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Dexamethasone |
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| Dexamethasone is a synthetic member of the glucocorticoid class of hormones. It acts as an anti-inflammatory and immunosuppressant. Its potency is about 40 times that of hydrocortisone. Dexamethasone is a synthetic adrenocortical steroid possessing basic glucocorticoid actions and effects. At equipotent anti-inflammatory doses, dexamethasone almost completely lacks the sodium retaining property of hydrocortisone and closely related derivatives of hydrocortisone. Dexamethasone is readily absorbed from the gastrointestinal tract. Pharmacological effects of dexamethasone are numerous and predominantly affect metabolism, including glucose homeostasis, promoting catabolism, suppression of the hypothalamus-pituitary-adrenal axis, suppression of growth. The metabolic clearance of dexamethasone is enhanced by the concurrent administration of phenobarbitone, phenytoin, and other drugs that induce hepatic enzyme function. The drug is readily absorbed into tissue, and rapidly distributed to kidneys, liver, muscle, and intestines. It is metabolized in the liver and primarily excreted by the kidneys. Naturally occurring glucocorticoids (hydrocortisone and cortisone), which also have salt-retaining properties, are used as replacement therapy in adrenocortical deficiency states. Their synthetic analogs including dexamethasone are primarily used for their potent anti-inflammatory effects in disorders of many organ systems. Glucocorticoids cause profound and varied metabolic effects. In addition, they modify the body’s immune responses to diverse stimuli. At equipotent anti-inflammatory doses, dexamethasone almost completely lacks the sodium-retaining property of hydrocortisone and closely related derivatives of hydrocortisone. |
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Functions and health benefits of dexamethasone |
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Dexamethasone stimulates synthesis of enzymes required to decrease the inflammatory response. Its primary efficacy is that of a strong antiinflammatory, as well as an antiallergic agent. Besides being an antiinflammatory, the drug will also suppress the immune response, stimulate bone marrow and influence fat, protein, and carbohydrate metabolism. Although it is able to cause
diuresis, there are more effective drugs for reducing edema. Dexamethasone is a strong anti-inflammatory agent. This drug works by preventing white blood cells from completing an inflammatory reaction. This drug can cause lymphocytes, a type of white blood cell, to break apart and die. The drug is sometimes given to reduce the likelihood that a person will have an allergic reaction to a chemotherapeutic agent, such as paclitaxel. Finally, this medicine is used to prevent nausea and vomiting from chemotherapy, in combination with other drugs. Dexamethasone interferes with the pathways responsible for nausea and vomiting related to chemotherapy. The drug has other uses such as part of a chemotherapy regime or to reduce swelling of the brain.
Dexamethasone is used to treat many inflammatory and autoimmune conditions. It is also given to cancer patients undergoing chemotherapy, to counteract certain side-effects of their antitumor treatment. In certain forms of brain disease, e.g. brain tumours or secondaries, dexamethasone is used to counteract the development of edema, which would eventually compress other brain structures. It is present in certain eye drops. Dexamethasone can be used for all conventional indications for glucocorticoids. It is also very efficient as an antiemetic agent in strongly emetogenic chemotherapy; it is thereby often combined with other antiemetic agents (e.g. ondansetron). It is also frequently used in context with different forms of shock, even though its use is sometimes viewed controversially (e.g. septic shock). Dexamethasone is also used in a diagnostic context, namely in its property to suppress the natural pituitary-adrenal axis. Patients presenting with clinical signs of glucocorticoid excess (Cushing's syndrome) are generally diagnosed by a 24h urine collection for cortisol or by a dexamethasone suppression test. During the latter, the response of the body to a high dose of glucocorticoids is monitored. Various forms are performed. In the most common form, a patient takes a nighttime dose of either 1 or 4 mg of dexamethasone, and the serum cortisol levels are measured in the morning. If the levels are relatively high (over 5 μg/dl or 150 nmol/l), then the test is positive and the patient has an autonomous source of either cortisol or ACTH, indicating Cushing's disease. Longer versions rely on urine collections on oral dexamethasone over various days. |
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Side effects of dexamethasone |
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Although side effects from dexamethasone are not common, they can occur. Chronic treatment with dexamethasone will lead to adrenal suppression. Adrenal glands produce necessary hormones and some steroids. Chronic use in children inhibits growth, and the lowest possible dose should be used over the shortest period of time. The most common side effects are depression, euphoria, hypertension, nausea, anorexia, decreased wound healing, acne, muscle wasting, bone pain, and increased susceptibility to infection. Other side-effects of dexamethasone include glaucoma, subcapsular cataract, gastrointestinal bleeding, pancreatitis, aseptic bone necrosis, osteoporosis, myopathies, obesity, edemas, hypertension, proteinuria, diabetes, sleep disturbances, psychiatric syndromes, delayed wound healing, atrophy and fragility of the skin, ecchymosis, pseudotumor cerebri. |
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Taking dexamethasone properly |
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Dexamethasone is given intravenously or orally. Dexamethasone pills should be taken with food or milk to protect the stomach from irritation. A liquid (elixir, solution, concentrated solution) is available if you cannot swallow pills. Those who have feeding tubes can also use the liquid. Flush the feeding tube before and after medicine is given. Dexamethasone also comes in solutions for treating infection in the eye, and nasal sprays, and intramuscular and IV infusions. If dose is ordered daily, it should be given in the morning to coincide with the bodyís normal secretion of cortisol.
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Contraindications, interactions, precautions |
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Dexamethasone may cause a change in how the white blood cells move in the bloodstream, causing an increase in the white blood cell count. This is normal. In addition, it usually causes a temporary increase in blood sugar level, and sometimes a drop in the blood potassium level. This is usually not a problem, and can be treated if needed. Abruptly stopping the drug can cause signs and symptoms of adrenal insufficiency, weakness, aches, fever, dizziness, lowering of blood pressure when changing position, difficulty breathing, and low blood sugar. The drug should be gradually discontinued. Corticosteroids may mask some signs of infection, and new infections may appear during their use. There may be decreased resistance and inability to localize infection when corticosteroids are used. Moreover, corticosteroids may affect the nitrobluetetrazolium test for bacterial infection and produce false negative results. Depending on the indication and the general condition, peptic ulcers, osteoporosis, psychoses, infectious diseases (e.g. herpes simplex, keratitis), diabetes and hypertension can be considered contraindications.
Corticosteroids should be used cautiously in patients with ocular herpes simplex because of possible corneal perforation. The lowest possible dose of corticosteroids should be used to control the condition under treatment, and when reduction in dosage is possible, the reduction should be gradual. Glucocorticoids may reduce salicylate blood levels. Phenytoin, phenobarbital, rifampin may increase the metabolism of glucocorticoids. Concomitant administration of glucocorticoids and cyclosporin may increase the blood levels of each, by mutually inhibiting the hepatic metabolism of each other. The clinical significance of this interaction is not clear. Glucocorticoids may also inhibit the hepatic metabolism of cyclophosphamide. Amphotericin B or potassium-depleting diuretics (furosemide, thiazides) when administered concomitantly with glucocorticoids may cause hypokalemia. When these drugs are used concurrently with digitalis glycosides, an increased chance of digitalis toxicity may occur should hypokalemia develop. |
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