Steroid Finished

A short course of oral steroids usually causes no side-effects. Side-effects are more likely to occur with a long course of oral steroids (more than 2-3 months), or if short courses are taken repeatedly. 

Endocrine disorders: Primary or secondary adrenocortical insufficiency (hydrocortisone or cortisone is the first choice; synthetic analogs may be used in conjunction with mineralocorticoids where applicable; in infancy mineralocorticoid supplementation is of particular importance), congenital adrenal hyperplasia, nonsuppurative thyroiditis, hypercalcemia associated with cancer.

Rheumatic disorders: As adjunctive therapy for short-term administration (to tide the patient over an acute episode or exacerbation) in: psoriatic arthritis; rheumatoid arthritis, including juvenile rheumatoid arthritis (selected cases may require low-dose maintenance therapy); ankylosing spondylitis; acute and subacute bursitis; acute nonspecific tenosynovitis; acute gouty arthritis; posttraumatic osteoarthritis; synovitis of osteoarthritis; epicondylitis.

Collagen diseases: During an exacerbation or as maintenance therapy in selected cases of: systemic lupus erythematosus, acute rheumatic carditis.

Dermatologic diseases: Pemphigus, bullous dermatitis herpetiformis, severe erythema multiforme (Stevens-Johnson syndrome), exfoliative dermatitis, mycosis fungoides, severe psoriasis, severe seborrheic dermatitis.

Allergic states: Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment: seasonal or perennial allergic rhinitis, serum sickness, bronchial asthma, contact dermatitis, atopic dermatitis, drug hypersensitivity reactions.

Ophthalmic diseases: Severe acute and chronic allergic and inflammatory processes involving the eye and its adnexa, such as: allergic conjunctivitis, keratitis, allergic corneal marginal ulcers, herpes zoster ophthalmicus, iritis and iridocyclitis, chorioretinitis, anterior segment inflammation, diffuse posterior uveitis and choroiditis, optic neuritis, sympathetic ophthalmia.

Respiratory diseases: Symptomatic sarcoidosis, Loeffler's syndrome not manageable by other means, berylliosis, fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculous chemotherapy, aspiration pneumonitis.

Hematologic disorders: Idiopathic thrombocytopenic purpura in adults, secondary thrombocytopenia in adults, acquired (autoimmune) hemolytic anemia, erythroblastopenia (RBC anemia), congenital (erythroid) hypoplastic anemia.

Procedures for isolation of steroids differ according to the chemical nature of the steroids and the scale and purpose of the isolation. Steroids are isolated from natural sources by extraction with organic solvents, in which they usually dissolve more readily than in the aqueous fluids of tissues. The source material often is treated initially with an alcoholic solvent, which dehydrates it, denatures (renders insoluble) proteins associated with the steroids, and dissolves many steroids. Saponification either of whole tissues or of substances extracted from them by alcohol splits the molecules of sterol esters, triglycerides, and other fatty esters and permits the extraction of the sterols by means of water-immiscible solvents, such as hexane or ether, with considerable purification. Intact sterol esters or hormonal steroids and their metabolites (compounds produced by biological transformation) that are sensitive to strong acids or alkalies, however, require essentially neutral conditions for isolation, and, although some procedures for analysis of urinary steroids employ acid treatment, milder hydrolysis, as by enzymes, is preferred. The acidity of some steroids allows them to be held in alkaline solution, while nonacidic impurities are extracted with organic solvents.

