Corticosteroids replacement therapy

Because most adrenal crises occur because of glucocorticoid dose reductions or lack of stress-related dose adjustments, patients receiving corticosteroid-replacement therapy should add 5 to 10 mg hydrocortisone (or equivalent) to their normal daily regimen shortly before strenuous activities such as exercise. During times of severe physical stress (e.g., febrile illnesses, after accidents), patients should be instructed to double their daily dose until recovery. 

Anti-inflammation, immunosuppression, corticosteroid replacement therapy PO 0 6-... 

Anti-inflammatory, corticosteroid replacement therapy Topical Apply 2 times/day for 2 wk. Foam Apply 2 times/day for 2 wk. 

Anti-inflammatory, immunosuppressant, corticosteroid replacement therapy Topical... 

Kyriazopoulou V, Parparousi O, Vagenakis AG. Rifampicin-induced adrenal crisis in Addisonian patients receiving corticosteroid replacement therapy. J Clin Endocrinol Metab 1984 59(6) 1204-6. 

Most adrenal crises occur secondary to glucocorticoid dose reduction or lack of stress-related dose adjustments. It is recommended that patients receiving corticosteroid-replacement therapy add 5 to... 

The adequacy of corticosteroid replacement therapy is judged by clinical criteria and biochemical measurements. The subjective well-being of the patient is an important clinical parameter in primary and secondary disease. In primary adrenal insufficiency, the disappearance of hyperpigmentation and the resolution of electrolyte abnormalities are valuable indicators of adequate replacement. Overtreatment may cause manifestations of Cushing s syndrome in children, linear growth may be decreased. Plasma ACTH levels may be used to monitor therapy in patients with primary adrenal insufficiency the early-morning ACTH level should not be suppressed, but should be less than 100 pg/mL (20 pmol/L). 

Information is limited but the interaction between dexamethasone and aminoglutethimide is established. The reduction in the serum corticosteroid levels can be enough to reduce or even abolish the effects of corticosteroid replacement therapy or to cause loss of control of a disease condition. This has been successfully accommodated by increasing the dosage of the dexamethasone. Hydrocortisone is routinely used with aminoglutethimide as replacement therapy, and would seem to be a suitable alternative to dexamethasone, where clinically appropriate. Other synthetic corticosteroids are predicted to interact in the same way as dexamethasone, but this needs confirmation. 

Do not take live virus vaccinations (eg, smallpox) because of the risk of a lack of antibody response This does not include patients receiving the corticosteroids as replacement therapy. 

Close monitoring of 24-hour urinary free cortisol levels and serum cortisol levels are essential to identify adrenal insufficiency in patients with Cushing s syndrome. Steroid secretion should be monitored with all drug therapy and corticosteroid replacement given if needed. 

Corticosteroids do not heal illnesses, but they are widely used in various conditions when it is necessary to utilize their anti-inflammatory, immunosuppressant, and mineralo-corticoid properties. In addition, they are used in replacement therapy for patients who have adrenal insufficiency. Corticosteroids can be used in vital situations for asthma, severe allergic reactions, and transplant rejections. They are effective in noninfectious granulomatous diseases such as sarcoidosis, collagen vascular disease, rheumatoid arthritis, and leukemia. Steroids are used as lotions, ointments, etc. in treating a number of dermatological and ophthalmologic diseases. 

Immunosuppression During therapy, do not use live virus vaccines (eg, smallpox). Do not immunize patients who are receiving corticosteroids, especially high doses, because of possible hazards of neurological complications and a lack of antibody response. This does not apply to patients receiving corticosteroids as replacement therapy. 

In patients with longstanding hypothyroidism and those with ischemic heart disease, rapid correction of hypothyroidism may precipitate angina, cardiac arrhythmias, or other adverse effects. For these patients, replacement therapy should be started at low initial doses, followed by slow titration to full replacement as tolerated over several months. If hypothyroidism and some degree of adrenal insufficiency coexist, an appropriate adjustment of the corticosteroid replacement must be initiated prior to thyroid hormone replacement therapy. This prevents acute adrenocortical insufficiency that could otherwise arise from a thyroid hormone-induced increase in the metabolic clearance rate of adrenocortical hormones. 

