Corticosteroids sensitization

Conversely, the in vitro treatment of normal murine thymocytes with Toj reduced their TdT content (Hu et al., 1982). In addition, both TF5 and Taj have been shown to reduce the density of corticosteroid receptors on murine cortical thymocytes (OsheroIF, 1981). These inductive capacities of thymosin j, P3, and 4 are consistent with their intrathymic localization within thymic epithelial cells (see Section 6.1). Thymosin aj is found within both medullary and subcapsular cortical epithelial cells. Thus, Tuj released in situ could be responsible for inducing both early and late stages of thymocyte differentiation and for promoting the subsequent loss of TdT activity and corticosteroid sensitivity. On the other hand, TP3 and TP4 are localized... 

Corticosteroid Sensitive 95% of thymocytes sensitive population of residual 5% resistant... 

The severity and type of symptoms in corticosteroid sensitivity are related to the dose of drug and the method of administration. Topical application of steroid creams occasionally produces local contact allergy (Coskey 1978 Brandao and Camarasa 1979), while systemic administration results in more severe generalized reactions. 

No treatment with corticosteroids, sensitization treatment for 20 days. 

Therapeutic studies have demonstrated a role for T cells in asthma airway inflammation. Prednisolone treatment in corticosteroid-sensitive asthmatics (CSA) results in improved lung function, reduced airway hyperresponsiveness (AHR), accompanied by a reduction in eosinophil counts, and a reduction in the numbers of CD4+ T cells expressing mRNA encoding IL-3, D -S, and granulocyte macrophage-colony stimulating factor (GM-CSF) but not IL-2, IL-4, or IFNy... 

The 21-hydroxyl group in the corticosteroid series can be protected as the base stable triphenylmethyl ether and tetrahydropyranyl ether. " " Mixed acetals from 21-alcohols are extremely acid sensitive compounds. ... 

There are few definitive data to substantiate the efficacy of LTRA therapy in refractory asthma, except for patients with aspirin-sensitive asthma. This is a fairly uncommon form of asthma that occurs generally in adults who often have no prior (i.e., childhood) history of asthma or atopy, may have nasal polyposis, and who often are dependent upon oral corticosteroids for control of their asthma. This syndrome is not specific to aspirin but is provoked by any inhibitors of the cycloxygenase-1 (COX-1) pathway. These patients have been shown to have a genetic defect that causes... 

Corticosteroids, such as beclomethasone (Beclovent), flu-nisolide (AeroBid), and triamcinolone (Azmacort), are given by inhalation and act to decrease the inflammatory process in the airways of the patient with asthma, hi addition, the corticosteroids increase the sensitivity of the p2-receptors. With increased sensitivity of the ( -receptors, the p2-receptor agonist drugs are more effective... 

Corticosteroid intrarectal foam, hydrocortisone acetate intrarectal foam Cortifoam Adjunctive therapy in treatment of ulcerative proctitis of the distal portion of the rectum Local pain or burning, rectal bleeding, apparent exacerbations or sensitivity reactions 1 applicatorful once or twice daily for 2 wk and every second day thereafter... 

In general, treatment of the asthma underlying NSAlDs sensitivity should follow standard asthma guidelines. This type of asthma is often severe and frequently high doses of inhaled corticosteroids and daily doses of oral corticosteroids are necessary. A special treatment option is a chronic desensitization to aspirin [8]. Desensitization and aspirin maintenance is routinely used in some centers for treatment of chronic rhinusinusitis with nasal polyposis. It is the only available procedure which allows AIA patients with ischemic heart disease to use aspirin. During the state of desensitization to aspirin, not only aspirin but almost all strong NSAIDs are tolerated, so desensitization and NSAID maintenance could be used for treatment of rheumatic disease or chronic pain syndromes. 

There are several underlying mechanisms responsible for posttransplant HTN. Some causes of HTN in transplant recipients may include renal dysfunction, increased sensitivity to endothelin-1 and angiotensin, increased density of glucocorticoid receptors in the vascular smooth muscle, and decreased production of vasodilatory prostaglandins.57 However, one of the most easily recognized causes of posttransplant HTN is the use of corticosteroids and calcineurin inhibitors.58,59 Corticosteroids usually cause sodium and water retention,57 thus increasing blood pressure, whereas calcineurin inhibitors are associated with a number of effects that may result in HTN, including... 

