Steroid induced aseptic necrosis

NSAIDS have antipyretic activity and can be used to treat fever. [75] [76] Fever is caused by elevated levels of prostaglandin E2 , which alters the firing rate of neurons within the hypothalamus that control thermoregulation. [75] [77] Antipyretics work by inhibiting the enzyme COX, which causes the general inhibition of prostanoid biosynthesis ( PGE2 ) within the hypothalamus . [75] [76] PGE2 signals to the hypothalamus to increase the body's thermal set point. [76] [78] Ibuprofen has been shown more effective as an antipyretic than paracetamol (acetaminophen). [77] [79] Arachidonic acid is the precursor substrate for cyclooxygenase leading to the production of prostaglandins F, D & E.

During conventional pharmacologic dose corticosteroid therapy, ACTH production is inhibited with subsequent suppression of cortisol production by the adrenal cortex. Recovery time for normal HPA activity is variable depending upon the dose and duration of treatment. During this time the patient is vulnerable to any stressful situation. Although it has been shown that there is considerably less adrenal suppression following a single morning dose of prednisolone (10 mg) as opposed to a quarter of that dose administered every six hours, there is evidence that some suppressive effect on adrenal activity may be carried over into the following day when pharmacologic doses are used. Further, it has been shown that a single dose of certain corticosteroids will produce adrenal cortical suppression for two or more days. Other corticoids, including methylprednisolone, hydrocortisone, prednisone, and prednisolone, are considered to be short acting (producing adrenal cortical suppression for 1¼ to 1½ days following a single dose) and thus are recommended for alternate day therapy.

Steroid induced aseptic necrosis

steroid induced aseptic necrosis


steroid induced aseptic necrosissteroid induced aseptic necrosissteroid induced aseptic necrosissteroid induced aseptic necrosissteroid induced aseptic necrosis