Corticosteroid potency

The vasoconstrictor assay is a highly reliable method used to determine the bioequivalence of topical corticosteroid preparations. By assessing skin blanching, the assay describes the delivery of the active agent through the skin barrier, intrinsic activity at the receptor, and the rate of clearance from the site of application. Vasoconstrictor rankings are generally good predictors of efficacy in clinical trials. Vasoconstrictor assays are not as predictive of outcomes in clinical practice because these assays do not account for a critical factor: how well patients use the medication. Patient compliance plays a vital role in corticosteroid potency.

Dexamethasone is given systemically to decrease inflammatory and immune responses. It is used in high doses in emergencies for anaphylactic reactions, spinal cord trauma or shock. It is used in lower doses to treat allergic reactions such as Chronic Obstructive Pulmonary Disease (COPD), hives, itching, inflammatory diseases including arthritis and to manage and treat immune mediated hemolytic anemia and thrombocytopenia. It sometimes is used systemically as a "performance-enhancing” drug because corticosteroids decrease inflammation, possibly enhance glucose metabolism (there is some debate about this) and may have some mood elevating properties. Other corticosteroids are preferred for intra articular use.

There is no agreed treatment for topical corticosteroid withdrawal, apart from ceasing the topical corticosteroid. However whether this should be tapered or abrupt has not been determined. Japanese reports suggest there is minimal difference in the outcome, so recommend immediate cessation. A tapering course of oral steroids is helpful, as the addiction appears to relate only to the use of topical corticosteroids. Oral tetracyclines and low-dose isotretinoin have been used in steroid rosacea and perioral /periorificial dermatitis .

An example of an acute hepatitis-like syndrome arising after pulse methylprednisolone therapy.  These episodes arise typically 2 to 4 weeks after a third or fourth cycle of pulse therapy, and range in severity from an asymptomatic and transient rise in serum aminotransferase levels to an acute hepatitis and even fulminant hepatic failure.  In this instance, the marked and persistent rise in serum enzymes coupled with liver histology suggesting chronic hepatitis led to a diagnosis of new-onset autoimmune hepatitis, despite the absence of serum autoantibodies or hypergammaglobulinemia.  Autoimmune hepatitis may initially present in this fashion, without the typical pattern of serum autoantibodies during the early, anicteric phase.  The diagnosis was further supported by the prompt improvements in serum enzymes with prednisone therapy.  The acute hepatitis-like syndrome that can occur after pulses of methylprednisolone is best explained as a triggering of an underlying chronic autoimmune hepatitis caused by the sudden and profound immunosuppression followed by rapid withdrawal.  This syndrome can be severe, and fatal instances have been reported.  Whether reinitiation of corticosteroid therapy with gradual tapering and withdrawal is effective in ameliorating the course of illness is unclear, but anecdotal reports such as this one suggest that they are beneficial and should be initiated promptly on appearance of this syndrome.  Long term follow up of such cases is also necessary to document that the autoimmune hepatitis does not relapse once corticosteroids are withdrawn again.

Corticosteroid potency

corticosteroid potency

An example of an acute hepatitis-like syndrome arising after pulse methylprednisolone therapy.  These episodes arise typically 2 to 4 weeks after a third or fourth cycle of pulse therapy, and range in severity from an asymptomatic and transient rise in serum aminotransferase levels to an acute hepatitis and even fulminant hepatic failure.  In this instance, the marked and persistent rise in serum enzymes coupled with liver histology suggesting chronic hepatitis led to a diagnosis of new-onset autoimmune hepatitis, despite the absence of serum autoantibodies or hypergammaglobulinemia.  Autoimmune hepatitis may initially present in this fashion, without the typical pattern of serum autoantibodies during the early, anicteric phase.  The diagnosis was further supported by the prompt improvements in serum enzymes with prednisone therapy.  The acute hepatitis-like syndrome that can occur after pulses of methylprednisolone is best explained as a triggering of an underlying chronic autoimmune hepatitis caused by the sudden and profound immunosuppression followed by rapid withdrawal.  This syndrome can be severe, and fatal instances have been reported.  Whether reinitiation of corticosteroid therapy with gradual tapering and withdrawal is effective in ameliorating the course of illness is unclear, but anecdotal reports such as this one suggest that they are beneficial and should be initiated promptly on appearance of this syndrome.  Long term follow up of such cases is also necessary to document that the autoimmune hepatitis does not relapse once corticosteroids are withdrawn again.

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