An allergy occurs when the body reacts to foreign particles it can't tolerate. These particles, such as tree pollen or dust mites, are called antigens, or allergens, and are normally harmless. But the immune system of a person with allergies views the allergens as harmful. Following the body’s first contact with an allergen, white blood cells produce antibodies that prepare the immune system for the same allergen the next time it enters the body. Antibodies attach themselves to cells such as basophils and mast cells. Later contact with even a small amount of the allergen triggers the cells to release chemicals such as leukotrienes, prostaglandins, and histamine. When these chemicals are released, they attach to the receptors of nearby cells. The binding causes swelling of nasal blood vessels and inflammation of membranes. This results in common allergy symptoms such as: • sneezing • itchiness • watery nose • and congestion Normally to reduce inflammation, the brain signals the adrenal glands to produce a hormone called cortisol. Cortisol works against allergens by acting on receptors in the cytoplasm of various cells. Once bound, cortisol-receptor complex enters into the nucleus. There it binds to the DNA and prevents the creation of proteins responsible for the release of inflammatory chemicals. As a result, when the allergen binds to the antibodies on the cell, the cell is not triggered to release inflammatory chemicals. Sometimes cortisol is not able to control the immune system response. In this case, nasal corticosteroids, synthetically-produced hormones similar to cortisol, may be prescribed. When inhaled, they bind to receptors and the complex works in the same way as cortisol. Therefore, when the allergen binds to the antibodies on the cell, the inflammatory chemicals are not released. As a result, the immune system’s response is decreased and symptoms are reduced. While effective, corticosteroids are not right for everyone and can cause minor as well as serious side effects, so a corticosteroid therapy should only be started under the care and guidance of a physician.
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.
In a pharmacokinetic study comparing flunisolide nasal solution (flunisolide nasal spray .025%) (29 mcg per spray) with flunisolide nasal solution (flunisolide nasal spray .025%) (25 mcg per spray), the original formulation, the two formulations were not bioequivalent. The total absorption of flunisolide nasal solution (29 mcg per spray) was 25% less than that of flunisolide nasal solution (25 mcg per spray), and the peak plasma concentration was 30% lower. The clinical significance of these differences is likely to be small, particularly since clinical efficacy is attributable to a local effect on nasal mucosa (see Pharmacodynamics ).