mobic and 7-hydroxy-5-11-dioxotetranorprostane-1-16-dioic-acid

mobic has been researched along with 7-hydroxy-5-11-dioxotetranorprostane-1-16-dioic-acid* in 1 studies

Trials

1 trial(s) available for mobic and 7-hydroxy-5-11-dioxotetranorprostane-1-16-dioic-acid

Article	Year
Effects of meloxicam and indomethacin on cyclooxygenase pathways in healthy volunteers. Journal of investigative medicine : the official publication of the American Federation for Clinical Research, 1997, Volume: 45, Issue:2 Meloxicam is a new NSAID with selectivity for the inducible cyclooxygenase (COX-2) in vitro. We compared the effects of therapeutically equivalent doses of meloxicam and indomethacin, a preferential inhibitor of the constitutive cyclooxygenase (COX-1), on platelet aggregation and platelet thromboxane formation, which are exclusively COX-1 dependent, physiological renal, and total body prostaglandin E2 (PGE2) production.. In a randomized cross-over design, 14 healthy female volunteers received meloxicam 7.5 mg per day for 6 days or indomethacin 25 mg three times per day for 3 days; the wash-out period was 5 days, and drug intake was adapted to the menstrual cycle. On the day before treatment and on the last day of each treatment period the following parameters were evaluated: maximum platelet aggregation and thromboxane B2 (TXB2) formation in response to 1.0 mmol/L arachidonic acid; 24-hour urinary excretion of PGE2 and 7 alpha-hydroxy-5, 11-diketo-tetranor-prosta-1, 16-dionic acid (PGE-M), the index metabolites of renal and total body PGE2 synthesis, respectively, were assessed by gas chromatography/tandem mass spectrometry.. Maximum platelet aggregation and TXB2 formation were almost completely inhibited by indomethacin (-87% and -99%, respectively; p < 0.001, each) as compared to control (100%), but remained unaffected by meloxicam (-1% and +4%, respectively). Meloxicam showed no significant effects on urinary PGE2 excretion (-13%) and only slight effects on PGE-M excretion (-22%; p < 0.05), whereas indomethacin reduced urinary PGE2 excretion (-43%; p < 0.05) as well as PGE-M excretion (-36%; p < 0.001).. Our data show, that meloxicam 7.5 mg per day is COX-1 sparing in humans in vivo. Topics: Adult; Anti-Inflammatory Agents, Non-Steroidal; Cross-Over Studies; Cyclooxygenase Inhibitors; Dinoprostone; Female; Humans; Indomethacin; Meloxicam; Platelet Aggregation; Prostaglandin-Endoperoxide Synthases; Prostaglandins; Therapeutic Equivalency; Thiazines; Thiazoles; Thromboxane B2	1997

Article

Year

Effects of meloxicam and indomethacin on cyclooxygenase pathways in healthy volunteers.

Journal of investigative medicine : the official publication of the American Federation for Clinical Research, 1997, Volume: 45, Issue:2

Meloxicam is a new NSAID with selectivity for the inducible cyclooxygenase (COX-2) in vitro. We compared the effects of therapeutically equivalent doses of meloxicam and indomethacin, a preferential inhibitor of the constitutive cyclooxygenase (COX-1), on platelet aggregation and platelet thromboxane formation, which are exclusively COX-1 dependent, physiological renal, and total body prostaglandin E2 (PGE2) production.. In a randomized cross-over design, 14 healthy female volunteers received meloxicam 7.5 mg per day for 6 days or indomethacin 25 mg three times per day for 3 days; the wash-out period was 5 days, and drug intake was adapted to the menstrual cycle. On the day before treatment and on the last day of each treatment period the following parameters were evaluated: maximum platelet aggregation and thromboxane B2 (TXB2) formation in response to 1.0 mmol/L arachidonic acid; 24-hour urinary excretion of PGE2 and 7 alpha-hydroxy-5, 11-diketo-tetranor-prosta-1, 16-dionic acid (PGE-M), the index metabolites of renal and total body PGE2 synthesis, respectively, were assessed by gas chromatography/tandem mass spectrometry.. Maximum platelet aggregation and TXB2 formation were almost completely inhibited by indomethacin (-87% and -99%, respectively; p < 0.001, each) as compared to control (100%), but remained unaffected by meloxicam (-1% and +4%, respectively). Meloxicam showed no significant effects on urinary PGE2 excretion (-13%) and only slight effects on PGE-M excretion (-22%; p < 0.05), whereas indomethacin reduced urinary PGE2 excretion (-43%; p < 0.05) as well as PGE-M excretion (-36%; p < 0.001).. Our data show, that meloxicam 7.5 mg per day is COX-1 sparing in humans in vivo.

Topics: Adult; Anti-Inflammatory Agents, Non-Steroidal; Cross-Over Studies; Cyclooxygenase Inhibitors; Dinoprostone; Female; Humans; Indomethacin; Meloxicam; Platelet Aggregation; Prostaglandin-Endoperoxide Synthases; Prostaglandins; Therapeutic Equivalency; Thiazines; Thiazoles; Thromboxane B2

1997