glucocorticoid (redirected from Gluco corticoid)

glucocorticoid /glu·co·cor·ti·coid/ (-kor´tĭ-koid)

1. any of the group of corticosteroids predominantly involved in carbohydrate metabolism, and also in fat and protein metabolism and many other activities (e.g., alteration of connective tissue response to injury and inhibition of inflammatory and allergic reactions); some also exhibit varying degrees of mineralocorticoid activity. In humans, the most important glucocorticoids are cortisol (hydrocortisone) and cortisone.

2. of, pertaining to, or resembling a glucocorticoid.

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glu·co·cor·ti·coid (glk-kôrt-koid)

n.

Any of a group of anti-inflammatory steroidlike compounds, such as hydrocortisone, that are produced by the adrenal cortex, are involved in carbohydrate, protein, and fat metabolism, and are used as anti-inflammatory agents.

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gluco·corti·coid adj.

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Glucocorticoid

Any of a group of corticosteroids (as hydrocortisone or dexamethasone) that are anti-inflammatory and immunosuppressive, and that are used widely in medicine (as in the alleviation of the symptoms of rheumatoid arthritis).

Mentioned in: Adrenal Virilism, Antipsychotic Drugs, Atypical, Corticosteroids, Inhaled, Croup

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glucocorticoid

[glo̅o̅′kōkôr′təkoid]

Etymology: Gk, glykys + L, cortex, bark; Gk, eidos, form

an adrenocortical steroid hormone that increases gluconeogenesis, exerts an antiinflammatory effect, and influences many body functions. The most important of the three glucocorticoids is cortisol (hydrocortisone). Corticosterone is less active, and cortisone is inactive until converted to cortisol. Glucocorticoids promote the release of amino acids from muscle, mobilize fatty acids from fat stores, and increase the ability of skeletal muscles to maintain contractions and avoid fatigue. These hormones are known to stabilize mitochondrial and lysosomal membranes, increase the production of adenosine triphosphate, promote the formation of certain liver enzymes, and decrease antibody production and the number of circulating eosinophils. A deficiency of glucocorticoids is characterized by hyperpigmentation (bronzing) of the skin, fasting hypoglycemia, weight loss, and apathy. An excess is associated with elevated serum glucose levels, thinning of the skin, ecchymosis, osteoporosis, poor wound healing, increased susceptibility to infection, and obesity. Glucocorticoid secretion is stimulated by the adrenocorticotropic hormone of the anterior pituitary, which in turn is regulated by the corticotropin-releasing hormone of the hypothalamus and circulating cortiosol levels (negative feedback). Synthetic or semisynthetic glucocorticoids, derived chiefly from cortisol, include prednisone, prednisolone, dexamethasone, methylprednisolone, triamcinolone, and betamethasone. Compare mineralocorticoid.

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glucocorticoid [gloo″ko-kor´tĭ-koid]

any corticoid substance that increases gluconeogenesis, raising the concentration of liver glycogen and blood glucose; the group includes cortisol, cortisone, and corticosterone. The release of glucocorticoids from the adrenal cortex is initially triggered by corticotropin-releasing hormone (CRH) elaborated by the hypothalamus. The target organ for this factor is the anterior lobe of the pituitary gland, which reacts to the presence of CRH by releasing corticotropin (ACTH). ACTH, in turn, stimulates the release of the glucocorticoids from the adrenal cortex. (See also adrenal gland.)

The principal glucocorticoid hormone is cortisol, which regulates the metabolism of proteins, carbohydrates, and lipids. Specifically, it increases the catabolism or breakdown of protein in bone, skin, muscle, and connective tissue. Cortisol also diminishes cellular utilization of glucose and increases the output of glucose from the liver.

Because of their effects on glucose levels and fat metabolism, all the glucocorticoids are referred to as anti-insulin diabetogenic hormones. They increase the blood sugar level, raise the concentration of plasma lipids, and, when insulin secretion is insufficient, promote formation of ketone bodies, thus contributing to ketoacidosis.

