<unk>  drugs currently being used act nonselectively, so in the long run they may impair many healthy anabolic processes. To prevent this, much research has been focused recently on the elaboration of selectively acting<unk>  drugs. Side effects include: * Immunodeficiency (see section below) * Hyperglycemia due to increased gluconeogenesis, insulin resistance, and impaired glucose tolerance ("steroid diabetes"); caution in those with diabetes mellitus * Increased skin fragility, easy bruising * Negative calcium balance due to reduced intestinal calcium absorption * Steroid-induced osteoporosis: reduced bone density (osteoporosis, osteonecrosis, higher fracture risk, slower fracture repair) * Weight gain due to increased visceral and truncal fat deposition (central obesity) and appetite stimulation; see corticosteroid-induced lipodystrophy * Hypercortisolemia with prolonged or excessive use (also known as, exogenous Cushing's syndrome) * Impaired memory and attention deficits * Adrenal insufficiency (if used for long time and stopped suddenly without a taper) * Muscle and tendon breakdown (proteolysis), weakness, reduced muscle mass and repair * Expansion of malar fat pads and dilation of small blood vessels in skin * Lipomatosis within the epidural space * Excitatory effect on central nervous system (euphoria, psychosis) * Anovulation, irregularity of menstrual periods * Growth failure, delayed puberty * Increased plasma amino acids, increased urea formation, negative nitrogen balance * Glaucoma due to increased ocular pressure * Cataracts * Topical steroid addiction In high doses, hydrocortisone (cortisol) and those<unk> s with appreciable mineralocorticoid potency can exert a mineralocorticoid effect as well, although in physiologic doses this is prevented by rapid degradation of cortisol by 11β-hydroxysteroid dehydrogenase isoenzyme 2 (11β-HSD2) in mineralocorticoid target tissues. Mineralocorticoid effects can include salt and water retention, extracellular fluid volume expansion, hypertension, potassium depletion, and metabolic alkalosis. Immunodeficiency<unk> s cause immunosuppression, decreasing the function and/or numbers of neutrophils, lymphocytes (including both B cells and T cells), monocytes, macrophages, and the anatomical barrier function of the skin. This suppression, if large enough, can cause manifestations of immunodeficiency, including T cell deficiency, humoral immune deficiency and neutropenia. + Main pathogens of concern in<unk> -induced immunodeficiency: Bacteria *Enterobacteriaceae including Salmonella species *Legionella micdadei *Listeria monocytogenes *Mycobacterium tuberculosis *Nontuberculous mycobacteria *Nocardia asteroides *Rhodococcus equi *Staphylococcus aureus *Streptococci Fungi *Aspergillus *Blastomyces *Candida species including Candida albicans *Coccidioides immitis *Cryptococcus neoformans *Fusarium species *Histoplasma capsulatum *Talaromyces marneffei *Pneumocystis jirovecii *Pseudallescheria boydii *Zygomycosis Viruses *Adenovirus *Cytomegalovirus *Herpes simplex virus *Human papillomavirus *Influenza/parainfluenza *Respiratory syncytial virus *Varicella zoster Other *Cryptosporidiosis/Isospora belli *Strongyloides stercoralis *Toxoplasma gondii Withdrawal In addition to the effects listed above, use of high-dose<unk> s for only a few days begins to produce suppression of the patient's adrenal glands suppressing hypothalamic corticotropin-releasing hormone leading to suppressed production of adrenocorticotropic hormone by the anterior pituitary. With prolonged suppression, the adrenal glands atrophy (physically shrink), and can take months to recover full function after discontinuation of the exogenous<unk> . During this recovery time, the patient is vulnerable to adrenal insufficiency during times of stress, such as illness. While suppressive dose and time for adrenal recovery vary widely, clinical guidelines have been devised to estimate potential adrenal suppression and recovery, to reduce risk to the patient. The following is one example: * If patients have been receiving daily high doses for five days or less, they can be abruptly stopped (or reduced to physiologic replacement if patients are adrenal-deficient). Full adrenal recovery can be assumed to occur by a week afterward. * If high doses were used for six to 10 days, reduce to replacement dose immediately and taper over four more days. Adrenal recovery can be assumed to occur within two to four weeks of completion of steroids. * If high doses were used for 11–30 days, cut immediately to twice replacement, and then by 25% every four days. Stop entirely when dose is less than half of replacement. Full adrenal recovery should occur within one to three months of completion of withdrawal. * If high doses were used more than 30 days, cut dose immediately to twice replacement, and reduce by 25% each week until replacement is reached. Then change to oral hydrocortisone or cortisone as a single morning dose, and gradually decrease by 2.5 mg each week. When the morning dose is less than replacement, the return of normal basal adrenal function may be documented by checking 0800 cortisol levels prior to the morning dose; stop drugs when 0800 cortisol is 10 μg/dl. Predicting the time to full adrenal recovery after prolonged suppressive exogenous steroids is difficult; some people may take nearly a year. * Flare-up of the underlying condition for which steroids are given may require a more gradual taper than outlined above.
Glucocorticoid
Adrenal steroid
Corticosteroid
Antiglucocorticoid
Xenohormone
Anticorticotropin
Phytosteroid
Neurohormone