Corticosteroids have a range of activity. They have potent antiinflammatory and immunosuppressive activity. Many synthetic drugs are available as corticosteroids. In appropriate doses, these are used as replacement therapy in adrenal insufficiency. The topical application of corticosteroids is safer when compared with systemic use. Corticosteroids should be used in smaller doses for the shortest duration of time. A high dose may be used for life-threatening syndromes or diseases. A tapering pattern of withdrawal should be followed to avoid complications of sudden withdrawal. Systemic therapy is indicated in a variety of conditions. These are administered by intraarticular injections with aseptic conditions for rheumatoid arthritis and osteoarthritis. In skin diseases, such as eczema, contact dermatitis, and psoriasis, corticosteroids are used topically. In some cases, steroids are combined with antimicrobial substances such as neomycin. 

Allergic reaction due to streptokinase overdose should be treated with corticosteroids and histamines. Severe hemorrhage requires discontinuation of streptokinase. Packed red blood cells are preferable for blood-replacement therapy, and volume expansion is advisable. Streptokinase may be used with caution with heparin, allopurinol, sex hormones, sulfonamides, tetracyclines, and dextran. 

Replacement therapy for secondary or tertiary adrenocortical insufficiency These deficiencies are caused by a defect either in CRF production by the hypothalamus or corticotropin production by the pituitary (see p. 247). [Note Under these conditions, the adrenal cortex synthesis of mineralocorticoids is less impaired than that of glucocorticoids.] The adrenal cortex responds to corticotropin administration by synthesizing and releasing the adrenal corticosteroids. Hydrocortisone is also used for these deficiencies. 

The Cochrane Library is a relatively new and growing electronic library that provides more than 850 summaries of published literature about pharmaceutical and other interventions to improve health. The Library adds new titles four times a year to its cumulative online and CD versions (the latter, available by subscription, offers more databases). The Library s 2000 Issue 3 contains evidence on dozens of clinical dilemmas, such as antibiotic treatment for traveler s diarrhea, antileukotriene agents compared to inhaled corticosteroids in the management of recurrent and/or chronic asthma, opioid antagonists for alcohol dependence, and bromocriptine versus levodopa in early Parkinson s disease. The Cochrane Library also updates earlier reviews when important new evidence becomes available. Among the newest updates are tacrine for Alzheimer s disease, tricyclic and related drugs for nocturnal enuresis in children, and nicotine replacement therapy for smoking cessation. 

Adverse drug reactions drugs that can predispose to thrush include broad-spectrum antibiotics, corticosteroids and drugs that can affect oestrogen levels, including oral contraceptives, hormone replacement therapy, tamoxifen and raloxifene. 

Secondary and tertiary adrenocortical insufficiencies can arise by inadequate ACTH production, especially following surgery around the pituitary gland or actual pituitary disease. Deficiency can also occur following cessation of long-term glucocorticoid therapy. In addition, inherited enzyme deficiencies that lead to corticosteroid synthesis inhibitions occur (e.g., 21-hydroxylase and 3-(3-hydroxylase deficiencies). All of these conditions require replacement therapy. 

Cortisone acetate or hydrocortisone usually is the corticosteroid of choice for replacement therapy in patients with adrenocortical insufficiency, because these drugs have both glucocorticoid and mineralocorticoid properties. Following oral administration, cortisone acetate and hydrocortisone acetate are completely and rapidly deacetylated by first-pass metabolism (37). Much of the oral cortisone, however, is inactivated by oxidative metabolism (Fig. 33.9) before it can be converted to hydrocortisone in the liver. The pharmacokinetics for hydrocortisone acetate is indistinguishable from that of orally administered hydrocortisone. Oral hydrocortisone is completely absorbed, with a bioavailability of greater than 95% and a half-life of 1 to 2 hours (23). The metabolism of hydrocortisone (Fig. 33.9) has been previously described. Cortisone acetate is slowly absorbed from IM injection sites over a period of 24 to 48 hours and is reserved for patients who are unable to take the drug orally. The acetate ester derivative demonstrates increased stability and has a longer duration of action when administered by IM injection. Thus, smaller doses can be used. Similarly, hydrocortisone may be dispensed as its 21-acetate (hydrocortisone acetate), which is superior to cortisone acetate when injected intra-articularly. Systemic absorption of hydrocortisone acetate from intra-articular injection sites usually is complete within 24 to 48 hours. When administered intrarectally, hydrocortisone is poorly absorbed (38,39). 

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