Other physiologic processes within the body can occur only in the presence of or with the “permission of€” the glucocorticoids. For example, the secretion of digestive enzymes by gastric cells and the normal excitability of myocardial and central nervous system neurons require a certain level of glucocorticoids.

Glucocorticoids also promote transport of amino acids into the extracellular compartment, making them more readily available for the production of energy. In times of stress the glucocorticoids influence the effectiveness of the catecholaminesdopamine, epinephrine, and norepinephrine. For example, the presence of cortisol is essential to norepinephrine-induced vasoconstriction and other physiologic phenomena necessary for survival under stress. This particular property of cortisol demonstrates the one identifiable relationship between hormones from the adrenal cortex and those from the adrenal medulla. One of the medullary hormones is norepinephrine, which is secreted in large quantities when the gland is stimulated by the sympathetic nervous system in response to stress.

Another effect of cortisol is that of dampening the body's inflammatory response to invasion by foreign agents. When present in large amounts, cortisol inhibits the release of histamine and counteracts potentially destructive reactions, such as increased capillary permeability and the migration of leukocytes. Since the immune response can damage body cells as well as those of foreign agents, the antiinflammatory protective mechanisms of cortisol help preserve the integrity of body cells at the site of the inflammatory response.

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glucocorticoid

any corticoid substance that increases gluconeogenesis, raising the concentration of liver glycogen and blood sugar, i.e. cortisol (hydrocortisone), cortisone and corticosterone. These substances are widely used as anti-inflammatory agents; they are effective at terminating pregnancy if it is in the late stages and they are used as a management tool in cattle for that purpose.

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dexamethasone sodium phosphate

Pharmacologic class: Glucocorticoid

Therapeutic class: Anti-inflammatory

Pregnancy risk category C

Action

Unclear. Reduces inflammation by suppressing polymorphonuclear leukocyte migration, reversing increased capillary permeability, and stabilizing leukocyte lysosomal membranes. Also suppresses immune response (by reducing lymphatic activity), stimulates bone marrow, and promotes protein, fat, and carbohydrate metabolism.

Availability

Elixir: 0.5 mg/5 ml

Oral solution: 0.5 mg/5 ml, 1 mg/ml

Solution for injection (sodium phosphate): 4 mg/ml, 10 mg/ml, 20 mg/ml, 24 mg/ml

Tablets: 0.25 mg, 0.5 mg, 0.75 mg, 1 mg, 1.5 mg, 2 mg, 4 mg, 6 mg

⊘Indications and dosages

➣ Allergic and inflammatory conditions

Adults: 0.75 to 9 mg/day (dexamethasone) P.O. as a single dose or in divided doses; in severe cases, much higher dosages may be needed. Dosage requirements vary and must be individualized based on disease and patient response.

➣ Cerebral edema

Adults: Initially, 10 mg (sodium phosphate) I.V., followed by 4 mg I.M. q 6 hours. Then reduce dosage gradually over 5 to 7 days.

➣ Suppression test for Cushing's syndrome

Adults: 1 mg P.O. at 11 P.M. or 0.5 mg P.O. q 6 hours for 48 hours (with urine collection testing, as ordered)

Off-label uses

• Acute altitude sickness
• Bacterial meningitis
• Bronchopulmonary dysplasia in preterm infants
• Hirsutism
• Suppression test for detection, diagnosis, or management of depression

Contraindications

• Hypersensitivity to drug, benzyl alcohol, bisulfites, EDTA, creatinine, polysorbate 80, or methylparaben
• Systemic fungal infections

Precautions

Use cautiously in:
• renal insufficiency, cirrhosis, diabetes mellitus, diverticulitis, GI disease, cardiovascular disease, hypoprothrombinemia, hypothyroidism, myasthenia gravis, glaucoma, osteoporosis, infections, underlying immunosuppression, psychotic tendencies
• pregnant or breastfeeding patients
• children.

