Corticosteroid

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(Redirected from
Systemic corticosteroids
)
Corticosteroid
Chemical class
Steroids
Legal status
In Wikidata

Corticosteroids are a class of

stress response, immune response, and regulation of inflammation, carbohydrate metabolism, protein catabolism, blood electrolyte levels, and behavior.[1]

Some common naturally occurring steroid hormones are

isomers). The main corticosteroids produced by the adrenal cortex are cortisol and aldosterone.[1]

Classes

Cortisol
Cortisone
Corticosterone
Aldosterone

Medical uses

Synthetic

skin diseases. Dexamethasone and its derivatives are almost pure glucocorticoids, while prednisone and its derivatives have some mineralocorticoid action in addition to the glucocorticoid effect. Fludrocortisone (Florinef) is a synthetic mineralocorticoid. Hydrocortisone (cortisol) is typically used for replacement therapy, e.g. for adrenal insufficiency and congenital adrenal hyperplasia
.

Medical conditions treated with systemic corticosteroids:[2][4]

Topical formulations are also available for the

skin, eyes (uveitis), lungs (asthma), nose (rhinitis), and bowels. Corticosteroids are also used supportively to prevent nausea, often in combination with 5-HT3 antagonists (e.g., ondansetron
).

Typical

hypertension (abnormally high blood pressure), steroid induced diabetes mellitus, psychosis, poor sleep, hypokalemia (low potassium levels in the blood), hypernatremia (high sodium levels in the blood) without causing peripheral edema, metabolic alkalosis and connective tissue weakness.[5]
Wound healing or ulcer formation may be inhibited by the immunosuppressive effects.

A variety of steroid medications, from anti-allergy nasal sprays (

central serous retinopathy (CSR).[6][7]

Corticosteroids have been widely used in treating people with traumatic brain injury.[8] A systematic review identified 20 randomised controlled trials and included 12,303 participants, then compared patients who received corticosteroids with patients who received no treatment. The authors recommended people with traumatic head injury should not be routinely treated with corticosteroids.[9]

Pharmacology

Corticosteroids act as agonists of the glucocorticoid receptor and/or the mineralocorticoid receptor.

In addition to their corticosteroid activity, some corticosteroids may have some progestogenic activity and may produce sex-related side effects.[10][11][12][13]

Pharmacogenetics

Asthma

Patients' response to inhaled corticosteroids has some basis in genetic variations. Two genes of interest are CHRH1 (corticotropin-releasing hormone receptor 1) and TBX21 (transcription factor T-bet). Both genes display some degree of polymorphic variation in humans, which may explain how some patients respond better to inhaled corticosteroid therapy than others.[14][15] However, not all asthma patients respond to corticosteroids and large sub groups of asthma patients are corticosteroid resistant.[16]

A study funded by the Patient-Centered Outcomes Research Institute of children and teens with mild persistent asthma found that using the control inhaler as needed worked the same as daily use in improving asthma control, number of asthma flares, how well the lungs work, and quality of life. Children and teens using the inhaler as needed used about one-fourth the amount of corticosteroid medicine as children and teens using it daily.[17][18]

Adverse effects

Lower arm of a 47-year-old female showing skin damage caused by topical corticosteroid use.

Use of corticosteroids has numerous side-effects, some of which may be severe:

  • Severe
    amoebic colitis: Fulminant amoebic colitis is associated with high case fatality and can occur in patients infected with the parasite Entamoeba histolytica after exposure to corticosteroid medications.[19]
  • Neuropsychiatric:
    anxiety,[21] depression. Therapeutic doses may cause a feeling of artificial well-being ("steroid euphoria").[22] The neuropsychiatric effects are partly mediated by sensitization of the body to the actions of adrenaline. Therapeutically, the bulk of corticosteroid dose is given in the morning to mimic the body's diurnal rhythm; if given at night, the feeling of being energized will interfere with sleep. An extensive review is provided by Flores and Gumina.[23]
  • Cardiovascular: Corticosteroids can cause sodium retention through a direct action on the kidney, in a manner analogous to the mineralocorticoid aldosterone. This can result in fluid retention and hypertension.
  • Metabolic: Corticosteroids cause a movement of body fat to the face and torso, resulting in "moon face", "buffalo hump", and "pot belly" or "beer belly", and cause movement of body fat away from the limbs. This has been termed corticosteroid-induced lipodystrophy. Due to the diversion of amino-acids to glucose, they are considered anti-anabolic, and long term therapy can cause muscle wasting (muscle atrophy).[24] Besides muscle atrophy, steroid myopathy includes muscle pains (myalgias), muscle weakness (typically of the proximal muscles), serum creatine kinase normal, EMG myopathic, and some have type II (fast-twitch/glycolytic) fibre atrophy.[25]
  • Endocrine: By increasing the production of glucose from amino-acid breakdown and opposing the action of insulin, corticosteroids can cause
    diabetes mellitus.[27]
  • Skeletal: Steroid-induced osteoporosis may be a side-effect of long-term corticosteroid use.[28][29][30] Use of inhaled corticosteroids among children with asthma may result in decreased height.[31]
  • Gastro-intestinal: While cases of
    peptic ulceration is relatively poor except for high doses taken for over a month,[32] the majority of doctors as of 2010 still believe this is the case, and would consider protective prophylactic measures.[33]
  • Eyes: chronic use may predispose to cataract and glaucoma. Clinical and experimental evidence indicates that corticosteroids can cause permanent eye damage by inducing central serous retinopathy (CSR, also known as central serous chorioretinopathy, CSC).[34] This should be borne in mind when treating patients with optic neuritis. There is experimental and clinical evidence that, at least in optic neuritis speed of treatment initiation is important.[35]
  • Vulnerability to infection: By suppressing immune reactions (which is one of the main reasons for their use in allergies), steroids may cause infections to flare up, notably candidiasis.[36]
  • Pregnancy: Corticosteroids have a low but significant
    contraindicated in pregnancy.[37]
  • Habituation: Topical steroid addiction (TSA) or
    red burning skin has been reported in long-term users of topical steroids (users who applied topical steroids to their skin over a period of weeks, months, or years).[38][39] TSA is characterised by uncontrollable, spreading dermatitis and worsening skin inflammation which requires a stronger topical steroid to get the same result as the first prescription. When topical steroid medication is lost, the skin experiences redness, burning, itching, hot skin, swelling, and/or oozing for a length of time. This is also called 'red skin syndrome' or 'topical steroid withdrawal' (TSW). After the withdrawal period is over the atopic dermatitis can cease or is less severe than it was before.[40]
  • In children the short term use of steroids by mouth increases the risk of vomiting, behavioral changes, and sleeping problems.[41]

