Vasoconstriction prostaglandin synthesis inhibition

NSAIDs are known to inhibit prostaglandin synthesis and as a result may decrease renal blood flow, which in certain circumstances can lead to renal failure. Renal impairment is more likely to occur in the presence of renal vasoconstrictors. Tacrolimus is known to cause renal vasoconstriction and thus the combined effects of ibuprofen and tacrolimus may have led to acute renal failure. Both patients also had a degree of liver impairment, which the authors suggest may have potentiated the toxicity of tacrolimus with ibuprofen. 

Topical corticosteroids (Table 16-1) may halt synthesis and mitosis of DNA in epidermal cells and appear to inhibit phospholipase A, lowering the amounts of arachidonic acid, prostaglandins, and leukotrienes in the skin. These effects, coupled with local vasoconstriction, reduce erythema, pruritus, and scaling. As antipsoriatic agents, they are best used adjunc-tively with a product that specifically functions to normalize epidermal hyperproliferation. 

Glucocorticosteroids are the most potent antiinflammatory agents available. They stabilize lysosomal membranes and reduce the concentration of proteolytic enzymes at the site of inflammation. They promote the synthesis of proteins called lipocortins which inhibit phospholipase-A2 and thus inhibit production of arachidonic acid, leukotrienes and prostaglandins. Furthermore, the expression of COX-II and through that the inflammatory effects of the licosanoids is inhibited. Glucocorticosteroids reduce the release of histamine from basophils, decrease capillary permeability and cause vasoconstriction. Glucocorticosteroids stimulate the loss of calcium with the urine and inhibit the resorption of calcium from the gut. 

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