Administration

• Give P.O. dose with food or milk.
• When giving I.M., inject deep into gluteal muscle; rotate sites as needed.
• For I.V. use, drug may be given undiluted as a single dose over 1 minute or added to dextrose or I.V. saline solutions and given as an intermittent infusion at prescribed rate.

Route	Onset	Peak	Duration
P.O.	Unknown	1-2 hr	2.75 days
I.V.	1 hr	1 hr	Variable
I.M. (sodium phosphate)	1 hr	1 hr	6 days

Adverse reactions

CNS: headache, malaise, vertigo, psychiatric disturbances, increased intracranial pressure, seizures

CV: hypotension, thrombophlebitis, myocardial rupture after recent myocardial infarction, thromboembolism

EENT: cataracts

GI: nausea, vomiting, abdominal distention, dry mouth, anorexia, peptic ulcer, bowel perforation, pancreatitis, ulcerative esophagitis

Metabolic: decreased carbohydrate tolerance, hyperglycemia, cushingoid appearance (moon face, buffalo hump), decreased growth (in children), latent diabetes mellitus, sodium and fluid retention, negative nitrogen balance, adrenal suppression, hypokalemic alkalosis

Musculoskeletal: muscle wasting, muscle pain, osteoporosis, aseptic joint necrosis, tendon rupture, long bone fractures

Skin: diaphoresis, angioedema, erythema, rash, pruritus, urticaria, contact dermatitis, acne, decreased wound healing, bruising, skin fragility, petechiae

Other: facial edema, weight gain or loss, increased susceptibility to infection, hypersensitivity reactions

Interactions

Drug-drug. Barbiturates, phenytoin, rifampin: decreased dexamethasone effects

Digoxin: increased risk of digoxin toxicity

Ephedrine: increased dexamethasone clearance

Estrogen, hormonal contraceptives: blocking of dexamethasone metabolism

Fluoroquinolones: increased risk of tendon rupture

Itraconazole, ketoconazole: increased dexamethasone blood level and effects

Live-virus vaccines: decreased antibody response to vaccine, increased risk of adverse reactions

Loop and thiazide diuretics: additive hypokalemia

Nonsteroidal anti-inflammatory drugs: increased risk of GI adverse effects

Somatrem, somatropin: decreased response to these drugs

Drug-diagnostic tests. Calcium, potassium: decreased levels

Cholesterol, glucose: increased levels

Nitroblue tetrazolium test: false-negative result

Drug-herbs. Echinacea: increased immune-stimulating effect

Ginseng: potentiation of immune-modulating response

Drug-behaviors. Alcohol use: increased risk of gastric irritation and GI ulcers

Patient monitoring

• Monitor blood glucose level closely in diabetic patients receiving drug orally.
• Monitor hemoglobin and potassium levels.
• Assess for occult blood loss.
☞ In long-term therapy, never discontinue drug abruptly. Dosage must be tapered gradually.

Patient teaching

☞ Instruct patient to immediately report sudden weight gain, swelling of face or limbs, excessive nervousness or sleep disturbances, excessive body hair growth, vision changes, difficulty breathing, muscle weakness, persistent abdominal pain, or change in stool color.
• Tell patient to take oral drug with or after meals.
• Advise patient to report vision changes.
• Inform patient that drug makes him more susceptible to infection. Advise him to avoid crowds and exposure to illness.
☞ Caution patient not to stop taking drug abruptly.
• As appropriate, review all other significant and life-threatening adverse reactions and interactions, especially those related to the drugs, tests, herbs, and behaviors mentioned above.

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glucocorticoid

Metabolism A steroid hormone that primarily affects carbohydrate metabolism and, to a lesser extent, fats and proteins Examples Cortisol–hydrocortisone, the major human glucocorticoid, cortisone; glucocorticoids are produced naturally in the adrenal cortex, less in the gonads, can be synthesized; they have anti-inflammatory and immunosuppressive effects