Glucocorticoid therapy

Glucocorticoid therapy

Treatment using corticoids that are anti-inflammatory and immunosuppressive.
Mentioned in: Myelofibrosis
References in periodicals archive ?
The impact of discontinuation of glucocorticoid therapy was also investigated.
The association between systemic glucocorticoid therapy and the risk of infection in patients with rheumatoid arthritis: systematic review and meta-analyses.
14) Systematic reviews and the prospective randomized controlled CAMERA-II (Computer-Assisted Management in Early Rheumatoid Arthritis) study have confirmed the added benefit of low-dose glucocorticoid therapy for limiting pro gressive joint damage.
Despite numerous studies addressing the mechanisms that mediate the response of lymphoid tumor cells to glucocorticoid therapy the mechanism of glucocorticoid resistance remain incompletely understood.
In past decades, this therapy was based on systemic use of glucocorticoid therapy with no evolution in sight.
While the current study does not propose using glucocorticoid pills right away, it opens the path for using glucocorticoid therapy along with light therapy to better synchronise the biological clock in people.
Dyslipidaemia, hyperglycaemia and hypertension are the most significant cardiovascular adverse effects resulting from glucocorticoid therapy, [6] but mechanistic insights are incomplete.
3) Treatment for esophageal symptoms includes dilation, topical glucocorticoid therapy, and systemic immunosuppression.
It is not generally realized that the dangerous side effect of glucocorticoid therapy occurs only with certain dosages and not with others.
Plenadren is proven in a pivotal Phase II/III trial to be effective and well tolerated compared to standard therapy, demonstrating a delivery of cortisol, which is more in line with the body's own cortisol profile[2] thus avoiding the unphysiological cortisol peaks seen with standard glucocorticoid therapy.
It is impossible to be certain about the role of oral steroids in the small bowel perforation in this case, but it would appear unlikely that glucocorticoid therapy would be responsible for patchy small bowel ischaemia.
If severe suppression of bone turnover is plausible as the pathogenic mechanism, long-term concomitant glucocorticoid therapy may play a role once bisphosphonate therapy is initiated.

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