Biosynthesis

Steroidogenesis
, including corticosteroid biosynthesis.

The corticosteroids are synthesized from

17α-hydroxylase
).

11β-hydroxylase (for corticosterone). These enzymes are nearly identical (they share 11β-hydroxylation and 18-hydroxylation functions), but aldosterone synthase is also able to perform an 18-oxidation. Moreover, aldosterone synthase is found within the zona glomerulosa at the outer edge of the adrenal cortex; 11β-hydroxylase is found in the zona fasciculata and zona glomerulosa
.

Classification of corticosteroids

By chemical structure

In general, corticosteroids are grouped into four classes, based on chemical structure. Allergic reactions to one member of a class typically indicate an intolerance of all members of the class. This is known as the "Coopman classification".[42][43]

The highlighted steroids are often used in the screening of allergies to topical steroids.[44]

Group A – Hydrocortisone type

Hydrocortisone, hydrocortisone acetate, cortisone acetate, tixocortol pivalate, prednisolone, methylprednisolone, and prednisone.

Group B – Acetonides (and related substances)

Amcinonide, budesonide, desonide, fluocinolone acetonide, fluocinonide, halcinonide, triamcinolone acetonide, and Deflazacort (O-isopropylidene derivative)

Group C – Betamethasone type

Beclometasone, betamethasone, dexamethasone, fluocortolone, halometasone, and mometasone.

Group D – Esters

Group D1 – Halogenated (less labile)

mometasone furoate
.

Group D2 – Labile prodrug esters

Ciclesonide, cortisone acetate, hydrocortisone aceponate, hydrocortisone acetate, hydrocortisone buteprate, hydrocortisone butyrate, hydrocortisone valerate, prednicarbate, and tixocortol pivalate.

By route of administration

Topical steroids

Main article: Topical steroid

For use topically on the skin, eye, and mucous membranes.

Topical corticosteroids are divided in potency classes I to IV in most countries (A to D in Japan). Seven categories are used in the United States to determine the level of potency of any given topical corticosteroid.

Inhaled steroids

For nasal mucosa, sinuses, bronchi, and lungs.[45]

This group includes:

There also exist certain combination preparations such as

Symbicort, containing budesonide and formoterol fumarate dihydrate (another long-acting bronchodilator).[46]
They are both approved for use in children over 12 years old.

Oral forms

Such as prednisone, prednisolone, methylprednisolone, or dexamethasone.[47]

Systemic forms

Available in injectables for intravenous and parenteral routes.[47]

History

Introduction of early corticosteroids[48][49][50]
Corticosteroid Introduced
Cortisone 1948
Hydrocortisone 1951
Fludrocortisone acetate
 1954[51]
Prednisolone 1955
Prednisone 1955[52]
Methylprednisolone 1956
Triamcinolone 1956
Dexamethasone 1958
Betamethasone 1958
Triamcinolone acetonide 1958
Fluorometholone 1959
Deflazacort 1969[53]

Tadeusz Reichstein, Edward Calvin Kendall, and Philip Showalter Hench were awarded the Nobel Prize for Physiology and Medicine in 1950 for their work on hormones of the adrenal cortex, which culminated in the isolation of cortisone.[54]

Initially hailed as a

adverse events of such a magnitude that the next major category of anti-inflammatory drugs, the nonsteroidal anti-inflammatory drugs (NSAIDs), was so named in order to demarcate from the opprobrium.[55] Corticosteroids were voted Allergen of the Year in 2005 by the American Contact Dermatitis Society.[56]

Mexican yams. His conversion of diosgenin into progesterone by a four-step process now known as Marker degradation was an important step in mass production of all steroidal hormones, including cortisone and chemicals used in hormonal contraception.[58]

In 1952, D.H. Peterson and H.C. Murray of

leukocyte adhesion cascade and the role of phospholipase A2 in the production of prostaglandins and leukotrienes
was fully understood in the early 1980s.

Etymology

The cortico- part of the name refers to the adrenal cortex, which makes these steroid hormones. Thus a corticosteroid is a "cortex steroid".

See also

References

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