Treatment of Childhood Bartter's Syndrome With Indomethacin

Littlewood, J M; Lee, M.R.; Meadow, S R

doi:10.1016/s0140-6736(76)90620-6

Cited by 11 publications

(5 citation statements)

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“…Pharmacologic suppression of prostaglandin formation addresses the underlying pathophysiology, and multiple clinical observational studies have shown benefit in the form of improved growth and electrolyte profile. [57][58][59][60] The use of selective COX-2 inhibitors has also been reported in BS. 6,[61][62][63] Commonly used NSAIDs in BS are indomethacin (1-4 mg/kg/d divided in 3-4 doses), ibuprofen (15-30 mg/ kg daily in 3 doses), and celecoxib (2-10 mg/kg/d in 2 doses).…”

Section: Nsaidsmentioning

confidence: 99%

Diagnosis and management of Bartter syndrome: executive summary of the consensus and recommendations from the European Rare Kidney Disease Reference Network Working Group for Tubular Disorders

Konrad

Nijenhuis

Ariceta

et al. 2021

Kidney International

106

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Section: Nsaidsmentioning

confidence: 99%

Diagnosis and management of Bartter syndrome: executive summary of the consensus and recommendations from the European Rare Kidney Disease Reference Network Working Group for Tubular Disorders

Konrad

Nijenhuis

Ariceta

et al. 2021

Kidney International

106

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“…Also prostaglandin E2 failed to influence in vitro sodium transport in the RBC. The inability of the prostaglandin synthetase inhibitors to influence the basic pathogenetic disturbances of transmembrane sodium transport could be the reason why indomethacin does not fully control all metabolic manifestations of Bartter's syndrome, despite the at -least partial clinical effectiveness of indomethacin treatment (Littlewood et al, 1977).…”

Section: Discussionmentioning

confidence: 99%

The Effect of Long-Term Treatment with Spironolactone on Sodium Pump Abnormalities in the Red Blood Cells of Patients with Bartter's Syndrome

Horký¹,

Schreiber²,

Dvořáková³

2009

Exp Clin Endocrinol Diabetes

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To elucidate the possible sodium transport alterations across the cell membranes in Bartter's syndrome and their influencing by spironolactone treatment Na+-K+-ATPase activity was studied by means of radioactive 86Rubidium influx into red blood cells (RBC) of patients with Bartter's syndrome prior to and after a long-term spironolactone administration. As compared with the control subjects and patients with primary aldosteronism the patients with Bartter's syndrome had a more than 5 times higher 86Rb uptake by the RBC, especially in the ouabain-sensitive component. A long-term spironolactone treatment led to the decrease of this high influx. Serum of patients with Bartter's syndrome incubated with healthy RBC distinctly increased their 86Rb influx. The increase nevertheless did not reach the values in the RBC of untreated patients with Bartter's syndrome. Even if our results do not allow to explain fully the mechanism responsible for the Na+-K+-ATPase changes in the RBC of these patients, analysis of the studied parameters demonstrated that none of the known humoral factors as aldosterone, renin, prostaglandins, or changes of the serum potassium were responsible for these abnormalities. The changes of sodium transport in RBC of patients with Bartter's syndrome could be a part of a more general disturbance of the transport mechanism and could significantly participate in the pathogenesis of this disease.

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“…These defects result in a stimulation of the renin-angiotensin system which in turn enhances the production of prostaglandins (PG) [2]. That PG play a role in the pathophysiology of Bartter syndrome is also shown by the therapeutic effect of PG synthesis inhibitors [6,10].…”

Section: Introductionmentioning

confidence: 99%

Exogenous prostaglandin administration and pseudo-Bartter syndrome

et al. 1989

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Biological abnormalities simulating Bartter syndrome were observed in a preterm neonate with complex cyanotic congenital heart disease, for which ductus arteriosus was maintained open by high doses of prostaglandin (PG) until a Blalock shunt could be performed. These abnormalities spontaneously disappeared after cessation of PG administration. We postulate that the natriuretic effect of exogenous administered PG could further increase sodium wasting already induced by the cardiopathy thus leading to pseudo-Bartter syndrome.

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Treatment of Childhood Bartter's Syndrome With Indomethacin

Cited by 11 publications

References 0 publications

Diagnosis and management of Bartter syndrome: executive summary of the consensus and recommendations from the European Rare Kidney Disease Reference Network Working Group for Tubular Disorders

Diagnosis and management of Bartter syndrome: executive summary of the consensus and recommendations from the European Rare Kidney Disease Reference Network Working Group for Tubular Disorders

The Effect of Long-Term Treatment with Spironolactone on Sodium Pump Abnormalities in the Red Blood Cells of Patients with Bartter's Syndrome

Exogenous prostaglandin administration and pseudo-Bartter syndrome

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