Heart's Dangerous Symphony: Torsade De Pointes Unleashed by Gitelman Syndrome-Induced Hypomagnesemia
Gitelman syndrome (GS) is a rare autosomal recessive salt-losing renal tubular disorder associated with a mutation of SLC12A3 or CLCNKB genes which encodes the thiazide-sensitive sodium-chloride co-transporter (NCCT) in the distal renal tubule. It is inherited as an autosomal recessive disorder. Hyp...
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Published in: | Cureus Vol. 15; no. 8; p. e44464 |
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Main Authors: | , , , , , , , |
Format: | Report |
Language: | English |
Published: |
01-08-2023
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Online Access: | Get full text |
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Summary: | Gitelman syndrome (GS) is a rare autosomal recessive salt-losing renal tubular disorder associated with a mutation of SLC12A3 or CLCNKB genes which encodes the thiazide-sensitive sodium-chloride co-transporter (NCCT) in the distal renal tubule. It is inherited as an autosomal recessive disorder. Hypokalemia, metabolic alkalosis, hypomagnesemia, hypocalciuria, and renin-angiotensin-aldosterone system (RAAS) activation are characteristics of GS. GS is often misdiagnosed or underdiagnosed owing to its low incidence and lack of awareness. Its prevalence is estimated to be around 1-10 per 40,000 people. We report a case of cardiac arrest secondary to torsade de pointes (TdP) because of GS-induced hypomagnesemia. Our case highlights the importance of clinicians being aware of the potential electrolyte abnormalities and complications associated with GS, as it can lead to catastrophic consequences if not identified and corrected earlier. |
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Bibliography: | ObjectType-Case Study-2 content type line 59 SourceType-Reports-1 ObjectType-Report-1 |
ISSN: | 2168-8184 2168-8184 |
DOI: | 10.7759/cureus.44464 |