ArticlePloS one2017
Increased urinary prostaglandin E2 metabolite: A potential therapeutic target of Gitelman syndrome.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Long-Term Indomethacin Treatment in a Chinese Child with Gitelman Syndrome: Case Report and Literature Review on its Efficacy and Tolerance.The American journal of case reports · 2023Review
- A case of Gitelman syndrome with homozygous SLC12A3 deletion presenting with epilepsy.Acta epileptologica · 2023Article
- Frequent SLC12A3 mutations in Chinese Gitelman syndrome patients: structure and function disorder.Endocrine connections · 2022Article
- Review and Analysis of Two Gitelman Syndrome Pedigrees Complicated with Proteinuria or Hashimoto's Thyroiditis Caused by Compound HeterozygousBioMed research international · 2021Article
- Simultaneous detection of small molecules, proteins and microRNAs using single molecule arrays.Chemical science · 2020Article
- Genetic Analysis of SLC12A3 Gene in Chinese Patients with Gitelman Syndrome.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Novel heterozygous missense mutation ofWorld journal of clinical cases · 2019Article
- Mechanism of Thiazide Diuretic Arterial Pressure Reduction: The Search Continues.Frontiers in pharmacology · 2019Review
- A novel SLC12A3 homozygous c2039delG mutation in Gitelman syndrome with hypocalcemia.BMC nephrology · 2018Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGitelman syndrome (GS), an inherited autosomal recessive salt-losing renal tubulopathy caused by mutations in SLC12A3 gene, has been associated with normal prostaglandin E2 (PGE2) levels since 1995 by a study involving 11 clinically diagnosed patients. However, it is difficult to explain why cyclooxygenase-2 (COX2) inhibitors, which pharmacologically reduce PGE2 synthesis, are helpful to patients with GS, and few studies performed in the last 20 years have measured PGE2 levels. The relationships between the clinical manifestations and PGE2 levels were never thoroughly analyzed.
methodsThis study involved 39 GS patients diagnosed by SLC12A3 gene sequencing. Plasma and 24-h urine samples as well as the clinical data were collected at admission. PGE2 and PGEM levels were detected in plasma and urine samples by enzyme immunoassays. The in vivo function of the sodium-chloride co-transporter (NCC) in GS patients was evaluated using a modified thiazide test. The association among PGE2 levels, clinical manifestations and the function of NCC in GS patients were analyzed.
resultsSignificantly higher levels of urinary and plasma PGEM were observed in GS patients than in the healthy volunteers. Higher urinary PGEM levels indicated more severe clinical manifestations and NCC dysfunction estimated by the increase of Cl- clearance. A higher PGEM level was found in male GS patients, who showed earlier onset age and more severe hypokalemia, hypochloremia and metabolic alkalosis than female GS patients. No relationship between renin angiotensin aldosterone system activation and PGEM level was observed.
conclusionsHigher urinary PGEM levels indicated more severe clinical manifestations and NCC dysfunction in GS patients. COX2 inhibition might be a potential therapeutic target in GS patients with elevated PGEM levels.
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