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Dexamethasone, inflammatory disease

Synthetic steroid with strong glucocorticoid-agonistic activity. Dexamethasone is over 10 times more potent than cortisol due to a higher binding affinity for glucocorticoid receptor and a decreased clearance rate of the compound. Due to its potency, dexamethasone is widely used in the clinics for the treatment of inflammatory diseases. [Pg.422]

Dexamethasone Synthetic glucocorticoid, lacks mineralocorticoid activity Used to treat range of inflammatory diseases. Used to treat some forms of asthma, also cerebral oedema and congenital adrenal hyperplasia... [Pg.23]

Dexamethasone (Eig. 8.3) is used for treatment of metabolic diseases in ruminants and for inflammatory diseases in a number of animal species. It is... [Pg.222]

A glucocorticoid-resistance model has been proposed to provide an explanation for how stress might influence diseases in which excessive inflammation is observed (e.g., allergies, autoimmune diseases, rheumatoid arthritis, and cardiovascular disease). In these cases, chronic stress diminishes the immune system s sensitivity to glucocorticoids that normally terminate the inflammatory response. For example, in a study of a group of 50 parents caring for a child undergoing treatment for pediatric cancer, whole blood of parents of cancer patients exhibited a lesser dexamethasone-dependent suppression of IL-6 production in vitro compared to parents of medically healthy children.94... [Pg.519]

The same strategy was applied in colon-specific delivery of two corticosteroids used to treat inflammatory bowel disease [20][21], Indeed, budeso-nide /3-D-glucuronide and dexamethasone /3-D-glucuronide underwent ready hydrolysis in the luminal contents of rat colon and caecum. Rat mucosal homogenates were less active, and hydrolysis in human fecal samples was quite low. Based on these and other studies, the prodrugs were found to be suitable candidates for delivery of corticosteroids to the large intestine. [Pg.684]

The first-line agents in the treatment of rheumatoid arthritis are non-steroidal anti-inflammatory drugs such as diclofenac. Diclofenac and indometacin, another NSAID, tend to have similar activity hov/ever, indometacin has a higher incidence of side-effects and therefore diclofenac is more appropriate for initial treatment. Sodium aurothiomalate is classified as a disease-modifying antirheumatic drug and is used as a second-line treatment in rheumatoid arthritis, but has been superseded by methotrexate, administered v/eekly. Paracetamol is often indicated in the management of osteoarthritis. Local intra-articular injections of dexamethasone may be administered for the relief of soft-tissue inflammatory conditions. [Pg.293]

A variety of debilitating diseases, such as rheumatoid arthritis, inflammatory myopathies, cancers, and a variety of immunological diseases are treated with the classic synthetic glucocorticoids, dexamethasone, and prednisone. However, long-term treatment with these drugs often leads to serious side effects such as fat redistribution, diabetes, vascular necrosis, and osteoporosis. There is currently an intense effort to identify new small molecules that are able to differentially modulate GR to retain the beneficial effects of glucocorticoids and reduce the incidence of unwanted side effects [10]. [Pg.918]

Modification of the pharmacokinetics through structural alterations has provided several new steroids with a better GR affinity and therapeutic index and a lower bioavailability than the older drugs (Fig. 33.14). The new inhaled/intranasal glucocorticosteroids like mometasone furoate, budesonide and fluticasone propionate are more lipophilic than those used in oral and systemic therapy and have greater affinity for the GR than does dexamethasone as a consequence of their greater lipophilicity (43). Several of the topical corticosteroids, such as mometasone furoate, BDP, triamcinolone acetonide, and flunisolide, were reintroduced as inhalation and intranasal dosage forms for treatment of respiratory diseases (e.g., asthma or rhinitis). Inhaled budesonide and flunisolide are readily absorbed from the airway mucosa into the blood and are rapidly biotransformed in the liver into inactive metabolites. Mometasone furoate and fluticasone propionate are very potent anti-inflammatory steroids with an oral bioavailability of less than 1%. Obviously, the risk of systemic side effects for these newer corticosteroids is greatly reduced when compared with ... [Pg.1335]

Additional evidence for a corticosteroid effect In an allergic respiratory disease was furnished by a study"" In 52 asthmatic patients, showing an Inverse relationship between severity of asthma and steroid reserves In the adrenal cortex. In view of the prominent anti-Inflammatory action of the corticosteroids. It has been proposed that the steroids act only on the Inflammatory components of bronchial obstruction."" However, recent animal studies Indicate other mechanisms may be Involved in the bronchodilator effects of corticosteroids. Carrillo and Aviado"" determined the effects of hydrocortisone and dexamethasone on the histamine content and the mechanical properties of the lungs, in both sensitized and non-sensltlzed rabbits, and concluded that the steroids Induce broncho-dllatlon both by depletion of lung histamine and by direct bronchlolar smooth muscle relaxant action. [Pg.73]

Treatment effect was assessed with the Inflammatory Neuropathy Cause and Treatment disabilities scale and the Rivermead Mobility Index and was categorised using the CIDP Disease Activity Status (CDAS) scale 39 of 40 patients were included with a median follow-up of 4.5 years. Cure (>5 years off treatment) or remission according to the CDAS criteria after one or two courses of pulsed dexamethasone or daily prednisolone was achieved in 10 of 39 patients (26%). [Pg.221]

Dexamethasone has been used to diminish the inflammatory injury which contributes to the chronic lung disease in oxygen- and ventilator-depen-dent neonates with bronchopulmonary dysplasia (BPD) (22,23). The use of corticosteroids in high doses would seem to create an additional risk for infection in these vulnerable children. There does not appear to be any definite increase in risk for the development of nosocomial LRI in dexamethasone-treated neonates (22-25). [Pg.205]


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See also in sourсe #XX -- [ Pg.89 ]




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