Adrenal corticosteroids

Prostatic cancer In clinical trials involving 350 patients with metastatic prostatic cancer, 11 deaths were reported within 2 weeks of starting high-dose ketoconazole (1200 mg/day). It is not known whether death was related to therapy. High ketoconazole doses are known to suppress adrenal corticosteroid secretion. Hypersensitivity reactions Anaphylaxis occurs rarely after the first dose. Hypersensitivity reactions, including urticaria, have been reported. 

Organ rejection prophylaxis Prophylaxis of organ rejection in patients receiving allogeneic liver or kidney transplants. It is recommended that tacrolimus be used concomitantly with adrenal corticosteroids. Because of the risk of anaphylaxis, reserve the injection for patients unable to take the capsules orally. 

In patients unable to take the capsules, therapy may be initiated with the injection. Administer the initial dose no sooner than 6 hours after transplantation. The recommended starting dose is 0.03 to 0.05 mg/kg/day as a continuous IV infusion. Give adult patients doses at the lower end of the dosing range. Concomitant adrenal corticosteroid therapy is recommended early posttransplantation. Proceed with continuous IV infusion only until the patient can tolerate oral administration. 

Administer Sancf/mmane with adrenal corticosteroids but not with other immunosuppressive agents. Increased susceptibility to infection and other possible development of lymphoma may result from immunosuppression. 

Allogeneic transplants For prophylaxis of organ rejection in kidney, liver, and heart allogeneic transplants. Gengraf and A/eora/have been used in combination with azathioprine and corticosteroids. Sanc//n n nne always is to be used with adrenal corticosteroids. Sandimmune a so may be used in the treatment of chronic rejection in patients previously treated with other immunosuppressive agents. Because of the risk of anaphylaxis, reserve Sandimmune injection for patients who are unable to... 

Bioequivalency Sandimmune capsules and oral solution have decreased bioavailability in comparison with A/eora/capsules, Neoral ora solution, Gengraf capsules, and Gengraf ora solution. Gengraf and Neoral are not bioequivalent to Sandimmune and cannot be used interchangeably without physician supervision. Adjunct therapy Adjunct therapy with adrenal corticosteroids is recommended. P.1163... 

The pharmacological actions of steroids are generally an extension of their physiological effects. Adrenal corticosteroids exert effects on almost every organ in the body. In normal physiological concentrations, they are... 

It is recommended that tacrolimus be used concomitantly with adrenal corticosteroids... 

Warnings Hepatotoxicity, primarily of the hepatocellular type, has been reported Anaphylaxis may occur after the first dose Deaths within 2 weeks of treatment initiation have been reported in patients with prostate cancer the role of ketoconazole in these deaths has not been ascertained, but it is known that ketoconazole can suppress adrenal corticosteroid secretion... 

Methylprednisolone Succinate and Acetate (Solu-Medrol, Depo-Medrol) [Steroid] Uses Tx inflammation d/t anaphylaxis and asthma suspected SCI Action Adrenal corticosteroid Dose Adults. Anaphylaxis/ status asthmaticus 125-250 mg IV/IM Suspected SCI Load w/ 30 mg/kg then inf... 

The two main classes of adrenal corticosteroids are properly known as glucocorticoids and mineralocorticoster-oids. The former are often known by shorter names and are commonly referred to as glucocorticoids , corticosteroids , corticoids , or even simply steroids the latter are often referred to as mineralocorticoids . Here we shall use the terms glucocorticoids and mineralocorticoids . When referring to both we shall use the term corticosteroids . 

Replacement therapy for secondary or tertiary adrenocortical insufficiency These deficiencies are caused by a defect either in CRF production by the hypothalamus or corticotropin production by the pituitary (see p. 247). [Note Under these conditions, the adrenal cortex synthesis of mineralocorticoids is less impaired than that of glucocorticoids.] The adrenal cortex responds to corticotropin administration by synthesizing and releasing the adrenal corticosteroids. Hydrocortisone is also used for these deficiencies. 

In its acute stages, benzene toxicity appears to be due primarily to the direct effects of benzene on the central nervous system, whereas the peripheral nervous system appears to be the target following chronic low-level exposures. In addition, because benzene may induce an increase in brain catecholamines, it may also have a secondary effect on the immune system via the hypothalamus-pituitary-adrenal axis (Hsieh et al. 1988b). Increased metabolism of catecholamines can result in increased adrenal corticosteroid levels, which are immunosuppressive (Hsieh et al. 1988b). 

Rats on a pantothenic acid-free diet show rapid depletion of adrenal corticosteroids, and reduced production of the steroids in isolated adrenal glands in response to stimulation with adrenocorticotrophic hormone (ACTH). This presumably reflects the role of acetyl CoA in the synthesis of steroids deficiency also results in atrophy of the seminiferous mbules of male rats and delayed sexual maturation in females. As deficiency progresses, there is enlargement, then congestion, and finally hemorrhage, of the adrenal cortex. In young animals, but not in adults, pantothenic acid deprivation eventually leads to necrosis of the adrenal cortex. 

Saprophytic colonization is found with increased incidence in patients with underlying pulmonary diseases, such as in advanced stages of chronic obstructive pulmonary disease, chronic asthma requiring administration of adrenal corticosteroids, primary ciliary dyskinesia syndrome and cystic fibrosis [4-7]. A.fumigatus is the predominant species cultured from the respiratory tract although other Aspergillus species may also be found occasionally. 

The adrenal corticosteroids have been extensively used to suppress many different aspects of the immune response. AU of the corticosteroids have similar mechanisms of action. They bind to specific corticosteroid binding proteins in the cytoplasm. These complexes are then transported into the nucleus where they bind to discrete portions of the cell s DNA. This binding results in derepression of regulatory genes and the subsequent transcription of new mRNA (Rhen and Cidlowski, 2005). Steroids inhibit the consequences of the immune response. They have several different actions in this regard. One of their most important effects is to transiently alter the number of circulating leukocytes. There is a rapid increase in the number of neutrophils and a concomitant decrease in the number of lymphocytes, monocytes, eosinophils and basophils (Krensky et al, 2005). 

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