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Stopping corticosteroid therapy
In autoimmune disease, clear end-points should be set before starting therapy. Corticosteroids may improve mood and give patients a feeling of general well-being unrelated to the effect on the disease being treated. Subjective assessments can therefore be misleading. Objective clinical parameters should be used to monitor the need for continuing or restarting therapy . proteinuria in nephritis, spirometry in asthma and creatinine kinase in myositis. Therapy should be tapered off. For example, with prednis(ol)one, the dose is reduced in steps of -5 mg every 3-7 days down to 15 mg/day. At that point, switch to alternate day therapy and reduce in mg steps over 2-3 weeks. This minimises the impact on mood and lessens the drop in general well-being.
Corticosteroids have been used as drug treatment for some time. Lewis Sarett of Merck & Co. was the first to synthesize cortisone, using a complicated 36-step process that started with deoxycholic acid, which was extracted from ox bile .  The low efficiency of converting deoxycholic acid into cortisone led to a cost of US $200 per gram. Russell Marker , at Syntex , discovered a much cheaper and more convenient starting material, diosgenin from wild Mexican yams . His conversion of diosgenin into progesterone by a four-step process now known as Marker degradation was an important step in mass production of all steroidal hormones, including cortisone and chemicals used in hormonal contraception .  In 1952, . Peterson and . Murray of Upjohn developed a process that used Rhizopus mold to oxidize progesterone into a compound that was readily converted to cortisone.  The ability to cheaply synthesize large quantities of cortisone from the diosgenin in yams resulted in a rapid drop in price to US $6 per gram, falling to $ per gram by 1980. Percy Julian's research also aided progress in the field.  The exact nature of cortisone's anti-inflammatory action remained a mystery for years after, however, until the leukocyte adhesion cascade and the role of phospholipase A2 in the production of prostaglandins and leukotrienes was fully understood in the early 1980s.