Dexamethasone systemic

Research conducted by Simons using antiglucocorticoids, including compounds which covalentiy bind to the GR (124), eg, dexamethasone 21-mesylate, has better defined the stmcture and function of the GR. Spiro C-17 oxetanes have shown potent antiglucocorticoid activity in whole cell systems (125,126). 

Commercially available electrotransport systems are bulky and limited to acute appHcations (96). One example, the Drionic system used for the treatment of hyperhidrosis (excessive perspiration), is presoaked in water for 30 min before each 20- to 30-min treatment. Another system, the Phoresor, approved for the deHvery of Hdocaine [137-58-6] for local anesthesia, and of dexamethasone [50-02-2] for treatment of local inflammation such as bursitis or tendinitis, is powered by a 9 V replaceable battery and features a disposable, fiHable dmg electrode. 

Allergic reactions to insulin include erythema, pruritus, and indurations,22 which usually are transient. For the more troublesome reactions, treatment options include dexamethasone, desensitization, or change in delivery system (i.e., insulin pump or inhaled insulin). 

C, cytarabine ASP, asparaginase CALCB, Cancer and Leukemia Croup B CNS, central nervous system CTX, cyclophosphamide DEX, dexamethasone DNR, daunorubicin DOX, doxorubicin IT, intrathecal captopurine MTX, methotrexate PRED, prednisone TG, thioguanine VCR, vincristine. 

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... 

SP produces a pronounced (4-fold) increase in the histamine content of the venus outflow of the perfused rat hindquarters [91] and, when injected intravenously in intact animals, it produces a significant increase in the level of plasma histamine and in the hematocrit and a pronounced fall in systemic blood pressure [102], In these experiments, pretreatment with the steroid, dexamethasone, reduced the SP-induced elevations in plasma histamine and hematocrit neurotensin and compound 48/80 were found to be similarly... 

One class of agents which inhibits LT production in stimulated cell systems, but probably not by direct 5-LO inhibition, is the anti-inflammatory corticosteroids, represented by dexamethasone (10) [30-34]. The well-known inhibition of PG production seen with eorticosteroids is not due to direct CO inhibition, but has been attributed to the inhibition of arachidon-ic acid mobilization by phospholipase A2, caused by enhanced biosynthesis of one or more proteins called lipocortins [35] (although this hypothesis is now being seriously questioned [36]). More recent evidence indicates the possibility of down-regulation of CO enzyme levels [37-39] similar mechanisms involving altered gene regulation could be involved in the observed effects on LT production as well. 

Melgert et al. [103] used this in vitro system to determine whether the drug targeting preparation containing the anti-inflammatory drug dexamethasone coupled to HS A, was still able to manifest its anti-inflammatory properties in hver slices. Dexamethasoncio-HSA and uncoupled dexamethasone showed effective inhibition of LPS-induced NO and TNFa pro-... 

Previous studies have reported that ERKs are characteristically associated with cell proliferation and protection from apoptosis (Bl, XI), while activation of JNK and p38 MAPK can promote apoptosis in many systems, including B lymphocytes (G5), cerebellar granule cells (K3), hematopoietic cells (K8), and neuronal cells (M3, XI). On the other hand, a recent report found that a pyridinyl imidazole, SB 202190, the specific inhibitor of p38 MAPK, by itself was sufficient to induce apoptosis in T lymphocyte Jurkat cells (N2). Moreover, Th-2-derived cytokine IL-5, the ERK activator and antiapoptotic factor for eosinophils, could also activate p38 MAPK in human eosinophils (BIO). We recently reported that cytokine IL-3, IL-5, and GM-CSF could prolong survival of human eosinophilic leukemic (EoL-1) cells through the transient activation of ERK (W15). On the other hand, activation of p38 MAPK in EoL-1 cells by the NSAID sodium salicylate (NaSal) could lead to apoptosis (W15). We also found that the suppression of ERK using ERK antisense phosphorothioate oligodeoxynucleotides could promote the apoptosis of peripheral blood eosinophils (W16). Moreover, we found that dexamethasone-induced apoptosis and activation of JNK and p38 MAPK activity in eosinophils are regulated by caspases (Z2). 

System (3) is a specific method for simultaneously measuring cortisone, hydrocortisone, prednisone, and prednisolone as endogenous glucocorticoids in plasma [151]. A 1 mL sample is extracted with 9 mL of 2 1 dichloromethane-ethyl ether. The extract is washed once with 2 mL of O.IM HCl, twice with 2 mL of O.IM NaOH, and dexamethasone is added as the internal standard. The column is 5 pm silica gel (25 cm x 3.2 mm), and the mobile phase is 1937 20 42 1 dichloromethane-tetrahydrofuran-methanol-anhydrous acetic acid eluted at a flow rate of 1.3 mL/min. Detection is by UV absorbance UV at 254 nm, and a limit of detection of 10 pg/L has been repotted. 

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