Pulse dose steroids lupus

In a small trial, 30 to 50 mg/kg/day PO in 2 divided doses resulted in significant disease improvement in children and adolescents with severe, refractory atopic dermatitis. A retrospective analysis of 14 patients aged 2 to 16 years who were treated with mycophenolate mofetil (MMF) for 2 to 24 months was performed. All subjects had severe atopic dermatitis (., extensive surface area affected with decreased quality of life including sleep disturbance, psychological distress, or impaired social functioning) refractory to topical therapy (., potent corticosteroids and calcineurin inhibitors) and/or oral/IM corticosteroids and cyclosporine. The initial dose range was between 12 and 40 mg/kg/day PO in 2 divided doses. Upward dose titration was continued until patients achieved disease clearance or a dose of 75 mg/kg/day (maximum daily dose = 3 g) was reached. Of the 14 patients, 4 experienced complete clearance, 4 had > 90% improvement, 5 had 60% to 90% improvement, and 1 patient had < 60% improvement. The maximum benefit of therapy was achieved after 8 to 12 weeks at MMF doses of 40 to 50 mg/kg/day in younger children and 30 to 40 mg/kg/day in adolescents; these doses were representative of approximately 1200 mg/m2. Although topical therapies were continued as needed, 9 patients were able to discontinue topical corticosteroids or decrease use to <= 2 days per week within 6 weeks. Therapy was well tolerated with no reports of complications of infection and no significant changes in laboratory values.

Because of the high risk of varicella infection in the immunocompromised patient, postexposure prophylaxis with varicella-zoster immune globulin is recommended in the nonimmune patient. Patient with varicella-zoster infection should be treated with acyclovir and carefully monitored. [ 28 ] Varicella immunization is safe and effective in patients with INS who are in remission and off steroid treatment (with the usual precautions for administering live viral vaccines to patients who have received steroids). [ 80 ]

30 mg/kg/dose (Max: 1 gram/dose) IV or IM once daily for 1 to 3 days. High-dose pulse steroids may be considered as an alternative to a second infusion of IVIG or for retreatment of patients who have had recurrent or recrudescent fever after additional IVIG, but should not be used as routine primary therapy with IVIG in patients with Kawasaki disease. Corticosteroid treatment has been shown to shorten the duration of fever in patients with IVIG-refractory Kawasaki disease or patients at high risk for IVIG-refractory disease. A reduction in the frequency and severity of coronary artery lesions has also been reported with pulse dose methylprednisolone treatment.

As a glucocorticoid , the lipophilic structure of prednisolone allows for easy passage through the cell membrane where it then binds to its respective glucocorticoid receptor (GCR) located in the cytoplasm. Upon binding, formation of the GC/GCR complex causes dissociation of chaperone proteins from the glucocorticoid receptor enabling the GC/GCR complex to translocate inside the nucleus. This process occurs within 20 minutes of binding. Once inside the nucleus, the homodimer GC/GCR complex binds to specific DNA binding-sites known as glucocorticoid response elements (GREs) resulting in gene expression or inhibition. Complex binding to positive GREs leads to synthesis of anti-inflammatory proteins while binding to negative GREs block the transcription of inflammatory genes. [28]

Pulse dose steroids lupus

pulse dose steroids lupus

As a glucocorticoid , the lipophilic structure of prednisolone allows for easy passage through the cell membrane where it then binds to its respective glucocorticoid receptor (GCR) located in the cytoplasm. Upon binding, formation of the GC/GCR complex causes dissociation of chaperone proteins from the glucocorticoid receptor enabling the GC/GCR complex to translocate inside the nucleus. This process occurs within 20 minutes of binding. Once inside the nucleus, the homodimer GC/GCR complex binds to specific DNA binding-sites known as glucocorticoid response elements (GREs) resulting in gene expression or inhibition. Complex binding to positive GREs leads to synthesis of anti-inflammatory proteins while binding to negative GREs block the transcription of inflammatory genes. [28]

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