Key result
Indomethacin is linked to superior urinary iPGE suppression and clinical correction vs aspirin or ibuprofen in Bartter's syndrome.
Why the study?
The role of prostaglandins in the pathogenesis of Bartter's syndrome and the comparative effects of different prostaglandin synthetase inhibitors were not fully characterized.
Observational (n=7)
Answers are grounded in this paper and cite their sources.
Supports differential NSAID effects in Bartter's syndrome; hypothesis-generating for indomethacin preference in larger controlled trials.
Urinary excretion of immunoreactive prostaglandin E (iPGE) was measurably increased in five of seven patients with Bartter's syndrome. The effects of indomethacin were compared with those of either aspirin or ibuprofen in four patients. Indomethacin produced notably greater suppression of urinary iPGE, greater sodium and potassium retention, greater increases in serum potassium, and decreases in plasma renin activity and in creatinine clearance than the other inhibitors. This demonstration that there is a close correlation between the suppression of urinary iPGE excretion and the extent of correction of the clinical abnormalities in Bartter's syndrome, regardless of the chemical structure of the prostaglandin synthetase inhibitor, is further evidence for the importance of prostaglandins in the pathogenesis of this syndrome.
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Robert E. Bowden (1978) conducted an observational in Bartter's syndrome (n=7). Indomethacin vs. Aspirin or ibuprofen was evaluated on Suppression of urinary immunoreactive prostaglandin E (iPGE) and correction of clinical abnormalities. Indomethacin produced notably greater suppression of urinary iPGE and correction of clinical abnormalities in Bartter's syndrome compared to aspirin or ibuprofen.
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