1995
DOI: 10.1016/0272-6386(95)90563-4
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Normal prostaglandinuria E2 in Gitelman's syndrome, the hypocalciuric variant of Bartter's syndrome

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Cited by 35 publications
(23 citation statements)
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“…Alternatively, long-term magnesium depletion may suppress the release of parathormone along with hypocalcemia and low 1,25(OH) 2 vitamin D 3 levels [18]. Although the urinary excretion of prostaglandin is normal or just slightly increased [19], the prostaglandin synthase inhibitor indomethacin reported was effective in GS [15, 20]. The catch-up growth supported the efficiency of potassium and magnesium supplementation with the combination of indomethacin.…”
Section: Discussionmentioning
confidence: 99%
“…Alternatively, long-term magnesium depletion may suppress the release of parathormone along with hypocalcemia and low 1,25(OH) 2 vitamin D 3 levels [18]. Although the urinary excretion of prostaglandin is normal or just slightly increased [19], the prostaglandin synthase inhibitor indomethacin reported was effective in GS [15, 20]. The catch-up growth supported the efficiency of potassium and magnesium supplementation with the combination of indomethacin.…”
Section: Discussionmentioning
confidence: 99%
“…[35,36] Long-term gastrointestinal side effects of indomethacin including chronic gastritis and gastric ulcers can be dose limited, and cyclooxygenase-2 selective inhibitors might be considered as an alternative. [37] Sodium chloride supplementation may be needed early in life, but high dietary salt intake is often sufficient in older children. Other medications to consider, depending on clinical and laboratory parameters, include ACE inhibitors, potassium-sparing diuretics (particularly spironolactone), and magnesium supplementation.…”
Section: Managementmentioning
confidence: 99%
“…Because patients with Gitelman syndrome do not typically show the increased prostaglandin production seen in patients with Bartter syndrome, [37] the same response to indomethacin is not seen. Hypomagnesemia is a more prominent component of Gitelman syndrome, so magnesium supplementation is routinely required.…”
Section: Managementmentioning
confidence: 99%
“…There is also only a mild increase of renal and systemic PGE 2 . Lüthy et al [105]found that urinary PGE 2 was not significantly higher in patients with Gitelman’s syndrome compared with a control group of healthy individuals. Parallel to this finding there is no increase of the prostaglandin excretion in patients taking thiazide diuretics (analogous to Gitelman’s syndrome), in contrast with patients taking loop diuretics (analogous to classic and neonatal subtypes), where the prostaglandin excretion is increased [106].…”
Section: Pathophysiologymentioning
confidence: 99%