Corticosteroid use in rheumatoid arthritis prevalence predictors correlates and outcomes

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up of such cases is also necessary to document that the autoimmune hepatitis does not relapse once corticosteroids are withdrawn again.

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.

Corticosteroids have been used as drug treatment for some time. Lewis Sarett of Merck & Co. was the first to synthesize cortisone, using a complicated 36-step process that started with deoxycholic acid, which was extracted from ox bile . [43] The low efficiency of converting deoxycholic acid into cortisone led to a cost of US $200 per gram. Russell Marker , at Syntex , discovered a much cheaper and more convenient starting material, diosgenin from wild Mexican yams . His conversion of diosgenin into progesterone by a four-step process now known as Marker degradation was an important step in mass production of all steroidal hormones, including cortisone and chemicals used in hormonal contraception . [44] In 1952, . Peterson and . Murray of Upjohn developed a process that used Rhizopus mold to oxidize progesterone into a compound that was readily converted to cortisone. [45] The ability to cheaply synthesize large quantities of cortisone from the diosgenin in yams resulted in a rapid drop in price to US $6 per gram, falling to $ per gram by 1980. Percy Julian's research also aided progress in the field. [46] The exact nature of cortisone's anti-inflammatory action remained a mystery for years after, however, until the leukocyte adhesion cascade and the role of phospholipase A2 in the production of prostaglandins and leukotrienes was fully understood in the early 1980s.

Data abstracted retrospectively from the charts at 11,359 clinic visits for 310 patients with SLE to the Montreal General Hospital were used to investigate the associations of recent corticosteroid dose and recent Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) score with 8 CHD risk factors (total serum cholesterol, high-density lipoprotein [HDL] cholesterol, low-density lipoprotein cholesterol, apolipoprotein B [Apo B], triglycerides, systolic blood pressure [BP], body mass index, and blood glucose) and the aggregate estimate of 2-year CHD risk. Separate multivariable linear regression models estimated the mutually-adjusted effects of average daily corticosteroid dose and average SLEDAI score within the past year on the current level of each risk factor while adjusting for age, sex, cumulative damage score, disease duration, and, where appropriate, use of relevant medications.

The cystic larvae of Taenia solium commonly infect the human nervous system, resulting in neurocysticercosis, a major contributor to seizure disorders in most of the world. Inflammation around the parasites is a hallmark of neurocysticercosis pathophysiology. Although mechanisms regulating this inflammation are poorly understood, anti-inflammatory drugs, particularly corticosteroids, have been long used alone or with anthelmintics to manage disease and limit neurological complications and perhaps damage to neural tissues. Only scarce controlled data exist to determine when and what type of corticosteroids and the treatment regime to use. This article revisits the mechanisms of action, rationale, evidence of benefit, safety and problems of corticosteroids in the context of neurocysticercosis, as well as alternative anti-inflammatory strategies to limit the damage caused by inflammation in the CNS.

Corticosteroid use in rheumatoid arthritis prevalence predictors correlates and outcomes

corticosteroid use in rheumatoid arthritis prevalence predictors correlates and outcomes

Data abstracted retrospectively from the charts at 11,359 clinic visits for 310 patients with SLE to the Montreal General Hospital were used to investigate the associations of recent corticosteroid dose and recent Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) score with 8 CHD risk factors (total serum cholesterol, high-density lipoprotein [HDL] cholesterol, low-density lipoprotein cholesterol, apolipoprotein B [Apo B], triglycerides, systolic blood pressure [BP], body mass index, and blood glucose) and the aggregate estimate of 2-year CHD risk. Separate multivariable linear regression models estimated the mutually-adjusted effects of average daily corticosteroid dose and average SLEDAI score within the past year on the current level of each risk factor while adjusting for age, sex, cumulative damage score, disease duration, and, where appropriate, use of relevant medications.

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