The impacts of contaminants on the structure of the immune system can be assessed by examining white blood cell (WBC) numbers and the mass and cellularity of immune organs, although these indicators are usually not as sensitive as measures of immune function. Avian immunotoxicity studies frequently assess total and (or) differential WBC counts [79], and immunosuppression can be indicated by reduced numbers of WBCs or elevated WBC numbers caused by recurrent infections. An elevated heterophil to lymphocyte ratio can indicate altered immune status in response to corticosteroid stress hormones or other factors [78,7 9], Exposure to lead shot or lead acetate has been shown to alter total and (or) differential WBC numbers in Japanese quail (Coturnix coturnix) and mallards [81-83], In western grebes (Aechmophorus occidentalis) from California, concentrations of mercury in the kidney were positively correlated with heterophil... 

Adverse reactions to sulfites appear to occur mainly among a small percentage of asthmatics, but it is possible for individuals without asthma to be sulfite sensitive. It is typically more of a problem in individuals with severe asthma who are also taking corticosteroid drugs to control their disease. Among these individuals, the prevalence of sulfite sensitivity is about 8%, while it is about 1% in asthmatics who are not dependent on steroids (Taylor and Bush, 1986). 

Lord et al. analyzed a mixture of steroids by CEC-ESI/MS and interfaced externally tapered CEC columns in both sheathless and sheath-flow arrangement. Sensitivity was found 20-fold higher in the sheathless configuration. The same conclusion was drawn by Warriner et ah, who evaluated CEC-nanospray/MS vs. CEC-microspray/MS with an ion trap using five corticosteroids. Cahours et al. used CEC-ESI/MS for a drug metabolism study and obtained a simultaneous baseline separation of flunitrazepam and its major metabolites. For CEC-ESI/MS coupling, the commercially available packed-CEC column was connected... 

WARNING May T risk of CV events GI bleeding Uses Osteoarthritis, RA, JRA Action NSAID w/ T COX-2 activity Dose Adults. 7.5-15 mg/d PO Feds (>2 y). 0.125 mg/kg/d, max 7.5 mg 4- in renal insuff take w/ food Caution [C, D (3rd tri) /-] Peptic ulcer, NSAID, or ASA sensitivity Disp Tabs, susp SE HA, dizziness, GI upset, GI bleeding, edema Interactions T Effects OF ASA, anticoagulants, corticosteroids, Li, EtOH, tobacco effects W/ cholestyramine 4-effects OF antihypertensives EMS T Effects of anticoagulants concurrent EtOH/tobacco use can T adverse GI effects (bleeding, D) T risk of photosensitivity Rxns OD May cause NA and lethargy activated charcoal may be effective... 

Corticosteroids suppress both humoral and cellular immunity. Single doses produce a redistribution of lymphocytes with a concentration dependent decrease of CD4 and CDS positive cells. This in vivo lymphopenic effect correlates with the in vitro inhibition of stimulated T-cell proliferation. Furthermore, corticosteroids are able to inhibit the expression of genes coding for IL-1, IL-2, IL-6, interferon a, and tumor necrosis factor, TNE-a. Chronic administration decreases the size and also the cellu-larity of lymphoid tissues like lymph nodes, spleen, and thymus. Corticosteroids have more effect on the primary immune response and are less effective against previously sensitized immune responses. Their suppressive effects are more pronounced for T-cell immune responses than for the humoral immune response. 

Prompt intensive treatment with corticosteroids may be lifesaving when an excessive inflammatory reaction has resulted in septic shock. A massive infusion of corticosteroids can restore cardiac output and reverse hypotension by sensitizing the response of adrenoceptors in the heart and blood vessels to the stimulating action of catecholamines. This protective role of steroids may be due to a direct effect on vascular smooth muscle. The combination of glucocorticoids and dopamine therapy preserves renal blood flow during shock. 

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