Oral corticosteroids asthma treatment

Oral and injectable systemic corticosterois are steroid hormones prescribed to decrease inflammation in diseases and conditions such as arthritis (rheumatoid arthritis, for example), ulcerative colitis, Crohn's disease, asthma, bronchitis, some skin rashes, and allergic or inflammatory conditions that involve the nose and eyes. Examples of systemic corticosteroids include hydrocortisone (Cortef), cortisone, prednisone (Prednisone Intensol), prednisolone (Orapred, Prelone), and methylprednisolone (Medrol, Depo-Medrol, Solu-Medrol). Some of the side effects of systemic corticosteroids are swelling of the legs, hypertension, headache, easy bruising, facial hair growth, diabetes, cataracts, and puffiness of the face.

Certain drugs such as troleandomycin (TAO), erythromycin ( Ery-Tab , EryPed 200), and clarithromycin ( Biaxin ) and ketoconazole ( Nizoral ) can reduce the ability of the liver to metabolize (breakdown) corticosteroids and this may lead to an increase in the levels and side effects of corticosteroids in the body. On the other hand, phenobarbital, ephedrine , phenytoin ( Dilantin ), and rifampin ( Rifadin , Rimactane ) may reduce the blood levels of corticosteroids by increasing the breakdown of corticosteroids by the liver. This may necessitate an increase of corticosteroid dose when they are used in combination with these drugs.

There is concern that P-glycoprotein mediated efflux contributes to steroid resistance. Therefore, this study examined bidirectional corticosteroid transport and induction capabilities for P-glycoprotein (P-gp) to understand which of the systemic and inhaled corticosteroids interacted with P-gp to the greatest extent. Hydrocortisone, prednisolone, prednisone, methylprednisolone, and dexamethasone represented systemically active drugs, while fluticasone propionate, beclomethasone dipropionate, ciclesonide and budesonide represented inhaled corticosteroids. Aldosterone and fludrocortisone represented mineralocorticoids. All drugs were detected using individually optimised HPLC protocols. Transport studies were conducted through Caco-2 monolayers. Hydrocortisone and aldosterone had efflux ratios below , while prednisone showed a P-gp mediated efflux ratio of only compared to its active drug, prednisolone, with an efflux ratio of . Dexamethasone and beclomethasone had efflux ratios of and respectively, while this increased to for methylprednisolone. Fluticasone showed an efflux ratio of . Protein expression studies suggested that all of the inhaled corticosteroids were able to induce P-gp expression, from to 2 times control levels. Most of the systemic corticosteroids had higher passive permeability (>20×10(-6) cm/s) compared to the inhaled corticosteroids (>5×10(-6) cm/s), except for budesonide, with permeability similar to the systemic corticosteroids. Inhaled corticosteroids are not transported by P-gp to the same extent as systemic corticosteroids. However, they are able to induce P-gp production. Thus, inhaled corticosteroids may have greater interactions with other P-gp substrates, but P-gp itself is less likely to influence resistance to the drugs.

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.

Oral corticosteroids asthma treatment

oral corticosteroids asthma treatment

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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