Corticosteroid mechanism of action pdf

Certain drugs such as troleandomycin (TAO), erythromycin ( Ery-Tab , EryPed 200), and clarithromycin ( Biaxin ) and ketoconazole ( Nizoral ) can reduce the ability of the liver to metabolize (breakdown) corticosteroids and this may lead to an increase in the levels and side effects of corticosteroids in the body. On the other hand, phenobarbital, ephedrine , phenytoin ( Dilantin ), and rifampin ( Rifadin , Rimactane ) may reduce the blood levels of corticosteroids by increasing the breakdown of corticosteroids by the liver. This may necessitate an increase of corticosteroid dose when they are used in combination with these drugs.

Acetaminophen belongs to a class of drugs called analgesics ( pain relievers) and antipyretics ( fever reducers). The exact mechanism of action of acetaminophen is not known. It may reduce the production of prostaglandins in the brain. Prostaglandins are chemicals that cause inflammation and swelling. Acetaminophen relieves pain by elevating the pain threshold, that is, by requiring a greater amount of pain to develop before a person feels it. It reduces fever through its action on the heat-regulating center of the brain. Specifically, it tells the center to lower the body's temperature when the temperature is elevated. The FDA approved acetaminophen in 1951.

The association linking corticosteroid therapy with the development of posterior subcapsular cataracts has been well documented. These drugs are widely used therapeutically, principally to capitalize on their ability to inhibit inflammatory responses. The literature on corticosteroid-induced posterior subcapsular cataracts is reviewed here. Data from the previously published series and individual lens susceptibility to corticoids do not allow the establishment of a direct factor relating cataract formation to corticosteroid dose and the duration of therapy; however, significant progress has been made in elucidating the mechanism by which corticoids bring about the development of these opacities. Exploration into the development of these lesions has shed light on the similarities these opacities share with other cataracts, especially with regard to location and pathogenesis.

Damage to the airway epithelium is one prominent feature of chronic asthma. Mucosal damage includes gap openings, partial denudation, and loss of ciliated cells. Apoptosis of the airway epithelium is increasingly recognized as a potential mechanism by which damage may occur. Corticosteroids (CSs) induce apoptosis in inflammatory cells, which in part explains their ability to suppress airway inflammation. However, CS therapy does not necessarily reverse epithelial damage. We examined whether CS therapy actually could induce airway epithelial apoptosis using culture models of primary airway epithelial cells and cell lines. The administration of CSs in low-micromolar concentrations induces apoptosis that involves the disruption of mitochondrial polarity, the activation of caspases, and the involvement of Bcl-2. Clear differences exist between CS-induced apoptosis in the cultured epithelium vs cultured hematopoietic cells in regard to time course and resistance to apoptosis. Our data suggest that the use of CSs, in concentrations that could be attained in vivo with the inhalation of potent preparations or with systemic administration, may be one factor in the airways remodeling and epithelial damage that is seen in many patients with chronic, persistent asthma.

Corticosteroid mechanism of action pdf

corticosteroid mechanism of action pdf

Damage to the airway epithelium is one prominent feature of chronic asthma. Mucosal damage includes gap openings, partial denudation, and loss of ciliated cells. Apoptosis of the airway epithelium is increasingly recognized as a potential mechanism by which damage may occur. Corticosteroids (CSs) induce apoptosis in inflammatory cells, which in part explains their ability to suppress airway inflammation. However, CS therapy does not necessarily reverse epithelial damage. We examined whether CS therapy actually could induce airway epithelial apoptosis using culture models of primary airway epithelial cells and cell lines. The administration of CSs in low-micromolar concentrations induces apoptosis that involves the disruption of mitochondrial polarity, the activation of caspases, and the involvement of Bcl-2. Clear differences exist between CS-induced apoptosis in the cultured epithelium vs cultured hematopoietic cells in regard to time course and resistance to apoptosis. Our data suggest that the use of CSs, in concentrations that could be attained in vivo with the inhalation of potent preparations or with systemic administration, may be one factor in the airways remodeling and epithelial damage that is seen in many patients with chronic, persistent asthma.

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