Pulse 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]

Novel approaches to the treatment of lupus nephritis, such as using adenosine analogues, and combinations of existing medications, are being studied. Indeed, many of these approaches are on their way to being put to use in the near future. Some of these treatments, involving the blocking of various molecules that stimulate the cells of inflammation, are being studied at the National Institutes of Health in Bethesda, Maryland. Finally, attempts are being made to completely reconstitute the immune system in patients with lupus by using bone marrow transplantation and stem cell transplantation. All of these approaches are in the very preliminary stages of development and are not yet accepted as useful. What is clear is that the treatment of lupus nephritis in decades to come will not be the same as it is today.

Over 90 percent of patients with systemic lupus erythematosus eventually have a cutaneous manifestation of the disease, including malar rash, discoid lupus erythematosus, alopecia or aphthous stomatitis. The usual therapy for cutaneous lupus erythematosus is strict use of sun block, judicious use of topical steroids (although fluorinated topical steroids should not be used on the face) and antimalarial therapy ( Table 4 ) . Some patients with very severe cases of discoid lupus erythematosus may not respond adequately to the usual dosage of hydroxychloroquine, which is 400 mg per day for a normal-sized adult. Quinacrine, in a dosage of 100 mg per day, can be added without increasing the risk of retinopathy, or the patient can be switched to chloroquine HCl (Aralen), in a dosage of 250 mg per day.

Retinal disease has a high morbidity and should be treated aggressively by an ophthalmologist. 16 , 17 Ophthalmic screening programs in SLE are controversial. Most physicians agree that patients on antimalarial or steroid regimens should receive a full dilated-eye examination on initiation of therapy then with routine examinations in low-risk patients and yearly for high-risk patients. High risk is defined by medication dosage (> mg per kg hydroxychloroquine or >3 mg per kg chloroquine), duration of use (more than five years), high body fat level, presence of renal or liver disease, presence of concomitant retinal disease, and age greater than 60 years. 16 , 18

Pulse steroids lupus

pulse steroids lupus

Retinal disease has a high morbidity and should be treated aggressively by an ophthalmologist. 16 , 17 Ophthalmic screening programs in SLE are controversial. Most physicians agree that patients on antimalarial or steroid regimens should receive a full dilated-eye examination on initiation of therapy then with routine examinations in low-risk patients and yearly for high-risk patients. High risk is defined by medication dosage (> mg per kg hydroxychloroquine or >3 mg per kg chloroquine), duration of use (more than five years), high body fat level, presence of renal or liver disease, presence of concomitant retinal disease, and age greater than 60 years. 16 , 18

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