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Corticosteroids are exogenous glucocorticoids important in immunosuppresion in a variety of illnesses. There

can possess both glucocorticoid and mineralcorticoid activity, though a reduction on MC activity is desirable.

These drugs are synthesized from cholic acid isolated from cattle or plants.





  • lungs
  • immune system
  • skin
  • transplants



  • increase surfactant and stabilize cell membranes
  • decrease prostaglandin and leukotrienes
  • increases pulmonary microvasculature
  • increases vitamin A

Immune System

Corticosteroids have profound effects on inflammation, reducing the concentration, distribution, and function of leukocytes and suppressing inflammatory cytokines and chemokines.

Following a dose of short-acting steroid, the number of circulating neutrophils increases, due to bone marrow mobilization and decreased extravasation, while the number of circulating lymphocytes, monocytes, eosinophils, and basophils decreases as they return to lymphoid tissue.

Macrophages and other APCs reduce their function


Topical steroids cause vasoconstriction, possibly by attenuating mast cell degranulation. Capillary permeability is also decreased through the reduction of histamine release.


Corticosteroids help control transplant rejection by reducing antigen expression in grafted tissue, delaying revascularization, and interfering with T cell sensitization and B cell activation.

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Like endogenous glucocorticoids, corticosteroids' effects are mediated by nuclear receptors, inhibiting the function of transcription factors such as AP1 or NF-kB. These TFs have broad action on regulation of growth factors and proinflammatory cytokines.

Corticosteroids influence most cells of the body. Major metabolic impacts are due to direct action of these drugs on the cell, but other important effects are mediated by insulin and glucagon.


Mediate many anti-inflammatory and immunosuppressive effects by inhibiting IL1beta, ppase A2, COX-2

Glucocorticoids must be activated by 11beta HSD1 (hydroxysteroid dehydrogenase).




Common Medications


  • overview
  • prednisone
  • topical steroids
  • Tab 2



Short- and medium-acting glucocorticoids

  • Hydrocortisone is a short acting molecule (8-12h) with both GC and MC activity
  • Prednisone is intermediate acting (12-36h) with stronger GC and weaker MC activity
  • prednisolone
  • methylprednisolone



  • traimcinolone
  • fluprednisolone



  • betamethasone
  • dexamethasone: long acting (24-72h) with very strong GC and no MC activity

stability is affected by C1,2 double bond, C9 F, and C16 hydroxylation or methylation


  • very similar to cortisone
  • given as prednosone; metabolized in the liver into prednisolone
  • prednisolone travels in blood bound to cortisone-bindign proteins
  • crosses plasma membrane alone
  • binds to receptors, activates transcription after binding to HREs
  • increases serum glucose, increasing insulin and lipogenesis
  • inhibits glucose uptake in muscle while stimulating hormone sensitive lipase, causing lipolysis
  • increased neutrophils, decreased B and T cells, monocytes, eosinophils and basophils
  • decreased IL-12 and IFN-gamma
  • complement
  • antibody production decreased by large doses but not by moderate
  • affects NCS - insomnia, euphoria
  • affects pituitary, suppresses ACTH
  • get peptic ulcers
  • decreases vitamin D
  • inhibits wound healing


topical steroids

potency ranking: group I: highest potency

ointments are usually strnger than a cream

Content 2

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Adverse Effects

The side effects of corticosteroids are numerous and can be serious. 50 mg for more than 7 days is bad for some reason.

short term

long term




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fungal/other infections

CBG levels are increased by estrogen, hyperthyroidism, diabetes

CBG levels are decreased by genetics, hypothyroidism, and protein deficiency states


Corticosteroid metabolism increased by barbiturates, phenytoin, mitotane, aminoglutethmide, rifampin.


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Guidance on Use

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Resources and References


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