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1 the primary pathophysiological mechanism in hypokalemic periodic paralysis.
2 utations confer susceptibility to thyrotoxic hypokalemic periodic paralysis.
3 ta may help explain the mechanism underlying hypokalemic periodic paralysis and the patient's worseni
4 m channel (CaV1.1) have been associated with hypokalemic periodic paralysis, but how the pathogenesis
5 ystem in patients with genetically confirmed hypokalemic periodic paralysis (Cav1.1-R1239H mutation,
6 cks resemble those of patients with familial hypokalemic periodic paralysis (hypoKPP) and resolve wit
8 sover trials, one involving 42 subjects with hypokalemic periodic paralysis (HypoPP) and the other in
12 result in a leak current through the VSD and hypokalemic periodic paralysis (HypoPP), but these have
13 nother disorder of sarcolemmal excitability, hypokalemic periodic paralysis (HypoPP), which is usuall
14 ith alterations in channel subunits, such as hypokalemic periodic paralysis in humans and the weaver
17 d in several human genetic diseases, such as hypokalemic periodic paralysis, myotonia, and long-QT an
18 ess in other variants of periodic paralysis (hypokalemic periodic paralysis or hyperkalemic periodic
19 ge-gated calcium channel of skeletal muscle (hypokalemic periodic paralysis), the neuronal P/Q-type v
21 897S) or CaV1.1-R2 (R900S, R1239H) linked to hypokalemic periodic paralysis type 1 and of CaV1.3-R3 (