute adverse effect of high-dose glucocorticoids.
  2. > 2 Weeks (Iatrogenic Cushing Syndrome)

C-cushings syndrome
R-retardation of growth
T-thin skin n easy brusibility
I-infections n immunosuppression
C-cataract n glaucoma
S-suppression of HPA axis
T-thinning n ulceration of gastric mucosa
E-Emotional disturbance
R-rise in BP
I- Increase in hair growth (hirsuitism)
O-others like fetal abnormalities n hypokalemia
D-diabetes mellitus precipitation

C/I: Peptic ulcer, heart disease or hypertension with heart failure, certain infectious illnesses such as varicella and tuberculosis, psychoses, diabetes, osteoporosis, or glaucoma


Glucocorticoid inhibitors

  1. Antagonists
    a. Mifepristone
    1. Glucocorticoid receptor antagonist
    2. Also has anti-progesterone activity   
  2. Synthesis inhibitors
    1. Aminoglutethimide (blocks conversion of cholesterol to pregnanolone)
    2. Metyrapone (blocks the enzyme named 11-hydroxylase).
    3. Ketoconazole is antiglucorticoid with antiandrogenic activity
    4. Trilostane: 17-hydroxysteroid dehydrogenase inhibitor that interferes with the synthesis of adrenal and gonadal hormones and is comparable to aminoglutethimide.
    5. Abiraterone: Abiraterone is an orally active steroid prodrug and has been studied in the treatment of refractory prostate cancer. It blocks 17-hydroxylase and 17,20-lyase, and predictably reduces synthesis of cortisol and gonadal steroids in the adrenal and gonadal steroids in the gonads.
    6. Mitotane: cytotoxic to adrenal cortex, was used in adrenal carcinoma but withdrawn due to toxicity, now available on compassionate basis.
  1. The most important mineralocorticoid in humans is aldosterone. However, small amounts of deoxycorticosterone are also formed and released.
  2. Fludrocortisone, a synthetic corticosteroid, is the most commonly prescribed salt-retaining hormone.
  3. Aldosterone is most potent mineralocorticoid but is not absorbed orally. Therefore, fludrocortisone is used.
Mineralocorticoids Antagonist
  1. Spironolactone: aldosterone receptor antagonist used in primary aldosteronism,
    1. Spironolactone is also an androgen antagonist hence used in hirsutism in women, as a diuretic in cardiovascular disease.
    2. Adverse effects reported for spironolactone include hyperkalemia, cardiac arrhythmia, menstrual abnormalities, gynecomastia, sedation, headache, gastrointestinal disturbances, and skin rashes.
  2. Eplerenone: another aldosterone antagonist is approved for the treatment of hypertension.
    *Like spironolactone, eplerenone has also been found to reduce mortality in heart failure. This aldosterone receptor antagonist is somewhat more selective than spironolactone and has no reported effects on androgen receptors.
  3. Drospirenone: a progestin in an oral contraceptive also antagonizes the effects of aldosterone.

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