Glucocorticoid-treatment does not influence the synthesis of thromboxane B2 and bicyclo-PGE2 in humans.
It has been reported that the anti-inflammatory action of glucocorticoids is due to the inhibition of phospholipases. Consequently, after high-dose steroid treatment in humans a decrease in cyclooxygenase products should be expected. In 15 patients (10 males, 5 females, 29-62 y) undergoing 6-methyl-prednisolone-treatment (40-80 mg daily) for various clinical reasons and in 5 healthy volunteers (4 male, 1 female, 28-37 y) receiving 500 mg 6-methyl-prednisolone daily for 3 days plasma- and serum-thromboxane B2 (TXB2), as well as bicyclo-prostaglandin E2 (bicyclo-PGE2) were monitored over 3 weeks. In the entire follow-up period, however, no significant change in either serum- or plasma-TXB2 or bicyclo-PGE2 could be measured in either, patients and volunteers, under glucocorticoid-treatment. These findings indicate that even high-dose glucocorticoid-treatment does not affect the serum- and plasma-metabolites of the eicosanoids examined. It is concluded that in humans a significant inhibition of phospholipases by glucocorticoids and subsequently reduced formation of cyclooxygenase products seems to be rather unlikely.
Sinzinger
H
H
Atherosclerosis Research Group (ASF), Austrian Academy of Sciences, Vienna.
Virgolini
I
I
Rauscha
F
F
Fitscha
P
P
D000328:Adult; D015232:Dinoprostone / Q000031:analogs & derivatives* / Q000096:biosynthesis / Q000097:blood; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology*; D006801:Humans; D008297:Male; D011863:Radioimmunoassay; D013929:Thromboxane B2 / Q000096:biosynthesis* / Q000097:blood
D005938:Glucocorticoids; D013929:Thromboxane B2; C025088:11-deoxy-15-keto-13,14-dihydro-11 beta,16-cycloprostaglandin E2; D015232:Dinoprostone