Abundant steroids usually are purified by repeated crystallization from solvents. Small-scale laboratory isolations for investigative or assay purposes usually exploit differing polarities of the steroid and of its impurities, which may be separated by partitioning between solvents differing in polarity or by chromatography (see below Determination of structure and methods of analysis). Occasionally, special reagents may selectively precipitate or otherwise sequester the desired steroid. A classical example is the precipitation of 3β-hydroxy sterols such as cholesterol by the natural steroid derivative digitonin. New steroids of great physiological interest often are isolated from tissue only with extreme difficulty, because they are usually trace constituents. In one example, 500 kg (1,100 pounds) of silkworm pupae yielded 25 mg (0.0008 ounce) of pure molting hormone, the steroid ecdysone (i.e., 20 × 106-fold purification). In such cases each isolation step is followed by an assay for the relevant physiological activity to ensure that the desired material is being purified. The percentage recovery of known steroid hormones during their assay in small biological samples usually is assessed by adding a trace of the same steroid in radioactive form to the initial sample, followed by radioassay (analysis based on radioactivity) after purification is complete. The efficiency of recovery of the radioactive steroid is assumed to be the same as that of the natural substance.

Steroidogenesis or steroid biosynthesis is a complex process; for the successful and continued production of steroid hormones, cell metabolism requires a sensitive balance among the various requisites. Basically, the following requirements should be met for steroid biosynthesis:

1. Adequate stores of precursors; namely, cholesterol, with efficient enzymes for utilizing the precursor pool.
2. Metabolic tools for generating substrates and cofactors required for steroid synthesis.
3. Stimulatory influences such as hormones must remain at a steady level.
4. Biotransformation and inhibitory factors must always be minimal.
Interference with any one or more of these processes might be sufficient to terminate or reduce steroid production. The skeletal process by which steroids are synthesized is as follows: The precursor of all steroids is cholesterol, which is of dietary origin or is synthesized by the organism from acetyl coezyme A. Steroid producing cells seem to rely mainly on the circulating sterol pool for their cholesterol.

Most of the cholesterol ready for conversion into steroids within steroid forming cells exists as esters of unsaturated fatty acids, presumably because the free sterol might readily diffuse from the cells into the intercellular fluid.

Esterification of cholesterol is catalyzed by two enzymes: Acyl CoA synthetase and sterol acyl transferase. Acyl CoA synthetase converts free fatty acids to CoA esters in the presence of CoA and ATP, while sterol acyl transferase directs the esterification of the fatty acid moiety to cholesterol. Once esterified, cholesterol is stored in cytoplasmic droplets along with smaller amounts of other lipids. But before this precursor pool can be utilized, the cholesterol must be liberated and that is accomplished by a sterol esterase. The esterol esterase hydrolyzes the cholesterol ester and cholesterol is thereby liberated for further utilization. The whole process of conversion and reversion of cholesterol to and from esters is rather obscure, and the factors regulating this process need further intensive study for proper resolution of the whole chain of events responsible for intracellular transfer of sterols and steroid esters from one organelle to another and for keeping free cholesterol ready for conversion into steroid hormones. 

Before prescribing a steroid, prescribers should perform a potassium hydroxide test to ensure that the disease to be treated is not a fungal infection, which may be aggravated by the use of steroids. Each steroid comes in a variety of potencies and preparations (which is determined by both the steroid itself and its concentration), so it’s important to know which one to prescribe and the duration and frequency of application. Low-potency corticosteroids can be prescribed for children and mild diseases. Due to the risk of skin thinning associated with topical steroids, only low-potency steroids should be used on areas such as the face and groin. Medium- to high-potency corticosteroids can be used for most areas of the body. For treating severe diseases or in areas with thick skin, super-potent steroids can be used.

As with any pharmaceutical, steroids also have risks whose likelihood increases with the dose and duration of therapy. The route of administration has been known to affect the type of adverse effect that patients may experience. Oral steroids may suppress the immune system, which can increase a patient’s risk of secondary infections. Inhaled steroids may induce gingival irritation and have systemic adverse effects, whereas topical formulations may result in skin thinning and color changes. Therefore, prescribers should carefully consider both the dose and duration when prescribing steroids—short-term, intermittent administration is typically recommended. The patient should generally be weaned off steroids by tapering the dose to allow the adrenal glands time to re-adapt after the cessation of corticosteroid therapy to help prevent adrenal insufficiency.