Presentation of antibodies when exposed to thermophilic Actinomyces.Examination procedures may include:
• taking a blood test• taking a chest x-ray• administering a breathing capacity test• administering an inhalation challenge• examining lung tissue• performing an immunological investigation• performing a lung function test• reviewing the clinical history

Treatment
Depending on the severity of the symptoms, FLD can last from one to two weeks, or it can last for the rest of ones life. Acute FLD has the ability to be treated because hypersensitivity to the antigens has not yet developed. The main treatment options are: rest and reducing the exposure to the antigens through masks and increased airflow in confined spaces where the antigens are present. Any exposure to the antigens once hypersensitivity has occurred can set off another chronic reaction. For chronic FLD, there are no true treatments because the patient has developed hypersensitivity meaning that their condition will last the rest of their life. Epidemiology
The growth of mold spores occurs when hay is not dried properly. The growth of these mold spores accumulates over time and will infect the host upon release from the source. When in the air, the farmer may inhale the particles and induce an allergic reaction. The hay at risk for increased volumes of spores is found at the bottom of the pile. The presence of Farmers Lung Disease peaks during late winter and early spring and is mostly seen after the harvest season when symptoms have set in. This disease is most prevalent in damp climates. See also
Organic dust toxic syndrome


== References ==
However, higher doses of dexamethasone override the export capacity of P-glycoprotein and enter the brain to produce central activation of GRs. In conjunction with the suppression of endogenous corticosteroids by dexamethasone, this results in skewed ratios of activation of peripheral versus central GRs as well as skewed ratios of activation of GRs versus MRs when compared to non-synthetic corticosteroids. These differences can have significant clinical relevance. Chemistry
Dexamethasone is a synthetic pregnane corticosteroid and derivative of cortisol (hydrocortisone) and is also known as 1-dehydro-9α-fluoro-16α-methylhydrocortisone or as 9α-fluoro-11β,17α,21-trihydroxy-16α-methylpregna-1,4-diene-3,20-dione. The molecular and crystal structure of dexamethasone has been determined by X-ray crystallography. It is a stereoisomer of betamethasone, the two compounds differing only in the spatial configuration of the methyl group at position 16 (see steroid nomenclature). Synthesis
To synthesize dexamethasone, 16β-methylprednisolone acetate is dehydrated to the 9,11-dehydro derivative. This is then reacted with a source of hypobromite, such as basic N-bromosuccinimide, to form the 9α-bromo-11β-hydrin derivative, which is then ring-closed to an epoxide. A ring-opening reaction with hydrogen fluoride in tetrahydrofuran gives dexamethasone. History
Dexamethasone was first synthesized by Philip Showalter Hench in 1957. It was introduced for medical use in 1958.On 16 June 2020, the RECOVERY Trial announced preliminary results stating that dexamethasone improves survival rates of hospitalized patients with COVID-19 receiving oxygen or on a ventilator. Benefits were only observed in patients requiring respiratory support; those who did not require breathing support saw a worse survival rate than the control group, although the difference may have been due to chance.