Open AccessHypokalemic paralysis due to thyrotoxicosis accompanied by Gitelman′s syndrome
Author(s) -
Süleyman Baldane,
Süleyman Hilmi İpekçi,
Seden Çelık,
Aycan Gündoğdu,
Levent Kebapçılar
Publication year - 2015
Publication title -
indian journal of nephrology/indian journal of nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.317
H-Index - 24
eISSN - 1998-3662
pISSN - 0971-4065
DOI - 10.4103/0971-4065.140719
Subject(s) - hypokalemia , medicine , gitelman syndrome , hypokalemic periodic paralysis , missense mutation , euthyroid , periodic paralysis , pediatrics , hyperaldosteronism , endocrinology , compound heterozygosity , bartter syndrome , gastroenterology , paralysis , mutation , surgery , thyroid , genetics , aldosterone , gene , hypomagnesemia , materials science , biology , magnesium , metallurgy
A 35-year-old male patient was admitted with fatigue and muscle weakness. He had been on methimazole due to thyrotoxicosis for 2 weeks. Laboratory tests showed overt hyperthyroidism and hypokalemia. Potassium replacement was started with an initial diagnosis of thyrotoxic hypokalemic periodic paralysis. Later on, despite the euthyroid condition and potassium chloride treatment, hypokalemia persisted. Further investigations revealed hyperreninemic hyperaldosteronism. The patient was considered to have Gitelman's syndrome (GS) and all genetic analysis was done. A c. 1145C>T, p. Thr382Met homozygote missense mutation located on solute carrier family 12, member gene 3, exon 9 was detected and GS was confirmed.