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10.1371/journal.pone.0180811 http://scihub22266oqcxt.onion/10.1371/journal.pone.0180811 28700713!5507263!28700713     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2017 ; 12 (7): e0180811 Nephropedia Template TP {{tp|p=28700713|t=2017. Increased urinary prostaglandin E2 metabolite: A potential therapeutic target of Gitelman syndrome |pdf=|usr=}}{{28700713}} gab.com Text Increased urinary prostaglandin E2 metabolite: A potential therapeutic target of Gitelman syndrome JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28700713 #FOAvip BACKGROUND: Gitelman 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. METHODS: This 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. RESULTS: Significantly 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. CONCLUSIONS: Higher 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. Twit Text FOAVip Increased urinary prostaglandin E2 metabolite: A potential therapeutic target of Gitelman syndrome ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28700713 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28700713 #FOAvip English Wikipedia <ref>{{Cite pmid|28700713}}</ref> Increased urinary prostaglandin E2 metabolite: A potential therapeutic target of Gitelman syndrome #MMPMID28700713 Peng X; Jiang L; Chen C; Qin Y; Yuan T; Wang O; Xing X; Li X; Nie M; Chen L PLoS One 2017[]; 12 (7): e0180811 PMID28700713show ga BACKGROUND: Gitelman 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. METHODS: This 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. RESULTS: Significantly 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. CONCLUSIONS: Higher 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. |Adolescent[MESH] |Adult[MESH] |Cyclooxygenase 2 Inhibitors/therapeutic use[MESH] |Cyclooxygenase 2/genetics/metabolism[MESH] |Dinoprostone/*blood/metabolism/*urine[MESH] |Female[MESH] |Gitelman Syndrome/*blood/drug therapy/genetics/*urine[MESH] |Humans[MESH] |Logistic Models[MESH] |Male[MESH] |Mutation/genetics[MESH] |Solute Carrier Family 12, Member 3/genetics/metabolism[MESH]Increased urinary prostaglandin E2 metabolite: A potential therapeutic(epmc).pdf DeepDyve Pubget Overpricing