Corticosteroid mechanism in asthma

Controlled clinical studies have shown that intranasal corticosteroids may cause a reduction in growth velocity in pediatric patients. This effect has been observed in the absence of laboratory evidence of HPA axis suppression, suggesting that growth velocity is a more sensitive indicator of systemic corticosteroid exposure in pediatric patients than some commonly used tests of HPA axis function. The long-term effects of this reduction in growth velocity associated with intranasal corticosteroids, including the impact on final adult height, are unknown. The potential for “catch-up” growth following discontinuation of treatment with intranasal corticosteroids has not been adequately studied. The growth of pediatric patients receiving intranasal corticosteroids, including DYMISTA, should be monitored routinely (., via stadiometry). The potential growth effects of prolonged treatment should be weighed against the clinical benefits obtained and the risks/benefits of treatment alternatives.

Persons who are using drugs that suppress the immune system (., corticosteroids) are more susceptible to infections than healthy individuals. Chickenpox and measles , for example, can have a more serious or even fatal course in susceptible children or adults using corticosteroids. In children or adults who have not had these diseases or been properly immunized, particular care should be taken to avoid exposure. How the dose, route, and duration of corticosteroid administration affect the risk of developing a disseminated infection is not known. The contribution of the underlying disease and/or prior corticosteroid treatment to the risk is also not known. If a patient is exposed to chickenpox, prophylaxis with varicella zoster immune globulin (VZIG) may be indicated. If a patient is exposed to measles, prophylaxis with pooled intramuscular immunoglobulin ( IG ) may be indicated (see the respective package inserts for complete VZIG and IG prescribing information). If chickenpox or measles develops, treatment with antiviral agents may be considered.

The anti-infective component in VASOCIDIN (sulfacetamide and prednisolone) Ophthalmic Solution is included to provide action against specific organisms susceptible to it. Sulfacetamide sodium is active in-vitro against susceptible strains of the following microorganisms: Escherichia coli , Staphylococcus aureus, Streptococcus (viridans group), Haemophilus influenzae, Klebsiella/Enterobacter species. The product does not provide adequate coverage against: Neisseria species, Pseudomonas species, Serratia marcescens . SEE INDICATIONS AND USAGE SECTION.

Corticosteroids affect the nervous system indirectly in a number of ways, by maintaining normal plasma glucose levels, adequate circulation, and normal electrolyte levels. Direct effects of corticosteroids on the central nervous system occur, but are not well defined. Corticosteroid levels influence mood, behavior, electroencephalograph patterns, memory consolidation, and brain excitability. Chronic glucocorticoid treatment causes cell death in hippocampal neurons in rats, and elevated glucocorticoid in the hippocampus is thought to play a role in altered cognition, dementia, and depression in aging humans. 62 Patients with Addison disease are subject to apathy, depression, irritability, and psychosis, 63 symptoms that are alleviated by glucocorticoid, but not mineralocorticoid, therapy. Cushing disease patients sometimes develop neuroses and psychoses that are reversible with the removal of excess hormone. 64 Increases in brain excitability in hypercorticism and after mineralocorticoid treatment are a result of electrolyte imbalances. However, increased brain excitability induced by cortisol is not due to changes in sodium concentration. Chronic glucocorticoid treatment can also result in pseudotumor cerebri, primarily in children. 65

Corticosteroid mechanism in asthma

corticosteroid mechanism in asthma

Corticosteroids affect the nervous system indirectly in a number of ways, by maintaining normal plasma glucose levels, adequate circulation, and normal electrolyte levels. Direct effects of corticosteroids on the central nervous system occur, but are not well defined. Corticosteroid levels influence mood, behavior, electroencephalograph patterns, memory consolidation, and brain excitability. Chronic glucocorticoid treatment causes cell death in hippocampal neurons in rats, and elevated glucocorticoid in the hippocampus is thought to play a role in altered cognition, dementia, and depression in aging humans. 62 Patients with Addison disease are subject to apathy, depression, irritability, and psychosis, 63 symptoms that are alleviated by glucocorticoid, but not mineralocorticoid, therapy. Cushing disease patients sometimes develop neuroses and psychoses that are reversible with the removal of excess hormone. 64 Increases in brain excitability in hypercorticism and after mineralocorticoid treatment are a result of electrolyte imbalances. However, increased brain excitability induced by cortisol is not due to changes in sodium concentration. Chronic glucocorticoid treatment can also result in pseudotumor cerebri, primarily in children. 65

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