Genetics Genetic mutations in the L-type calcium channel α1-subunit (Cav1.1) have been described in Southern Chinese with<unk> . The mutations are located in a different part of the gene from those described in the related condition familial<unk>  paralysis. In<unk> , the mutations described are single-nucleotide polymorphisms located in the hormone response element responsive to thyroid hormone, implying that transcription of the gene and production of ion channels may be altered by increased thyroid hormone levels. Furthermore, mutations have been reported in the genes coding for potassium voltage-gated channel, Shaw-related subfamily, member 4 (Kv3.4) and sodium channel protein type 4 subunit alpha (Na41.4). Of people with<unk> , 33% from various populations were demonstrated to have mutations in KCNJ18, the gene coding for Kir2.6, an inward-rectifier potassium ion channel. This gene, too, harbors a thyroid response element. Certain forms of human leukocyte antigen (HLA)—especially B46, DR9, DQB1*0303, A2, Bw22, AW19, B17, and DRW8—are more common in<unk> . Linkage to particular forms of HLA, which plays a central role in the immune response, might imply an immune system cause, but it is uncertain whether this directly causes<unk>  or whether it increases the susceptibility to Graves' disease, a known autoimmune disease. Thyroid disease The most common underlying form of thyroid disease associated with<unk>  is Graves' disease, a syndrome due to an autoimmune reaction that leads to overproduction of thyroid hormone.<unk>  has also been described in people with other thyroid problems such as thyroiditis, toxic nodular goiter, toxic adenoma, TSH-producing pituitary adenoma, excessive ingestion of thyroxine or iodine, and amiodarone-induced hyperthyroidism.
Thyrotoxic periodic paralysis
Hypokalemic periodic paralysis
Hyperkalemic periodic paralysis
Zaki syndrome
Thyrotoxic myopathy
Ketosis-prone diabetes
Aicardi–Goutières syndrome
Bartter syndrome