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.
The mean age of the patients at the start of the INF was years (range 2–20 years). At the initiation of INF, 62% (21/34) of patients were ≥10 years of age. The mean duration of uveitis prior to INF treatment was years (2–8 years). The mean duration of steroid treatment prior to start of disease modifying antirheumatic drugs (DMARD) therapy was 2 years (– years). Prior to INF therapy, all patients had been treated with steroids. This included 15/34 (44%) patients that received topical steroids and 19/34 (56%) patients that were on both topical and systemic steroids. The average dose of systemic steroid was mg/kg, and the maximum dose was 20 mg per day for a mean period of months. Topical prednisone administration varied significantly from every hour while awake to once a day. Based on the dosage given, there were 6 (18%) patients assigned to the LD group, 19 (56%) patients to the MD group, and 9 (26%) patients to the HD group. Dosing was determined by the primary pediatric rheumatologist on the basis of disease duration, disease activity at the time of presentation, and prior medication failures.