Steroid conversion tables

The cause of Cushing syndrome (endogenous hypercortisolism rather than exogenous hypercortisolism resulting from medication) is overproduction of cortisol due to either a primary adrenal disease (eg, adenoma, carcinoma, nodular hyperplasia) or an excess of corticotropin (from a pituitary tumor or an ectopic source). The most frequently diagnosed subtype of hypercortisolism is corticotropin-dependent Cushing disease resulting from a pituitary corticotroph adenoma. It most commonly occurs in women in the third to fifth decades of life. Insidious in onset, it usually occurs 2-5 years before a clinical diagnosis is made.

When activated macrophages start to secrete IL-1, which synergistically with CRH increases ACTH, [10] T-cells also secrete glucosteroid response modifying factor (GRMF), as well as IL-1; both increase the amount of cortisol required to inhibit almost all the immune cells. [11] Immune cells then assume their own regulation, but at a higher cortisol setpoint. The increase in cortisol in diarrheic calves is minimal over healthy calves, however, and falls over time. [58] The cells do not lose all their fight-or-flight override because of interleukin-1's synergism with CRH. Cortisol even has a negative feedback effect on interleukin-1 [10] —especially useful to treat diseases that force the hypothalamus to secrete too much CRH, such as those caused by endotoxic bacteria. The suppressor immune cells are not affected by GRMF, [11] so the immune cells' effective setpoint may be even higher than the setpoint for physiological processes. GRMF affects primarily the liver (rather than the kidneys) for some physiological processes. [59]

Steroid conversion tables

steroid conversion tables


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